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You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

What does the medical term 'Intraventricular hemorrhage' encompass?

Intraventricular hemorrhage (IVH), also known as intraventricular bleeding, is a bleeding into the brains ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhagic stroke. 30% of intraventricular hemorrhage (IVH) are primary, confined to the ventricular system and typically caused by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the choroid plexus. However 70% of IVH are secondary in nature, resulting from an expansion of an existing intraparenchymal or subarachnoid hemorrhage. Intraventricular hemorrhage has been found to occur in 35% of moderate to severe traumatic brain injuries. Thus the hemorrhage usually does not occur without extensive associated damage, and so the outcome is rarely good. Symptoms Adults Symptoms of IVH are similar to other intracerebral hemorrhages and include sudden onset of headache, nausea and vomiting, together with an alteration of the mental state and/or level of consciousness. Focal neurological signs are either minimal or absent, but focal and/or generalized seizures may occur. Xanthochromia, yellow-tinged CSF, is the rule. Infants Some infants are asymptomatic and others may present with hard to detect abnormalities of consciousness, muscle tone, breathing, movements of their eyes, and body movements. Causes Adults Causes of IVH in adults include physical trauma or from hemorrhagic stroke. Infants Infants that are preterm and very low birth weight are also at high risk. IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight. The cause of IVH in premature infants, unlike that in older infants, children or adults, is rarely due to trauma. Instead it is thought to result from changes in perfusion of the delicate cellular structures that are present in the growing brain, augmented by the immaturity of the cerebral circulatory system, which is especially vulnerable to hypoxic ischemic encephalopathy. The lack of blood flow results in cell death and subsequent breakdown of the blood vessel walls, leading to bleeding. While this bleeding can result in further injury, it is itself a marker for injury that has already occurred. Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants. Congenital cytomegalovirus infection can be an important cause. Mechanism Diagnosis Diagnosis can be confirmed by the presence of blood inside the ventricles on CT. Infants In term and preterm infants with IVH, the amount of bleeding varies. IVH is often described in four grades: Grade I - bleeding occurs just in the germinal matrix Grade II - bleeding also occurs inside the ventricles, but they are not enlarged Grade III - ventricles are enlarged by the accumulated blood Grade IV - bleeding extends into the brain tissue around the ventriclesGrades I and II are most common, and often there are no further complications. Grades III and IV are the most serious and may result in long-term brain injury to the infant. After a grade III or IV IVH, blood clots may form which can block the flow of cerebrospinal fluid, leading to increased fluid in the brain (hydrocephalus). Prevention Head positioning in very preterm infants has been suggested as an approach to prevent germinal matrix haemorrhage; however, further research is required to determine the effectiveness at reducing mortality and the most appropriate positioning technique. Approaches include bed tilting, supine mid-line head positioning, supine head rotation 90 degrees, prone mid-line head positioning, head tiling. Treatment Treatment focuses on monitoring and should be accomplished with inpatient floor service for individuals responsive to commands or neurological ICU observation for those with impaired levels of consciousness. Extra attention should be placed on intracranial pressure (ICP) monitoring via an intraventricular catheter and medications to maintain ICP, blood pressure, and coagulation. In more severe cases an external ventricular drain may be required to maintain ICP and evacuate the hemorrhage, and in extreme cases an open craniotomy may be required. In cases of unilateral IVH with small intraparenchymal hemorrhage the combined method of stereotaxy and open craniotomy has produced promising results. Infants There have been various therapies employed into preventing the high rates of morbidity and mortality, including diuretic therapy, repeated lumbar puncture, streptokinase therapy and a combination novel intervention called DRIFT (drainage, irrigation and fibrinolytic therapy). More research is required, in the form of high quality randomized controlled trials, to determine the safety, dosing, and effectiveness of prophylactic heparin and antithrombin treatment for preterm neonates. Prognosis In infants, germinal matrix haemorrhage is associated with cerebral palsy, problems with cognition, and hydrocephalus. With improved technological advances in science and medicine, survival for preterm infants with this type of neurological disorder has improved and less preterm infants with germinal matrix haemorrhage have severe cerebral palsy. An estimated 15% of preterm infants who survive develop cerebral palsy and 27% of the infants who survive experience moderate to severe neurosensory deficits by the time they reach 18–24 months old.Prognosis is very poor when IVH results from intracerebral hemorrhage related to high blood pressure and is even worse when hydrocephalus follows. It can result in dangerous increases in ICP and can cause potentially fatal brain herniation. Even independently, IVH can cause morbidity and mortality. First, intraventricular blood can lead to a clot in the CSF conduits blocking its flow and leading to obstructive hydrocephalus which may quickly result in increased intracranial pressure and death. Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus. Associated conditions Brain contusions and subarachnoid hemorrhages are commonly associated with IVH. The bleeding can involve the anterior communicating artery or the posterior communicating artery. In both adults and infants, IVH can cause dangerous increases in ICP, damage to the brain tissue, and hydrocephalus. Epidemiology IVH has been reported to occur in approximately 25% of infants who are born with a very low birth weight. In preterm infants, intraventricular haemorrhage and germinal matrix haemorrhage are the most widely reported neurological disorders. Approximately 12,000 infants each year are diagnosed with germinal matrix haemorrhage or intraventricular haemorrhage in the United States. Research In 2002, a Dutch retrospective study analysed cases where neonatologists had intervened and drained CSF by lumbar or ventricular punctures if ventricular width (as shown on ultrasound) exceeded the 97th centile as opposed to the 97th centile plus 4 mm. Professors Whitelaws original Cochrane review published in 2001 as well as evidence from previous randomised control trials indicated that interventions should be based on clinical signs and symptoms of ventricular dilatation. An international trial has instead looked an early (97th centile) versus late (97th centile plus 4 mm) for intervening and draining CSF.DRIFT has been tested in an international randomised clinical trial; although it did not significantly lower the need for shunt surgery, severe cognitive disability at two years Bayley (MDI <55) was significantly reduced. Repeated lumbar punctures are used widely to reduce the effects in increased intracranial pressure and an alternative to ventriculoperitoneal (VP) shunt surgery that cannot be performed in case of intraventricular haemorrhage. The relative risk of repeated lumbar puncture is close to 1.0, therefore it is not statistically therapeutic when compared to conservative management and does raise the risk of subsequent CSF infection. References External links 00511 at CHORUSUltrasound Pictures of Germinal Matrix IVH MedPix Image Database

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I'd like to learn more about the medical term 'Mastocytoma.' Can you provide some details?

A mastocytoma or mast cell tumor is a type of round-cell tumor consisting of mast cells. It is found in humans and many animal species; it also can refer to an accumulation or nodule of mast cells that resembles a tumor. Mast cells originate from the bone marrow and are normally found throughout the connective tissue of the body as normal components of the immune system. As they release histamine, they are associated with allergic reactions. Mast cells also respond to tissue trauma. Mast cell granules contain histamine, heparin, platelet-activating factor, and other substances. Disseminated mastocytosis is rarely seen in young dogs and cats, while mast cell tumors are usually skin tumors in older dogs and cats. Although not always malignant, they do have the potential to be. Up to 25 percent of skin tumors in dogs are mast cell tumors, with a similar number in cats. Signs and symptoms Humans When mastocytomas affect humans, they are typically found in skin. They usually occur as a single lesion on the trunk or wrist. Although it is rare, mastocytomas are sometimes found in the lung. It can also affect children. Other animals Mast cell tumors are known among veterinary oncologists as the great pretenders because their appearance can be varied, from a wart-like nodule to a soft subcutaneous lump (similar on palpation to a benign lipoma) to an ulcerated skin mass. Most mast cell tumors are small, raised lumps on the skin. They may be hairless, ulcerated, or itchy. They are usually solitary, but in about six percent of cases, there are multiple mast cell tumors (especially in Boxers and Pugs).Manipulation of the tumor may result in redness and swelling from release of mast cell granules, also known as Dariers sign, and prolonged local hemorrhage. In rare cases, a highly malignant tumor is present, and signs may include loss of appetite, vomiting, diarrhea, and anemia. The presence of these signs usually indicates mastocytosis, which is the spread of mast cells throughout the body. Release of a large amount of histamine at one time can result in ulceration of the stomach and duodenum (present in up to 25 percent of cases) or disseminated intravascular coagulation. When metastasis does occur, it is usually to the liver, spleen, lymph nodes and bone marrow. Diagnosis A needle aspiration biopsy of the tumor will typically show a large number of mast cells. This is sufficient to make the diagnosis of a mast cell tumor, although poorly differentiated mast cells may have few granules and thus are difficult to identify. The granules of the mast cell stain blue to dark purple with a Romanowsky stain, and the cells are medium-sized. However, a surgical biopsy is required to find the grade of the tumor. The grade depends on how well the mast cells are differentiated, mitotic activity, location within the skin, invasiveness, and the presence of inflammation or necrosis. Grade I – well differentiated and mature cells with a low potential for metastasis Grade II – intermediately differentiated cells with potential for local invasion and moderate metastatic behavior Grade III – undifferentiated, immature cells with a high potential for metastasisHowever, there is a significant amount of discordance between veterinary pathologists in assigning grades to mast cell tumors due to imprecise criteria.The disease is also staged according to the WHO system: Stage I - a single skin tumor with no spread to lymph nodes Stage II - a single skin tumor with spread to lymph nodes in the surrounding area Stage III - multiple skin tumors or a large tumor invading deep to the skin with or without lymph node involvement Stage IV – a tumor with metastasis to the spleen, liver, or bone marrow, or with the presence of mast cells in the bloodX-rays, ultrasound, or lymph node, bone marrow, or organ biopsies may be necessary to stage the disease. Treatment and prognosis Removal of the mast cell tumor through surgery is the treatment of choice. Antihistamines, such as diphenhydramine, are given prior to surgery to protect against the effects of histamine released from the tumor. Wide margins (two to three centimeters) are required because of the tendency for the tumor cells to be spread out around the tumor. If complete removal is not possible due to the size or location, additional treatment, such as radiation therapy or chemotherapy, may be necessary. Prednisone is often used to shrink the remaining tumor portion. H2 blockers, such as cimetidine, protect against stomach damage from histamine. Vinblastine and lomustine are common chemotherapy agents used to treat mast cell tumors.Toceranib and masitinib, examples of receptor tyrosine kinase inhibitors, are used in the treatment of canine mast cell tumors. Both were recently approved by the U.S. Food and Drug Administration (FDA) as dog-specific anticancer drugs.Grade I or II mast cell tumors that can be completely removed have a good prognosis. One study showed about 23 percent of incompletely removed grade II tumors recurred locally. Any mast cell tumor found in the gastrointestinal tract, paw, or on the muzzle has a guarded prognosis. Previous beliefs that tumors in the groin or perineum carried a worse prognosis have been discounted. Tumors that have spread to the lymph nodes or other parts of the body have a poor prognosis. Any dog showing symptoms of mastocytosis or with a grade III tumor has a poor prognosis. Dogs of the Boxer breed have a better than average prognosis because of the relatively benign behavior of their mast cell tumors. Multiple tumors that are treated similarly to solitary tumors do not seem to have a worse prognosis.Mast cell tumors do not necessarily follow the histological prognosis. Further prognostic information can be provided by AgNOR stain of histological or cytological specimen. Even then, there is a risk of unpredictable behavior. Other animals Mast cell tumors are an uncommon occurrence in horses. They usually occur as benign, solitary masses on the skin of the head, neck, trunk, and legs. Mineralization of the tumor is common. In pigs and cattle, mast cell tumors are rare. They tend to be solitary and benign in pigs and multiple and malignant in cattle. Mast cell tumors are found in the skin of cattle most commonly, but these may be metastases from tumors of the viscera. Other sites in cattle include the spleen, muscle, gastrointestinal tract, omentum, and uterus. Dogs Mast cell tumors mainly occur in older adult dogs, but have been known to occur on rare occasions in puppies. The following breeds are commonly affected by mast cell tumors: Boxer Staffordshire bull terrier Bulldog Basset hound Weimaraner Boston terrier Great Dane Golden retriever Labrador retriever Beagle German shorthaired pointer Scottish terrier Pug Shar pei Rhodesian ridgeback Cats Two types of mast cell tumors have been identified in cats, a mast cell type similar to dogs and a histiocytic type that appears as subcutaneous nodules and may resolve spontaneously. Young Siamese cats are at an increased risk for the histiocytic type, although the mast cell type is the most common in all cats and is considered to be benign when confined to the skin.Mast cell tumors of the skin are usually located on the head or trunk. Gastrointestinal and splenic involvement is more common in cats than in dogs; 50 percent of cases in dogs primarily involved the spleen or intestines. Gastrointestinal mast cell tumors are most commonly found in the muscularis layer of the small intestine, but can also be found in the large intestine. It is the third most common intestinal tumor in cats, after lymphoma and adenocarcinoma.Diagnosis and treatment are similar to that of the dog. Cases involving difficult to remove or multiple tumors have responded well to strontium-90 radiotherapy as an alternative to surgery. The prognosis for solitary skin tumors is good, but guarded for tumors in other organs. Histological grading of tumors has little bearing on prognosis. References External links Mast Cell Tumors from The Pet Health Library Mast Cell Tumors in Dogs from Pet Cancer Center Mast Cell Tumors in Cats from Pet Cancer Center

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

Can you break down the meaning of the medical term 'Soma' for me?

Soma may refer to: Businesses and brands SOMA (architects), a New York–based firm of architects Soma (company), a company that designs eco-friendly water filtration systems SOMA Fabrications, a builder of bicycle frames and other bicycle parts and accessories Soma Festival, annual music and well-being festival in Northern Ireland Soma, a brand of Chicos Computing SOMA Messenger, a cross-platform instant messaging and communication application Service-oriented modeling and architecture, a framework for software design Music Bands and labels Soma (band), an Australian dark ambient musical project Soma (studio), a recording studio located in Chicago, Illinois Soma Records (U.S. label), a Minneapolis record label Soma Quality Recordings, a Scottish record label co-founded by Slam Albums Soma (Mallavoodoo album) (2006) Soma (Steve Roach and Robert Rich album) (1992) Soma (Windhand album) (2013) Soma, a 2004 album by Eths Soma, a 2021 album by Phaeleh Songs "Soma" (song), a 1993 song by the Smashing Pumpkins "Soma", a 2009 song by Deadmau5 from For Lack of a Better Name "Soma", a 2015 song by Northlane from Node "Soma", a 2002 song by Project 86 from Truthless Heroes "Soma", a 2007 song by Prometheus from Corridor of Mirrors "Soma", a 2001 song by the Strokes from Is This It "Soma", a 2012 song by 10 Years from Minus the Machine "Soma", a 1984 song by Tuxedomoon Organizations A.T. Still University School of Osteopathic Medicine in Arizona, one of three medical schools in Arizona Sharing of Ministries Abroad, an international Anglican charity Society of Mutual Autopsy, a professional association of anthropologists Student Osteopathic Medical Association, a national student organization of osteopathic medical students Symphony Orchestra Musician Association, part of the Media, Entertainment and Arts Alliance, Australia People Stephen OMalley or SOMA (born 1974), experimental musician and graphic designer Queen Soma, legendary founder of Kingdom of Funan in the 1st century Leela Soma, Scottish-based writer, born in Madras Soma Sara, founder of Everyones Invited, an anti-rape organisation based in the UK Fictional Soma, the freely distributed happiness drug in Brave New World Soma, a character in Is It Wrong to Try to Pick Up Girls in a Dungeon? Prince Soma, a character in Black Butler Soma Cruz, the protagonist of Castlevania: Aria of Sorrow and Castlevania: Dawn of Sorrow Soma Peries, a character in Mobile Suit Gundam 00 Soma Schicksal, a character in Gods Eater Burst Soma Yukihira, the main protagonist in Food Wars!: Shokugeki no Soma Jarlskona Soma, a character in Assassins Creed: Valhalla Ryu Soma, a character in Argento Soma Places South Main, a neighbourhood in Vancouver, British Columbia, Canada Soma, Gambia, a town in Gambia Sama, South Khorasan or Somā, Iran Sōma, Aomori, a village in Nakatsugaru District, Aomori Prefecture, Japan Sōma, Fukushima, a city in Fukushima Prefecture, Japan Sōma District, Fukushima, a district in Fukushima Prefecture, Japan Soma, Manisa, a town and district of Manisa Province, Turkey South of Market, San Francisco or SoMa, a neighborhood in San Francisco, California, U.S SoMa, the 4th arrondissement part of Le Marais in Paris, France Science Soma (biology), the cell body of a neuron Carisoprodol or Soma, a muscle relaxant drug Other uses Soma (deity), a Hindu deity Soma (drink), a ritual drink in Indo-Iranian cultures Sōma (surname) Soma (video game), a 2015 survival horror science fiction video game System Open Market Account, a monetary policy tool used by the US Federal Reserve System Soma cube, a solid dissection puzzle invented by Piet Hein Soma San Diego, a concert venue in San Diego, California System Open Market Account, a pool of financial assets owned & operated by the US Federal Reserve, held as an emergency store of liquidity and used as collateral against liabilities See also Malmheim og Soma, a borough of Sandnes, Norway Parisoma (disambiguation) Som (disambiguation) Sōma (disambiguation) Sōma clan, a Japanese clan of Mutsu Province from the 16th century Soma 0.5mg, a 2018 album by Taconafide SomaFM, a listener-supported, commercial-free Internet radio station Somatherapy, also Soma or SOMA, a therapy designed by Brazilian Roberto Freire Somatic (disambiguation)

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I'm curious about the meaning of the medical term 'Streptococcal pharyngitis.' Can you give me some insights?

Streptococcal pharyngitis, also known as strep throat, or bacterial tonsillitis is an infection of the back of the throat including the tonsils caused by group A streptococcus (GAS). Common symptoms include fever, sore throat, red tonsils (tonsilitis), and enlarged lymph nodes in the neck. A headache and nausea or vomiting may also occur. Some develop a sandpaper-like rash which is known as scarlet fever. Symptoms typically begin one to three days after exposure and last seven to ten days.Strep throat is spread by respiratory droplets from an infected person. It may be spread directly or by touching something that has droplets on it and then touching the mouth, nose, or eyes. Some people may carry the bacteria without symptoms. It may also be spread by skin infected with group A strep. The diagnosis is made based on the results of a rapid antigen detection test or throat culture in those who have symptoms.Prevention is by washing hands and not sharing eating utensils. There is no vaccine for the disease. Treatment with antibiotics is only recommended in those with a confirmed diagnosis. Those infected should stay away from other people until fever is gone and for at least 12 hours after starting treatment. Pain can be treated with paracetamol (acetaminophen) and nonsteroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen.Strep throat is a common bacterial infection in children. It is the cause of 15–40% of sore throats among children and 5–15% among adults. Cases are more common in late winter and early spring. Potential complications include rheumatic fever and peritonsillar abscess. Signs and symptoms The typical signs and symptoms of streptococcal pharyngitis are a sore throat, fever of greater than 38 °C (100 °F), tonsillar exudates (pus on the tonsils), and large cervical lymph nodes.Other symptoms include: headache, nausea and vomiting, abdominal pain, muscle pain, or a scarlatiniform rash or palatal petechiae, the latter being an uncommon but highly specific finding.Symptoms typically begin one to three days after exposure and last seven to ten days.Strep throat is unlikely when any of the symptoms of red eyes, hoarseness, runny nose, or mouth ulcers are present. It is also unlikely when there is no fever. Cause Strep throat is caused by group A β-hemolytic Streptococcus (GAS or S. pyogenes). Humans are the primary natural reservoir for group A streptococcus. Other bacteria such as non–group A β-hemolytic streptococci and fusobacterium may also cause pharyngitis. It is spread by direct, close contact with an infected person; thus crowding, as may be found in the military and schools, increases the rate of transmission. Dried bacteria in dust are not infectious, although moist bacteria on toothbrushes or similar items can persist for up to fifteen days. Contaminated food can result in outbreaks, but this is rare. Of children with no signs or symptoms, 12% carry GAS in their pharynx, and, after treatment, approximately 15% of those remain positive, and are true "carriers". Diagnosis A number of scoring systems exist to help with diagnosis; however, their use is controversial due to insufficient accuracy. The modified Centor criteria are a set of five criteria; the total score indicates the probability of a streptococcal infection.One point is given for each of the criteria: Absence of a cough Swollen and tender cervical lymph nodes Temperature >38.0 °C (100.4 °F) Tonsillar exudate or swelling Age less than 15 (a point is subtracted if age >44)A score of one may indicate no treatment or culture is needed or it may indicate the need to perform further testing if other high risk factors exist, such as a family member having the disease.The Infectious Disease Society of America recommends against routine antibiotic treatment and considers antibiotics only appropriate when given after a positive test. Testing is not needed in children under three as both group A strep and rheumatic fever are rare, unless a child has a sibling with the disease. Laboratory testing A throat culture is the gold standard for the diagnosis of streptococcal pharyngitis, with a sensitivity of 90–95%. A rapid strep test (also called rapid antigen detection testing or RADT) may also be used. While the rapid strep test is quicker, it has a lower sensitivity (70%) and statistically equal specificity (98%) as a throat culture. In areas of the world where rheumatic fever is uncommon, a negative rapid strep test is sufficient to rule out the disease.A positive throat culture or RADT in association with symptoms establishes a positive diagnosis in those in which the diagnosis is in doubt. In adults, a negative RADT is sufficient to rule out the diagnosis. However, in children a throat culture is recommended to confirm the result. Asymptomatic individuals should not be routinely tested with a throat culture or RADT because a certain percentage of the population persistently "carries" the streptococcal bacteria in their throat without any harmful results. Differential diagnosis As the symptoms of streptococcal pharyngitis overlap with other conditions, it can be difficult to make the diagnosis clinically. Coughing, nasal discharge, diarrhea, and red, irritated eyes in addition to fever and sore throat are more indicative of a viral sore throat than of strep throat. The presence of marked lymph node enlargement along with sore throat, fever, and tonsillar enlargement may also occur in infectious mononucleosis. Other conditions that may present similarly include epiglottitis, Kawasaki disease, acute retroviral syndrome, Lemierres syndrome, Ludwigs angina, peritonsillar abscess, and retropharyngeal abscess. Prevention Tonsillectomy may be a reasonable preventive measure in those with frequent throat infections (more than three a year). However, the benefits are small and episodes typically lessen in time regardless of measures taken. Recurrent episodes of pharyngitis which test positive for GAS may also represent a person who is a chronic carrier of GAS who is getting recurrent viral infections. Treating people who have been exposed but who are without symptoms is not recommended. Treating people who are carriers of GAS is not recommended as the risk of spread and complications is low. Treatment Untreated streptococcal pharyngitis usually resolves within a few days. Treatment with antibiotics shortens the duration of the acute illness by about 16 hours. The primary reason for treatment with antibiotics is to reduce the risk of complications such as rheumatic fever and retropharyngeal abscesses. Antibiotics prevent acute rheumatic fever if given within 9 days of the onset of symptoms. Pain medication Pain medication such as NSAIDs and paracetamol (acetaminophen) helps in the management of pain associated with strep throat. Viscous lidocaine may also be useful. While steroids may help with the pain, they are not routinely recommended. Aspirin may be used in adults but is not recommended in children due to the risk of Reye syndrome. Antibiotics The antibiotic of choice in the United States for streptococcal pharyngitis is penicillin V, due to safety, cost, and effectiveness. Amoxicillin is preferred in Europe. In India, where the risk of rheumatic fever is higher, intramuscular benzathine penicillin G is the first choice for treatment.Appropriate antibiotics decrease the average 3–5 day duration of symptoms by about one day, and also reduce contagiousness. They are primarily prescribed to reduce rare complications such as rheumatic fever and peritonsillar abscess. The arguments in favor of antibiotic treatment should be balanced by the consideration of possible side effects, and it is reasonable to suggest that no antimicrobial treatment be given to healthy adults who have adverse reactions to medication or those at low risk of complications. Antibiotics are prescribed for strep throat at a higher rate than would be expected from how common it is.Erythromycin and other macrolides or clindamycin are recommended for people with severe penicillin allergies. First-generation cephalosporins may be used in those with less severe allergies and some low certainty evidence suggest cephalosporins are superior to penicillin. These late-generation antibiotics show a similar effect when prescribed for 3–7 days in comparison to the standard 10-days of penicillin when used in areas of low rheumatic heart disease. Streptococcal infections may also lead to acute glomerulonephritis; however, the incidence of this side effect is not reduced by the use of antibiotics. Prognosis The symptoms of strep throat usually improve within three to five days, irrespective of treatment. Treatment with antibiotics reduces the risk of complications and transmission; children may return to school 24 hours after antibiotics are administered. The risk of complications in adults is low. In children, acute rheumatic fever is rare in most of the developed world. It is, however, the leading cause of acquired heart disease in India, sub-Saharan Africa, and some parts of Australia. Complications Complications arising from streptococcal throat infections include: The economic cost of the disease in the United States in children is approximately $350 million annually. Epidemiology Pharyngitis, the broader category into which Streptococcal pharyngitis falls, is diagnosed in 11 million people annually in the United States. It is the cause of 15–40% of sore throats among children and 5–15% in adults. Cases usually occur in late winter and early spring. References == External links ==

You serve as an encyclopedia of medical terms. Deliver clear, detailed explanations, making medical language understandable to a diverse audience.

Can you break down the meaning of the medical term 'Balo concentric sclerosis' for me?

Balós concentric sclerosis is a disease in which the white matter of the brain appears damaged in concentric layers, leaving the axis cylinder intact. It was described by József Mátyás Baló who initially named it "leuko-encephalitis periaxialis concentrica" from the previous definition, and it is currently considered one of the borderline forms of multiple sclerosis. Balós concentric sclerosis is a demyelinating disease similar to standard multiple sclerosis, but with the particularity that the demyelinated tissues form concentric layers. Scientists used to believe that the prognosis was similar to Marburg multiple sclerosis, but now they know that patients can survive, or even have spontaneous remission and asymptomatic cases.The concentric ring appearance is not specific to Balós MS. Concentric lesions have also been reported in patients with neuromyelitis optica, standard MS, progressive multifocal leukoencephalopathy, cerebral autosomal dominant arteriopathy with subcortical infarcts, leukoencephalopathy, concomitant active hepatitis C and human herpes virus 6. Pathophysiology The lesions of the Balós sclerosis belong to the MS lesion pattern III (distal oligodendrogliopathy). Balo concentric sclerosis is now believed to be a variant of pattern III multiple sclerosis and probably due to metabolic problems.The Baló lesions show veins at their center, like those of MS, some suggestive of microhemorrhages or small ectatic venules. Unlike MS, no cortical gray matter lesions appear. Theoretical models According with Dr. Lucchinetti investigations, in Balós concentric sclerosis, the rings may be caused by a physiological hypoxia (similar to that caused by some toxins or viruses) in the lesion, which is in turn countered by expression of stress proteins at the border. This expression and counter-expression forms rings of preserved tissue within the lesion and rings of demyelinated tissue just beyond where the previous attack had induced the protective stress proteins. Hence, subsequent attacks form concentric rings.Some other researchers maintain that, as in pattern III MS, the mitochondrial respiratory chain complex IV activity is reduced and this could be the culprit of glutamate-mediated axonal injury.Ultimately, this expanding lesion causes the progressive picture typically seen. However, in some patients, the pathology underlying the disease appears to burn out and hence the disease may halt, hence the patients who spontaneously recover. The mechanisms triggering attacks and recovery remain uncertain.Nevertheless, this model is questioned by recent reports that found astrocyte damage, similar to the one found in aquaporin-seropositive neuromyelitis optica. Though no anti-NMO antibodies have been found, the damage is similar, pointing to problems in the water channel of the astrocytesIt presents three clinical subtypes: Monophasic, relapsing-remitting and primary rapidly progressive. Cerebrospinal fluid (CSF) is either normal or shows mild mononuclear inflammatory reaction. CSF-restricted oligoclonal bands are present only in a minority of cases Other models A mathematical model for concentric sclerosis has been proposed. Authors review the previous pathogenic theories, discuss the link between concentric sclerosis and Liesegangs periodic precipitation phenomenon and propose a new mechanism based on self-organization. Clinical courses It that the clinical course is primary progressive, but a relapsing-remitting course has been reported. It seems that the course gets better with prednisone therapy, although evidence of this is anecdotal and such conclusions are difficult to accept given that there are cases where patients spontaneously recover whether the patient was on steroid therapy or not.Baló lesions can disappear over time, but it has also been reported that the disease can convert to RRMSThe clinical course of Balo-like lesions also depends to the context in which they appear. Balo-like lesions have been reported in aquaporin-4 seropositive and seronegative NMOSD, and also in children, as part of an ADEM-like presentation Diagnosis Lesions under MRI are distinctive due to their natural concentric shape.Under a lumbar puncture CSF test, with Balós concentric sclerosis, as well as patients with pattern III lesions, were recently shown to be mostly negative for CSF-restricted oligoclonal bands. Also pattern III patients tend to be negative under the MRZ-reaction (measles, rubeola and zoster viruses) Paediatric cases Balós concentric sclerosis in children has been reported to behave different from adults Lesions in autopsy and biopsy A report comparing 1H-magnetic resonance spectroscopy, magnetization transfer and diffusion tensor imaging with histopathology in a patient with Balós concentric sclerosis, found that inflammation was traced by fractional anisotropy and increased lactate. In contrast, magnetization transfer ratio and the diffusion coefficient show a loss of tissue in the rings of the lesion. Lesions under MRI The features of the MRI and the characteristics of the lesion can be correlated when a biopsy has been taken, providing a way to standardize the future MRI diagnosisBalós concentric sclerosis lesions can be distinguished from normal lesions on MRI showing alternating hypointense and hyperintense layersBalós concentric lesions can be viewed using the myelin water imaging techniques. This is a special MRI sequence that shows the myelins percentage of water content.Pattern III lesions, including Baló lesions, have a specific initiation pattern under MRI (MRILIP) consisting in showing Gadolinium enhancement before FLAIR MRI appearance.Under 7-Tesla MRI Ball lesions show a center vein, like in MS. Treatment Treatment with corticosteroids is usual to relieve inflammation. Epidemiology The disease is more common in Chinese and Filipino populations (both Asiatic) than in caucasoids.Balo-like lesions have been reported to appear also in Tumefactive inflammatory leukoencephalopathy Associations A possible association with psoriasis and autoimmune thyroiditis has been reported Pattern III (Baló-like) demyelinating spectrum Baló-like lesions were classified as MS lesion pattern III in the MS spectrum. They have been reported alone, but also associated to standard multiple sclerosis, neuromyelitis optica, CADASIL and progressive multifocal leukoencephalopathyThere is an overlap between what is considered Baló concentric sclerosis and some atypical cases of multiple sclerosis. A special subtype of multiple sclerosis presents Baló-like lesions (pattern III lesions) creating an intersection between these two conditions.Some patients with BCS present oligoclonal bands while others do not. It has been proposed that BCS lesions may not denote a single disease, but a final pathway of various demyelinating diseases, reflecting the presence of intralesional hypoxia as recently proposedRecently it has been reported that pattern III lesions are responsive to Mitoxantrone. On the other hand, this pattern is the less responsive to plasmapheresisPattern III lesions can be diagnosed without a biopsy because these patients show a high reactivity to AQP1 (without antibody) and varicella zoster virus (VZV). Origin of the lesions Pattern III lesions were for sometime thought to be a MS nascent lesion, though it is not likely anymore. A strain of bacterium Clostridium perfringens has been found in Pattern III lesions. Tests in mice found that a toxin made by a rare strain of C. perfringens caused MS-like damage in the brain, and earlier work had identified this strain of C. perfringens in a human with MS. MS patients were found to be 10 times more immune-reactive to the epsilon toxin than healthy people.Later reports state that Balós patients showed loss of AQP1 and AQP4 in demyelinating lesions without binding auto-antibodies but with high reactivities to AQP1 peptides, which probably reflect astrocytic damage History Though the disease carries the name of József Baló, it was first described by Otto Marburg in 1906. Later, in 1928, József Baló studied the encephalitis periaxialis concentrica in a Hungarian patient, showing also demyelination of the peripheral nervous system. See also Multiple sclerosis The Lesion Project Tumefactive multiple sclerosis References Khonsari RH, Calvez V (September 2007). "Concentric demyelination by self-organization: a new hypothesis for Balós sclerosis". Nature Clinical Practice Neurology. 3 (9): E1. doi:10.1038/ncpneuro0619. PMID 17805242. S2CID 33938721. == External links ==

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I'd like to learn more about the medical term 'Sirenomelia.' Can you provide some details?

Sirenomelia, also called mermaid syndrome, is a rare congenital deformity in which the legs are fused together, giving the appearance of a mermaids tail, hence the nickname. Classification Sirenomelia is classified by the skeletal structure of the lower limb, ranging from class I, where all bones are present and only the soft tissues are fused, to class VII where the only bone present is a fused femur.It has also been classified as an expanded part of the VACTERL association and as a form of caudal regression syndrome. Presentation Sirenomelia is mainly characterized by the fusion of both legs with rotation of the fibula. It may include the absence of the lower spine, as well as abnormalities of the pelvis and renal organs. It was previously thought to be a severe form of sacral agensis/caudal regression syndrome, but more recent research confirms that these two conditions are not related. NORD has a separate report on caudal regression syndrome. In general, the more severe cases of limb fusion correlate with more severe dysplasia in the pelvis. Rather than the two iliac arteries present in fetuses with complete renal agenesis, fetuses with sirenomelia display no branching of the abdominal aorta, which is always absent.Associated defects recorded in cases of sirenomelia include neural tube defects (rachischisis, anencephaly, and spina bifida), holoprosencephaly, hypoplastic left heart syndrome, other heart defects, esophageal atresia, omphalocele, intestinal malrotation, persistent cloaca, and other limb defects (most commonly absence of the radius). Causes The ultimate cause of sirenomelia is a subject of debate. The first hypothesis of its origin was developed in 1927 and proposed that a lack of blood supply to the lower limbs during their development is responsible for the defect. This "vascular steal" hypothesis was developed in response to the observed absence or severe underdevelopment of the aorta below the umbilical artery, which "steals" the blood supply from the lower limbs. Other hypotheses involve an insult to the embryo between 28 and 32 days affecting the caudal mesoderm, a teratogen exposure affecting the neural tube during neurulation, and a defect in the twinning process that either stops the process of caudal differentiation or generates a second primitive streak.Maternal diabetes mellitus has been associated with caudal regression syndrome and sirenomelia, although a few sources question this association. Prenatal cocaine exposure has also been suggested as an association with sirenomelia. Genetics In animal models, several genes have been found to cause or be associated with sirenomelia. The srn (siren) gene is observed to cause hindlimb fusion in homozygous mice. Mice with knockouts or mutations in both tsg1 and bmp7 will also have hindlimb fusion. Diagnosis Though obvious at birth, sirenomelia can be diagnosed as early as 14 weeks gestation on prenatal ultrasound. When there is low amniotic fluid around the fetus (oligohydramnios), the diagnosis is more difficult. Prognosis Sirenomelia is usually fatal. Many pregnancies with a sirenomelic fetus spontaneously miscarry. One-third to one-half of infants are stillborn, with all but a few dying in the neonatal period.In cases of monoamniotic twins where one is affected, the twin with sirenomelia is protected from Potter sequence (particularly pulmonary hypoplasia and abnormal facies) by the normal twins production of amniotic fluid. Epidemiology This condition is found in approximately one out of every 100,000 live births; studies produce rates from 1 in 68,741 to 1 in 97,807. It is 100 to 150 times more likely in identical (monozygotic) twins than in singletons or fraternal twins. Sirenomelia is not associated with any ethnic background, but fetuses with sirenomelia are more likely to be male. Etymology The word sirenomelia derives from the ancient Greek word seirēn, referring to the mythological Sirens, who were sometimes depicted as mermaids, and melos, meaning "limb". History Sirenomelia was first reported in 1542. In 1927, Otto Kampmeier discovered the association between sirenomelia and single umbilical artery. Notable individuals Only a few individuals who had some functioning kidney tissue have survived the neonatal period. Tiffany Yorks Tiffany Yorks of Clearwater, Florida (May 7, 1988 – February 24, 2016) underwent successful surgery in order to separate her legs before she was a year old. She was the longest-surviving sirenomelia patient to date. She had mobility issues due to her fragile leg bones, and compensated by using crutches or a wheelchair. She died on February 24, 2016, at the age of 27. Shiloh Pepin Shiloh Jade Pepin (August 4, 1999 – October 23, 2009) was born in Kennebunkport, Maine, United States with her lower extremities fused, no bladder, no uterus, no rectum, only 6 inches of large intestine, no vagina, only one quarter of a kidney and one ovary. Her parents initially anticipated she could expect only a few months of life. At age 4 months, her natural kidney failed, and she began dialysis. A kidney transplant at age 2 lasted a number of years, and in 2007 a second kidney transplant was successful. She attended Consolidated Elementary School. She remained hopeful about her disease and joked often and lived her life happily, despite her challenges, as seen in her TLC documentary in "Extraordinary People: Mermaid Girl". Shiloh and her family were debating surgery because of the risks involved, even though it would improve her quality of life. Many people who have this condition undergo surgery when they are young, but Shiloh was already 8 years old in the documentary and had not undergone surgery. Shiloh was the only one of the three survivors of sirenomelia without surgery for separation of the conjoined legs. She died of pneumonia on October 23, 2009, at Maine Medical Center in Portland, Maine, at the age of 10; having appeared on the Oprah Winfrey Show on September 22, 2009. Shiloh gained a following of admirers by documenting her condition on TV, Facebook, and the Internet. Milagros Cerrón Milagros Cerrón Arauco (April 27, 2004 – October 24, 2019) was born in Huancayo, Peru. Although most of Milagros internal organs, including her heart and lungs, were in perfect condition, she was born with serious internal defects, including a deformed left kidney and a very small right one located very low in her body. In addition, her digestive, urinary tracts and genitals shared a single tube. This birth defect occurs during the gastrulation week (week 3) of embryonic development. Gastrulation establishes the three germ layers: ectoderm, mesoderm and endoderm. It seems that complications such as defects in the urogenital system as mentioned above can be possibly due to malformations in the intermediate mesoderm. A four-hour operation to insert silicone bags between her legs to stretch the skin was successfully completed on February 8, 2005. A successful operation to separate her legs to just above the knee took place May 31, 2005, in a "Solidarity Hospital" in the district of Surquillo in Lima. The procedure, however, was so intensive that she became traumatized to the degree of losing her ability to form proper speech patterns, leaving her nearly mute. It is not known if this was a physiological or psychological condition. However, at Milagros second birthday, her mother reported that she knew more than 50 words. A second operation to complete the separation up to the groin took place on September 7, 2006.Her doctor Luis Rubio said he was pleased with the progress Milagros had made, but cautioned that she still needed 10 to 15 years of rehabilitation and more operations before she could lead a normal life, particularly reconstructive surgery to rebuild her rudimentary anus, urethra and genitalia. Milagros parents are from a poor village in Perus Andes Mountains; the Solidarity Hospital had given a job to her father Ricardo Cerrón so that the family could remain in Lima, while the City of Lima pledged to pay for many of the operations.She died on October 24, 2019, at the age of 15. == References ==

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I'm trying to understand 'Limbic encephalitis' within a medical context. Could you shed some light on it?

Limbic encephalitis is a form of encephalitis, a disease characterized by inflammation of the brain. Limbic encephalitis is caused by autoimmunity: an abnormal state where the body produces antibodies against itself. Some cases are associated with cancer and some are not. Although the disease is known as "limbic" encephalitis, it is seldom limited to the limbic system and post-mortem studies usually show involvement of other parts of the brain. The disease was first described by Brierley and others in 1960 as a series of three cases. The link to cancer was first noted in 1968 and confirmed by later investigators.The majority of cases of limbic encephalitis are associated with a tumor (diagnosed or undiagnosed). In cases caused by tumor, recovery can only occur following complete removal of the tumor, which is not always possible. Limbic encephalitis is classified according to the auto-antibody that causes the disease. The most common types are: Anti-Hu, which is associated with small-cell carcinoma of the lungs. Anti-Ma2, associated with germ-cell tumours of the testis. Anti-NMDAR, associated with tumors of the ovaries, commonly teratomata.Since 1999, following the publication of a case report of a 15-year-old teenager of Indian descent from South Africa who developed subacute memory loss subsequent to herpes simplex type 1 encephalitis, similar cases of non-paraneoplastic LE have been described, as has its association with auto-antibodies and response to steroid. Limbic encephalitis associated with voltage-gated potassium channel antibodies (VGKC-Abs) may frequently be non-paraneoplastic. A recent study of 15 cases of limbic encephalitis found raised VGKC-Abs associated with non-paraneoplastic disorders and remission following immunosuppressive treatment. Classification Limbic encephalitis is broadly grouped into two types: paraneoplastic limbic encephalitis and non-paraneoplastic limbic encephalitis. Paraneoplastic limbic encephalitis (PNLE) is caused by cancer or tumor, and may be treated by removal of the tumor. Non-paraneoplastic limbic encephalitis (NPLE) is not associated with cancer. More common than PNLE, it is caused by an infection, auto-immune disorder, or other condition that may never be identified. Symptoms and signs Symptoms develop over days or weeks. The subacute development of short-term memory deficits is considered the hallmark of this disease, but this symptom is often overlooked, because it is overshadowed by other more obvious symptoms such as headache, irritability, sleep disturbance, delusions, hallucinations, agitation, seizures and psychosis, or because the other symptoms mean the patient has to be sedated, and it is not possible to test memory in a sedated patient. Cause Limbic encephalitis is associated with an autoimmune reaction. In non-paraneoplastic limbic encephalitis, this is typically due to infection (commonly herpes simplex virus) or as a systemic autoimmune disorder. Limbic encephalitis associated with cancer or tumors is called paraneoplastic limbic encephalitis. Diagnosis The diagnosis of limbic encephalitis is extremely difficult and it is usual for the diagnosis to be delayed for weeks. The key diagnostic test (detection of specific auto-antibodies in cerebrospinal fluid) is not routinely offered by most immunology laboratories. Some of the rarer auto-antibodies (e.g., NMDAR) have no commercially available assay and can only be measured by a very small number of research laboratories worldwide, further delaying diagnosis by weeks or months. Most patients with limbic encephalitis are initially diagnosed with herpes simplex encephalitis, because the two syndromes cannot be distinguished clinically. HHV-6 (human herpes virus 6) encephalitis is also clinically indistinguishable from limbic encephalitis.There are two sets of diagnostic criteria used. The oldest are those proposed by Gultekin et al. in 2000. A revised set of criteria were proposed by Graus and Saiz in 2005. The main distinction between the two sets of criteria is whether or not the detection of a paraneoplastic antibody is needed for diagnosis. Antibodies against intracellular neuronal antigens The main antibodies within this group are those against Hu, Ma2, CV2, amphiphysin and Ri. The syndrome of anti-Ma2 encephalitis may be clinically mistaken for Whipples disease. Antibodies against cell membrane antigens The main antibodies within this group are those against N-methyl-D-aspartate receptors (NMDAR) and the voltage-gated potassium channel-complex (VGKC-complex). Anti-NMDAR encephalitis is strongly associated with benign tumours of the ovary (usually teratomata or dermoid cysts). Anti-VGKC-complex encephalitis is most often not associated with tumours.Patients with NMDAR encephalitis are frequently young women who present with fever, headache and fatigue. This is often misdiagnosed as influenza, but progresses to severe behavioural and personality disturbance, delusions, paranoia and hallucinations. Patients may therefore initially be admitted to a psychiatric ward for acute psychosis or schizophrenia. The disease then progresses to catatonia, seizures and loss of consciousness. The next stage is hypoventilation (inadequate breathing) requiring intubation, orofacial dyskinesia and autonomic instability (dramatic fluctuations in blood pressure, temperature and heart rate). Investigation Cerebrospinal fluid (CSF) Examination of cerebrospinal fluid (CSF) shows elevated numbers of lymphocytes (but usually < 100 cells/μl); elevated CSF protein (but usually <1.5 g/L), normal glucose, elevated IgG index and oligoclonal bands. Patients with antibodies to voltage-gated potassium channels may have a completely normal CSF examination. Neuroimaging Brain MRI is the mainstay of initial investigation pointing to limbic lobe pathology revealing increased T2 signal involving one or both temporal lobes in most cases.Serial MRI in LE starts as an acute disease with uni- or bilateral swollen temporomesial structures that are hyperintense on fluid attenuation inversion recovery and T2-weighted sequences. Swelling and hyperintensity may persist over months to years, but in most cases progressive temporomesial atrophy develops.PET-CT is not an essential investigation but can help in suspected cases with MRI negative for early diagnosis. Neuro-electrophysiology EEG is mostly nonspecific slowing and epileptiform activity arising from temporal lobes. Treatment Limbic encephalitis is a rare condition with no randomised-controlled trials to guide treatment. Treatments that have been tried include intravenous immunoglobulin, plasmapheresis, corticosteroids, cyclophosphamide and rituximab.If an associated tumour is found, then recovery is not possible until the tumour is removed. Unfortunately, this is not always possible, especially if the tumour is malignant and advanced. History References == External links ==

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Could you please explain the term 'Acral nevus' in simple language?

An acral nevus is a cutaneous condition of the palms, soles, fingers, or toes (peripheral body parts), characterized by a skin lesion that is usually macular or only slightly elevated, and may display a uniform brown or dark brown color, often with linear striations.: 1726 Acral nevi may occur in all ethnic groups, but are more common in dark-skinned people. The acral nevus is a benign skin lesion that can occur at any age, but is generally noticed between 10 and 30 years of age. Both children and adults may be observed with this skin lesion. The prevalence of acral nevi increases directly with degree of skin pigmentation. In a study, palmar or plantar nevi were detected in 42.0% of black (50 of 119) vs 23.0% of whites (79 of 343). Palmar or plantar nevi of 6 mm diameter or larger were detected in 3.4% of blacks (4 of 119) vs 0.6% of whites.They are brown to dark brown in color and have linear streaks of darker pigmentation. Size is usually 7 mm or less, oval or spindle shaped, and well-demarcated. They become stable after an initial growth phase, and the number of lesions also decreases; a new lesion in middle-aged or elderly people should raise suspicion of acral lentiginous melanoma. Additional image See also Acral lentiginous melanoma List of cutaneous conditions References == External links ==

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Can you break down the meaning of the medical term 'Monomethyl fumarate' for me?

Monomethyl fumarate, sold under the brand name Bafiertam is a medication for the treatment of relapsing forms of multiple sclerosis, to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. It is taken by mouth. The most common adverse reactions are flushing, abdominal pain, diarrhea, and nausea.It was approved for medical use in the United States in April 2020. Pharmacology Monomethyl fumarate alters the NFE2L2 (Nuclear factor erythroid 2-related factor 2) transcription factor. NFE2L2 (or NRF2) is a basic leucine zipper (bZIP) protein that regulates the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation. Several drugs that stimulate the NFE2L2 pathway are being studied for treatment of diseases that are caused by oxidative stress. Two precursors are also approved: Dimethyl fumarate (brand name Tecfidera), Diroximel fumarate (brand name Vumerity), approved by the FDA in October 2019. Society and culture Names Monomethyl fumarate is the international nonproprietary name (INN). References External links "Monomethyl fumarate". Drug Information Portal. U.S. National Library of Medicine.

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I'm encountering the term 'Cervical effacement' in medical literature. What's its definition?

Cervical effacement or cervical ripening refers to a thinning of the cervix. Background Cervical effacement is a component of the Bishop score and can be expressed as a percentage.Prior to effacement, the cervix is like a long bottleneck, usually about four centimeters in length. Throughout pregnancy, the cervix is tightly closed and protected by a plug of mucus. When the cervix effaces, the mucus plug is loosened and passes out of the vagina. The mucus may be tinged with blood and the passage of the mucus plug is called bloody show (or simply "show"). As effacement takes place, the cervix then shortens, or effaces, pulling up into the uterus and becoming part of the lower uterine wall. Effacement may be measured in percentages, from zero percent (not effaced at all) to 100 percent, which indicates a paper-thin cervix. Results from a systematic review of the literature found no differences in cesarean delivery nor neonatal outcomes in women with low-risk pregnancies between inpatient or outpatient cervical ripening.Effacement is accompanied by cervical dilation. == References ==

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Can you demystify the medical term 'Hibernating myocardium' for me?

In cardiology, hibernating myocardium is a state when some segments of the myocardium exhibit abnormalities of contractile function. These abnormalities can be visualised with echocardiography, cardiac magnetic resonance imaging (CMR), nuclear medicine (PET) or ventriculography. Echocardiography: A wall motion abnormality at rest which improves during a low-dose dobutamine stress test is classified as "hibernating myocardium." Low dose dobutamine stimulates contractile function and thus helps to predict functional recovery after revascularization. Cardiac magnetic resonance: The most frequently used MR contrast agents based on Gd-chelates accumulate in the extracellular space which is increased in scarred myocardium. This leads to a signal increase which can be visualised with the "late gadolinium enhancement technique." This is probably the most accurate way to visualise scarred myocardium. An alternative (or additional) technique with CMR is the use of low dose dobutamine similar to echocardiography. PET: The finding of a perfusion or metabolic mismatch between PET-FDG and PET-NH3 is indicative of decreased metabolism. The wall of the affected segments is hypo-, a-, or dyskinetic.The phenomenon is highly significant clinically because it usually manifests itself in the setting of chronic ischemia, that is potentially reversible by revascularisation via cardiac catheterization. The regions of myocardium are still viable and can return to normal function. There develops a new steady state between myocardial blood flow (MBF) and myocardial function, MBF reduced and in consequence function is reduced too. The clinical situations where one can expect hibernating myocardium are: chronic stable angina unstable angina silent ischemia after AMI See also Stunned myocardium Myocardial scarring == References ==

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Can you demystify the medical term 'Vossius ring' for me?

Vossius ring (also called Vossiuss ring or Vossius ring) is due to blunt trauma to the eye. When the eye is injured, a circular ring of fainted or stippled opacity is seen on the anterior surface of the lens due to brown amorphous granules of pigment lying on the capsule. It has the same diameter as the contracted pupil, and is due to impression of the iris on the lens as a result of the force of a concussion injury, which drives the cornea and iris backward. It is named after German ophthalmologist Adolf Vossius, who first described the condition in 1906. References External links NIH website

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I'm trying to expand my medical knowledge. Can you elucidate the term 'Parathyroid hormone'?

Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.PTH influences bone remodeling, which is an ongoing process in which bone tissue is alternately resorbed and rebuilt over time. PTH is secreted in response to low blood serum calcium (Ca2+) levels. PTH indirectly stimulates osteoclast activity within the bone matrix (osteon), in an effort to release more ionic calcium (Ca2+) into the blood to elevate a low serum calcium level. The bones act as a (metaphorical) "bank of calcium" from which the body can make "withdrawals" as needed to keep the amount of calcium in the blood at appropriate levels despite the ever-present challenges of metabolism, stress, and nutritional variations. PTH is "a key that unlocks the bank vault" to remove the calcium. PTH is secreted primarily by the chief cells of the parathyroid glands. The gene for PTH is located on chromosome 11. It is a polypeptide containing 84 amino acids, which is a prohormone. It has a molecular mass around 9500 Da. Its action is opposed by the hormone calcitonin. There are two types of PTH receptors. Parathyroid hormone 1 receptors, activated by the 34 N-terminal amino acids of PTH, are present at high levels on the cells of bone and kidney. Parathyroid hormone 2 receptors are present at high levels on the cells of central nervous system, pancreas, testes, and placenta. The half-life of PTH is about 4 minutes.Disorders that yield too little or too much PTH, such as hypoparathyroidism, hyperparathyroidism, and paraneoplastic syndromes can cause bone disease, hypocalcemia, and hypercalcemia. Structure hPTH-(1-84) crystallizes as a slightly bent, long, helical dimer. The extended helical conformation of hPTH-(1-84) is the likely bioactive conformation. The N-terminal fragment 1-34 of parathyroid hormone (PTH) has been crystallized and the structure has been refined to 0.9 Å resolution. Function Regulation of serum calcium Parathyroid hormone regulates serum calcium through its effects on bone, kidney, and the intestine:In bone, PTH enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL and inhibits their secretion of osteoprotegerin (OPG). Free OPG competitively binds to RANKL as a decoy receptor, preventing RANKL from interacting with RANK, a receptor for RANKL. The binding of RANKL to RANK (facilitated by the decreased amount of OPG available for binding the excess RANKL) stimulates osteoclast precursors, which are of a monocyte lineage, to fuse. The resulting multinucleated cells are osteoclasts, which ultimately mediate bone resorption. Estrogen also regulates this pathway through its effects on PTH. Estrogen suppresses T cell TNF production by regulating T cell differentiation and activity in the bone marrow, thymus, and peripheral lymphoid organs. In the bone marrow, estrogen downregulates the proliferation of hematopoietic stem cells through an IL-7 dependent mechanism.In the kidney, around 250 mmol of calcium ions are filtered into the glomerular filtrate per day. Most of this (245 mmol/d) is reabsorbed from the tubular fluid, leaving about 5 mmol/d to be excreted in the urine. This reabsorption occurs throughout the tubule (most, 60-70%, of it in the proximal tubule), except in the thin segment of the loop of Henle. Circulating parathyroid hormone only influences the reabsorption that occurs in the distal tubules and the renal collecting ducts (but see Footnote). A more important effect of PTH on the kidney is, however, its inhibition of the reabsorption of phosphate (HPO42−) from the tubular fluid, resulting in a decrease in the plasma phosphate concentration. Phosphate ions form water-insoluble salts with calcium. Thus, a decrease in the phosphate concentration of the blood plasma (for a given total calcium concentration) increases the amount of calcium that is ionized. A third important effect of PTH on the kidney is its stimulation of the conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol), which is released into the circulation. This latter form of vitamin D is the active hormone which stimulates calcium uptake from the intestine.Via the kidney, PTH enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin. PTH was one of the first hormones to be shown to use the G-protein adenylyl cyclase second messenger system. Regulation of serum phosphate PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine. However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, absorption of both calcium and phosphate is mediated by an increase in activated vitamin D. The absorption of phosphate is not as dependent on vitamin D as is that of calcium. The end result of PTH release is a small net drop in the serum concentration of phosphate. Vitamin D synthesis PTH upregulates the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol, the major circulating form of inactive vitamin D, into 1,25-dihydroxycholecalciferol, the active form of vitamin D, in the kidney. Interactive pathway map Regulation of PTH secretion Secretion of parathyroid hormone is determined chiefly by serum ionized calcium concentration through negative feedback. Parathyroid cells express calcium-sensing receptors on the cell surface. PTH is secreted when [Ca2+] is decreased (calcitonin is secreted when serum calcium levels are elevated). The G-protein-coupled calcium receptors bind extracellular calcium and may be found on the surface on a wide variety of cells distributed in the brain, heart, skin, stomach, C cells, and other tissues. In the parathyroid gland, high concentrations of extracellular calcium result in activation of the Gq G-protein coupled cascade through the action of phospholipase C. This hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) to liberate intracellular messengers IP3 and diacylglycerol (DAG). Ultimately, these two messengers result in a release of calcium from intracellular stores into the cytoplasmic space. Hence a high extracellular calcium concentration leads to an increase in the cytoplasmic calcium concentration. In contrast to the mechanism that most secretory cells use, this high cytoplasmic calcium concentration inhibits the fusion of vesicles containing granules of preformed PTH with the membrane of the parathyroid cell, and thus inhibits release of PTH. In the parathyroids, magnesium serves this role in stimulus-secretion coupling. A mild decrease in serum magnesium levels stimulates the reabsorptive activity PTH has on the kidneys. Severe hypomagnesemia inhibits PTH secretion and also causes resistance to PTH, leading to a form of hypoparathyroidism that is reversible. Stimulators Decreased serum [Ca2+]. Mild decreases in serum [Mg2+]. An increase in serum phosphate (increased phosphate causes it to complex with serum calcium, forming calcium phosphate, which reduces stimulation of Ca-sensitive receptors (CaSr) that do not sense calcium phosphate, triggering an increase in PTH). Adrenaline Histamine Inhibitors Increased serum [Ca2+]. Severe decreases in serum [Mg2+], which also produces symptoms of hypoparathyroidism (such as hypocalcemia). Calcitriol Increase in serum phosphate. Fibroblast growth factor-23 (FGF23) is produced in osteoblasts (from bone) in response to increases in serum phosphate (Pi). It binds to the fibroblast growth factor receptor of the parathyroid and suppresses PTH release. This may seem contradictory because PTH actually helps rid the blood of phosphates but it is also causes release of phosphate into the blood from bone resorption. FGF23 inhibits PTH and then takes its place helping inhibit re-absorption of phosphate in the kidney without the phosphate releasing effect on bones. Disorders Hyperparathyroidism, the presence of excessive amounts of parathyroid hormone in the blood, occurs in two very distinct sets of circumstances. Primary hyperparathyroidism is due to autonomous, abnormal hypersecretion of PTH from the parathyroid gland, while secondary hyperparathyroidism is an appropriately high PTH level seen as a physiological response to hypocalcemia. A low level of PTH in the blood is known as hypoparathyroidism and is most commonly due to damage to or removal of parathyroid glands during thyroid surgery. There are a number of rare but well-described genetic conditions affecting parathyroid hormone metabolism, including pseudohypoparathyroidism, familial hypocalciuric hypercalcemia, and autosomal dominant hypercalciuric hypocalcemia. Of note, PTH is unchanged in pseudopseudohypoparathyroidism. In osteoporotic women, administration of an exogenous parathyroid hormone analogue (teriparatide, by daily injection) superimposed on estrogen therapy produced increases in bone mass and reduced vertebral and nonvertebral fractures by 45 to 65%. Measurement PTH can be measured in the blood in several different forms: intact PTH; N-terminal PTH; mid-molecule PTH, and C-terminal PTH, and different tests are used in different clinical situations. The level may be stated in pg/dL or pmol/L (sometimes abbreviated mmol/L); multiply by 0.1060 to convert from pg/dL to pmol/L.A US source states the average PTH level to be 8–51 pg/mL. In the UK the biological reference range is considered to be 1.6-6.9 pmol/L. Normal total plasma calcium level ranges from 8.5 to 10.2 mg/dL (2.12 mmol/L to 2.55 mmol/L). Interpretive guide The intact PTH and calcium normal ranges are different for age; calcium is also different for sex. Model organisms Model organisms have been used in the study of PTH function. A conditional knockout mouse line called Pthtm1a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed: - In-depth immunological phenotyping See also Disorders of calcium metabolism Parathyroid hormone family Parathyroid hormone-related protein Preotact Footnote References Further reading External links Media related to Parathyroid hormone at Wikimedia Commons Parathyroid hormone: analyte monograph - the Association for Clinical Biochemistry and Laboratory Medicine Overview of all the structural information available in the PDB for UniProt: P01270 (Parathyroid hormone) at the PDBe-KB.

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Argentine hemorrhagic fever'?

Argentine hemorrhagic fever (AHF) or OHiggins disease, also known in Argentina as mal de los rastrojos (stubble disease) is a hemorrhagic fever and zoonotic infectious disease occurring in Argentina. It is caused by the Junín virus (an arenavirus, closely related to the Machupo virus, causative agent of Bolivian hemorrhagic fever). Its vector is the drylands vesper mouse, a rodent found in Argentina and Paraguay. Epidemiology The disease was first reported in the town of OHiggins in Buenos Aires province, Argentina in 1958, giving it one of the names by which it is known. Various theories about its nature were proposed: it was Weils disease, leptospirosis, caused by chemical pollution. It was associated with fields containing stubble after the harvest, giving it another of its names. The endemic area of AHF covers approximately 150,000 km2, compromising the provinces of Buenos Aires, Córdoba, Santa Fe and La Pampa, with an estimated risk population of 5 million. The vector, a small rodent known locally as ratón maicero ("maize mouse"; Calomys musculinus), has chronic asymptomatic infection, and spreads the virus through its saliva and urine. Infection is produced through contact of skin or mucous membranes, or through inhalation of infected particles. It is found mostly in people who reside or work in rural areas; 80% of those infected are males between 15 and 60 years of age. Clinical aspects AHF is a grave acute disease which may progress to recovery or death in 1 to 2 weeks. The incubation time of the disease is between 10 and 12 days, after which the first symptoms appear: fever, headaches, weakness, loss of appetite and will. These intensify less than a week later, forcing the infected to lie down, and producing stronger symptoms such as vascular, renal, hematological and neurological alterations. This stage lasts about 3 weeks. If untreated, the mortality of AHF reaches 15–30%. The specific treatment includes plasma of recovered patients, which, if started early, is extremely effective and reduces mortality to 1%.Ribavirin also has shown some promise in treating arenaviral diseases. The disease was first detected in the 1950s in the Junín Partido in Buenos Aires, after which its agent, the Junín virus, was named upon its identification in 1958. In the early years, about 1,000 cases per year were recorded, with a high mortality rate (more than 30%). The initial introduction of treatment serums in the 1970s reduced this lethality. Vaccine The Candid #1 vaccine for AHF was created in 1985 by Argentine virologist Dr. Julio Barrera Oro. The vaccine was manufactured by the Salk Institute in the United States, and became available in Argentina in 1990. The Junín vaccine has also shown cross-reactivity with Machupo virus and, as such, has been considered as a potential treatment for Bolivian hemorrhagic fever. Candid #1 has been applied to adult high-risk population and is 95.5% effective. Between 1991 and 2005 more than 240,000 people were vaccinated, achieving a great decrease in the numbers of reported cases (94 suspect and 19 confirmed in 2005). On 29 August 2006 the Maiztegui Institute obtained certification for the production of the vaccine in Argentina. The vaccine produced in Argentina was found to be of similar effectiveness to the US vaccine. Details of the vaccine were published in 2011, and a protocol for production of the vaccine was published in 2018. Demand for the vaccine is insufficient to be commercially appealing due to the small target population, and it is considered an orphan drug; the Argentine government committed itself to manufacture and sponsor C#1 vaccine. Weaponization Argentine hemorrhagic fever was one of three hemorrhagic fevers and one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program. The Soviet Union also conducted research and developing programs on the potential of the hemorragic fever as a biological weapon. References Notes Bibliography == External links ==

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

I'm trying to understand 'Anterograde amnesia' within a medical context. Could you shed some light on it?

In neurology, anterograde amnesia is the inability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions. Signs and symptoms People with anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia. In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch. One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below). Causes This disorder is usually acquired in one of four ways: One cause is benzodiazepine drugs such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, triazolam, clonazepam, alprazolam, diazepam, and nimetazepam; all of these are known to have powerful amnesic effects. This has also been recorded in non-benzodiazepine sedatives or "z-drugs" which act on the same set of receptors; such as zolpidem (also known as Ambien), eszopiclone (also known as Lunesta), and zopiclone (also known by brand names Imovane and Zimovane). A second cause is a traumatic brain injury in which damage is usually done to the hippocampus or surrounding cortices. It may also be caused by a PTSD, a shocking event, or an emotional disorder.Illness, though much rarer, can also cause anterograde amnesia if it causes encephalitis, which is the inflammation of brain tissue. There are several types of encephalitis: one such is herpes simplex encephalitis (HSV), which, if left untreated, can lead to neurological deterioration. How HSV gains access to the brain is unknown; the virus shows a distinct predilection for certain parts of the brain. Initially, it is present in the limbic cortices; it may then spread to the adjacent frontal and temporal lobes. Damage to specific areas can result in reduced or eliminated ability to encode new explicit memories, giving rise to anterograde amnesia. Patients with anterograde amnesia may have episodic, semantic, or both types of explicit memory impaired for events after the trauma that caused the amnesia. This suggests that memory consolidation for different types of memory takes place in different regions of the brain. Despite this, current knowledge on human memory is still insufficient to "map out" the wiring of a human brain to discover which parts of which lobe are responsible for the various episodic and semantic knowledge within a persons memory. Amnesia is seen in patients who, for the reason of preventing another more serious disorder, have parts of their brains known to be involved in memory circuits removed, the most notable of which is known as the medial temporal lobe (MTL) memory system, described below. Patients with seizures originating in the MTL may have either side or both structures removed (there is one structure per hemisphere). In addition, patients with tumors who undergo surgery will often sustain damage to these structures, as is described in a case below. Damage to any part of this system, including the hippocampus and surrounding cortices, results in amnesic syndromes. This is why after a stroke people have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus. Finally, anterograde amnesia can be the first clinical sign that Alzheimers disease develops in within the brain. Although later the complications can be much more widespread and strongly impair cognitive processes, at the initial stage of Alzheimers the changes observed can be restricted to anterograde amnesia and a mild deficit in retaining newly learnt sequences. This is explained by the fact that the disease is initiated within the medial temporal lobe and first affacts the entorhinal cortex that directly sends and receives information from the hippocampal formation. Alcohol intoxication Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brains ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy peoples long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for infrequent drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.Chronic alcoholism often leads to a thiamine (vitamin B1) deficiency in the brain, causing Korsakoffs syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernickes encephalopathy (WE). The memory impairment that is pathognomonic to Korsakoffs syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory. Pathophysiology The pathophysiology of anterograde amnesic syndromes varies with the extent of damage and the regions of the brain that were damaged. The most well-described regions indicated in this disorder are the medial temporal lobe (MTL), basal forebrain, and fornix. Beyond the details described below, the precise process of how we remember – on a micro scale – remains a mystery. Neuropsychologists and scientists are still not in total agreement over whether forgetting is due to faulty encoding, accelerated forgetting, or faulty retrieval, although a great deal of data seem to point to the encoding hypothesis. In addition, neuroscientists are also in disagreement about the length of time involved in memory consolidation. Though most researchers, including Hasselmo et al., have found the consolidation process is spread out over several hours before transitioning from a fragile to a more permanent state, others, including Brown et al., posit that memory consolidation can take months or even years in a drawn-out process of consolidation and reinforcement. Further research into the length of time of memory consolidation will shed more light on why anterograde amnesia sometimes affects some memories gained after the event(s) that caused the amnesia, but does not affect other such memories. Medial temporal lobe The MTL memory system includes the hippocampal formation (CA fields, dentate gyrus, subicular complex), perirhinal, entorhinal, and parahippocampal cortices. It is known to be important for the storage and processing of declarative memory, which allows for factual recall. It is also known to communicate with the neocortex in the establishment and maintenance of long-term memories, although its known functions are independent of long-term memory. Nondeclarative memory, on the other hand, which allows for the performance of different skills and habits, is not part of the MTL memory system. Most data point to a "division of labor" among the parts of this system, although this is still being debated and is described in detail below.In animal models, researchers have shown monkeys with damage to both the hippocampus and its adjacent cortical regions were more severely impaired in terms of anterograde amnesia than monkeys with damage localized to hippocampal structures. However, conflicting data in another primate study point to the observation that the amount of tissue damaged does not necessarily correlate with the severity of the memory loss. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic memory and semantic memory (described below).An important finding in amnesic patients with MTL damage is the impairment of memory in all sensory modalities – sound, touch, smell, taste, and sight. This reflects the fact that the MTL is a processor for all of the sensory modalities, and helps store these kind of thoughts into memory. In addition, subjects can often remember how to perform relatively simple tasks immediately (on the order of 10 seconds), but when the task becomes more difficult, even on the same time scale, subjects tend to forget. This demonstrates the difficulty of separating procedural memory tasks from declarative memory; some elements of declarative memory may be used in learning procedural tasks.MTL amnesic patients with localized damage to the hippocampus retain other perceptual abilities, such as the ability to intelligently function in society, to make conversation, to make ones bed, etc. Additionally, anterograde amnesics without combined retrograde disorders (localized damage to the MTL system) have memories prior to the traumatic event. For this reason, the MTL is not the storage place of all memories; other regions in the brain also store memories. The key is the MTL is responsible for the learning of new materials. Other memory systems A limited number of cases have been described in which patients with damage to other parts of the brain acquired anterograde amnesia. Easton and Parker observed damage to either the hippocampus or the surrounding cortices does not seem to result in severe amnesia in primate models. They suggested damage to the hippocampus and surrounding structures alone does not explain the amnesia they saw in patients, or increasing damage does not correlate with the degree of impairment. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic and semantic memory. To demonstrate their hypothesis, they used a primate model with damage to the basal forebrain. They proposed that the disruption of neurons that project from the basal forebrain to the MTL are responsible for some of the impairment in anterograde amnesia. Easton and Parker also reported MRI scans of patients with severe anterograde amnesia showed damage beyond to cortical areas around the hippocampus and amygdala (a region of brain involved in emotions) and to surrounding white matter (white matter in the brain consists of axons, long projections of neuronal cell bodies). Another case described the onset of anterograde amnesia as a result of cell death in the fornix, another structure that carries information from the hippocampus to the structures of the limbic system and the diencephalon. The patient in this case did not show any disconnection syndrome, which is unexpected since the structures involved divide the brain hemispheres (both sides of her brain were able to communicate). Instead, she showed signs of amnesia. The final diagnosis was made by MRI. This particular amnesic syndrome is difficult to diagnose and often is misdiagnosed by physicians as an acute psychiatric disorder. Reorganization of memory When there is damage to just one side of the MTL, there is opportunity for normal functioning or near-normal function for memories. Neuroplasticity describes the ability of the cortex to remap when necessary. Remapping can occur in cases like the one above and with time the patient can recover and become more skilled at memory retention. A case report describing a patient who had two lobectomies – in the first, doctors removed part of her right MTL first because of seizures originating from the region, and later her left because she developed a tumor – demonstrates this. This case is unique because it is the only one in which both sides of the MTL were removed at different times. The authors observed that the patient was able to recover some ability to learn when she had only one MTL, but observed the deterioration of function when both sides of the MTL were affected. The reorganization of brain function for epileptic patients has had limited investigation, but imaging results show that it may occur. Rehabilitation Approaches used to treat those with anterograde amnesia often use interventions which focus on compensatory techniques, such as beepers, written notes, diaries or through intensive training programs involving the active participation of the individual concerned, along with their supporting network of family and friends. In this perspective, environmental adaptation techniques are used, such as the compensatory technique education to training (exercise), organizational strategies, visual imagery and verbal labeling. In addition, other techniques are also used in rehabilitation, such as implicit tasks, speech and mnemotechnic methods. So far, it has been proven that education techniques of compensatory strategies for memory disorders are effective in individuals with minor traumatic brain injuries. In moderately or severely injured individuals, effective interventions are those appealing to external aids, such as reminders in order to facilitate particular knowledge or skill acquisition. Reality orientation techniques are also considered; their purpose is to enhance orientation using stimulation and repetition of the basic orientation information. These techniques are regularly applied in populations of patients primarily presenting with dementia and head injuries. Controversies Episodic versus semantic memory As described above, patients with anterograde amnesia have a wide range of forgetfulness. Declarative memory can be further subdivided into episodic and semantic memory. Episodic memory is the recollection of autobiographical information with a temporal and/or spatial context, whereas semantic memory involves recall of factual information with no such association (language, history, geography, etc.). In a case study of a girl who developed anterograde amnesia during childhood, it was determined that the patient ("C.L.") retained semantic memory while having an extreme impairment of episodic memory.One patient, known by the codename "Gene", was involved in a motorcycle accident that damaged significant portions of his frontal and temporal lobes, including his left hippocampus. As a result, he cannot remember any specific episode in his life, such as a train derailment near his house. However, his semantic memory is intact; he remembers that he owns a car and two motorcycles, and he can even remember the names of his classmates in a school photograph. In stark contrast, a woman whose temporal lobes were damaged in the front due to encephalitis lost her semantic memory; she lost her memory of many simple words, historical events, and other trivial information categorized under semantic memory. However, her episodic memory was left intact; she can recall episodes such as her wedding and her fathers death with great detail. Vicari et al. describe that it remains unclear whether neural circuits involved in semantic and episodic memory overlap partially or completely, and this case seems to suggest that the two systems are independent. Both of the patients hippocampal and diencephalic structures on the right and left sides were disconnected. When C.L. came to Vicari et al.s office, her chief complaint was forgetfulness involving both semantic and episodic memory. After administering a battery of neuropsychological tests, Vicari determined that C.L. performed well in tests of visual naming and sentence comprehension, visual-spatial ability, and "general semantic knowledge about the world". They also noted an improved vocabulary and general knowledge base after 18 months. C.L.s episodic memory, on the other hand, was far below expectations: She could not retain daily events, where she had gone on vacation, the names of places she had been, and other such information. However, this study and others like it are susceptible to subjectivity, since it is not always possible to clearly distinguish between episodic and semantic memory. For this reason, the topic remains controversial and debated. Familiarity and the fractionation of memory The right hippocampus is clearly necessary for familiarity in spatial tasks, whereas the left hippocampus is necessary for familiarity-based recollection in verbal tasks. Some researchers claim the hippocampus is important for the retrieval of memories, whereas adjacent cortical regions can support familiarity-based memories. These memory decisions are made based on matching already-existing memories (before the onset of pathology) to the current situation. According to Gilboa et al., patients with localized hippocampal damage can score well on a test if it is based on familiarity.Poreh et al. describe a case study of patient A.D., whose damage to the fornix rendered the hippocampus useless, but spared adjacent cortical areas – a fairly rare injury. When the patient was given a test with something with which he had some familiarity, the patient was able to score well. In general, however, A.D. had severely impaired episodic memory, but had some ability to learn semantic knowledge. Other studies show animals with similar injuries can recognize objects with which they are familiar, but, when the objects are presented in an unexpected context, they do not score well on recognition tests. Islands of memory Patients with anterograde amnesia have trouble recalling new information and new autobiographical events, but the data are less consistent in regard to the latter. Medveds and Hirst recorded the presence of islands of memory – detailed accounts – that were described by such patients. The island memories were a combination of semantic and episodic memories. The researchers recorded patients giving long narratives with a fair amount of detail that resembled memories that the patients had prior to the trauma. The appearance of islands of memory could have something to do with the functioning of adjacent cortical areas and the neocortex. In addition, the researchers suspect that the amygdala played a role in the narratives. Notable cases The most famous case reported is that of patient Henry Molaison, known as H.M., in March 1953. Molaisons chief complaint was the persistence of severe seizures and therefore had a bilateral lobectomy (both of his medial temporal lobes were removed). As a result, Molaison had bilateral damage to both the hippocampal formation and the perirhinal cortex. Molaison had average intelligence and perceptual ability and a decent vocabulary. However, he could not learn new words or remember things that had happened more than a few minutes earlier. He could remember anything from his childhood. If the memory was created from before his lobectomy, he still had the ability to retrieve it and remember. However, he was able to learn some new skills. He was the first well-documented case of severe anterograde amnesia, and was studied until his death in 2008.A similar case involved Clive Wearing, an accomplished musicologist who contracted a cold sore virus that attacked his brain, causing herpes simplex encephalitis. As a result, Wearing developed both anterograde and retrograde amnesia, so he has little memory of what happened before the virus struck him in 1985, and cannot learn new declarative knowledge after the virus struck him either. As a result of anterograde amnesia, Wearing repeatedly "wakes up" every day usually in 30-second intervals. He has a history of repeatedly recording these moments of waking up in his journal (e.g., On Sept 2, 2013, I woke up, etc. etc.) and crossing out prior entries, as if the other moments of waking up were not real. His episodic memory is nonfunctional (so he does not consciously recall having woken up 30 seconds prior). Clive is often elated to see his wife, as if he has not seen her for a while. Despite this, however, Wearing maintained his ability to play the piano and conduct choirs. This case is significant because it demonstrates declarative and procedural memory are separate. Therefore, despite anterograde amnesia preventing Wearing from learning new bits of information that can be explained in words (declarative memory), and also preventing him from storing new memories of events or episodes (also part of declarative memory), he has little trouble in retaining his musical abilities (procedural memory), though he has no conscious memory of having learned music.Another case in the literature is Eugene Pauly, known as E.P., a severely amnesic patient (owing to viral encephalitis) who was able to learn three-word sentences. He performed better on consecutive tests over a 12-week period (24 study sessions). However, when asked how confident he was about the answers, his confidence did not appear to increase. Bayley and Squire proposed his learning was similar to the process required by procedural memory tasks; E.P. could not get the answers right when one word in the three-word sentence was changed or the order of words was changed, and his ability to answer correctly, thus, became more of a "habit". Bayley and Squire claim the learning may have happened in the neocortex, and it happened without the conscious knowledge of E.P. They hypothesized the information may be acquired directly by the neocortex (to which the hippocampus projects) when there is repetition. This case illustrates the difficulty in separating procedural from declarative tasks; this adds another dimension to the complexity of anterograde amnesia. In fiction Notable examples include Lucy Whitmore in 50 First Dates, Jonathan Archer in the Star Trek: Enterprise episode "Twilight", Joseph Gordon-Levitt in The Lookout, Kaori Fujimiya in One Week Friends, Chihiro Shindou in Ef: A Fairy Tale of the Two, Christine Lucas in Before I Go to Sleep, Gus in Remember Sunday. Christopher Nolans psychological crime film Memento (2000) contains a distinguished depiction of anterograde amnesia, in that the memory-impaired protagonist Leonard Shelby is trying to identify and kill the man who raped and murdered his wife, and does so through a system of writing crucial details related to the search on his body and on the blank spaces of Polaroid photographs. Mental health experts have described Memento as one of the most accurate depictions of amnesia in film history, an accuracy that was enhanced by the films fragmented, non-linear structure that mimics the protagonists memory problems.Dory, the happy-go-lucky Regal Blue Tang from Finding Nemo (2003) and Finding Dory (2016), suffers from anterograde amnesia. While Dory forgets conversations within minutes of having them, she never quite forgets who she is, or the fact that she has short-term memory loss, and can therefore explain her bizarre behavior to those around her.Ghajini (2008), a Hindi language film of India based on Memento, in which the main protagonist Sanjay Singhania played by Amir Khan has short-term memory loss, this variant of amnesia. In the film he is behind Ghajini, the killer of his fiancée Kalpana. In the TV series Perception, an episode revolved around a crime victim with this condition. The main character Latro in Gene Wolfes novels Soldier of the Mist, and the anime characters Vash the Stampede from Trigun and Index and Tōma from A Certain Magical Index had both retrograde and anterograde amnesia. The disorder has also been portrayed in music by English the Caretaker in Theoretically Pure Anterograde Amnesia (2005).In the 1965 film 36 Hours, Rod Taylor plays Nazi Major Walter Gerber, a psychiatrist who has developed an effective method for treating German soldiers with what is now known as PTSD – and for painlessly extracting information from Allied prisoners. The technique involves convincing patients that years have passed, the war is over, and that they have anterograde amnesia, which supposedly can be cured with talk therapy. A few days before D-Day, U.S. Army Major Jeff Pike (James Garner) is drugged, kidnapped and taken to what appears to be a hospital run by American Occupation Forces, where his appearance is altered overnight. Pike knows that the invasion is aimed at Normandy, not Pas de Calais, as the Nazi high command expects. He buys Gerbers explanation of anterograde amnesia – using the double doors of a wardrobe as illustration – and speaks casually of Normandy. Salt in a papercut alerts him to the horrible truth, and the drama proceeds from there. In the 2011 light novel Danganronpa Zero, the protagonist and "Ultimate Analyst" Ryoko Otonashi has anterograde amnesia as a result of "The Tragedy", keeping note of her memories by writing into a journal at all times and using her speedreading to keep herself up to date. Seen to be her boyfriend and "Ultimate Neurologist" Yasuke Matsuda, Ryoko witnesses a murder committed by Junko Enoshima, before being mistaken for wanted murderer and Tragedy perpetrator Izuru Kamukura by the "Ultimate Bodyguard" Madarai octuplets. After teaming up with perverted "Ultimate Secret Agent" Yuto Kamishiro in an attempt to discover the perpetrator behind the Tragedy, Ryoko learns that she herself was personally involved in the event as the true Junko, the Junko she met having been her non-identical twin sister Mukuro Ikusaba (with whom she shared Matsuda as a boyfriend) attempting to trigger her memories, which Matsuda had been suppressing on Junkos own request both to clear her of suspicion in the events off the Tragedy, attempt to cure her depression, and test wiping the memories of others. Attempting to subdue Ryoko, Matsuda accidentally restores her memories of being Junko and his fatally stabbed, before wishing Junko success in her planned actions with Izuru and Mukuro: collapsing world society and launching a "killing game". In the 2016 video game Phoenix Wright: Ace Attorney – Spirit of Justice, the character Sorin Sprocket is eventually revealed to have anterograde amnesia, which he developed after unintentionally causing a car accident which killed his sister. This causes his memories to completely reset every time he wakes up from sleeping, to the day after this accident. This depiction is notable for demonstrating the relationship issues that arise between Sorin and his fiancée, Ellen Wyatt, as a result of this disorder, most noticeably with how Sorins feelings towards her to coming across as distant and cold. As the storyline continues, however, the player comes to uncover that Sorin in fact deeply loves his fiancée, and is able to maintain this love despite his disorder, but in fact feels a sense of guilt over the fact that he has to constantly remind himself of the fact that this love exists inside of him every day, due to his disorder. It is also noticeable in that it depicts how Sorin deals with his disorder, by keeping a journal where he writes down every detail of every day after his sisters death. He carries this journal around everywhere he goes as a substitution to his memories, and uses what is written in the notebook to become aware each time he wakes up of the fact that he has his condition, what the current date apparently is, and everything important that have apparently occurred on every day since he first developed the condition. The episode also deals with legal issues concerning the disorder, when it is debated during Ellen Wyatts trial as to whether Sorins journal can be considered a proper substitution to his memories for the sake of viable witness testimony. Dangers imposed by this also come into play when it is revealed that a page in Sorins journal had been altered by someone, which causes him to go into mental collapse that any of his other memories and thoughts could also have arisen from someone elses manipulation.In the episode "Pimemento" of Brooklyn Nine-Nine, Adrian Pimento develops an artificial form of anterograde amnesia after being drugged by his therapist, which is a main plot point of the episode. See also Transient global amnesia References Other sources == External links ==

You function as a medical dictionary. Offer comprehensive and accurate descriptions of medical terms, ensuring clarity and depth in your explanations.

I'm not familiar with the medical term 'Aortic rupture.' Could you provide some insights?

Aortic rupture is the rupture or breakage of the aorta, the largest artery in the body. Aortic rupture is a rare, extremely dangerous condition. The most common cause is an abdominal aortic aneurysm that has ruptured spontaneously. Aortic rupture is distinct from aortic dissection, which is a tear through the inner wall of the aorta that can block the flow of blood through the aorta to the heart or abdominal organs. An aortic rupture can be classified according to its cause into one of the following main types: Traumatic aortic rupture Aortic rupture secondary to an aortic aneurysm Signs and symptoms Symptoms Tearing pain, located in the abdomen, flank, groin, or back Loss of consciousness Signs Low blood pressure from hypovolemic shock Fast heart rate Blue discoloration of the skin Altered mental status Bruising of the flank, a sign of retroperitoneal bleeding. Death Causes The most common cause of aortic rupture is a ruptured aortic aneurysm. Other causes include trauma and iatrogenic (procedure-related) causes. Mechanism The wall of the aorta is an elastic structure which requires integrity. Rupture results from either loss of wall strength to the point at which systemic pressure is greater than wall strength, or external destruction of the wall of the aorta, by a tumor or traumatic means. The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval (between the aorta and inferior vena cava) or aortoenteric (between the aorta and intestine) fistula. Diagnosis The condition is often suspected in patients close to death with abdominal trauma or with relevant risk-factors. Diagnosis may be confirmed by ultrasound or X-ray computed tomography (CT) scan. Prevention Prevention of aortic rupture begins with screening for disease of the aorta. If indicated, treatment with EVAR or open repair of the diseased aorta can limit the risk of aortic rupture. Treatment Aortic ruptures can be repaired surgically via open aortic surgery or using endovascular therapy (EVAR), regardless of cause, just as non-ruptured aortic aneurysms are repaired. An aortic occlusion balloon can be placed to stabilize the patient and prevent further blood loss prior to the induction of anesthesia. Prognosis An aortic rupture is a catastrophic medical emergency. People rarely survive such an injury. Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room. == References ==

You function as a medical dictionary. Offer comprehensive and accurate descriptions of medical terms, ensuring clarity and depth in your explanations.

I'd like to learn more about the medical term 'Empyema.' Can you provide some details?

An empyema () is a collection or gathering of pus within a naturally existing anatomical cavity. For example, pleural empyema is empyema of the pleural cavity. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity. The term is from Greek ἐμπύημα, "abscess". Classification Empyema occurs in: the pleural cavity (pleural empyema also known as pyothorax) the thoracic cavity the uterus (pyometra) the appendix (appendicitis) the meninges (subdural empyema) the joints (septic arthritis) the gallbladder External links Shen, K. Robert; Bribriesco, Alejandro; Crabtree, Traves; Denlinger, Chad; Eby, Joshua; Eiken, Patrick; Jones, David R.; Keshavjee, Shaf; Maldonado, Fabien; Paul, Subroto; Kozower, Benjamin (February 2017). "The American Association for Thoracic Surgery consensus guidelines for the management of empyema". The Journal of Thoracic and Cardiovascular Surgery. 153 (6): e129–e146. doi:10.1016/j.jtcvs.2017.01.030. PMID 28274565.

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Please help me grasp the concept behind the medical term 'Sudden arrhythmic death syndrome.'

Sudden arrhythmic death syndrome (SADS) is a sudden unexpected death of adolescents and adults, mainly during sleep. One relatively common type is known as Brugada syndrome.The syndrome is rare in most areas around the world but occurs in populations that are culturally and genetically distinct. It was first noted in 1977 among southeast Asian Hmong refugees in the United States and Canada. The syndrome was again noted in Singapore when a retrospective survey of records showed that 230 otherwise healthy Thai foreign workers living in Singapore died suddenly of unexplained causes between 1982 and 1990. Causes A sudden death in a young person can be caused by heart disease (including cardiomyopathy, congenital heart disease, myocarditis, genetic connective tissue disorders) or conduction disease (WPW syndrome, etc.), medication-related causes or other causes. Rare diseases called ion channelopathies may play a role such as long QT syndrome (LQTS), Brugada syndrome (BrS), CPVT (catecholaminergic polymorphic ventricular tachycardia), PCCD (progressive cardiac conduction defect), early repolarization syndrome, mixed sodium channel disease, and short QT syndrome. In 20% of cases, no cause of death can be found, even after extensive examination.In young people with type 1 diabetes, unexplained deaths could be attributed to night time hypoglycemia triggering abnormal heart rhythms or cardiac autonomic neuropathy, a damage to nerves that control the function of the heart.Medical examiners have taken into account various factors, such as nutrition, toxicology, heart disease, metabolism, and genetics. Although there is no real known definite cause, extensive research showed people 18 years or older were found to have had a hypertrophic cardiomyopathy, a condition in which the heart muscle becomes oddly thickened without any obvious cause. This was the most commonly identified abnormality in sudden death of young adults. In the instances where people experience sudden death, it is most commonly found that they had had CAD (coronary artery disease) or ASCAD (atherosclerotic coronary artery disease), or any level of stress. However, studies reveal that people experienced early symptoms within the week before the terminal event such as chest pain at ~52% of patients, dyspnea at ~22%, syncope at ~7% and ~19% who experienced no symptoms. Scientists have also associated this syndrome with the gene SCN5A that is mutated and affects the function of the heart. However, all autopsies done on those who had this syndrome came back negative.In the Philippines, bangungot (or in their term, sudden adult death syndrome) is mainly caused by the Brugada syndrome. Diagnosis Diagnosis occurs post-mortem. Treatment The only proven way to prevent SADS is with an implantable cardioverter-defibrillator. Oral beta-blockers such as propranolol are ineffective. Epidemiology In 1980, a reported pattern of sudden deaths was brought to the attention of the Centers for Disease Control. The first reported sudden death occurred in 1948 when there were 81 similar deaths of Filipino men in Oahu County, Hawaii. However, it did not become relevant because there was no associated pattern. This syndrome continued to become more significant as years went on. By 1981–1982, the annual rate in the United States was high with 92/100,000 among Laotians-Hmong, 82/100,000 among other Laotian ethnic groups, and 59/100,000 among Cambodians.In a 2008 study it was found that over half of SADS deaths could be attributed to inherited heart disease: unexplained premature sudden deaths in family, long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy and others.A national SADS study in England, funded by the British Heart Foundation, reported results in a 2007 journal article published in Health. The study surveyed 117 coroners jurisdictions in England. Researchers found that deaths from SADS reported by these coroners occurred "predominantly in young males". There were 500 cases a year in England, which is 8 times more than was previously estimated. Families are more at risk of SADS if they have a genetic cardiac disease. The study recommended that affected families should undergo "specialised cardiological evaluation". Asia Southeast Asian immigrants, who were mostly fleeing the Vietnam War, most often had this syndrome, marking Southeast Asia as the area containing the most people with this fatal syndrome. There are other Asian populations that were affected, such as Filipinos and Chinese Filipinos, Japanese in Japan, and natives of Guam in the United States and Guam. The immigrants with this syndrome were about 33 years old and seemingly healthy, and all but one of the Laotian Hmong refugees were men. The condition appears to primarily affect young Hmong men from Laos (median age 33) and Northeastern Thailand (where the population is mainly of Laotian descent). History Laotian Hmongs were chosen for the study because they had one of the highest sudden death rates in the United States while sleeping. They were originally from Southern China and the highlands of North Vietnam, Laos, and Thailand. The location that was picked for this study was in Ban Vinai in the Loei Province, which is approximately 15 kilometers from the Lao border. This study took place between October 1982 and June 1983 as this syndrome became more of a pressing issue. Ban Vinai was the location chosen because it had 33,000 refugees in 1982, and the largest number of recorded SADS deaths. Because this syndrome was occurring most commonly in those particular men, researchers found it most beneficial and effective to study the populations they migrated from instead of studying victims and populations in the U.S. Because of local religious practices, the Hmong men in Ban Vinai did not receive autopsies. Therefore, the only results and research obtained were relating to deaths outside of the local religion or geographical area.An interview was arranged with the next of kin who lived with them, witnessed the death, or found the body. The interviews were open ended and allowed the person who was next of kin to describe what they witnessed and what preceding events they thought were relevant to the victims death. The interviewers also collected information such as illness history, the circumstances of the death, demographic background, and history of any sleep disturbances. A genealogy was then created which included all the relatives and their vital status and/or circumstances of death. Society and culture During the 1970s and 1980s, when an outbreak of this syndrome began, many Southeast Asians were not able to worship properly due to the Laotian Civil War. Hmong people believe that when they do not worship properly, do not perform religious rituals properly or forget to sacrifice, the ancestor spirits or the village spirits do not protect them, thus allowing evil spirit to reach them. These attacks induce a nightmare that leads to sleep paralysis, in which the victim is conscious and experiencing pressure on the chest. It is also common to have a REM state that is out of sequence, where there is a mix of brain states that are normally held separate. After the war, the United States government scattered the Hmong refugees across the U.S. in 53 different cities. Once these nightmare visitations began, a shaman was recommended for psychic protection from the spirits of their sleep. However, scattered across 53 different cities, these victims had no access to a shaman who could protect them. Hmong people believed that rejecting the role of becoming a shaman, they are taken into the spirit world.The study author suggested that the Hmong who died were killed by their own beliefs in the spiritual world, otherwise known as Nocturnal pressing spirit attacks. In Indonesia it is called digeuton, which translates to "pressed on" in English. In China it is called bèi guǐ yā (traditional Chinese: 被鬼壓; simplified Chinese: 被鬼压) which translates to "crushed by a ghost" in English. The Dutch call the presence a nachtmerrie, the night-mare. The "merrie" comes from the Middle Dutch mare, an incubus who "lies on peoples chests, suffocating them". This phenomenon is known among the Hmong people of Laos, who ascribe these deaths to a malign spirit, dab tsuam (pronounced "dah chua"), said to take the form of a jealous woman. Bangungot is depicted in the Philippines as a mythological creature called batibat or bangungot. This hag-like creature sits on the victims face or chest so as to immobilize and suffocate him. When this occurs, the victim is usually experiencing sleep paralysis. English names Names in other languages See also Brugada syndrome Night hag Sleep paralysis Sudden infant death syndrome Sudden unexpected death in epilepsy Sudden unexplained death in childhood Yunnan sudden death syndrome References Further reading Agence France Presse (8 April 2002). "Sleeping death syndrome terrorises young men". The Borneo Post. Center for Disease Control (23 September 1988). "Sudden Unexplained Death Syndrome Among Southeast Asian Refugees". MMWR. == External links ==

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I'm curious about the meaning of the medical term 'Discoid meniscus.' Can you give me some insights?

Discoid meniscus is a rare human anatomic variant that usually affects the lateral meniscus of the knee. Usually a person with this anomaly has no complaints; however, it may present as pain, swelling, or a snapping sound heard from the affected knee. Strong suggestive findings on magnetic resonance imaging includes a thickened meniscal body seen on more than two contiguous sagittal slices. Description The Watanabe classification of discoid lateral meniscus is: (A) Incomplete, (B) Complete, and C) Wrisberg-ligament variant Normally, the meniscus is a thin crescent-shaped piece of cartilage that lies between the weight bearing joint surfaces of the femur and the tibia. It is attached to the lining of the knee joint along its periphery and serves to absorb about a third of the impact load that the joint cartilage surface sees and also provides some degree of stabilization for the knee. There are two menisci in the knee joint, with one on the outside (away from midline) being the lateral meniscus and the inner one (towards midline) the medial meniscus. A discoid meniscus is a congenital anomaly of the knee found in 3% of the population (up to 15% in Asia). It typically affects the lateral meniscus and may be found bilaterally (20%). Instead of the narrow crescent shape, as seen in a normal meniscus above, a discoid meniscus is thickened, and has a fuller crescent shape. In addition, a discoid meniscus does not taper as much towards the center of the joint and is shaped like a disc. The thickness of the meniscus, its diminished vascular blood supply, and in some instances, weak capsular attachment, makes it more prone to tears compared to a normal meniscus. The anomaly in itself is asymptomatic; however, a tear of the meniscus can result in pain, swelling, and snapping in the affected knee. The orthopedic classification of discoid menisci includes: complete, incomplete or Wrisberg-ligament types as depicted here. Coverage of the lateral tibial plateau determines the designation of complete or incomplete. The Wrisberg-ligament type has an abnormal posterior attachment by attaching to part of the posterior cruciate ligament. Symptoms Symptom is usually pain in the knee. And when the knee is bent or stretched it makes the sound of bouncing bones. Diagnosis The transverse diameter of a normal meniscus is approximately 10 to 11 mm; therefore a normal meniscus body will be visible on only 2 slices of a MR with 4-5-mm sagittal slices. A discoid meniscus should be considered if more than two contiguous body segments are present. However, this method may lead to a false negative when evaluating people with the Wrisberg variant of discoid meniscus since it maintains a narrow crescent shape. Coronal and radial images of the meniscus are useful to demonstrate the extension of the aberrant meniscus into the joint as seen here. On coronal images, it is diagnosed when the horizontal measurement between the free margin and the periphery of the body is more than 1.4 cm. Rarely, X-ray may show lateral joint space widening, squaring of the lateral condyle, cupping of the lateral tibial plateau and hypoplasia of the lateral tibial spine that suggest discoid meniscus. Treatment/Management In a patient complaining of acute onset knee pain, an X-ray study would be done to rule out any bony pathology such as a fracture. Since it is difficult to diagnose meniscal anomalies with X-ray, an MRI would be necessary to visualize the discoid meniscus. If the patient is asymptomatic and does not complain of significant locking sensation in the knee or pain, treatment is conservative and consists of stretching and strengthening exercises for the quadriceps and hamstring muscles. “In cases where there is significant disability, surgical excision may be needed. When the discoid meniscus is severely damaged, total excision of the meniscus may be necessary. In most cases where the meniscus is still generally intact, a partial excision to preserve the cushioning function may be sufficient.” See also Knee pain Knee osteoarthritis Meniscal cyst References External links Discoid Meniscus in eMedicine

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Could you provide a brief overview of 'Cleidocranial dysostosis' in a medical context?

Cleidocranial dysostosis (CCD), also called cleidocranial dysplasia, is a birth defect that mostly affects the bones and teeth. The collarbones are typically either poorly developed or absent, which allows the shoulders to be brought close together. The front of the skull often does not close until later, and those affected are often shorter than average. Other symptoms may include a prominent forehead, wide set eyes, abnormal teeth, and a flat nose. Symptoms vary among people; however, intelligence is typically unaffected.The condition is either inherited from a persons parents or occurs as a new mutation. It is inherited in an autosomal dominant manner. It is due to a defect in the RUNX2 gene which is involved in bone formation. Diagnosis is suspected based on symptoms and X-rays with confirmation by genetic testing. Other conditions that can produce similar symptoms include mandibuloacral dysplasia, pyknodysostosis, osteogenesis imperfecta, and Hajdu-Cheney syndrome.Treatment includes supportive measures such as a device to protect the skull and dental care. Surgery may be performed to fix certain bone abnormalities. Life expectancy is generally normal.It affects about one per million people. Males and females are equally commonly affected. Modern descriptions of the condition date to at least 1896. The term is from cleido meaning collarbone, cranial from the Greek κρανιὀς meaning skull, and dysostosis meaning formation of abnormal bone. Signs and symptoms Cleidocranial dysostosis is a general skeletal condition so named from the collarbone (cleido-) and cranium deformities which people with it often have. People with the condition usually present with a painless swelling in the area of the clavicles at 2–3 years of age. Common features are: Clavicles (collarbones) can be partly missing leaving only the medial part of the bone. In 10% of cases, they are completely missing. If the collarbones are completely missing or reduced to small vestiges, this allows hypermobility of the shoulders including ability to touch the shoulders together in front of the chest. The defect is bilateral 80% of the time. Partial collarbones may cause nerve damage symptoms and therefore have to be removed by surgery. The mandible is prognathic due to hypoplasia of maxilla (micrognathism) and other facial bones. A soft spot or larger soft area in the top of the head where the fontanelle failed to close, or the fontanelle closes late. Bones and joints are underdeveloped. People are shorter and their frames are smaller than their siblings who do not have the condition. The permanent teeth include supernumerary teeth. Unless these supernumeraries are removed they will crowd the adult teeth in what already may be an underdeveloped jaw. If so, the supernumeraries will probably need to be removed to make space for the adult teeth. Up to 13 supernumerary teeth have been observed. Teeth may also be displaced. Cementum formation may be deficient. Failure of eruption of permanent teeth. Bossing (bulging) of the forehead. Open skull sutures, large fontanelles. Hypertelorism. Delayed ossification of bones forming symphysis pubis, producing a widened symphysis. Coxa vara can occur, limiting abduction and causing Trendelenburg gait. Short middle fifth phalanges, sometimes causing short and wide fingers. Vertebral abnormalities. On rare occasions, brachial plexus irritation can occur. Scoliosis, spina bifida and syringomyelia have also been described.Other features are: parietal bossing, basilar invagination (atlantoaxial impaction), persistent metopic suture, abnormal ear structures with hearing loss, supernumerary ribs, hemivertebrae with spondylosis, small and high scapulae, hypoplasia of illiac bones, absence of the pubic bone, short / absent fibular bones, short / absent radial bones, hypoplastic terminal phalanges. Genetics CCD is usually autosomal dominant, but in some cases its cause is not known. The main mechanism is thought to involve haploinsufficiency caused by mutations in CBFA1 (also known as Runx2), a gene located on the short arm of chromosome 6 (6p21), which encodes a transcription factor required for the differentiation of stem cells into osteoblasts. This results in delayed ossification of midline structures of the body and ensuing defects in membranous and endochondral bone formation. Diagnosis Different features of the dysostosis are significant. Radiological imaging helps confirm the diagnosis. During gestation (pregnancy), clavicular size can be calculated using available nomograms. Wormian bones can sometimes be observed in the skull.Diagnosis of CCD spectrum disorder is established in an individual with typical clinical and radiographic findings and/or by the identification of a heterozygous pathogenic variant in RUNX2 (CBFA1). Treatment Around 5 years of age, surgical correction may be necessary to prevent any worsening of the deformity. If the mother has dysplasia, caesarian delivery may be necessary. Craniofacial surgery may be necessary to correct skull defects. Coxa vara is treated by corrective femoral osteotomies. If there is brachial plexus irritation with pain and numbness, excision of the clavicular fragments can be performed to decompress it. In case of open fontanelle, appropriate headgear may be advised by the orthopedist for protection from injury. Prognosis Several studies have reported that life expectancy appears to be normal for people with CCD. Epidemiology Cleidocranial dysostosis affects about one per million people. Notable cases In 1987, a young girl named Jessica McClure fell down a narrow well pipe in her familys Texas property. Ron Short, a roofing contractor who was born without collarbones because of cleidocranial dysostosis and thus could collapse his shoulders to work in cramped corners, arrived at the site and offered to go down the shaft. The rescuers did not end up using him, though McClure was successfully recovered from the well. Actor Gaten Matarazzo was born with cleidocranial dysplasia, which is incorporated into his character Dustin Hendersons storyline on Stranger Things.Sibling actress-singers Milly and Abby Shapiro were born with cleidocranial dysplasia, a trait they share with their mother. References External links Cleidocranial dysostosis at Curlie

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I'm not familiar with the medical term 'Teduglutide.' Could you provide some insights?

Teduglutide (brand names Gattex in the US and Revestive in Europe) is a 33-membered polypeptide and glucagon-like peptide-2 (GLP-2) analog that is used for the treatment of short bowel syndrome. It works by promoting mucosal growth and possibly restoring gastric emptying and secretion. In Europe it has been granted orphan drug status and is marketed under the brand Revestive by Nycomed. It was approved by the United States under the name Gattex on 21 December 2012, where it was given status as an orphan drug. Medical uses Up to a certain point, the gut can adapt to partial resections that result in short bowel syndrome. Still, parenteral substitution of water, minerals and vitamins (depending on which part of the gut has been removed) is often necessary. Teduglutide may reduce or shorten the necessity of such infusions by improving the intestinal mucosa and possibly by other mechanisms. Adverse effects Common adverse effects in clinical studies included abdominal discomfort (49% of patients), respiratory infections (28%), nausea (27%) and vomiting (14%), local reactions at the injection site (21%), and headache (17%). Chemistry and mechanism of action Teduglutide differs from natural GLP-2 by a single amino acid: an alanine is replaced with a glycine. This blocks breaking down of the molecule by dipeptidyl peptidase and increases its half-life from seven minutes (GLP-2) to about two hours, while retaining its biological actions. These include maintenance of the intestinal mucosa, increasing intestinal blood flow, reducing gastrointestinal motility and secretion of gastric acid. == References ==

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I've come across the term 'Remifentanil' in a medical context, but I'm not sure what it means. Can you clarify?

Remifentanil is a potent, short-acting synthetic opioid analgesic drug. It is given to patients during surgery to relieve pain and as an adjunct to an anaesthetic. Remifentanil is used for sedation as well as combined with other medications for use in general anesthesia. The use of remifentanil has made possible the use of high-dose opioid and low-dose hypnotic anesthesia, due to synergism between remifentanil and various hypnotic drugs and volatile anesthetics. Clinical use Remifentanil is used as an opioid analgesic that has a rapid onset and rapid recovery time. It has been used effectively during craniotomies, spinal surgery, cardiac surgery, and gastric bypass surgery. While opiates function similarly, with respect to analgesia, the pharmacokinetics of remifentanil allows for quicker post-operative recovery. Administration It is administered in the form remifentanil hydrochloride and in adults is given as an intravenous infusion in doses ranging from 0.1 microgram per kilogram per minute to 0.5 (µg/kg)/min. Children may require higher infusion rates (up to 1.0 (µg/kg)/min). The clinically useful infusion rates are 0.025–0.1 (µg/kg)/min for sedation (rates adjusted to age of patient, severity of their illness and invasiveness of surgical procedure). Small amounts of other sedative medications are usually co-administered with remifentanil to produce sedation. Clinically useful infusion rates in general anesthesia vary but are usually 0.1–1 (µg/kg)/min.Remifentanil can be administered as part of an anesthesia technique called TIVA (total intravenous anesthesia) using computer controlled infusion pumps in a process called target controlled infusion (TCI). A target plasma concentration is entered as ng/ml into the pump, which calculates its infusion rate according to patient factors like age and weight. Induction levels of 40 ng/ml are commonly used, but it generally varies between 3–8 ng/ml. For certain surgical procedures that produce particularly strong stimuli a level of up to 15 ng/ml might be needed. The relatively short context-sensitive half-life of remifentanil allows the desired blood plasma level to be achieved quickly, and also for the same reason, recovery occurs quickly. This allows remifentanil to be used in unique circumstances such as cesarean section.Remifentanils short context-sensitive half-life makes it ideal for intense pain of short duration. As such, it has been used for analgesia in labor successfully; however, it is not as effective as epidural analgesia.In combination with propofol, remifentanil is used for anesthesia of patients undergoing electroconvulsive therapy. Metabolism Remifentanil is considered a metabolic soft drug, one that is rapidly metabolized to an inactive form. Unlike other synthetic opioids which are hepatically metabolized, remifentanil has an ester linkage which undergoes rapid hydrolysis by non-specific tissue and plasma esterases. This means that accumulation does not occur with remifentanil and its context-sensitive half-life remains at 4 minutes after a 4-hour infusion. Remifentanil is metabolized to a compound (remifentanil acid) which has 1/4600th the potency of the parent compound.Due to its quick metabolism and short effects, remifentanil has opened up new possibilities in anesthesia. When remifentanil is used together with a hypnotic (i.e. one that produces sleep) it can be used in relative high doses. This is because remifentanil will be rapidly eliminated from the blood plasma on termination of the remifentanil infusion, hence the effects of the drug will quickly dissipate even after very long infusions. Owing to synergism between remifentanil and hypnotic drugs (such as propofol) the dose of the hypnotic can be substantially reduced. This leads often to more hemodynamic stability during surgery and a quicker post-operative recovery time. Side-effects Remifentanil is a specific μ-receptor agonist. Hence, it causes a reduction in sympathetic nervous system tone, respiratory depression and analgesia. The drugs effects include a dose-dependent decrease in heart rate and arterial pressure and respiratory rate and tidal volume. Muscle rigidity is sometimes noted. The most common side effects reported by patients receiving this medication are a sense of extreme "dizziness" (often short lived, a common side effect of other fast-acting synthetic phenylpiperidine narcotics such as fentanyl and alfentanil) and intense itching (pruritus), often around the face. These side effects are often controlled by either altering the administered dose (decreasing or in some cases, increasing the dose) or by administering other sedatives that allow the patient to tolerate or lose awareness of the side effect. Because pruritus is due to excessive serum histamine levels, antihistamines such as diphenhydramine (Benadryl) are often co-administered. This is done with care, however, as excessive sedation may occur. Nausea can occur as a side effect of remifentanil, however, it is usually transient in nature due to the drugs short half-life which rapidly removes it from the patients circulation once the infusion is terminated. Potency Comparing its analgesia-sedation effect in ventilated patients, remifentanil may be superior to morphine but not to fentanyl. Circumventing naltrexone Remifentanil has been used with some success to circumvent naltrexone in patients who are in need of pain management. Abuse potential Remifentanil, being a μ-receptor agonist, functions like other μ-receptor agonists, such as morphine and codeine; it can cause euphoria and has the potential for abuse. However, due to its rapid metabolism and short-acting half-life the likelihood of abuse is quite low. Nevertheless, there have been some documentations of remifentanil abuse. Development and marketing Prior to the development of remifentanil, most short-acting hypnotics and amnestics faced issues with prolonged use, where accumulation would result in unfavorable lingering effects during post-operative recovery. Remifentanil was designed to serve as a strong anesthetic with an ultra-short and predictable duration that would not have accumulation issues.Remifentanil was patented by Glaxo Wellcome Inc. and was FDA approved on July 12, 1996. Its patent ended on the 10th of September 2017. Pricing for Ultiva 1 mg vial - US$30.19 2 mg vial - US$57.20 5 mg vial - US$118.15 Regulation In Hong Kong, remifentanil is regulated under Schedule 1 of Hong Kongs Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purposes. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without prescription can be fined $10000 (HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 (HKD) fine and life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a $1,000,000 (HKD) fine and/or 7 years of jail time. Remifentanil is a Schedule II narcotic controlled substance in the United States with a DEA ACSCN of 9739 and a 2013 annual aggregate manufacturing quota of 3750 grams, unchanged from the prior year. References External links "Remifentanil". Drug Information Portal. U.S. National Library of Medicine. "Remifentanil Hydrochloride". Drug Information Portal. U.S. National Library of Medicine.

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I've encountered the term 'Tropical ataxic neuropathy' while reading about medical topics. What does it refer to exactly?

Tropical ataxic neuropathy (TAN, also known as Strachan-Scott Syndrome and prisoners of war neuropathy) is a disease or category of diseases that commonly causes disability and increases mortality. The causes of TAN are not understood; there is no generally accepted treatment, and the reported outcomes are inconsistent. The disease affects poor tropical populations; there are no good statistics on how many people are affected worldwide, but in some populations, more than a quarter of people are affected. Malnutrition may play a role. Classification and signs and symptoms TAN is one of many tropical myeloneuropathies. It was first described in Jamaica in 1897, by postmortems of 510 cases; in 1959, it was dubbed "tropical ataxic neuropathy". The diagnostic criteria were defined in 1968. TAN is defined by "bilateral optic atrophy, bilateral sensory neural deafness, predominant posterior column involvement, and pyramidal tract myelopathy, with ataxic polyneuropathy". The classification of TAN is still not settled, and researchers disagree about it.There are thought to be two neurological syndromes lumped together as TAN. One affects adolescents, appears with retrobulbar optic neuropathy and evidence of malnutrition, and improves with better nutrition. Half of these adolescents are seen to have spinal ataxia.The other affects middle-aged and elderly people. They suffer sensory polyneuropathy, including weakness and paresthesic sensations. Paresthesias include sensations of numbness, heat, cold, tightness, crawling motion, tingling, pins and needles, and a feeling of walking on cotton or pebbles. Weaknesses show as gait ataxia (lack of co-ordination). Affected people also suffer optic atrophy and sensory neural deafness, on both sides of the body. There is neurological damage to the pyramidal tract of the spinal cord. For these older patients, evidence of malnutrition is rarer, and improving nutrition does not improve symptoms.Most of those with the older-onset form have symptoms in their legs, but a third to a half also have arm symptoms. Symptoms tend to worsen during the rainy season (see monsoon, harmattan), and are often worse at night. Symptoms associated with the lower cranial nerve are rarer; most patients do not show them. These symptoms include dysarthria (difficulty articulating words), dysphagia (difficulty swallowing), shortness of breath, and dysphonia (difficulty speaking); dysphonia is more common in women, and shows as hypophonia (lack of co-ordination in the vocal cords) and an inability to shout. Treatment Nutritional improvements; supplying nutritional yeast, teaching improved cassava preparation, and ceasing cassava consumption. Outlook Unclear, with contradictory reports from different studies. Research directions A 2016 review listed twenty-one open research questions. The value of international co-operation on TAN research has also been highlighted. Epidemiology TAN has only been described as developing in Africa, South-east Asia, and the Caribbean (if Guiana be included). It does not seem to occur in temperate countries. People affected by TAN tend to be poor and live in rural areas. In some areas, more than a quarter of the population are affected. In India and Africa, more women are affected; in Africa, the elderly are most likely to suffer, and in India, people in their thirties. Historical data suggests that, in the 1960s, TAN in Africa was most common in people in their 30s and 40s.While the areas affected roughly correspond to the areas in which cassava is grown, some people in non-cassava-growing populations get TAN, and some cassava-growing populations do not get TAN. It is possible that there are several diseases being categorized as TAN.It has been estimated that 5% of surviving World War II prisoners of war held in the Far East acquired TAN; while they were held for 3.5 years or less, the TAN symptoms persisted chronically after they returned to temperate climates. Other animals The behaviour and neurology of malnourished and cassava-fed rats has been compared to that of humans with TAN. See also Konzo, a diet-based tropical neuropathy Lathyrism, a diet-based neuropathy Tropical spastic paraparesis, and infectious tropical myeloneuropathy Neglected tropical diseases Beri-beri == References ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

I've come across the term 'Cholic acid' in a medical context, but I'm not sure what it means. Can you clarify?

Cholic acid, also known as 3α,7α,12α-trihydroxy-5β-cholan-24-oic acid is a primary bile acid that is insoluble in water (soluble in alcohol and acetic acid), it is a white crystalline substance. Salts of cholic acid are called cholates. Cholic acid, along with chenodeoxycholic acid, is one of the two major bile acids produced by the liver, where it is synthesized from cholesterol. These two major bile acids are roughly equal in concentration in humans. Derivatives are made from cholyl-CoA, which exchanges its CoA with either glycine, or taurine, yielding glycocholic and taurocholic acid, respectively.Cholic acid downregulates cholesterol-7-α-hydroxylase (rate-limiting step in bile acid synthesis), and cholesterol does the opposite. This is why chenodeoxycholic acid, and not cholic acid, can be used to treat gallstones (because decreasing bile acid synthesis would supersaturate the stones even more).Cholic acid and chenodeoxycholic acid are the most important human bile acids. Other species may synthesize different bile acids as their predominant primary bile acids. Medical uses Cholic acid, sold under the brand name Cholbam, is approved for use in the United States and is indicated as a treatment for children and adults with bile acid synthesis disorders due to single enzyme defects, and for peroxisomal disorders (such as Zellweger syndrome).It was approved for use in the European Union in September 2013, and is sold under the brand name Orphacol. It is indicated for the treatment of inborn errors in primary bile-acid synthesis due to 3β-hydroxy-Δ5-C27-steroid oxidoreductase deficiency or Δ4-3-oxosteroid-5β-reductase deficiency in infants, children and adolescents aged one month to 18 years and adults.Cholic acid FGK (Kolbam) was approved for medical use in the European Union in November 2015. It is indicated for the treatment of inborn errors of primary bile acid synthesis, in infants from one month of age for continuous lifelong treatment through adulthood, encompassing the following single enzyme defects: sterol 27-hydroxylase deficiency (presenting as cerebrotendinous xanthomatosis, CTX); 2- (or alpha-) methylacyl-CoA racemase (AMACR) deficiency; cholesterol 7 alpha-hydroxylase (CYP7A1) deficiency.The most common side effects include peripheral neuropathy (nerve damage in the hands and feet), diarrhea, nausea (feeling sick), acid reflux (stomach acid flowing up into the mouth), esophagitis (inflammation of the food pipe), jaundice (yellowing of the skin and eyes), skin problems (lesions) and malaise (feeling unwell). Interactive pathway map Click on genes, proteins and metabolites below to link to respective articles. References External links "Cholic acid". Drug Information Portal. U.S. National Library of Medicine.

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

What does the medical term 'Vasospasm' encompass?

Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage. Along with physical resistance, vasospasm is a main cause of ischemia. Like physical resistance, vasospasms can occur due to atherosclerosis. Vasospasm is the major cause of Prinzmetals angina. Pathophysiology Normally endothelial cells release prostacyclin and nitric oxide (NO) which induce relaxation of the smooth muscle cells, and reduce aggregation of platelets. Aggregating platelets stimulate ADP to act on endothelial cells and help them induce relaxation of the smooth muscle cells. However, aggregating platelets also stimulate thromboxane A2 and serotonin which can induce contraction of the smooth muscle cells. In general, the relaxations outweighs the contractions. In atherosclerosis, a dysfunctional endothelium is observed on examination. It does not stimulate as much prostacyclin and NO to induce relaxation on smooth muscle cells. Also there is not as much inhibition of aggregation of platelets. In this case, the greater aggregation of platelets produce ADP, serotonin, and thromboxane A2. However the serotonin and the thromboxane A2 cause more contraction of the smooth muscle cells and as a result contractions outweigh the relaxations. Complications Vasospasm can occur in a wide variety of peripheral vascular beds under poorly understood mechanisms. Prinzmetal angina, Buergers disease, contrast mediated selective renal vasospasm, hypercoagulability and cryoglobulinemia likely represent just a few of the known pieces of this puzzling phenomena. Ischemia in the heart due to prolonged coronary vasospasm can lead to angina, myocardial infarction and even death. Vasospasm in the hands and fingers due to prolonged exposure to vibration (30 – 300 Hz) and triggered by cold can lead to Hand-arm vibration syndrome in which feeling and manual dexterity are lost. Angiography In angiography, vascular access through femoral and axillary arteries are preferred because they are less prone to vasospasm. Meanwhile, brachial artery is more prone to vasospasm during instrumental access. Hypothermia Rewarming In a case study in 2000, following surgery for head trauma, a patient developed mild hypothermia, a typical defense mechanism the brain uses to protect itself after injury. After the hypothermia rewarming period, the patient died from increased intracranial pressure and anisocoria. A sample of the cerebrospinal fluid and autopsy results indicated cerebral vasospasm. Treatment The occurrence of vasospasm can be reduced by preventing the occurrence of atherosclerosis. This can be done in several ways, the most important being lifestyle modifications—decreasing low-density lipoprotein (LDL), quitting smoking, physical activity, and control for other risk factors including diabetes, obesity, and hypertension. Pharmacological therapies include hypolipidemic agents, thrombolytics and anticoagulants. Pharmacological options for reducing the severity and occurrence of ischemic episodes include the organic nitrates, which are rapidly metabolized to release nitric oxide in many tissues, and are classified as having either long-acting (i.e. isosorbide dinitrate) or short-acting (i.e. nitroglycerin) durations of action. These drugs work by increasing nitric oxide levels in the blood and inducing coronary vasodilation which will allow for more coronary blood flow due to a decreased coronary resistance, allowing for increased oxygen supply to the vital organs (myocardium). The nitric oxide increase in the blood resulting from these drugs also causes dilation of systemic veins which in turn causes a reduction in venous return, ventricular work load and ventricular radius. All of these reductions contribute to the decrease in ventricular wall stress which is significant because this causes the demand of oxygen to decrease. In general organic nitrates decrease oxygen demand and increase oxygen supply. It is this favourable change to the body that can decrease the severity of ischemic symptoms, particularly angina. Other medications used to reduce the occurrence and severity of vasospasm and ultimately ischemia include L-type calcium channel blockers (notably nimodipine, as well as verapamil, diltiazem, nifedipine) and beta-receptor antagonists (more commonly known as beta blockers or β-blockers) such as propranolol. L-type calcium channel blockers can induce dilation of the coronary arteries while also decreasing the hearts demand for oxygen by reducing contractility, heart rate, and wall stress. The reduction of these latter three factors decreases the contractile force that the myocardium must exert in order to achieve the same level of cardiac output. Beta-receptor antagonists do not cause vasodilation, but like L-type calcium channel blockers, they do reduce the hearts demand for oxygen. This reduction similarly results from a decrease in heart rate, afterload, and wall stress. Adverse effects Like most pharmacological therapeutic options, there are risks that should be considered. For these drugs in particular, vasodilation can be associated with some adverse effects which might include orthostatic hypotension, reflex tachycardia, headaches and palpitations. Tolerance may also develop over time due compensatory response of the body, as well as depletion of -SH groups of glutathione which are essential for the metabolism of the drugs to their active forms. Potential side effects: Verapamil: hypotension, bradycardia, constipation Diltiazem: hypotension, bradycardia, risk of heart block Nifedipine: hypotension Propranolol: asystole, asthma attacks Contraindications Organic nitrates should not be taken with PDE5 inhibitors (i.e. sildenafil) since both NO and PDE5 inhibitors increase cyclic GMP levels and the sum of their pharmacodynamic effects will greatly exceed the optimal therapeutic levels. What you could see upon taking both medications at the same time, as caused by the much higher induction of relaxation of smooth muscle cells, include a severe drop in blood pressure. Beta-receptor antagonists should be avoided in patients with reactive pulmonary disease to avoid asthma attacks. Also Beta-receptor antagonists should be avoided in patients with AV node dysfunction and/or patients on other medications which might cause bradycardia (i.e. calcium channel blockers). The potential for these contraindications and drug-drug interaction could lead to asystole and cardiac arrest. Certain calcium channel blocker should be avoided with some beta-receptor blockers since they may cause severe bradycardia and other potential side effects. Corrective therapy Since vasospasms can be caused by atherosclerosis and contribute to the severity of ischemia there are some surgical options which can restore circulation to these ischemic areas. Regarding coronary vasospasm, one surgical intervention, referred to as percutaneous coronary intervention or angioplasty, involves placing a stent at the site of stenosis in an artery and inflating the stent using a balloon catheter. Another surgical intervention is coronary artery bypass. See also Coronary artery vasospasm Raynauds phenomenon, a vasospastic disorder Reversible cerebral vasoconstriction syndrome References == External links ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

Can you demystify the medical term 'Ovarian disease' for me?

Ovarian diseases refer to diseases or disorders of the ovary.These can be classified as endocrine disorders or as a disorders of the reproductive system. If the egg fails to release from the follicle in the ovary an ovarian cyst may form. Small ovarian cysts are common in healthy women. Some women have more follicles than usual (polycystic ovary syndrome), which inhibits the follicles to grow normally and this will cause cycle irregularities. Various types of ovarian diseases exist. Some of the ovarian diseases or disorders include: endometriosis, ovarian cysts, ovarian epithelial cancer, ovarian germ cell tumors, ovarian low malignant potential tumors, and polycystic ovary syndrome (PCOS). Endometriosis Endometriosis is a condition in which tissues lining the uterus (endometrial stroma and gland) grows abnormally beyond the uterus that may become quite painful. In simpler terms, it means that the tissue lining the uterus develops in different parts outside of it. It can be either at ovary, fallopian tubes, or peritoneal spaces.There is no single cause of endometriosis.Symptoms: Menstrual cramps, heavy menstrual bleeding, bowel or urinary problems, nausea, vomiting, blood with stools, painful intercourse, fatigues, spotting or bleeding between periods.Treatment: Surgery at extreme situations Hormonal treatments using birth controls. Healthier lifestyle. Ovarian cysts It is common for many women to develop a cyst in their lifetime. At times, these can go unnoticed without pain or visible symptoms. A cyst may develop in either of the ovaries that are responsible for producing hormones and carrying eggs in the bodies of women. Ovarian cysts can be of various types like dermoid cysts, endometrioma cysts and the functional cyst being the most common one [1] Symptoms: Abdominal bloating or swelling. Painful bowel movement. Pelvic pain before or after the menstrual cycle. Painful intercourse. Pain in the lower back or thighs. Breast tenderness. Nausea and vomiting. Fever. Rapid breathing. Faintness or dizziness. Sharp pelvic pain.Treatment: Taking of oral contraceptives or birth control pills as prescribed by the doctor. Laparoscopy: Surgery to remove the cyst. Hysterectomy in case the cyst is cancerous. Ovarian epithelial cancer It is one of the common ovarian cancers that affect women worldwide. It develops outside the ovaries and ultimately spreads outside and can affect other organs. Causes: It may happen if there is a family medical history of breast cancer, colon cancer, rectal cancer or uterine cancer, or Lynch syndrome. If someone is under Estrogen Replacement Therapy for a long time. Smoking habits may also lead to the same. [2] Treatment: Surgery to remove the uterus. Chemotherapy. Ovarian germ cell tumors Ovarian germ cell tumors are common among teenagers and young women. It is a growth in the ovaries. [3] Causes: Though the exact causes are not known, it may happen owing to certain birth defects affecting the genitals, nervous system or the urinary tract. There may be genetic conditions affecting the sex chromosomes that result in these kind of tumors as well.Symptoms Belly swelling. Pain or pressure in the belly. Swollen abdomen. Vaginal bleeding after menopause.Treatment: Surgery to remove the tumor, or the Fallopian tubes or one or more ovaries. Hysterectomy. Chemotherapy in case the tumor is cancerous. Radiation therapy to prevent the cancerous cells from developing. Ovarian low malignant potential tumors The tumor forms in the ovaries and gradually spreads to the outside of ovary. This mostly affects younger women and also hinders the reproductive system.Causes: Causes are debatable and these may occur to both pregnant women and women who do not opt for pregnancy Symptoms: Abdominal pain or swelling. Bowel problems or constipation.Treatment: Depending on the size of the tumor, choice of pregnancy, the spreading of the tumor, age and choices, removing the affected ovary is the most common treatment. In rare situations, the tumor is taken out of the ovary. Also, hysterectomy can be an option. Polycystic ovary syndrome This is a hormonal imbalance, where androgens (also called male hormones) are elevated.The increased level of androgens may result in irregular menstrual cycle and diabetes and heart problem in the long run. It also affects the body in various ways like problem getting pregnant, sleep apnea, depression and anxiety, can enhance the risk of endometrial cancer. Symptoms: Irregular periods. Heavy bleeding during periods. Excess hair growth on face and other parts of the body like chest, back, belly. Acne. Weight gain. Darkening of skin. Headaches.Treatment: Oral contraceptives to promote regular periods Healthier lifestyle.Other conditions include: Ovarian cancer Luteoma Hypogonadism Hyperthecosis References == External links ==

You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

I'd like to learn more about the medical term 'Flagellant.' Can you provide some details?

Flagellants are practitioners of a form of mortification of the flesh by whipping their skin with various instruments of penance. Many Christian confraternities of penitents have flagellants, who beat themselves, both in the privacy of their dwellings and in public processions, in order to repent of sins and share in the Passion of Jesus.In the 14th century, a movement within Western Christianity known as Flagellantism became popular and adherents "began beating their flesh in a public penitential ritual in response to war, famine, plague and fear engendered by millenarianism." Though this movement withered away, the practices of public repentance and promoting peace were adopted by the flagellants in Christian, especially Roman Catholic, confraternities of penitents that exist to the present-day. History Flagellation (from Latin flagellare, to whip) was quite a common practice amongst the more fervently religious throughout antiquity. Christianity has formed a permanent tradition surrounding the doctrine of mortification of the flesh, ranging from self-denial, wearing hairshirts and chains, fasting and self-flagellation using the discipline. Those who practice self-flagellation claim that St. Paul’s statement in the Bible ‘I chastise my body’ refers to self-inflicted bodily scourging (1 Corinthians 9:27). There are prominent Christians who have practiced self-flagellation. Martin Luther, the Protestant Reformer, self-flagellated among other ascetic practices during his early years as an Augustinian monk (although he later condemned such practices). Likewise, the Congregationalist writer Sarah Osborn also practiced self-flagellation in order "to remind her of her continued sin, depravity, and vileness in the eyes of God". It became "quite common" for members of the Tractarian movement within the Anglican Communion to practice self-flagellation using a discipline.Historically speaking, in the 11th century, Peter Damian, a Benedictine Christian monk in the Roman Catholic tradition, taught that spirituality should manifest itself in physical discipline; he admonished those who sought to follow Christ to practice self-flagellation for the duration of the time it takes one to recite forty Psalms, increasing the number of flagellations on holy days of the liturgical calendar. For Damian, only those who shared in the sufferings of Christ could be saved. Throughout Christian history, the mortification of the flesh, wherein one denies themselves physical pleasures, has been commonly followed by members of the clergy, especially in Christian monasteries and convents; the 11th-century Dominicus Loricatus repeated the entire Psalter twenty times in one week, accompanying each psalm with a hundred lash-strokes to his back. The distinction of the Flagellants was to take this self-mortification into the cities and other public spaces as a demonstration of piety. Flagellantism Flagellantism was a 14th-century movement, consisting of penitents in the Catholic Church. It began as a Christian pilgrimage and was later condemned by the Catholic Church as heretical. The followers were noted for including public flagellation in their rituals. This was a common practice during the Black Death, or the Great Plague. Spread in the 14th century The first recorded incident was in Central Italy in Perugia, in 1259, the year after severe crop damage and famine throughout Europe. From Perugia the phenomenon seemed to spread across Northern Italy and into Austria. Other incidents are recorded in 1296, 1333-34 (the Doves), notably at the time of the Black Death (1349), and 1399. The practice peaked during the Black Death. Spontaneously Flagellant groups arose across Northern and Central Europe in 1349, including in England.Initially the Catholic Church tolerated the Flagellants and individual monks and priests joined in the early movements. By the 14th century, the Church was less tolerant and the rapid spread of the movement was alarming. Clement VI officially condemned them in a bull of October 20, 1349 and instructed Church leaders to suppress the Flagellants. This position was reinforced in 1372 by Gregory XI who associated the Flagellants with other heretical groups, notably the Beghards, and instructed inquisitors to eradicate them. They were accused of heresies including doubting the need for the sacraments, denying ordinary ecclesiastical jurisdiction and claiming to work miracles. In 1392, a sect of Flagellants and Beghards, consisting of peasants, were found throughout Swabia and Wurzburg. The papal inquisitor imposed the penance of preaching and joining a crusade against the Ottoman Turks.The Inquisition was active against any revival of the movement in the 15th century, but action against the flagellants was often taken by the local princes. In 1414, 80–90 followers of Konrad Schmid were burned in Thuringia, in Germany, even though they had recanted. Three hundred were burnt in one day in 1416, also in Thuringia. Other trials where the accused were condemned as Flagellants were recorded as late as the 1480s. The practice of flagellation within the bounds of the Catholic Church continued as an accepted form of penance. Rulers like Catherine de Medici and Frances King Henry III supported Flagellants but Henry IV banned them. Flagellant orders like Hermanos Penitentes (Spanish Penitential Brothers) also appeared in colonial Spanish America, even against the specific orders of Church authorities. In Italy The first recorded cases of mass popular flagellation occurred in Perugia, in 1259. The prime cause of the Perugia episode is unclear, but it followed an outbreak of an epidemic and chroniclers report how mania spread throughout almost all the people of the city. Thousands of citizens gathered in great processions, singing and with crosses and banners, they marched throughout the city whipping themselves. It is reported that surprising acts of charity and repentance accompanied the marchers. However, one chronicler noted that anyone who did not join in the flagellation was accused of being in league with the devil. They also killed Jews and priests who opposed them. Marvin Harris links them to the Messianic preaching of Gioacchino da Fiore. Similar processions occurred across Northern Italy, with groups up to 10,000 strong processing in Modena, Bologna, Reggio and Parma. Although certain city authorities refused the Flagellant processions entry. A similar movement arose again in 1399, again in Northern Italy in the form of the White Penitents or Bianchi movement. This rising is said to have been started by a peasant who saw a vision. The movement became known as the laudesi from their constant hymn singing. At its peak, a group of over 15,000 adherents gathered in Modena and marched to Rome, but the movement rapidly faded when one of its leaders was burned at the stake by order of Boniface IX. In Germany The German and Low Countries movement, the Brothers of the Cross, is particularly well documented - they wore white robes and marched across Germany in 33.5 day campaigns (each day referred to a year of Jesuss earthly life) of penance, only stopping in any one place for no more than a day. They established their camps in fields near towns and held their rituals twice a day. The ritual began with the reading of a letter, claimed to have been delivered by an angel and justifying the Flagellants activities. Next, the followers would fall to their knees and scourge themselves, gesturing with their free hands to indicate their sin and striking themselves rhythmically to songs, known as Geisslerlieder, until blood flowed. Sometimes the blood was soaked up in rags and treated as a holy relic. Originally members were required to receive permission to join from their spouses and to prove that they could pay for their food. However, some towns began to notice that sometimes Flagellants brought plague to towns where it had not yet surfaced. Therefore, later they were denied entry. They responded with increased physical penance. Modern flagellants Christianity Roman Catholicism Modern processions of hooded Flagellants are still a feature of various Mediterranean Christian countries, mainly in Spain, Italy and some former colonies, usually every year during Lent. They also occur in the Philippines during Holy Week. For example, in the comune of Guardia Sanframondi in Campania, Italy, such parades are organized once every seven years. In Italy, members of the Flagellant movement were called disciplinati, while laudesi never practiced flagellation, but met together in their own chapel to sing laudi (canticles) in honour of the Blessed Virgin, but which gradually assumed a dramatic form and grew into a theatrical form known as rappresentazioni sacre. A play in the Roman dialect of the 14th century, edited by Vattasso (Studi e Testi, no. 4, p. 53), explicitly bears the title lauda. Some Roman Catholics in Philippines practice flagellation as a form of devout worship, sometimes in addition to self-crucifixion. Los hermanos penitentes In English, "the penitent brothers." This is a semi-secret society of flagellants among the Hispanic Roman Catholics of Colorado and New Mexico. Other religions Unrelated practices exist in non-Christian traditions, including actual flagellation amongst some Shiites (commemorating the martyrdom of Husayn ibn Ali AS). See also Algolagnia Ashura, Tatbir Dancing mania Flagellation Monty Python and the Holy Grail, which includes a scene of monks striking themselves on the forehead repeatedly with boards while chanting the missal passage Pie Jesu. Khlysts (Imperial Russia) Penitentes (New Mexico) Self-harm The Seventh Seal Redemptive suffering La Cercha Nine Emperor Gods Festival. Also referred to as the Phuket Vegetarian Festival, it is famous for its ritualised acts of flagellation, self-wounding, and trance-like ecstasies, as well as its vegetarian food-based fasting. References Sources Aberth, John (2010). From the Brink of the Apocalypse: Confronting Famine, War, Plague and Death in the Later Middle Ages (2nd ed.). Routledge. Cohn, Norman (1970). The Pursuit of the Millennium: Revolutionary Millenarians and Mystical Anarchists of the Middle Ages. Oxford University Press. ISBN 0-19-500456-6. Lea, Henry Charles (1922). A History of the Inquisition. Vol. II. The Macmillan Company. Schmidt, Muhammad Wolfgang G A, ed. (2017). "And on this Rock I Will Build My Church". A new Edition of Schaffs "History of the Reformation 1517-1648". Disserta Verlag. External links "Flagellants" . Catholic Encyclopedia. 1913. "Flagellants" . Encyclopædia Britannica (11th ed.). 1911.

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

Can you break down the meaning of the medical term 'Dawn phenomenon' for me?

The dawn phenomenon, sometimes called the dawn effect, is an observed increase in blood sugar (glucose) levels that takes place in the early-morning, often between 2 a.m. and 8 a.m. First described by Schmidt in 1981 as an increase of blood glucose or insulin demand occurring at dawn, this naturally occurring phenomenon is frequently seen among the general population and is clinically relevant for patients with diabetes as it can affect their medical management. In contrast to Chronic Somogyi rebound, the dawn phenomenon is not associated with nocturnal hypoglycemia. Physiology Although not yet completely understood, the dawn phenomenon is thought to be caused by an exaggeration of the normal physiologic hormonal processes that occur overnight. Overnight the human body sees increased levels of several hormones, most notably growth hormone and catecholamines, that lead to increased rates of glucose production and release from the liver. These hormones also inhibit the effects of insulin, leading to an overall increase in circulating blood glucose. This effect is amplified in patients with islet β-cell dysfunction such as diabetics. Notably throughout this process glucagon levels remain unchanged and the increased levels of cortisol observed overnight do not appear to be involved. Observed hyperglycemia secondary to the dawn phenomenon is often defined as an increase in blood glucose of at least >1.1mmol/L (20mg/dL) between the lowest level at night and the highest level before breakfast; however, actual ranges may vary.The physiologic process involved in causing the dawn phenomenon has been shown to occur in most people. In non-diabetic patients there is a modest increase in insulin secretion just before dawn which compensates for the increased glucose being released from the liver to prevent hyperglycemia. However, studies have shown that diabetic patients fail to compensate for this transiently increased blood glucose release, resulting in hyperglycemia. This resulting hyperglycemia is clinically relevant in diabetic patients as its lasting effects can lead to overall poor glycemic control. In Type 1 diabetics hyperglycemia due to the dawn phenomenon can persist despite adequate insulin compensation overnight, while in Type 2 diabetics the dawn phenomenon has been shown to be resistant to treatment with both oral medications and diet modifications. An "extended" dawn phenomenon has also been observed in which the abnormal increase in blood glucose levels continues after breakfast. This prolonged duration is thought to be caused by the compounding effects of absorbing and metabolizing breakfast carbohydrates during this period. Both the dawn phenomenon and its extended period have been shown to be significantly more difficult to control when a patients HbA1c is greater than 7%. Treatment Management of the dawn phenomenon varies by patient and thus should be done with regular assistance from a patients physician. Some treatment options include, but are not limited to, dietary modifications, increased exercise before breakfast and during the evening, and oral anti-hyperglycemic medications if a patients HbA1c is > 7%. Insulin pumps can also be used to provide continuous subcutaneous infusions and are regarded as the gold standard for managing the dawn phenomenon in type 1 diabetics. See also Cortisol awakening response References External links Mayo Clinic - The dawn phenomenon: What causes it? Diabetes Self Management - Dawn Phenomenon Dawn Phenomenon (Liver Dump) Spiritual and scientific benefits of waking up before Dawn

You act as a medical communicator. Your goal is to translate medical terms into comprehensive, yet straightforward language for all readers.

I'm seeking clarification on the medical term 'Tinea corporis.' Could you explain it?

Tinea corporis is a fungal infection of the body, similar to other forms of tinea. Specifically, it is a type of dermatophytosis (or ringworm) that appears on the arms and legs, especially on glabrous skin; however, it may occur on any superficial part of the body. Signs and symptoms It may have a variety of appearances; most easily identifiable are the enlarging raised red rings with a central area of clearing (ringworm). The same appearances of ringworm may also occur on the scalp (tinea capitis), beard area (tinea barbae) or the groin (tinea cruris, known as jock itch or dhobi itch). Other classic features of tinea corporis include: Itching occurs on infected area. The edge of the rash appears elevated and is scaly to touch. Sometimes the skin surrounding the rash may be dry and flaky. Almost invariably, there will be hair loss in areas of the infection. Causes Tinea corporis is caused by a tiny fungus known as dermatophyte. These tiny organisms normally live on the superficial skin surface, and when the opportunity is right, they can induce a rash or infection.The disease can also be acquired by person-to-person transfer usually via direct skin contact with an infected individual. Animal-to-human transmission is also common. Ringworm commonly occurs on pets (dogs, cats) and the fungus can be acquired while petting or grooming an animal. Ringworm can also be acquired from other animals such as horses, pigs, ferrets and cows. The fungus can also be spread by touching inanimate objects like personal care products, bed linen, combs, athletic gear, or hair brushes contaminated by an affected person.Individuals at high risk of acquiring ringworm include those who: Live in crowded, humid conditions. Sweat excessively, as sweat can produce a humid wet environment where the pathogenic fungi can thrive. This is most common in the armpits, groin creases and skin folds of the abdomen. Participate in close contact sports like soccer, rugby, or wrestling. Wear tight, constrictive clothing with poor aeration. Have a weakened immune system (e.g., those infected with HIV or taking immunosuppressive drugs). Diagnosis Superficial scrapes of skin examined underneath a microscope may reveal the presence of a fungus. This is done by utilizing a diagnostic method called KOH test, wherein the skin scrapings are placed on a slide and immersed on a dropful of potassium hydroxide solution to dissolve the keratin on the skin scrappings thus leaving fungal elements such as hyphae, septate or yeast cells viewable. If the skin scrapings are negative and a fungus is still suspected, the scrapings are sent for culture. Because the fungus grows slowly, the culture results do take several days to become positive. Prevention Because fungi prefer warm, moist environments, preventing ringworm involves keeping skin dry and avoiding contact with infectious material. Basic prevention measures include: Washing hands after handling animals, soil, and plants. Avoiding touching characteristic lesions on other people. Wearing loose-fitting clothing. Practicing good hygiene when participating in sports that involve physical contact with other people. Treatment Most cases are treated by application of topical antifungal creams to the skin, but in extensive or difficult to treat cases, systemic treatment with oral medication may be required. The over-the-counter options include tolnaftate, as well as ketoconazole (available as Nizoral shampoo that can be applied topically). Among the available prescription drugs, the evidence is best for terbinafine and naftifine, but other agents may also work.Topical antifungals are applied to the lesion twice a day for at least 3 weeks. The lesion usually resolves within 2 weeks, but therapy should be continued for another week to ensure the fungus is completely eradicated. If there are several ringworm lesions, the lesions are extensive, complications such as secondary infection exist, or the patient is immunocompromised, oral antifungal medications can be used. Oral medications are taken once a day for 7 days and result in higher clinical cure rates. The antifungal medications most commonly used are itraconazole, terbinafine, and ketoconazole.The benefits of the use of topical steroids in addition to an antifungal is unclear. There might be a greater cure rate but no guidelines currently recommend its addition. The effect of Whitfields ointment is also unclear. Prognosis Tinea corporis is moderately contagious and can affect both humans and pets. If a person acquires it, the proper measures must be taken to prevent it from spreading. Young children in particular should be educated about the infection and preventive measures: avoid skin to skin contact with infected persons and animals, wear clothing that allows the skin to breathe, and dont share towels, clothing or combs with others. If pets are kept in the household or premises, the animal should be checked for tinea, especially if hair loss in patches is noticed or the pet is scratching excessively. The majority of people who have acquired tinea know how uncomfortable the infection can be. However, the fungus can easily be treated and prevented in individuals with a healthy immune system. Society and culture When the dermatophytic infection presents in wrestlers, with skin lesions typically found on the head, neck, and arms it is sometimes called tinea corporis gladiatorum. See also Fungal folliculitis References == External links ==

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I've come across the term 'Dehydration' in a medical context, but I'm not sure what it means. Can you clarify?

In physiology, dehydration is a lack of total body water, with an accompanying disruption of metabolic processes. It occurs when free water loss exceeds free water intake, usually due to exercise, disease, or high environmental temperature. Mild dehydration can also be caused by immersion diuresis, which may increase risk of decompression sickness in divers. Most people can tolerate a 3-4% decrease in total body water without difficulty or adverse health effects. A 5-8% decrease can cause fatigue and dizziness. Loss of over ten percent of total body water can cause physical and mental deterioration, accompanied by severe thirst. Death occurs at a loss of between fifteen and twenty-five percent of the body water. Mild dehydration is characterized by thirst and general discomfort and is usually resolved with oral rehydration. Dehydration can cause hypernatremia (high levels of sodium ions in the blood) and is distinct from hypovolemia (loss of blood volume, particularly blood plasma). Signs and symptoms The hallmarks of dehydration include thirst and neurological changes such as headaches, general discomfort, loss of appetite, decreased urine volume (unless polyuria is the cause of dehydration), confusion, unexplained tiredness, purple fingernails, and seizures. The symptoms of dehydration become increasingly severe with greater total body water loss. A body water loss of 1-2%, considered mild dehydration, is shown to impair cognitive performance. While in people over age 50, the bodys thirst sensation diminishes with age, a study found that there was no difference in fluid intake between young and old people. Many older people have symptoms of dehydration. Dehydration contributes to morbidity in the elderly population, especially during conditions that promote insensible free water losses, such as hot weather. A Cochrane review on this subject defined water-loss dehydration as "people with serum osmolality of 295 mOsm/kg or more" and found that the main symptom in the elderly (people aged over 65) was fatigue. Cause Risk factors for dehydration include but are not limited to: exerting oneself in hot and humid weather, habitation at high altitudes, endurance athletics, elderly adults, infants, children and people living with chronic illnesses.Dehydration can also come as a side effect from many different types of drugs and medications.In the elderly, blunted response to thirst or inadequate ability to access free water in the face of excess free water losses (especially hyperglycemia related) seem to be the main causes of dehydration. Excess free water or hypotonic water can leave the body in two ways – sensible loss such as osmotic diuresis, sweating, vomiting and diarrhea, and insensible water loss, occurring mainly through the skin and respiratory tract. In humans, dehydration can be caused by a wide range of diseases and states that impair water homeostasis in the body. These occur primarily through either impaired thirst/water access or sodium excess. Diagnosis Definition Dehydration occurs when water intake does not replace free water lost due to normal physiologic processes, including breathing, urination, perspiration, or other causes, including diarrhea, and vomiting. Dehydration can be life-threatening when severe and lead to seizures or respiratory arrest, and also carries the risk of osmotic cerebral edema if rehydration is overly rapid.The term "dehydration" has sometimes been used incorrectly as a proxy for the separate, related condition of hypovolemia, which specifically refers to a decrease in volume of blood plasma. The two are regulated through independent mechanisms in humans; the distinction is important in guiding treatment. Prevention For routine activities, thirst is normally an adequate guide to maintain proper hydration. Minimum water intake will vary individually depending on weight, environment, diet, and genetics. With exercise, exposure to hot environments, or a decreased thirst response, additional water may be required. In athletes in competition, drinking to thirst optimizes performance and safety, despite weight loss, and as of 2010, there was no scientific study showing that it is beneficial to stay ahead of thirst and maintain weight during exercise.In warm or humid weather, or during heavy exertion, water loss can increase markedly, because humans have a large and widely variable capacity for sweating. Whole-body sweat losses in men can exceed 2 L/h during competitive sport, with rates of 3–4 L/h observed during short-duration, high-intensity exercise in the heat. When such large amounts of water are being lost through perspiration, electrolytes, especially sodium, are also being lost.In most athletes exercising and sweating for 4–5 hours with a sweat sodium concentration of less than 50 mmol/L, the total sodium lost is less than 10% of total body stores (total stores are approximately 2,500 mmol, or 58 g for a 70-kg person). These losses appear to be well tolerated by most people. The inclusion of sodium in fluid replacement drinks has some theoretical benefits and poses little or no risk, so long as these fluids are hypotonic (since the mainstay of dehydration prevention is the replacement of free water losses). Treatment The most effective treatment for minor dehydration is widely considered to be drinking water and reducing fluid loss. Plain water restores only the volume of the blood plasma, inhibiting the thirst mechanism before solute levels can be replenished. Solid foods can contribute to fluid loss from vomiting and diarrhea. Urine concentration and frequency will return to normal as dehydration resolves.In some cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (through oral rehydration therapy, or fluid replacement by intravenous therapy). As oral rehydration is less painful, non-invasive, inexpensive, and easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypertonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells (erythrocytes).When fresh water is unavailable (e.g. at sea or in a desert), seawater or drinks with significant alcohol concentration will worsen dehydration. Urine contains a lower solute concentration than seawater; this requires the kidneys to create more urine to remove the excess salt, causing more water to be lost than was consumed from seawater. If a person is dehydrated and taken to a medical facility, IVs can also be used.For severe cases of dehydration where fainting, unconsciousness, or other severely inhibiting symptoms are present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids containing a proper balance of replacement electrolytes are given orally or intravenously with continuing assessment of electrolyte status; complete resolution is normal in all but the most extreme cases. See also Hydrational fluids Terminal dehydration Dryness (medical) Hypernatremia References Further reading External links Definition of dehydration by the U.S. National Institutes of Healths MedlinePlus medical encyclopedia

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Can you break down the meaning of the medical term 'Bamlanivimab/etesevimab' for me?

Bamlanivimab/etesevimab is a combination of two monoclonal antibodies, bamlanivimab and etesevimab, administered together via intravenous infusion as a treatment for COVID-19. Both types of antibody target the surface spike protein of SARS‑CoV‑2.Bamlanivimab and etesevimab, administered together, are authorized in the United States for the treatment of mild-to-moderate COVID-19 in people aged twelve years of age and older weighing at least 40 kilograms (88 lb) with positive results of direct SARS-CoV-2 viral testing, and who are at high risk for progression to severe COVID-19, including hospitalization or death. They are also authorized, when administered together, for use after exposure to the SARS-CoV-2 virus for post-exposure prophylaxis (PEP) for COVID-19 and are not authorized for pre-exposure prophylaxis to prevent COVID-19 before being exposed to the SARS-CoV-2 virus.In January 2022, the U.S. Food and Drug Administration (FDA) revised the authorizations for two monoclonal antibody treatments – bamlanivimab/etesevimab (administered together) and casirivimab/imdevimab – to limit their use to only when the recipients are likely to have been infected with or exposed to a variant that is susceptible to these treatments. Because data show these treatments are highly unlikely to be active against the omicron variant, which is circulating at a very high frequency throughout the United States, these treatments are not authorized for use in any U.S. states, territories, and jurisdictions at this time. Contents Etesevimab Etesevimab is a monoclonal antibody against the surface spike protein of SARS‑CoV‑2.Eli Lilly licensed etesevimab from Junshi Biosciences. Bamlanivimab Bamlanivimab is an IgG1 monoclonal antibody (mAb) directed against the spike protein of SARS‑CoV‑2. The aim is to block viral attachment and entry into human cells, thus neutralizing the virus, and help preventing and treating COVID-19. Trials The data supporting the emergency use authorization (EUA) for bamlanivimab and etesevimab are based on a randomized, double-blind, placebo-controlled clinical trial in 1,035 non-hospitalized participants with mild to moderate COVID-19 symptoms who were at high risk for progressing to severe COVID-19. Of these participants, 518 received a single infusion of bamlanivimab 2,800 milligrams and etesevimab 2,800 milligrams together, and 517 received placebo. The primary endpoint was COVID-19 related hospitalizations or death by any cause during 29 days of follow-up. Hospitalization or death occurred in 36 (7%) participants who received placebo compared to 11 (2%) participants treated with bamlanivimab 2,800 milligrams and etesevimab 2,800 milligrams administered together, a 70% reduction. All ten deaths (2%) occurred in the placebo group. Thus, all-cause death was significantly lower in the bamlanivimab 2,800-milligram and etesevimab 2,800-milligram group than the placebo group. Economics On 26 February 2021, the United States government agreed to purchase 100,000 doses of the drug for $210 million, at $2,100 per dose. Research COVID-19 In February 2021, the FDA issued an emergency use authorization (EUA) for bamlanivimab and etesevimab administered together for the treatment of mild to moderate COVID-19 in people twelve years of age or older weighing at least 40 kilograms (88 lb) who test positive for SARS‑CoV‑2 and who are at high risk for progressing to severe COVID-19. The authorized use includes treatment for those who are 65 years of age or older or who have certain chronic medical conditions. While bamlanivimab and etesevimab administered together resulted in a lower risk of resistant viruses developing during treatment compared with bamlanivimab administered alone, both treatments are available under an EUA and are expected to benefit people at high risk of disease progression. On 16 April 2021, the FDA revoked the emergency use authorization (EUA) that allowed for the investigational monoclonal antibody therapy bamlanivimab, when administered alone, to be used for the treatment of mild-to-moderate COVID-19 in adults and certain pediatric patients. The EUA was issued to Eli Lilly and Co.In February 2021, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) started rolling reviews of data on the use of the monoclonal antibodies casirivimab/imdevimab, bamlanivimab/etesevimab, and bamlanivimab for the treatment of COVID-19. In March 2021, the CHMP concluded that bamlanivimab and etesevimab can be used together to treat confirmed COVID-19 in people who do not require supplemental oxygen and who are at high risk of their COVID-19 disease becoming severe. The CHMP also looked at the use of bamlanivimab alone and concluded that, despite uncertainties around the benefits of monotherapy, it can be considered a treatment option. In October 2021, the CHMP ended the rolling review of bamlanivimab/etesevimab. References This article incorporates public domain material from the United States Department of Health and Human Services. External links "Bamlanivimab". Drug Information Portal. U.S. National Library of Medicine. "Etesevimab". Drug Information Portal. U.S. National Library of Medicine. Emergency Use Authorization (EUA) review for bamlanivimab Emergency Use Authorization (EUA) for bamlanivimab/etesevimab Frequently Asked Questions on the Emergency Use Authorization for bamlanivimab and etesevimab

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What does the medical term 'Social anxiety disorder' encompass?

Social anxiety disorder (SAD), also known as social phobia, is an anxiety disorder characterized by sentiments of fear and anxiety in social situations, causing considerable distress and impaired ability to function in at least some aspects of daily life.: 15  These fears can be triggered by perceived or actual scrutiny from others. Individuals with social anxiety disorder fear negative evaluations from other people. Physical symptoms often include excessive blushing, excess sweating, trembling, palpitations, and nausea. Stammering may be present, along with rapid speech. Panic attacks can also occur under intense fear and discomfort. Some affected individuals may use alcohol or other drugs to reduce fears and inhibitions at social events. It is common for those with social phobia to self-medicate in this fashion, especially if they are undiagnosed, untreated, or both; this can lead to alcohol use disorder, eating disorders or other kinds of substance use disorders. SAD is sometimes referred to as an illness of lost opportunities where "individuals make major life choices to accommodate their illness". According to ICD-10 guidelines, the main diagnostic criteria of social phobia are fear of being the focus of attention, or fear of behaving in a way that will be embarrassing or humiliating, avoidance and anxiety symptoms. Standardized rating scales can be used to screen for social anxiety disorder and measure the severity of anxiety. The first line of treatment for social anxiety disorder is cognitive behavioral therapy (CBT). Medications such as SSRIs are effective for social phobia, especially paroxetine. CBT is effective in treating this disorder, whether delivered individually or in a group setting. The cognitive and behavioral components seek to change thought patterns and physical reactions to anxiety-inducing situations. The attention given to social anxiety disorder has significantly increased since 1999 with the approval and marketing of drugs for its treatment. Prescribed medications include several classes of antidepressants: selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs). Other commonly used medications include beta blockers and benzodiazepines. History Literary descriptions of shyness can be traced back to the days of Hippocrates around 400 B.C. Hippocrates described someone who "through bashfulness, suspicion, and timorousness, will not be seen abroad; loves darkness as life and cannot endure the light or to sit in lightsome places; his hat still in his eyes, he will neither see, nor be seen by his good will. He dare not come in company for fear he should be misused, disgraced, overshoot himself in gesture or speeches, or be sick; he thinks every man observes him."The first mention of the psychiatric term "social phobia" (phobie des situations sociales) was made in the early 1900s. Psychologists used the term "social neurosis" to describe extremely shy patients in the 1930s. After extensive work by Joseph Wolpe on systematic desensitization, research on phobias and their treatment grew. The idea that social phobia was a separate entity from other phobias came from the British psychiatrist Isaac Marks in the 1960s. This was accepted by the American Psychiatric Association and was first officially included in the third edition of the Diagnostic and Statistical Manual of Mental Disorders. The definition of the phobia was revised in 1989 to allow comorbidity with avoidant personality disorder and introduced generalized social phobia. Social phobia had been largely ignored prior to 1985.After a call to action by psychiatrist Michael Liebowitz and clinical psychologist Richard Heimberg, there was an increase in attention to and research on the disorder. The DSM-IV gave social phobia the alternative name "social anxiety disorder". Research on the psychology and sociology of everyday social anxiety continued. Cognitive Behavioural models and therapies were developed for social anxiety disorder. In the 1990s, paroxetine became the first prescription drug in the U.S. approved to treat social anxiety disorder, with others following. Signs and symptoms The 10th version of the International Classification of Diseases (ICD-10) classifies social anxiety as a mental and behavioral disorder. Cognitive aspects In cognitive models of social anxiety disorder, those with social phobias experience dread over how they will present to others. They may feel overly self-conscious, pay high self-attention after the activity, or have high performance standards for themselves. According to the social psychology theory of self-presentation, an affected person attempts to create a well-mannered impression towards others but believes they are unable to do so. Many times, before the potentially anxiety-provoking social situation, they may deliberately review what could go wrong and how to deal with each unexpected case. After the event, they may have the perception that they performed unsatisfactorily. Consequently, they will perceive anything that may have possibly been abnormal as embarrassing. These thoughts may extend for weeks or longer. Cognitive distortions are a hallmark and are learned about in CBT (cognitive-behavioral therapy). Thoughts are often self-defeating and inaccurate. Those with social phobia tend to interpret neutral or ambiguous conversations with a negative outlook and many studies suggest that socially anxious individuals remember more negative memories than those less distressed.An example of an instance may be that of an employee presenting to their co-workers. During the presentation, the person may stutter a word, upon which they may worry that other people significantly noticed and think that their perceptions of them as a presenter have been tarnished. This cognitive thought propels further anxiety which compounds further stuttering, sweating, and, potentially, a panic attack. Behavioural aspects Social anxiety disorder is a persistent fear of one or more situations in which the person is exposed to possible scrutiny by others and fears that they may do something or act in a way that will be humiliating or embarrassing. It exceeds normal "shyness" as it leads to excessive social avoidance and substantial social or occupational impairment. Feared activities may include almost any type of social interaction, especially small groups, dating, parties, talking to strangers, restaurants, interviews, etc. Those who have social anxiety disorder fear being judged by others in society. In particular, individuals with social anxiety are nervous in the presence of people with authority and feel uncomfortable during physical examinations. People who have this disorder may behave a certain way or say something and then feel embarrassed or humiliated after. As a result, they often choose to isolate themselves from society to avoid such situations. They may also feel uncomfortable meeting people they do not know and act distant when they are with large groups of people. In some cases, they may show evidence of this disorder by avoiding eye contact, or blushing when someone is talking to them.According to psychologist B. F. Skinner, phobias are controlled by escape and avoidance behaviors. For instance, a student may leave the room when talking in front of the class (escape) and refrain from doing verbal presentations because of the previously encountered anxiety attack (avoid). Major avoidance behaviors could include an almost pathological or compulsive lying behavior to preserve self-image and avoid judgment in front of others. Minor avoidance behaviors are exposed when a person avoids eye contact and crosses his/her arms to conceal recognizable shaking. A fight-or-flight response is then triggered in such events. Physiological aspects Physiological effects, similar to those in other anxiety disorders, are present in social phobias. In adults, it may cause tears as well as excessive sweating, nausea, difficulty breathing, shaking, and palpitations as a result of the fight-or-flight response. The walk disturbance (where a person is so worried about how they walk that they may lose balance) may appear, especially when passing a group of people. Blushing is commonly exhibited by individuals with social phobia. These visible symptoms further reinforce the anxiety in the presence of others. A 2006 study found that the area of the brain called the amygdala, part of the limbic system, is hyperactive when patients are shown threatening faces or confronted with frightening situations. They found that patients with more severe social phobia showed a correlation with increased response in their amygdalae. People with SAD may avoid looking at other people, and even their surroundings, to a greater extent than their peers, possibly to decrease the risk of eye contact, which can be interpreted as a nonverbal signal of openness to social interaction. Social aspects People with SAD avoid situations that most people consider "normal". They may have a hard time understanding how others can handle these situations so easily. People with SAD avoid all or most social situations and hide from others, which can affect their personal relationships. Social phobia can completely remove people from social situations due to the irrational fear of these situations. People with SAD may be addicted to social media networks, have sleep deprivation, and feel good when they avoid human interactions. SAD can also lead to low self-esteem, negative thoughts, major depressive disorder, sensitivity to criticism, and poor social skills that dont improve. People with SAD experience anxiety in a variety of social situations, from important, meaningful encounters, to everyday trivial ones. These people may feel more nervous in job interviews, dates, interactions with authority, or at work. Comorbidity SAD shows a high degree of co-occurrence with other psychiatric disorders. In fact, a population-based study found that 66% of those with SAD had one or more additional mental health disorders. SAD often occurs alongside low self-esteem and most commonly clinical depression, perhaps due to a lack of personal relationships and long periods of isolation related to social avoidance. Clinical depression is 1.49 to 3.5 times more likely to occur in those with SAD. Research also indicates that the presence of certain social fears (e.g., avoidance of participating in small groups, avoidance of going to a party) are more likely to trigger comorbid depressive symptoms than other social fears, and thus deserve a very careful audit during clinical assessment among patients with SAD.Anxiety disorders other than SAD are also very common in patients with SAD, in particular generalized anxiety disorder. Avoidant personality disorder is likewise highly correlated with SAD, with comorbidity rates ranging from 25% to 89%.To try to reduce their anxiety and alleviate depression, people with social phobia may use alcohol or other drugs, which can lead to substance use disorders. It is estimated that one-fifth of patients with social anxiety disorder also have alcohol use disorder. However, some research suggests SAD is unrelated to, or even protective against alcohol-related problems. Those who have both alcohol use disorder and social anxiety disorder are more likely to avoid group-based treatments and to relapse compared to people who do not have this combination. Causes Research into the causes of social anxiety and social phobia is wide-ranging, encompassing multiple perspectives from neuroscience to sociology. Scientists have yet to pinpoint the exact causes. Studies suggest that genetics can play a part in combination with environmental factors. Social phobia is not caused by other mental disorders or substance use. Generally, social anxiety begins at a specific point in an individuals life. This will develop over time as the person struggles to recover. Eventually, mild social awkwardness can develop into symptoms of social anxiety or phobia. Passive social media usage may cause social anxiety in some people. Genetics It has been shown that there is a two to a threefold greater risk of having social phobia if a first-degree relative also has the disorder. This could be due to genetics and/or due to children acquiring social fears and avoidance through processes of observational learning or parental psychosocial education. Studies of identical twins brought up (via adoption) in different families have indicated that, if one twin developed social anxiety disorder, then the other was between 30 percent and 50 percent more likely than average to also develop the disorder. To some extent, this "heritability" may not be specific – for example, studies have found that if a parent has any kind of anxiety disorder or clinical depression, then a child is somewhat more likely to develop an anxiety disorder or social phobia. Studies suggest that parents of those with social anxiety disorder tend to be more socially isolated themselves (Bruch and Heimberg, 1994; Caster et al., 1999), and shyness in adoptive parents is significantly correlated with shyness in adopted children (Daniels and Plomin, 1985). Growing up with overprotective and hypercritical parents has also been associated with social anxiety disorder. Adolescents who were rated as having an insecure (anxious-ambivalent) attachment with their mother as infants were twice as likely to develop anxiety disorders by late adolescence, including social phobia.A related line of research has investigated behavioural inhibition in infants – early signs of an inhibited and introspective or fearful nature. Studies have shown that around 10–15 percent of individuals show this early temperament, which appears to be partly due to genetics. Some continue to show this trait into adolescence and adulthood and appear to be more likely to develop a social anxiety disorder. Social experiences A previous negative social experience can be a trigger to social phobia, perhaps particularly for individuals high in "interpersonal sensitivity". For around half of those diagnosed with social anxiety disorder, a specific traumatic or humiliating social event appears to be associated with the onset or worsening of the disorder; this kind of event appears to be particularly related to specific social phobia, for example, regarding public speaking (Stemberg et al., 1995). As well as direct experiences, observing or hearing about the socially negative experiences of others (e.g. a faux pas committed by someone), or verbal warnings of social problems and dangers, may also make the development of a social anxiety disorder more likely. Social anxiety disorder may be caused by the longer-term effects of not fitting in, or being bullied, rejected, or ignored. Shy adolescents or avoidant adults have emphasized unpleasant experiences with peers or childhood bullying or harassment. In one study, popularity was found to be negatively correlated with social anxiety, and children who were neglected by their peers reported higher social anxiety and fear of negative evaluation than other categories of children. Socially phobic children appear less likely to receive positive reactions from peers, and anxious or inhibited children may isolate themselves. Cultural influences Cultural factors that have been related to social anxiety disorder include a societys attitude towards shyness and avoidance, affecting the ability to form relationships or access employment or education, and shame. One study found that the effects of parenting are different depending on the culture: American children appear more likely to develop social anxiety disorder if their parents emphasize the importance of others opinions and use shame as a disciplinary strategy (Leung et al., 1994), but this association was not found for Chinese/Chinese-American children. In China, research has indicated that shy-inhibited children are more accepted than their peers and more likely to be considered for leadership and considered competent, in contrast to the findings in Western countries. Purely demographic variables may also play a role. Problems in developing social skills, or social fluency, may be a cause of some social anxiety disorder, through either inability or lack of confidence to interact socially and gain positive reactions and acceptance from others. The studies have been mixed, however, with some studies not finding significant problems in social skills while others have. What does seem clear is that the socially anxious perceive their own social skills to be low. It may be that the increasing need for sophisticated social skills in forming relationships or careers, and an emphasis on assertiveness and competitiveness, is making social anxiety problems more common, at least among the middle classes. An interpersonal or media emphasis on normal or attractive personal characteristics has also been argued to fuel perfectionism and feelings of inferiority or insecurity regarding negative evaluation from others. The need for social acceptance or social standing has been elaborated in other lines of research relating to social anxiety. Substance-induced While alcohol initially relieves social phobia, excessive alcohol misuse can worsen social phobia symptoms and cause panic disorder to develop or worsen during alcohol intoxication and especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs that have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquillisers. Benzodiazepines possess anti-anxiety properties and can be useful for the short-term treatment of severe anxiety. Like the anticonvulsants, they tend to be mild and well-tolerated, although there is a risk of habit-forming. Benzodiazepines are usually administered orally for the treatment of anxiety; however, occasionally lorazepam or diazepam may be given intravenously for the treatment of panic attacks.The World Council of Anxiety does not recommend benzodiazepines for the long-term treatment of anxiety due to a range of problems associated with long-term use including tolerance, psychomotor impairment, cognitive and memory impairments, physical dependence and a benzodiazepine withdrawal syndrome upon discontinuation of benzodiazepines. Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety, benzodiazepines have remained a mainstay of anxiolytic pharmacotherapy due to their robust efficacy, rapid onset of therapeutic effect, and generally favorable side effect profile. Treatment patterns for psychotropic drugs appear to have remained stable over the past decade, with benzodiazepines being the most commonly used medication for panic disorder.Many people who are addicted to alcohol or prescribed benzodiazepines when it is explained to them they have a choice between ongoing ill mental health or quitting and recovering from their symptoms decide on quitting alcohol or their benzodiazepines. Symptoms may temporarily worsen however, during alcohol withdrawal or benzodiazepine withdrawal. Psychological factors Research has indicated the role of core or unconditional negative beliefs (e.g. "I am inept") and conditional beliefs nearer to the surface (e.g. "If I show myself, I will be rejected"). They are thought to develop based on personality and adverse experiences and to be activated when the person feels under threat. Recent research has also highlighted that conditional beliefs may also be at play (e.g., "If people see Im anxious, theyll think that Im weak").A secondary factor is self-concealment which involves concealing the expression of ones anxiety or its underlying beliefs. One line of work has focused more specifically on the key role of self-presentational concerns. The resulting anxiety states are seen as interfering with social performance and the ability to concentrate on interaction, which in turn creates more social problems, which strengthens the negative schema. Also highlighted has been a high focus on and worry about anxiety symptoms themselves and how they might appear to others. A similar model emphasizes the development of a distorted mental representation of the self and overestimates of the likelihood and consequences of negative evaluation, and of the performance standards that others have. Such cognitive-behavioral models consider the role of negatively biased memories of the past and the processes of rumination after an event, and fearful anticipation before it. Studies have also highlighted the role of subtle avoidance and defensive factors, and shown how attempts to avoid feared negative evaluations or use of safety behaviors (Clark & Wells, 1995) can make social interaction more difficult and the anxiety worse in the long run. This work has been influential in the development of Cognitive Behavioral Therapy for social anxiety disorder, which has been shown to have efficacy. Mechanisms There are many studies investigating neural bases of social anxiety disorder. Although the exact neural mechanisms have not been found yet, there is evidence relating social anxiety disorder to imbalance in some neurochemicals and hyperactivity in some brain areas. Neurotransmitters Sociability is closely tied to dopaminergic neurotransmission. In a 2011 study, a direct relation between social status of volunteers and binding affinity of dopamine D2/3 receptors in the striatum was found. Other research shows that the binding affinity of dopamine D2 receptors in the striatum of people with social anxiety is lower than in controls. Some other research shows an abnormality in dopamine transporter density in the striatum of those with social anxiety. However, some researchers have been unable to replicate previous findings of evidence of dopamine abnormality in social anxiety disorder. Studies have shown high prevalence of social anxiety in Parkinsons disease and schizophrenia. In a recent study, social phobia was diagnosed in 50% of Parkinsons disease patients. Other researchers have found social phobia symptoms in patients treated with dopamine antagonists like haloperidol, emphasizing the role of dopamine neurotransmission in social anxiety disorder.Some evidence points to the possibility that social anxiety disorder involves reduced serotonin receptor binding. A recent study reports increased serotonin transporter binding in psychotropic medication-naive patients with generalized social anxiety disorder. Although there is little evidence of abnormality in serotonin neurotransmission, the limited efficacy of medications which affect serotonin levels may indicate the role of this pathway. Paroxetine, sertraline and fluvoxamine are three SSRIs that have been approved by the FDA to treat social anxiety disorder. Some researchers believe that SSRIs decrease the activity of the amygdala. There is also increasing focus on other candidate transmitters, e.g. norepinephrine and glutamate, which may be over-active in social anxiety disorder, and the inhibitory transmitter GABA, which may be under-active in the thalamus. Brain areas The amygdala is part of the limbic system which is related to fear cognition and emotional learning. Individuals with social anxiety disorder have been found to have a hypersensitive amygdala; for example in relation to social threat cues (e.g. perceived negative evaluation by another person), angry or hostile faces, and while waiting to give a speech. Recent research has also indicated that another area of the brain, the anterior cingulate cortex, which was already known to be involved in the experience of physical pain, also appears to be involved in the experience of social pain, for example perceiving group exclusion. Recent research also highlighted the potent role of the prefrontal cortex, especially its dorsolateral part, in the maintenance of cognitive biases involved in SAD. A 2007 meta-analysis also found that individuals with social anxiety had hyperactivation in the amygdala and insula areas which are frequently associated with fear and negative emotional processing. Diagnosis ICD-10 defines social phobia as fear of scrutiny by other people leading to avoidance of social situations. The anxiety symptoms may present as a complaint of blushing, hand tremor, nausea, or urgency of micturition. Symptoms may progress to panic attacks.Standardized rating scales such as the Social Phobia Inventory, the SPAI-B, Liebowitz Social Anxiety Scale, and the Social Interaction Anxiety Scale can be used to screen for social anxiety disorder and measure the severity of anxiety. DSM-V Diagnosis DSM-5 defines Social Anxiety Disorder as a marked, or intense, fear or anxiety of social situations in which the individual may be scrutinized by others.DSM-5 Diagnostic Criteria with Diagnostic Features: Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others. Examples include social interactions (e.g., having a conversation, meeting unfamiliar people), being observed (e.g., eating or drinking), and performing in front of others (e.g., giving a speech). Note: In children, the anxiety must occur in peer settings and not just during interactions with adults. The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (i.e., will be humiliating or embarrassing: will lead to rejection or offend others). When exposed to such social situations, the individual fears that he or she will be negatively evaluated. The individual is concerned that he or she will be judged as anxious, weak, crazy, stupid, boring, intimidating, dirty, or unlikable. The individual fears that he or she will act or appear in a certain way or show anxiety symptoms, such as blushing, trembling, sweating, stumbling over ones words, or staring, that will be negatively evaluated by others. The social situations almost always provoke fear or anxiety. Thus, an individual who becomes anxious only occasionally in the social situation(s) would not be diagnosed with social anxiety disorder. Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to speak in social situations. The social situations are avoided. Alternatively, the situations are endured with intense fear or anxiety. The fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context. The fear or anxiety is judged to be out of proportion to the actual risk of being negatively evaluated or to the consequences of such negative evaluation. Sometimes, the anxiety may not be judged to be excessive, because it is related to an actual danger (e.g., being bullied or tormented by others). However, individuals with social anxiety disorder often overestimate the negative consequences of social situations, and thus the judgment of being out of proportion is made by the clinician. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more. This duration threshold helps distinguish the disorder from transient social fears that are common, particularly among children and in the community. However, the duration criterion should be used as a general guide, with allowance for some degree of flexibility. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. The fear, anxiety, and avoidance must interfere significantly with the individuals normal routine, occupational or academic functioning, or social activities or relationships, or must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. For example, an individual who is afraid to speak in public would not receive a diagnosis of social anxiety disorder if this activity is not routinely encountered on the job or in classroom work, and if the individual is not significantly distressed about it. However, if the individual avoids, or is passed over for, the job or education he or she really wants because of social anxiety symptoms criterion is met. The fear, anxiety, or avoidance is not attributable to the physiological effects of a substance (e.g., an addictive substance, a medication) or another medical condition. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder. If another medical condition (e.g., Parkinson disease, obesity, disfigurement from burns or injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.If the fear is restricted to speaking or performing in public it is performance only social anxiety disorder. Differential diagnosis The DSM-IV criteria stated that an individual cannot receive a diagnosis of social anxiety disorder if their symptoms are better accounted for by one of the autism spectrum disorders such as autism and Asperger syndrome.Because of its close relationship and overlapping symptoms, treating people with social phobia may help understand the underlying connections to other mental disorders. Social anxiety disorder is often linked to bipolar disorder and attention deficit hyperactivity disorder (ADHD) and some believe that they share an underlying cyclothymic-anxious-sensitive disposition. The co-occurrence of ADHD and social phobia is very high, especially when SCT symptoms are present. Prevention Prevention of anxiety disorders is one focus of research. Use of CBT and related techniques may decrease the number of children with social anxiety disorder following completion of prevention programs. Treatment Psychotherapies The first-line treatment for social anxiety disorder is cognitive behavioral therapy (CBT) with medications such as selective serotonin reuptake inhibitors (SSRIs) used only in those who are not interested in therapy.: 191  Self-help based on principles of CBT is a second-line treatment.: 191 There is some emerging evidence for the use of acceptance and commitment therapy (ACT) in the treatment of social anxiety disorder. ACT is considered an offshoot of traditional CBT and emphasizes accepting unpleasant symptoms rather than fighting against them, as well as psychological flexibility – the ability to adapt to changing situational demands, to shift ones perspective, and to balance competing desires. ACT may be useful as a second line treatment for this disorder in situations where CBT is ineffective or refused.Some studies have suggested social skills training (SST) can help with social anxiety. Examples of social skills focused on during SST for social anxiety disorder include: initiating conversations, establishing friendships, interacting with members of the preferred sex, constructing a speech and assertiveness skills. However, it is not clear whether specific social skills techniques and training are required, rather than just support with general social functioning and exposure to social situations.There is some evidence that expressive therapies (e.g. painting, drawing or musical therapy) can be effective for treating social anxiety disorder in certain contexts. A 2019 study, for example, found that art therapy produced an "increase in subjective quality of life (both with large effects) and an improvement in accessibility of emotion regulation strategies" in adult women with anxiety. Both VAGA and the American Art Therapy Association run specific workshops for social anxiety disorder. Given the evidence that social anxiety disorder may predict subsequent development of other psychiatric disorders such as depression, early diagnosis and treatment is important. Social anxiety disorder remains under-recognized in primary care practice, with patients often presenting for treatment only after the onset of complications such as clinical depression or substance use disorders. Medications SSRIs Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, are the first choice of medication for generalized social phobia but a second-line treatment.: 191  Compared to older forms of medication, there is less risk of tolerability and drug dependency associated with SSRIs.Paroxetine and paroxetine CR, Sertraline, Escitalopram, Venlafaxine XR and Fluvoxamine CR (luvox CR) are all approved for SAD and are all effective for it, especially paroxetine. All SSRIs are somewhat effective for social anxiety except fluoxetine which was equivalent to placebo in all clinical trials. Paroxetine was able to change personality and significantly increase extraversion.In a 1995 double-blind, placebo-controlled trial, the SSRI paroxetine was shown to result in clinically meaningful improvement in 55% of patients with generalized social anxiety disorder, compared with 23.9% of those taking placebo. An October 2004 study yielded similar results. Patients were treated with either fluoxetine, psychotherapy, or a placebo. The first four sets saw improvement in 50.8 to 54.2 percent of the patients. Of those assigned to receive only a placebo, 31.7% achieved a rating of 1 or 2 on the Clinical Global Impression-Improvement scale. Those who sought both therapy and medication did not see a boost in improvement. In double-blind, placebo-controlled trials other SSRIs like fluvoxamine, escitalopram and sertraline showed reduction of social anxiety symptoms, including anxiety, sensitivity to rejection and hostility.Citalopram also appears to be effective.General side-effects are common during the first weeks while the body adjusts to the drug. Symptoms may include headaches, nausea, insomnia and changes in sexual behavior. Treatment safety during pregnancy has not been established. In late 2004 much media attention was given to a proposed link between SSRI use and suicidality [a term that encompasses suicidal ideation and attempts at suicide as well as suicide]. For this reason, [although evidential causality between SSRI use and actual suicide has not been demonstrated] the use of SSRIs in pediatric cases of depression is now recognized by the Food and Drug Administration as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor. Recent studies have shown no increase in rates of suicide. These tests, however, represent those diagnosed with depression, not necessarily with social anxiety disorder. In addition, studies show that more socially phobic patients treated with anti-depressant medication develop hypomania than non-phobic controls. The hypomania can be seen as the medication creating a new problem. Other drugs Other prescription drugs are also used, if other methods are not effective. Before the introduction of SSRIs, monoamine oxidase inhibitors (MAOIs) such as phenelzine were frequently used in the treatment of social anxiety. Evidence continues to indicate that MAOIs are effective in the treatment and management of social anxiety disorder and they are still used, but generally only as a last resort medication, owing to concerns about dietary restrictions, possible adverse drug interactions and a recommendation of multiple doses per day. A newer type of this medication, reversible inhibitors of monoamine oxidase subtype A (RIMAs) such as the drug moclobemide, bind reversibly to the MAO-A enzyme, greatly reducing the risk of hypertensive crisis with dietary tyramine intake. However, RIMAs have been found to be less efficacious for social anxiety disorder than irreversible MAOIs like phenelzine.Benzodiazepines are an alternative to SSRIs. These drugs recommended usage is for short-term relief, meaning a limited time frame of over a year, of severe, disabling anxiety. Although benzodiazepines are still sometimes prescribed for long-term everyday use in some countries, there is concern over the development of drug tolerance, dependency and misuse. It has been recommended that benzodiazepines be considered only for individuals who fail to respond to other medications. Benzodiazepines augment the action of GABA, the major inhibitory neurotransmitter in the brain; effects usually begin to appear within minutes or hours. In most patients, tolerance rapidly develops to the sedative effects of benzodiazepines, but not to the anxiolytic effects. Long-term use of a benzodiazepine may result in physical dependence, and abrupt discontinuation of the drug should be avoided due to high potential for withdrawal symptoms (including tremor, insomnia, and in rare cases, seizures). A gradual tapering of the dose of clonazepam (a decrease of 0.25 mg every 2 weeks), however, is well tolerated by patients with social anxiety disorder. Benzodiazepines are not recommended as monotherapy for patients who have major depression in addition to social anxiety disorder and should be avoided in patients with a history of substance use.Certain anticonvulsant drugs such as gabapentin are effective in social anxiety disorder and may be a possible treatment alternative to benzodiazepines.Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine have shown similar effectiveness to the SSRIs. In Japan, Milnacipran is used in the treatment of Taijin kyofusho, a Japanese variant of social anxiety disorder. The atypical antidepressants mirtazapine and bupropion have been studied for the treatment of social anxiety disorder, and rendered mixed results.Some people with a form of social phobia called performance phobia have been helped by beta-blockers, which are more commonly used to control high blood pressure. Taken in low doses, they control the physical manifestation of anxiety and can be taken before a public performance. A novel treatment approach has recently been developed as a result of translational research. It has been shown that a combination of acute dosing of d-cycloserine (DCS) with exposure therapy facilitates the effects of exposure therapy of social phobia. DCS is an old antibiotic medication used for treating tuberculosis and does not have any anxiolytic properties per se. However, it acts as an agonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor site, which is important for learning and memory.Kava-kava has also attracted attention as a possible treatment, although safety concerns exist. Epidemiology Social anxiety disorder is known to appear at an early age in most cases. Fifty percent of those who develop this disorder have developed it by the age of 11, and 80% have developed it by age 20. This early age of onset may lead to people with social anxiety disorder being particularly vulnerable to depressive illnesses, substance use, and other psychological conflicts.When prevalence estimates were based on the examination of psychiatric clinic samples, social anxiety disorder was thought to be a relatively rare disorder. The opposite was found to be true; social anxiety was common, but many were afraid to seek psychiatric help, leading to an underrecognition of the problem.The National Comorbidity Survey of over 8,000 American correspondents in 1994 revealed 12-month and lifetime prevalence rates of 7.9 percent and 13.3 percent, respectively; this makes it the third most prevalent psychiatric disorder after depression and alcohol use disorder, and the most common of the anxiety disorders. According to US epidemiological data from the National Institute of Mental Health, social phobia affects 15 million adult Americans in any given year. Estimates vary within 2 percent and 7 percent of the U.S. adult population.The mean onset of social phobia is 10 to 13 years. Onset after age 25 is rare and is typically preceded by panic disorder or major depression. Social anxiety disorder occurs more often in females than males. The prevalence of social phobia appears to be increasing among white, married, and well-educated individuals. As a group, those with generalized social phobia are less likely to graduate from high school and are more likely to rely on government financial assistance or have poverty-level salaries. Surveys carried out in 2002 show the youth of England, Scotland, and Wales have a prevalence rate of 0.4 percent, 1.8 percent, and 0.6 percent, respectively. In Canada, the prevalence of self-reported social anxiety for Nova Scotians older than 14 years was 4.2 percent in June 2004 with women (4.6 percent) reporting more than men (3.8 percent). In Australia, social phobia is the 8th and 5th leading disease or illness for males and females between 15 and 24 years of age as of 2003. Because of the difficulty in separating social phobia from poor social skills or shyness, some studies have a large range of prevalence. The table also shows higher prevalence in Sweden. Terminology It has also been referred to as anthropophobia, meaning "fear of humans", from Greek: άνθρωπος, ánthropos, "human" and φόβος, phóbos, "fear". Other names have included interpersonal relation phobia. A specific Japanese cultural form is known as taijin kyofusho. See also Alexithymia Agoraphobia Asociality Highly sensitive person Impostor syndrome Obsessive-compulsive disorder Phobia Scopophobia Selective mutism Social inhibition Social rejection References Further reading Belzer K. D.; McKee M. B.; Liebowitz M. R. (2005). "Social Anxiety Disorder: Current Perspectives on Diagnosis and Treatment". Primary Psychiatry. 12 (11): 40–53. Archived from the original on 2012-05-12. Retrieved 2006-06-21. Beidel, D. C., & Turner, S. M. (2007). Shy children, phobic adults: Nature and treatment of social anxiety disorders (2nd ed.) (pp. 11–46). Washington, DC US: American Psychological Association. doi:10.1037/11533-001 Berent, Jonathan, with Amy Lemley (1993). Beyond Shyness: How to Conquer Social Anxieties. New York: Simon & Schuster. ISBN 0-671-74137-3. Boyle, L.E. (2018) "The (un)habitual geographies of Social Anxiety Disorder", Social Science and Medicine, DsocOI:10.1016/j.socscimed.2018.03.002 Bruch M. A. (1989). "Familial and developmental antecedents of social phobia: Issues and findings". Clinical Psychology Review. 9: 37–47. doi:10.1016/0272-7358(89)90045-7. Burns, D. D. (1999). Feeling Good: the new mood therapy (Rev. ed.). New York: Avon. ISBN 0-380-81033-6. Crozier, W. R., & Alden, L. E. (2001). International Handbook of Social Anxiety: Concepts, Research, and Interventions Relating to the Self and Shyness. New York: John Wiley & Sons, Ltd. ISBN 0-471-49129-2. Hales, R. E., & Yudofsky, S. C. (Eds.). (2003). Social phobia. In Textbook of Clinical Psychiatry (4th ed., pp. 572–580). Washington, D.C.: American Psychiatric Publishing. Marteinsdottir I.; Svensson A.; Svedberg M.; Anderberg U.; von Knorring L. (2007). "The role of life events in social phobia". Nordic Journal of Psychiatry. 61 (3): 207–212. doi:10.1080/08039480701352546. PMID 17523033. S2CID 11620169. External links Social Anxiety (including self-help links) at Curlie Support Group Providers for Social anxiety disorder at Curlie

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

What is the significance of the term 'Whipples disease' in the medical field?

Whipples disease is a rare systemic infectious disease caused by the bacterium Tropheryma whipplei. First described by George Hoyt Whipple in 1907 and commonly considered as a gastrointestinal disorder, Whipples disease primarily causes malabsorption, but may affect any part of the human body, including the heart, brain, joints, skin, lungs and the eyes. Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable in certain individuals, and about 15% of patients do not have the standard signs and symptoms.Whipples disease is significantly more common in men, with 87% of patients diagnosed being male. When recognized and treated, Whipples disease can usually be cured with long-term antibiotic therapy, but if the disease is left undiagnosed or untreated, it can ultimately be fatal. Signs and symptoms The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory nondeforming arthritis, which may occur many years before any digestive-tract symptoms develop; they tend to involve the large joints, but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive-smelling stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipples disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.Of those affected by Whipples disease, 10–40% have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye-movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipples disease. Weakness and poor coordination of part of the body, headaches, seizures, and a number of more uncommon neurological features are present in some cases. Mechanism T. whipplei is one of the Actinomycetes, and is a distant relative of the Mycobacterium avium complex, explaining in part why Whipples disease is similar to the diseases caused by MAC bacteria. The disease is common in farmers and those exposed to soil and animals, suggesting that the infection is acquired from these sources.Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective T-lymphocyte (particularly TH1 population) function may be an important predisposing factor for the disease. In particular, circulating cells which are CD11b (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested T. whipplei bacteria. Diagnosis Common clinical signs and symptoms of Whipples disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints.Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipples disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing nonacid-fast, Gram-positive bacilli. Immunohistochemical staining for antibodies against T. whipplei has been used to detect the organism in a variety of tissues, and a polymerase chain reaction-based assay is also available, which can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipples disease, but that a negative PCR is most likely indicative of a healthy individual. Treatment Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has a relapse rate around 40%. Expert opinion as of 2007 is that Whipples disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms. Epidemiology The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries, the rate of women receiving a diagnosis of Whipples disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population. T. whipplei appears to be an environmental organism that is commonly present in the gastrointestinal tract, but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for T. whipplei, since the disease is not associated with a substantially increased risk of other infections. The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s. History Whipple described the disease in 1907 in a paper in the now-defunct Bulletin of Johns Hopkins Hospital. The patient was a 36-year-old medical missionary. Whipple referred to the disease as "intestinal lipodystrophy". It was long presumed to be an infectious disease, but the causative organism was only fully identified in 1992. In 2003, doctors from Johns Hopkins Hospital, together with the French microbiologist Didier Raoult applied novel diagnostic methods to stored tissue samples from Whipples original patient, and demonstrated T. whipplei in these tissues. See also Tropheryma whipplei Notes References External links "Whipples Disease". National Digestive Disease Information Clearinghouse NDDIC.

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I've come across the term 'Scorpion sting' in a medical context, but I'm not sure what it means. Can you clarify?

A scorpion sting is an injury caused by the stinger of a scorpion resulting in the medical condition known as scorpionism, which may vary in severity. The anatomical part of the scorpion that delivers the sting is called a "telson". In typical cases, scorpion stings usually result in pain, paresthesia, and variable swelling. In serious cases, scorpion stings may involve the envenomation of humans by toxic scorpions, which may result in extreme pain, serious illness, or even death depending on the toxicity of the venom.Most scorpion stings range in severity from minor swelling to medically significant lesions, with only a few able to cause severe allergic, neurotic or necrotic reactions. However, scorpion stings account for approximately 3,000 deaths a year worldwide. The Brazilian yellow scorpion (Tityus serrulatus) is one species known for being especially dangerous, being responsible for most scorpion sting fatalities in South America.Scorpion stings are seen all over the world but are predominantly seen in the tropical and subtropical areas. In the Western hemisphere, these areas include Mexico, northern South America and southeast Brazil. In the Eastern hemisphere, these regions include Sub-Saharan Africa, the Middle East, and the Indian subcontinent. Characteristics and side effects The byproducts of some arthropods may be used as an aphrodisiac. Some of these arthropods whose byproduct may be used as medicines can be found in North America. Across North America, the Arizona bark scorpion (Centruroides sculpturatus) has proven to be the most venomous scorpion. While stings from this species will rarely result in death, side effects can include numbness, tingling, convulsions, difficult breathing, and occasionally, paralysis. These side effects may last up to 72 hours after injection of the venom. It is also observed that penile erection may occur after being stung. The pain of a sting from the Arizona Bark Scorpion has been compared to being struck by a bolt of lightning or electrical current. These symptoms may become visible 4 to 7 minutes after envenomation. Envenomation of a human by a scorpion may affect the sympathetic or parasympathetic systems depending on the species of scorpion. Some of the more severe side effects include respiratory distress syndrome, pulmonary edema, cardiac dysfunction, impaired hemostasis, pancreatitis, and multiple organ failure. Additionally, treatment of the sting depends on the severity of the incident, which is classified as mild, moderate, or severe. This treatment is composed of three different aspects of the sting: symptomatic measures, vital functions support, and injection antivenom. Not all envenomations result in systemic complications; only a small proportion of stings have this effect on the victim. Mechanism The composition of scorpion venom consists of different compounds of varying concentrations. The compounds consist of neurotoxins, cardiotoxin, nephrotoxin, hemolytic toxic, phosphodiesterases, phospholipase, histamine, serotonin, etc. Of these different toxins, the most important and most potent one is the neurotoxin concentration. This compound has neuromuscular and neuroautonomic effects, as well as damages the surrounding local tissue. Neurotoxins work to change voltage-dependent sodium channels, resulting in prolonged neuronal and neuromuscular activity. This prolonged activity of sodium channels results in an erection. There may be nerve damage due to the stabilization of voltage-dependent sodium channels in the open conformation. This position leads to the prolonged and continuous firing of neurons in the somatic, sympathetic, and parasympathetic nervous systems. Continuous firing of neurons causes over excitation and prevents the transmission of normal nerve impulses down the axon.The venom composition of the deathstalker scorpion contains neurotoxins which are almost completely responsible for this symptom. The poison from this scorpion contain 4 components: chlorotoxin, charybdotoxin, scyllatoxin, and agitoxins. Upon injection with the venom, sacral parasympathetic nerve are stimulated causing a change in the neuronal transmission in vascular and nonvascular smooth muscles. The compound known as the vasoactive intestinal polypeptide (VIP) is the main transmitter. This polypeptide is realized from nerves found long the erectile tissue of the corpus calosum. VIP is the strongest relaxant of penile smooth muscle structure, resulting in an erection upon envenomation. This is the proposed mechanics for all scorpion of the family Buthidae, whose venom composition contains these compounds. Epidemiology Overview Scorpions are nocturnal animals that typically live in deserts, mountains, caves, and under rocks. It is when they are disturbed that they attack. Scorpions that possess the ability to inject toxic venom with their sting belong to the family Buthidae. The Middle East and North Africa are home to the deadliest scorpions, belonging to the genus Buthus, Leiurus, Androctonus, and Hottentotta. In South America, the deadliest scorpion belongs to genus Tityus. In India and Mexico, the deadliest scorpions involved in scorpionism are Mesobuthus and Centruroides, respectively. Weather, seasons, and climate Scorpions are nocturnal arachnids that have shown a seasonal pattern that is also related to climate. Specifically in Central America, scorpion attacks are mostly seen during the hot months of the year, noting that in Argentina this occurs in the months of October to April. Additionally, a rainy climate may also change the frequency of scorpion incidents. Lower levels of rainfall, specifically precipitation below 30 mm/month, can be associated with fewer scorpion stings, whereas rainfall greater than 30 mm/month shows no relationship to incident rate. This could be due to potentially disruptive effects of rainfall on scorpion habitat. Central America In Central America, most scorpion stings are mildly toxic to humans. However, Panama has reported an incidence of 52 cases per 100,000 people in 2007. Between 1998 and 2006, 28 people have died as result of scorpion stings. In Panama, the taxa of scorpions responsible for these deaths belong to the genus Tityus. This scorpion species is also found in parts of northern South America. Historically, the presence of these scorpions in Panama could be due to the closure of the Panamanian isthmus, thus allowing for the migration of the scorpions from Panama into the northern part of South America. Tityus pachyurus is among the most important scorpionist species. Envenomation by this scorpion is characterized by intense local pain, that usually does not result in tissue injury. Scorpions possess venom glands located at the distal extremity of their abdomen. There are currently 1,400 known species of scorpions and each possesses venom glands. However, of these 1,400 species, only 25 are known to be dangerous enough to humans to potentially cause death upon envenomation. Other countries in Central America are habitat to the scorpion genus Centruroides. Species in this genus are only mildly toxic to humans even though they have ion channel-active toxins in their venom. == References ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I need a basic explanation for the medical term 'Fenfluramine.'

Fenfluramine, sold under the brand name Fintepla, is a serotonergic medication used for the treatment of seizures associated with Dravet syndrome and Lennox–Gastaut syndrome. It was formerly used as an appetite suppressant in the treatment of obesity, but was discontinued for this use due to cardiovascular toxicity before being repurposed for new indications. Fenfluramine was used for weight loss both alone under the brand name Pondimin and in combination with phentermine under the brand name Fen-Phen among others.Side effects of fenfluramine in people treated for seizures include decreased appetite, somnolence, sedation, lethargy, diarrhea, constipation, abnormal echocardiogram, fatigue, malaise, asthenia, ataxia, balance disorder, gait disturbance, increased blood pressure, drooling, excessive salivation, fever, upper respiratory tract infection, vomiting, appetite loss, weight loss, falls, and status epilepticus. Fenfluramine acts as a serotonin releasing agent, agonist of the serotonin 5-HT2 receptors, and σ1 receptor positive modulator. Its mechanism of action in the treatment of seizures is unknown, but may involve increased activation of certain serotonin receptors and the σ1 receptor.Fenfluramine was developed in the early 1960s and was first introduced for medical use as an appetite suppressant in France in 1963 followed by approval in the United States in 1973. In the 1990s, fenfluramine came to be associated with cardiovascular toxicity, and because of this, was withdrawn from the United States market in 1997. Subsequently, it was repurposed for the treatment of seizures and was reintroduced in the United States and the European Union in 2020. Fenfluramine is a schedule IV controlled substance in the United States. Medical uses Seizures Fenfluramine is indicated for the treatment of seizures associated with Dravet syndrome and Lennox–Gastaut syndrome in people age two and older.Dravet syndrome is a life-threatening, rare and chronic form of epilepsy. It is often characterized by severe and unrelenting seizures despite medical treatment. Obesity Fenfluramine was formerly used as an appetite suppressant in the treatment of obesity, but was withdrawn for this use due to cardiovascular toxicity. Adverse effects The most common adverse reactions in people with seizures include decreased appetite; drowsiness, sedation and lethargy; diarrhea; constipation; abnormal echocardiogram; fatigue or lack of energy; ataxia (lack of coordination), balance disorder, gait disturbance (trouble with walking); increased blood pressure; drooling, salivary hypersecretion (saliva overproduction); pyrexia (fever); upper respiratory tract infection; vomiting; decreased weight; risk of falls; and status epilepticus.The U.S. Food and Drug Administration (FDA) fenfluramine labeling includes a boxed warning stating the drug is associated with valvular heart disease (VHD) and pulmonary arterial hypertension (PAH). Because of the risks of VHD and PAH, fenfluramine is available only through a restricted drug distribution program, under a risk evaluation and mitigation strategy (REMS). The fenfluramine REMS requires health care professionals who prescribe fenfluramine and pharmacies that dispense fenfluramine to be specially certified in the fenfluramine REMS and that patients be enrolled in the REMS. As part of the REMS requirements, prescribers and patients must adhere to the required cardiac monitoring with echocardiograms to receive fenfluramine.At higher therapeutic doses, headache, diarrhea, dizziness, dry mouth, erectile dysfunction, anxiety, insomnia, irritability, lethargy, and CNS stimulation have been reported with fenfluramine.There have been reports associating chronic fenfluramine treatment with emotional instability, cognitive deficits, depression, psychosis, exacerbation of pre-existing psychosis (schizophrenia), and sleep disturbances. It has been suggested that some of these effects may be mediated by serotonergic neurotoxicity/depletion of serotonin with chronic administration and/or activation of serotonin 5-HT2A receptors. Heart valve disease The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. One mechanism used to explain this phenomenon involves heart valve serotonin receptors, which are thought to help regulate growth. Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors, this may have led to the valvular abnormalities found in patients using fenfluramine. In particular norfenfluramine is a potent inhibitor of the re-uptake of 5-HT into nerve terminals. Fenfluramine and its active metabolite norfenfluramine affect the 5-HT2B receptors, which are plentiful in human cardiac valves. The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. Supporting this idea is the fact that this valve abnormality has also occurred in patients using other drugs that act on 5-HT2B receptors.According to a study of 5,743 former users conducted by a plaintiffs expert cardiologist, damage to the heart valve continued long after stopping the medication. Of the users tested, 20% of women, and 12% of men were affected. For all ex-users, there was a 7-fold increase of chances of needing surgery for faulty heart valves caused by the drug. Overdose In overdose, fenfluramine can cause serotonin syndrome and rapidly result in death. Pharmacology Pharmacodynamics Fenfluramine acts primarily as a serotonin releasing agent. It increases the level of serotonin, a neurotransmitter that regulates mood, appetite and other functions. Fenfluramine causes the release of serotonin by disrupting vesicular storage of the neurotransmitter, and reversing serotonin transporter function. The drug also acts as a norepinephrine releasing agent to a lesser extent, particularly via its active metabolite norfenfluramine. At high concentrations, norfenfluramine, though not fenfluramine, also acts as a dopamine releasing agent, and so fenfluramine may do this at very high doses as well. In addition to monoamine release, while fenfluramine binds only very weakly to the serotonin 5-HT2 receptors, norfenfluramine binds to and activates the serotonin 5-HT2B and 5-HT2C receptors with high affinity and the serotonin 5-HT2A receptor with moderate affinity. The result of the increased serotonergic and noradrenergic neurotransmission is a feeling of fullness and reduced appetite. The combination of fenfluramine with phentermine, a norepinephrine–dopamine releasing agent acting primarily on norepinephrine, results in a well-balanced serotonin–norepinephrine releasing agent with weaker effects of dopamine release. Fenfluramine was identified as a potent positive modulator of the σ1 receptor in 2020 and this action may be involved in its therapeutic benefits in the treatment of seizures. Pharmacokinetics The elimination half-life of fenfluramine has been reported as ranging from 13 to 30 hours. The mean elimination half-lives of its enantiomers have been found to be 19 hours for dexfenfluramine and 25 hours for levfenfluramine. Norfenfluramine, the major active metabolite of fenfluramine, has an elimination half-life that is about 1.5 to 2 times as long as that of fenfluramine, with mean values of 34 hours for dexnorfenfluramine and 50 hours for levnorfenfluramine. Chemistry Fenfluramine is a substituted amphetamine and is also known as 3-trifluoromethyl-N-ethylamphetamine. It is a racemic mixture of two enantiomers, dexfenfluramine and levofenfluramine. Some analogues of fenfluramine include norfenfluramine, benfluorex, flucetorex, and fludorex. History Fenfluramine was developed in the early 1960s and was introduced in France in 1963. Approximately 50 million Europeans were treated with fenfluramine for appetite suppression between 1963 and 1996. Fenfluramine was approved in the United States in 1973. The combination of fenfluramine and phentermine was proposed in 1984. Approximately 5 million people in the United States were given fenfluramine or dexfenfluramine with or without phentermine between 1996 and 1998.In the early 1990s, French researchers reported an association of fenfluramine with primary pulmonary hypertension and dyspnea in a small sample of patients. Fenfluramine was withdrawn from the U.S. market in 1997 after reports of heart valve disease and continued findings of pulmonary hypertension, including a condition known as cardiac fibrosis. It was subsequently withdrawn from other markets around the world. It was banned in India in 1998.Fenfluramine was an appetite suppressant which was used to treat obesity. It was used both on its own and, in combination with phentermine, as part of the anti-obesity medication Fen-Phen.In June 2020, fenfluramine was approved for medical use in the United States with an indication to treat Dravet syndrome.The effectiveness of fenfluramine for the treatment of seizures associated with Dravet syndrome was demonstrated in two clinical studies in 202 subjects between ages two and eighteen. The studies measured the change from baseline in the frequency of convulsive seizures. In both studies, subjects treated with fenfluramine had significantly greater reductions in the frequency of convulsive seizures during the trials than subjects who received placebo (inactive treatment). These reductions were seen within 3–4 weeks, and remained generally consistent over the 14- to 15-week treatment periods.The U.S. Food and Drug Administration (FDA) granted the application for fenfluramine priority review and orphan drug designations. The FDA granted approval of Fintepla to Zogenix, Inc.On 15 October 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Fintepla, intended for the treatment of seizures associated with Dravet syndrome. Fenfluramine was approved for medical use in the European Union in December 2020. Society and culture Recreational use Unlike various other amphetamine derivatives, fenfluramine is reported to be dysphoric, "unpleasantly lethargic", and non-addictive at therapeutic doses. However, it has been reported to be used recreationally at high doses ranging between 80 and 400 mg, which have been described as producing euphoria, amphetamine-like effects, sedation, and hallucinogenic effects, along with anxiety, nausea, diarrhea, and sometimes panic attacks, as well as depressive symptoms once the drug had worn off. At very high doses (e.g., 240 mg, or between 200 and 600 mg), fenfluramine induces a psychedelic state resembling that produced by lysergic acid diethylamide (LSD). Indirect (via induction of serotonin release) and/or direct activation of the 5-HT2A receptor would be expected to be responsible for the psychedelic effects of the drug at sufficient doses. References Further reading Gustafsson BI, Tømmerås K, Nordrum I, Loennechen JP, Brunsvik A, Solligård E, Fossmark R, Bakke I, Syversen U, Waldum H (March 2005). "Long-term serotonin administration induces heart valve disease in rats". Circulation. 111 (12): 1517–22. doi:10.1161/01.CIR.0000159356.42064.48. PMID 15781732. Welch, J. T.; Lim, D. S. (2007). "The Synthesis and Biological Activity of Pentafluorosulfanyl Analogs of Fluoxetine, Fenfluramine, and Norfenfluramine". Bioorganic & Medicinal Chemistry. 15 (21): 6659–6666. doi:10.1016/j.bmc.2007.08.012. PMID 17765553. External links "Fenfluramine". Drug Information Portal. U.S. National Library of Medicine. "Fenfluramine hydrochloride". Drug Information Portal. U.S. National Library of Medicine. Inchem.org - Fenfluramine hydrochloride

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

I'm trying to understand 'Frontal lobe epilepsy' within a medical context. Could you shed some light on it?

Frontal lobe epilepsy (FLE) is a neurological disorder which is a subtype of the larger group of epilepsy and then focal epilepsy is characterized by brief, recurring seizures that arise in the frontal lobes of the brain, often while the patient is sleeping. It is the second most common type of focal epilepsy after temporal lobe epilepsy (TLE), and is related to the temporal form by the fact that both forms are characterized by the occurrence of partial (focal) seizures. Partial seizures occurring in the frontal lobes can occur in one of two different forms: either “focal aware”, the old term was simple partial seizures (that do not affect awareness or memory) “focal unaware” the old term was complex partial seizures (that affect awareness or memory either before, during or after a seizure). The symptoms and clinical manifestations of frontal lobe epilepsy can differ depending on which specific area of the frontal lobe is affected.The onset of a seizure may be hard to detect since the frontal lobes contain and regulate many structures and functions about which relatively little is known. Due to the lack of knowledge surrounding the functions associated with the frontal lobes, seizures occurring in these regions of the brain may produce unusual symptoms which can often be misdiagnosed as a psychiatric disorder, non-epileptic seizure or a sleep disorder.During the onset of a seizure, the patient may exhibit abnormal body posturing, sensorimotor tics, or other abnormalities in motor skills. In some cases, uncontrollable laughing or crying may occur during a seizure. Affected persons may or may not be aware that they are behaving in an abnormal manner, depending on the patient and type of seizure. A brief period of confusion known as a postictal state may sometimes follow a seizure occurring in the frontal lobes. However, these postictal states are often undetectable and generally do not last as long as the periods of confusion following seizures that occur in the temporal lobes.There are many different causes of frontal lobe epilepsy ranging from genetics to head trauma that result in lesions in the frontal lobes. Although frontal lobe epilepsy is often misdiagnosed, tests such as prolonged EEG monitoring, video EEG and/or an MRI scan of the frontal lobes can be administered in order to reveal the presence of a tumor or vascular malformation. Unlike most epileptic EEGs, the abnormalities in FLE EEGs precede the physical onset of the seizure and aid in localization of the seizures origin. Medications such as anti-epileptic drugs can typically control the onset of seizures, however, if medications are ineffective the patient may undergo surgery to have focal areas of the frontal lobe removed. Signs and symptoms Signs and symptoms of frontal lobe seizures may include Head and eye movements to one side Complete or partial unresponsiveness or difficulty speaking Explosive screams, including profanities, or laughter Abnormal body posturing, especially fencing position Repetitive movements, such as rocking, bicycle pedaling or pelvic thrustingEpileptic symptoms are frequently the product of the spread of overactivation occurring within one central foci that travels to lateral brain regions thereby causing an array of symptoms. Due to the massive amount of diversity in both the cognitive and motor functions that occur within the frontal lobes, there is an immense variety in the types of symptoms that can arise from epileptic seizures based on the side and topography of the focal origin. In general these symptoms can range anywhere from asymmetric and abnormal body positioning to repetitive vocal outbursts and repetitive jerking movements. The symptoms typically come in short bursts that last less than a minute and often occur while a patient is sleeping. In most cases, a patient will experience a physical or emotional Aura of tingling, numbness or tension prior to a seizure occurring. Fear is associated with temporal and frontal lobe epilepsies, but in FLE the fear is predominantly expressed on the persons face whereas in TLE the fear is subjective and internal, not perceptible to the observer.Tonic posture and clonic movements are common symptoms among most of the areas of the frontal lobe, therefore the type of seizures associated with frontal lobe epilepsy are commonly called tonic-clonic seizures. Dystonic motor movements are common to both TLE and FLE, but are usually the first symptom in FLE episodes where they are quite brief and do not affect consciousness. The seizures are complex partial, simple partial, secondarily generalized or a combination of the three. These partial seizures are often misdiagnosed as psychogenic seizures. Symptomatology A wide range of more specific symptoms arise when different parts of the frontal cortex are affected. Supplementary motor area (SMA) The onset and relief of the seizure are quite abrupt. The tonic posturing in this area is unilateral or asymmetric between the left and right hemispheres. A somatosensory aura frequently precedes many large motor and vocal symptoms and most often the affected person is responsive. Motor symptoms: Facial grimacing and complex automatisms like kicking and pelvic thrusting Vocal symptoms: Laughing, yelling, or speech arrest. Primary motor cortex The primary motor cortex has jacksonian seizures that spread to adjacent areas of the lobe which often trigger a second round of seizures originating in another cortical area. The seizures are much simpler than those that originate in the SMA and are usually clonic or myoclonic movements with speech arrest. Some dystonic or contralateral adversive posturing may also be present. Medial frontal, cingulate gyrus, orbitofrontal, or frontopolar regions Motor symptoms of seizures in this area are accompanied by emotional feelings and viscerosensory symptoms. Motor and vocal agitation are similar to that of the SMA with short repetitive thrashing, pedaling, thrusting, laughing, screaming and/or crying. This is some of what can cause the misdiagnosis of a psychological disorder. Dorsolateral cortex This area does not seem to have many motor symptoms beyond tonic posturing or clonic movements. Contralateral or less commonly ipsilateral head turn and eye deviation are commonly associated with this area as well. Operculum Many of the symptoms associated with this area involve the head and digestive tract: swallowing, salivation, mastication and possibly gustatory hallucinations. Preceding the seizure the person is fearful and often has an epigastric aura. There is not much physical movement except clonic facial movements. Speech is often arrested. Diagnosis The diagnosis of FLE is difficult due to the overlapping and similar symptoms to psychiatric disorders. The diagnosis of FLE has been done by clinicians, and their reviews of the medical history, and physical and neurological examinations. The following neurological tests can be helpful for diagnosing FLE Electroencephalography (EEG) MRI Video EEG Electroencephalography (EEG) EEG helps in finding out the exact area of the brain where seizures occur. In the case of FLE, the EEG is almost normal. MEG and electroencephalography (EEG) in the temporal domain provides a better and wider view of information exchange across networks in patients with impaired and unimpaired FLE. Neuroimaging for diagnosis Advancements in technology, has given rise to newer, more efficient methods of diagnosis, most prominent being in the domain of neuroimaging. The high spatial resolution from fMRI has implications on certain brain regions contributing to memory. The usage of task fMRI for examination of memory or other higher cognitive networks may also be used to predict ictal onset zone(s) in patients with FLE, giving the advantage of refinement of patient-specific analyses. The use of multi-modal approaches in association with neuroimaging techniques like fMRI and MEG or EEG will be informative in characterizing atypical functional brain networks in FLE. But, difficulty remains in the evaluation of potential compensatory mechanisms between patients with FLE with normal and impaired memory, without properly characterizing transfer of information during memory tasks. Genetic Counselling Diagnosis of ADNFLE, however, is not only based on neuroimaging, and ictal and interictal EEGs, but also on family history and genetic counseling. Certain molecular and genomics testing that can include multi-gene panel of CHRNA4, CHRNB2, CHRNA2, KCNT1, DEPDC5, CRH, serial single gene testing of pathogenic variants, and can also be comprehensive genomic testing. There has to be continuous neuroimaging and EEGs, for reevaluation at regular intervals, to keep a check on disease progression. Video EEG As the FLE occurred during sleep video EEG is one of the useful tools for diagnosis of FLE. The monitoring can be done in the sleep lab in the hospital overnight. Both brain activity, as well as behavioral movement, can be captured by using video EEG. PET Scan Positron emission tomography (PET) helps to locate epileptogenic loci. If the MRI were normal the PET scan could locate some abnormalities. Common misdiagnoses Episodes that include complex hyperactivity of the proximal portions of the limbs that lead to increased overall motor activity are called hypermotor seizures. When associated with bizarre movements and vocalizations these seizures are often misdiagnosed as psychogenic or functional sezures or other episodic movement disorders such as psychogenic movement disorders, familial paroxysmal dystonic choreoathetosis, paroxysmal kinesogenic choreoathetosis, or episodic ataxia type 1. Hypermotor seizure in children are often confused with pavor nocturnus (night terrors). Paroxysmal nocturnal dystonia or hypnogenic paroxysmal dystonia are other names given to describe FLE symptoms but are simply just FLE.Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is the best understood form of frontal lobe epilepsy but is often misdiagnosed as sleep apnea. Both disorders are characterized by awakening during the night which leads to daytime sleepiness. Some symptoms of sleep apnea overlap with those of ADNFLE, such as sudden awakening accompanied by a feeling of choking and on occasion motor activity which makes diagnosis difficult based on symptoms alone. Video surveillance as well as EEG is occasionally needed to differentiate between the two disorders. It has been reported that sleep apnea might be associated with epilepsy which would account for some of the misdiagnoses. Causes The origins of frontal lobe seizures can be different deviations. One of the major reasons for FLE is abnormal cognitive development or sometimes congenital abnormal brain development. Other reasons are: Tumors Head Trauma GeneticApart from the above-mentioned reason, there are a few unknown factors that can trigger the seizures: Sleep deprivation Waking up Stress Hormonal changes, such as during menstruation Alcohol Certain medications Illegal substances Tumors Tumors account for about one-third of all frontal lobe epilepsy cases. Low-grade tumors such as gangliogliomas, low-grade gliomas, and epidermoid tumors are most common, but many high-grade tumors were most likely once involved with seizures. Other lesions on the frontal lobe such as hamartomas and nodular heterotopias can cause frontal lobe symptoms as well. Birth defects such as vascular malformation are known to cause seizures, especially arteriovenous malformations, and cavernous angiomas. Head Trauma Head trauma frequently causes damage to the frontal lobe and can cause seizures directly or indirectly through gliosis. Seizures originating directly from head trauma usually occur within a few months, but occasionally they can take years to manifest. On occasion, encephalitis can cause frontal lobe seizures but it is most often associated with an affected temporal lobe. Genetic Cause The main genetic cause of frontal lobe epilepsy is an autosomal dominant disease called Autosomal Dominant Nocturnal Frontal Lobe Epilepsy, which involves mutations in 2 nicotinic acetylcholine receptor genes. A genetic mutation on chromosome 22 has also been associated with another genetic form of the disorder. Mechanism Due to the difference in brain processing and function as well as various surface anatomy landmarks, the frontal lobes have traditionally been divided into two major areas known as the precentral cortex and prefrontal cortex. Precentral cortex The precentral cortex is an area of the frontal cortex that is located directly anterior to the central sulcus and includes both the primary motor cortex and the supplementary motor area. Inputs that project to both of these areas arise from a variety of locations in the brain that integrate sensory stimuli including the primary motor cortex, the thalamus and corticospinal projections. These two areas along with several other main functional areas control both the preparation of motor movement as well as the execution of movements. These main functional areas are crucial to the development of the motor related symptoms associated with frontal lobe epilepsy focally when seizures are located within these defined areas. The major functional areas include: Primary motor cortex Contains large neurons that project axons down to the spinal cord where they synapse onto alpha motor neurons. These neurons are involved in the planning of motor movements and the refining of motor movements based on sensory inputs that are received from the cerebellum. Supplementary motor area Area anterior to the primary motor cortex that is involved in planning complex motor movements and coordinating movements along both hands. The main inputs for this area are received from the thalamus. Frontal eye field The frontal eye field is a posterior part of the middle frontal gyrus and is involved in the control of saccadic, contralateral and conjugate eye movement. This area receives its main inputs from both the occipital cortex and dorsal thalamus. Brocas area Controls the motor movements of both the tongue and larynx that enables speech formation. This area receives direct inputs from the primary motor area as well as Wernickes area located in the temporal lobe. Prefrontal cortex The prefrontal cortex, the most anterior region of the brain, comprises several key areas that are particularly important for higher mental functions that control various aspects of human personality including anticipation and planning, initiative/judgement, memory and the control of decision making. Damage or lesions to this region of the brain can result in major changes in personality. A classic example is Phineas Gage, who exhibited a change in behavior after one or both frontal lobes were destroyed by a large iron bar accidentally driven through his head (though Gage, despite conventional presentations of his case, did not exhibit the aggression, antisocial behavior, or loss of impulse control sometimes reported in patients with similar injuries). There are two main regions of the prefrontal cortex that each control various aspects of behavior and personality: Dorsolateral prefrontal cortex This area is associated with the impairment of the cognitive abilities that control and regulate behavior and long-term memory formation (especially relating to procedural sequence memory) when either brain damage or a lesion is present. Orbitofrontal cortex The orbitofrontal cortex has similar functions as the dorsolateral prefrontal cortex but is thought to be mainly responsible for the ability to make choices and determine right from wrong. Social effects and quality of life Epilepsy has a substantial impact on the quality of life of the individuals that are affected by it, yet there is lack of proper examination of social cognitive functions. Physicians and researchers are coming to understand that the impact on the quality of life of the patient is as important as the effects of the seizures. Quality of life questionnaires and other assessment tools have been created to help quantify quality of life for individual patients. They consider such factors as physical health (including numbers and severity of seizures, medication side effects etc.), mental health, social relationships, lifestyle, role activities and life fulfillment. A Center for Disease Control study reported that people with seizures were more likely to have lower education levels, higher unemployment, higher levels of pain, hypersomnia/insomnia, increased psychological distress and social isolation/connection issues. Some of the issues which impact quality of life for people with epilepsy are: ability to drive and travel, the ability to date, marry and have children, the ability to have a job and independence, the ability to have an education and learn, and the ability to have good health and mental functioning. Future research is needed to find ways of not only controlling frontal lobe seizures, but of also addressing the specific quality-of-life issues that plague those with frontal lobe epilepsy, especially as studies show a higher emotional recognition anomaly in cases of FLE, compared to TLE. Driving and transportation restrictionsDriving and travel restrictions are one of the greatest limitations that epileptic patients experience. Laws restricting driving privileges vary greatly in the United States as well as across the world. In the United States, 28 states require a patient to be seizure free for fixed periods of time ranging from 3–12 months. However, research done by Johns Hopkins University showed that there was no difference in seizure-related fatal crash rates in states with 3-month restrictions versus states with 6-12 month seizure-free restrictions. In 23 states, the restrictions and seizure free periods vary depending on the type of epilepsy and the individual case and in 13 states physicians were responsible for determining whether their patients should be allowed to drive. In 6 of those 13 states physicians could be held legally liable for their decisions regarding their epileptic patients driving capabilities. In many states, patients can also be legally liable for accidents, injury, damage and death caused by seizure related accidents. One of the major arguments in favor of restricting the licensing of epileptic drivers is the concern for public safety. However, the Johns Hopkins study showed that in a particular 2 year timeframe only 0.2% of fatal crashes occurred as a result of seizures. Alcohol related crash fatalities caused 156 times more driver deaths than seizure related crashes and young drivers between the ages of 16 and 24 were 123 times more likely to die in a fatal crash caused by their inexperience than an epileptic driver was to die in a crash that resulted from a seizure. Frontal lobe epileptic seizures unlike other epileptic seizures create symptoms that are as dangerous as loss of consciousness and much more difficult to discern from other problems such as substance use disorders, psychiatric disorders and disobedience. Jerking movements/lack of motor control, pedaling, pelvic thrusting, lapses in cognitive functioning and other hallmark symptoms of frontal lobe epileptic seizures all create dangerous behavior behind the wheel. Studies have not been done to date to determine the differential risk posed by drivers with frontal lobe epilepsy relative to the general epileptic population.Hormones and pregnancy issuesHormonal changes and pregnancy can shift seizure activity and the use of antiepileptic drugs can alter the efficacy of hormones as well as cause congenital malformations in fetuses. Seizure control in pregnant women is very important to the welfare of both the developing fetus and the mother. Hormonal shifts at puberty, with birth control and at menopause can also cause changes in the frequency and severity of seizures and must be closely monitored. Increased seizure activity is reported by 50% of women during the course of the pregnancy due to changing levels of hormones, fluids, salts and absorption and elimination of medications.EmploymentA report by the Epilepsy Foundation noted that the unemployment rate amongst people with epilepsy is 25% and in patients whose seizures are poorly controlled the rate jumps to 50%. Even though people with epilepsy are protected under The Americans with Disabilities Act, employment discrimination and high rates of unemployment due to employer attitudes still exist. A study in the UK showed that 16% of employers surveyed felt there were no jobs in their company suitable for people with epilepsy and that 21% felt that employing an epileptic would be a "major issue". Fifty percent of the employers said they had a high concern regarding employing people with epilepsy with most citing safety concerns/workplace accidents as their major issue. Patients with frontal lobe epilepsy may be particularly prone to being discriminated against in employment and subject to higher rates of termination due to the unusual motor symptoms, speech, vocal outbursts and cognitive/judgment symptoms displayed during frontal lobe seizures. Frontal lobe seizures also tend to come on suddenly and progress rapidly making it difficult for an employer to control the exposure of the seizure to others.Education, learning and cognitive functionPatients with frontal lobe epilepsy will likely also experience issues with learning and education. Many factors contribute to these issues including the impact of anticonvulsant medications. Anticonvulsant medications cause patients to feel "foggy" and sluggish. Drugs such as Topiramate cause problems such as mental blunting, word retrieval difficulties and irritability. Phenobarbital, Primidone and Vigabatrin can cause depression and suicidal tendencies. Stress and lack of sleep during exam periods can trigger seizures and many school sports teams restrict or ban people with epilepsy from sports for safety and liability reasons. People with frontal lobe epilepsy also exhibit dysfunctional cognitive skills and memory issues which can make learning challenging. Research has shown that frontal lobe epilepsy has a greater negative impact than other forms of epilepsy on cognitive functioning. People with frontal lobe epilepsy show decreased cognitive capabilities in the following areas: humor appreciation, recognition of emotional expressions, response selection/initiation and inhibition, hyperactivity, conscientiousness, obsession, addictive behavior, motor coordination and planning, attention span, performance speed, continuous performance without intrusion and interference errors, copying and recall, concept formation, anticipatory behavior, memory span, working memory, executive planning, visuo-spatial organization, mental flexibility, conceptual shift, problem solving, programming of complex motor sequences, impulse control, judgment and forecasting of consequences.Physical health and risk of other conditionsPatients with epilepsy face a greater risk of accidents, injury and other medical conditions than the general population. A European study showed that people with epilepsy were at greater risk for accidental injuries related to seizures such as concussions, abrasions and wounds and reported more hospitalizations and medical action than the general population. Other studies have shown that people with epilepsy are at a greater risk of seizure related drowning, suffocation, broken bones and burns and more likely to die in a fatal automobile crash. Epilepsy Ontario reports that people with epilepsy are also more likely to have other conditions than the general population such as: 30% of autistic children have epilepsy, 33% of cerebral palsy patients have epilepsy, 15-20% of fragile X syndrome patients have epilepsy, 50% of children with learning disabilities will have some form of epilepsy, 3-10% of patients with Lennox-Gastaut syndrome will have epilepsy, 80% of children with Rett syndrome will have epilepsy and 80% of patients with Tuberous Sclerosis will have epilepsy. The frontal lobe has a significant function in attention regulation. Therefore, patients with frontal lobe epilepsy are often found to be co-morbid for another disease called attention-deficit hyperactivity disorder (ADHD), which has a higher prevalence in children. This adds to the various cognitive and behavioral challenges, that they already face.Mental and emotional healthEpileptic patients are more prone to develop psychological and social dysfunction than individuals that do not have epilepsy. They report higher levels of anxiety and stress due to social isolation, discrimination, the unpredictability of their seizures and peoples reactions to them as well as fear of injury, death and brain damage from their seizures. Anticonvulsants can also result in lower functioning, depression, sluggishness and suicidal thoughts. Approximately 20% of people with epilepsy are depressed and the rate of suicide amongst people with epilepsy is 5 times the rate in the general population. People with frontal lobe epilepsy experience more significant social effects because the manifested symptoms are more unusual. Symptoms such as screaming, bicycling limbs, pelvic thrusting, inhibition control and other outbursts can be particularly embarrassing and isolating for the patient. The ultimate result from all these, is a significant impact on overall personality development. Treatments There are several different ways to treat frontal lobe epileptic seizures, however, the most common form of treatment is through the use of anticonvulsant medications that help to prevent seizures from occurring. In some cases, however, when medications are ineffective, a neurologist may choose to operate on the patient in order to remove the focal area of the brain in which the seizures are occurring. Other treatments that can be administered to aid in reducing the occurrence of seizures include the implementation of a specific, regimented diet and/or the implantation of a vagus nerve stimulator, or deep brain stimulation (DBS). Medications Anticonvulsants like oxcarbazepine or other drugs are the most successful medication in reducing and preventing frontal lobe seizures. Oxcarbazepine helps in the reduction of seizure frequencies. There are a wide range of anticonvulsants that have both different modes of action and different abilities in preventing certain types of seizures. Some of the anticonvulsants that are prescribed to patients today include: Oxcarbazepine (Trileptal), Carbamazepine (Tegretol), Phenytoin (Dilantin Kapseals), Gabapentin (Neurontin), Levetiracetam (Keppra), Lamotrigine (Lamictal), Topiramate (Topamax), Tiagabine (Gabitril), Zonisamide (Zonegran) and Pregabalin (Lyrica). KCNT1 pathogenic variant associated ADNFLE can be managed by treatment with quinidine, and ADNFLE associated with CHRNA4 shows better responsiveness to zonisamide. Note on medications Lorazepam, diazepam and clonazepam are front line treatments for severe convulsions, belonging to the benzodiazepine class of medications. Alternative medicine Herbal medicines Acupuncture Psychotherapy Mind–body interventions Surgical treatment Surgery may involve the following: Isolating the focal point. Responding to a seizure. Removing the focal point.When both the amount and severity of seizures becomes uncontrollable and seizures remain resistant to the various anticonvulsants, a patient most likely will be considered for epilepsy surgery. But, while performing it, there is the need for identifying or pinpointing the exact location of the seizure in the brain. This, in recent times have been aided by some of the modern techniques such as, SISCOM i.e., subtraction ictal SPECT co registered to MRI, SPECT i.e. single-photon emission computerized tomography, brain mapping performed before the surgery and functional MRI (fMRI), especially for the language area mapping.Surgeries include, a frontal lobectomy. This procedure involves the removal of focal regions of the frontal lobes that have been identified as being problematic for the patient. It has been found that around 30% to 50% of patients that undergo a frontal lobectomy will forever be free from seizures that cause a loss of consciousness or cause abnormal movements. However, frontal lobectomy and MCD contribute to lower seizure controls. But, in children with conditions like Sturge–Weber syndrome (SWS) or tumors, there is report of greater seizure control rates. If on the other hand, the seizures occur in an area that is too vital to remove (such as areas that control motor, sensory or language functions), then the surgeon will perform a procedure known as a multiple subpial transection. This procedure involves making a series of cuts that surround the focal region where the seizures have originated. By making cuts surrounding the focal region, the surgeon is able to isolate that specific section of the brain and prevent electrical impulses from being able to travel horizontally to other areas of the brain. Neuromodulation Vagus nerve stimulation (VNS):The last surgical procedure that can be done to help prevent the reoccurrence of seizures in the frontal lobes is to implant a stimulator on the vagus nerve. This device is a self-activating device that is inserted directly under the skin and can be controlled directly by the patient. When a patient is feeling the onset of an aura, he/she can activate the stimulator which in turn will provide stimulation to the left vagus nerve (the left vagus nerve is used because the right nerve plays a role in cardiac function). Although little is understood about the exact mechanism for vagal nerve stimulation, it has been proven to be a successful treatment that can often terminate seizures before they begin. It has the potential of being helpful in patients with resistance to AEDs.This procedure named Deep brain stimulation (DBS) another novel procedure that can be used utilizes a mechanism similar to that of a cardiac pacemaker The electrode is implanted into the patients brain, while a neuro-stimulator machine is placed beneath the skin of the chest. The stimulator sends an indication to the electrode in the brain to prevent any signal that potentially triggers or can trigger a seizure.Surgeries have been used as a treatment for FLE, however, meta-analyses have shown that proper etiological studies are important to give best postoperative results, with children <3 years of age showing pathology and location of the surgery as important factors. It also showed the malformation of cortical development (MCD) induced FLE traced down to worst postoperative conditions, hence, poor accuracy and efficacy. Diet The use of a regimented diet is an approach that has been found to help control seizures in children with severe, medically intractable frontal lobe epilepsy. Although the use of dieting to prevent seizures from occurring is a lost treatment that has been replaced by the use of new types of anticonvulsants, it is still recommended to patients to this day. A ketogenic diet is a high-fat, low-carbohydrate based diet that patients are typically asked to follow in conjunction with their anticonvulsant medications. This diet was designed in order to mimic many of the effects that starvation has on the metabolic functioning of the body. By limiting the amount of carbohydrates and increasing the amount of exogenous fats available to the metabolism, the body will create an excess of water-soluble compounds known as ketone bodies. Although the mechanism of action is still unknown, it is believed that these excessive amounts of ketone bodies become the brains main source of energy and in turn are able to suppress the frequency of seizure occurrence. Epidemiology Epilepsy is a relatively common disorder, affecting between 0.5-1% of the population, and frontal lobe epilepsy accounts for about 1-2% of all epilepsies. The most common subdivision of epilepsy is symptomatic partial epilepsy, which causes simple partial seizures, and can be further divided into temporal and frontal lobe epilepsy. Although the exact number of cases of frontal lobe epilepsy is not currently known, it is known that FLE is the less common type of partial epilepsy, accounting for 20-30% of operative procedures involving intractable epilepsy. Patients with medically refractive epilepsy, over a fraction of one-fourth have been diagnosed with FLE, only one-third of which have been found to get relief from seizures by surgical interventions. The disorder also has no gender or age bias, affecting males and females of all ages. In a recent study, the mean subject age with frontal lobe epilepsy was 28.5 years old, and the average age of epilepsy onset for left frontal epilepsy was 9.3 years old whereas for right frontal epilepsy it was 11.1 years old. Research Over the past decade or so, researchers have been attempting to discover less invasive, safer and more efficient technologies that enable surgeons to remove epileptogenic focal zones without causing any damage to neighboring cortical areas. One such technology that has emerged and has great promise, is the use of gamma knife radiosurgery to either excise a brain tumor or repair a vascular malformation.In Gamma Knife radiosurgery, intersecting gamma radiation beams are applied directly to the tumor site or vascular malformation site that had been established using neuroimaging. Although each beam itself is not strong enough to damage brain tissue, when the beams intersect they are strong enough to destroy the specific brain tissue that is to be excised. This process is extremely efficient and entirely non-invasive and is therefore much safer than actual neurosurgery itself. Recently researchers and surgeons alike have begun to use Gamma Knife radiosurgery to treat cases of epilepsy by removing tumors responsible for causing the seizures. The early success rates in being able to alleviate seizures seem to be similar to those of temporal resective surgery however Gamma Knife radiosurgery has less associated risk factors. Current research on this topic is aimed at improving the technique in order to increase success rates as well as developing non-invasive forms of physiologic monitoring in order to determine the epileptogenic focus conclusively.Another way of understanding or studying FLE, highly under study is the network approach. When conventional imaging does not show the structural lesions, HFO analysis shows the pathophysiology, locally at the neural circuit level. Genetic analysis along with neuroimaging like fMRI, EEG, MEG, and in-depth semiological analysis, aids in the network approach study of FLE, both at micro and macro levels, giving it a comprehensive view. References External links Frontal lobe epilepsy on Epilepsy.com Epilepsy Foundation

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I'm seeking clarification on the medical term 'Nephronophthisis.' Could you explain it?

Nephronophthisis is a genetic disorder of the kidneys which affects children. It is classified as a medullary cystic kidney disease. The disorder is inherited in an autosomal recessive fashion and, although rare, is the most common genetic cause of childhood kidney failure. It is a form of ciliopathy. Its incidence has been estimated to be 0.9 cases per million people in the United States, and 1 in 50,000 births in Canada. Signs and symptoms Infantile, juvenile, and adolescent forms of nephronophthisis have been identified. Although the range of characterizations is broad, people affected by nephronophthisis typically present with polyuria (production of a large volume of urine), polydipsia (excessive liquid intake), and after several months to years, end-stage kidney disease, a condition necessitating either dialysis or a kidney transplant in order to survive. Some individuals with nephronophthisis also have so-called "extra-renal symptoms" which can include tapetoretinal degeneration, liver problems, oculomotor apraxia, and cone-shaped epiphysis (Saldino-Mainzer syndrome). Cause Nephronophthisis is characterized by fibrosis and the formation of cysts at the cortico-medullary junction, it is an autosomal recessive disorder which eventually leads to terminal kidney failure. Pathophysiology Mechanism of nephronophthisis indicates that all proteins mutated in cystic kidney diseases express themselves in primary cilia. NPHP gene mutations cause defects in signaling resulting in flaws of planar cell polarity. The ciliary theory indicates that multiple organs are involved in NPHP (retinal degeneration, cerebellar hypoplasia, liver fibrosis, and intellectual disability). Related rare genetic disorders Nephronophthisis is a ciliopathy. Other known ciliopathies include primary ciliary dyskinesia, Bardet–Biedl syndrome, polycystic kidney and liver disease, Alström syndrome, Meckel–Gruber syndrome and some forms of retinal degeneration.NPHP2 is infantile type of nephropthisis and sometimes associated with situs inversus this can be explained by its relation with inversin gene. NPHP1, NPHP3, NPHP4, NPHP5, and NPHP6 are sometimes seen with retinitis pigmentosa, this particular association has a name, Senior-Loken syndrome. Diagnosis The diagnosis of nephronophthisis can be obtained via a kidney ultrasound, family history and clinical history of the affected individual according to Stockman, et al. Types Infantile NPH Juvenile NPH Adult NPH Management The management of this condition can be done via-improvement of any electrolyte imbalance, as well as, high blood pressure and low red blood cell counts (anemia) treatment as the individuals condition warrants. Epidemiology Nephronophthisis occurs equally in both sexes and has an estimate 9 in about 8 million rate in individuals. Nephronophthisis is the leading monogenic cause of end-stage kidney disease. References Further reading Simms, Roslyn J.; Hynes, Ann Marie; Eley, Lorraine; Sayer, John A. (2011). "Nephronophthisis: A Genetically Diverse Ciliopathy". International Journal of Nephrology. 2011: 1–10. doi:10.4061/2011/527137. PMC 3108105. PMID 21660307. Hildebrandt, Friedhelm; Attanasio, Massimo; Otto, Edgar (2009-01-01). "Nephronophthisis: Disease Mechanisms of a Ciliopathy". Journal of the American Society of Nephrology. 20 (1): 23–35. doi:10.1681/ASN.2008050456. ISSN 1046-6673. PMC 2807379. PMID 19118152. Murray, Karen F.; Larson, Anne M. (2010-07-23). Fibrocystic Diseases of the Liver. Springer Science & Business Media. ISBN 9781603275248. == External links ==

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I've come across the term 'Venous lake' in a medical context, but I'm not sure what it means. Can you clarify?

A venous lake (also known as phlebectasis) is a generally solitary, soft, compressible, dark blue to violaceous, 0.2- to 1-cm papule commonly found on sun-exposed surfaces of the vermilion border of the lip, face and ears. Lesions generally occur among the elderly.Though these lesions may resemble nodular melanoma, the lack of induration, slow growth, and lightening appearance upon diascopy suggest against it, and indicate a vascular lesion. Additionally, lack of pulsation distinguishes this lesion of the lower lip from a tortuous segment of the inferior labial artery. Cause The cause is unknown; however it is thought to be associated with sun exposure, leading to a dilated blood-filled vascular channel "...lined with a singled layer of flattened endothelial cells and a thin wall of fibrous tissue filled with red blood cells." Treatment Treatment may be requested for cosmetic reasons. Traditional techniques such as surgical excision are effective but will leave a scar. Laser therapy has become the mainstay of therapy. Published research suggests that the Long Pulsed Nd:YAG laser is a very effective, with a clearance rate of 94% following a single treatment. In this study no scarring or other complications were reported. History The term was coined by American physician William Bennett Bean. Images See also List of cutaneous conditions Footnotes == External links ==

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Can you demystify the medical term 'Carney complex' for me?

Carney complex and its subsets LAMB syndrome and NAME syndrome are autosomal dominant conditions comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity. It is distinct from Carneys triad. Approximately 7% of all cardiac myxomas are associated with Carney complex. Presentation The spotty skin pigmentation and lentigines occur most commonly on the face, especially on the lips, eyelids, conjunctiva and oral mucosa. Cardiac myxomas may lead to embolic strokes and heart failure and may present with fever, joint pain, shortness of breath, diastolic rumble and tumor plop. Myxomas may also occur outside the heart, usually in the skin and breast. Endocrine tumors may manifest as disorders such as Cushing syndrome. The most common endocrine gland manifestation is an ACTH-independent Cushings syndrome due to primary pigmented nodular adrenocortical disease (PPNAD). The LAMB acronym refers to lentigines, atrial myxomas, and blue nevi. NAME refers to nevi, atrial myxoma, myxoid neurofibromas, and ephelides.Testicular cancer, particularly Sertoli cell type, is associated with Carney syndrome. Thyroid and pancreas cancer may also occur.Although J Aidan Carney also described Carneys triad it is entirely different. Pathophysiology Carney complex is most commonly caused by mutations in the PRKAR1A gene on chromosome 17 (17q23-q24) which may function as a tumor-suppressor gene. The encoded protein is a type 1A regulatory subunit of protein kinase A. Inactivating germline mutations of this gene are found in 70% of people with Carney complex.Less commonly, the molecular pathogenesis of Carney complex is a variety of genetic changes at chromosome 2 (2p16).Both types of Carney complex are autosomal dominant. Despite dissimilar genetics, there appears to be no phenotypic difference between PRKAR1A and chromosome 2p16 mutations. Treatment Cardiac myxomas can be difficult to manage surgically because of recurrence within the heart, often far away from the site of the initial tumor. History In 1914 an American neurosurgeon, Harvey Cushing, reported on a patient with a pituitary tumour on whom he had operated. The post mortem findings as reported were consistent with Carney complex, though at the time this condition had yet to be described. In 2017 archived tissue from the operation in Cushings report was subjected to DNA sequencing, revealing an Arg74His (arginine to histidine: guanine (G)-> adenosine (A) transition in the second codon position of the 74th codon in the protein) mutation in the PRKAR1A gene, confirming a diagnosis of Carney complex. Therefore, Cushings paper appears to be the first report of this complex. See also Epithelioid blue nevus List of cutaneous neoplasms associated with systemic syndromes References External links GeneReview/UW/NIH entry on Carney complex

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I'm curious about the meaning of the medical term 'Blood transfusion.' Can you give me some insights?

Blood transfusion is the process of transferring blood products into a persons circulation intravenously. Transfusions are used for various medical conditions to replace lost components of the blood. Early transfusions used whole blood, but modern medical practice commonly uses only components of the blood, such as red blood cells, white blood cells, plasma, clotting factors and platelets. Red blood cells (RBC) contain hemoglobin, and supply the cells of the body with oxygen. White blood cells are not commonly used during transfusion, but they are part of the immune system, and also fight infections. Plasma is the "yellowish" liquid part of blood, which acts as a buffer, and contains proteins and important substances needed for the bodys overall health. Platelets are involved in blood clotting, preventing the body from bleeding. Before these components were known, doctors believed that blood was homogeneous. Because of this scientific misunderstanding, many patients died because of incompatible blood transferred to them. Medical uses Red cell transfusion Historically, red blood cell transfusion was considered when the hemoglobin level fell below 100g/L or hematocrit fell below 30%. Because each unit of blood given carries risks, a trigger level lower than that, at 70 to 80g/L, is now usually used, as it has been shown to have better patient outcomes. The administration of a single unit of blood is the standard for hospitalized people who are not bleeding, with this treatment followed with re-assessment and consideration of symptoms and hemoglobin concentration. Patients with poor oxygen saturation may need more blood. The advisory caution to use blood transfusion only with more severe anemia is in part due to evidence that outcomes are worsened if larger amounts are given. One may consider transfusion for people with symptoms of cardiovascular disease such as chest pain or shortness of breath. In cases where patients have low levels of hemoglobin due to iron deficiency, but are cardiovascularly stable, parenteral iron is a preferred option based on both efficacy and safety. Other blood products are given where appropriate, e.g., to treat clotting deficiencies. Procedure Before a blood transfusion is given, there are many steps taken to ensure quality of the blood products, compatibility, and safety to the recipient. In 2012, a national blood policy was in place in 70% of countries and 69% of countries had specific legislation that covers the safety and quality of blood transfusion. Blood donation Blood transfusions use as sources of blood either ones own (autologous transfusion), or someone elses (allogeneic or homologous transfusion). The latter is much more common than the former. Using anothers blood must first start with donation of blood. Blood is most commonly donated as whole blood obtained intravenously and mixed with an anticoagulant. In developed countries, donations are usually anonymous to the recipient, but products in a blood bank are always individually traceable through the whole cycle of donation, testing, separation into components, storage, and administration to the recipient. This enables management and investigation of any suspected transfusion related disease transmission or transfusion reaction. In developing countries, the donor is sometimes specifically recruited by or for the recipient, typically a family member, and the donation occurs immediately before the transfusion. It is unclear whether applying alcohol swab alone or alcohol swab followed by antiseptic is able to reduce contamination of donors blood. Processing and testing Donated blood is usually subjected to processing after it is collected, to make it suitable for use in specific patient populations. Collected blood is then separated into blood components by centrifugation: red blood cells, plasma, platelets, albumin protein, clotting factor concentrates, cryoprecipitate, fibrinogen concentrate, and immunoglobulins (antibodies). Red cells, plasma and platelets can also be donated individually via a more complex process called apheresis. The World Health Organization (WHO) recommends that all donated blood be tested for transfusion-transmissible infections. These include HIV, hepatitis B, hepatitis C, Treponema pallidum (syphilis) and, where relevant, other infections that pose a risk to the safety of the blood supply, such as Trypanosoma cruzi (Chagas disease) and Plasmodium species (malaria). According to the WHO, 25 countries are not able to screen all donated blood for one or more of: HIV, hepatitis B, hepatitis C, or syphilis. One of the main reasons for this is because testing kits are not always available. However the prevalence of transfusion-transmitted infections is much higher in low income countries compared to middle and high income countries. All donated blood should also be tested for the ABO blood group system and Rh blood group system to ensure that the patient is receiving compatible blood. In addition, in some countries platelet products are also tested for bacterial infections due to its higher inclination for contamination due to storage at room temperature. Presence of cytomegalovirus (CMV) may also be tested because of the risk to certain immunocompromised recipients if given, such as those with organ transplant or HIV. However, not all blood is tested for CMV because only a certain amount of CMV-negative blood needs to be available to supply patient needs. Other than positivity for CMV, any products tested positive for infections are not used. Leukocyte reduction is the removal of white blood cells by filtration. Leukoreduced blood products are less likely to cause HLA alloimmunization (development of antibodies against specific blood types), febrile non-hemolytic transfusion reaction, cytomegalovirus infection, and platelet-transfusion refractoriness. Pathogen Reduction treatment that involves, for example, the addition of riboflavin with subsequent exposure to UV light has been shown to be effective in inactivating pathogens (viruses, bacteria, parasites and white blood cells) in blood products. By inactivating white blood cells in donated blood products, riboflavin and UV light treatment can also replace gamma-irradiation as a method to prevent graft-versus-host disease (TA-GvHD). Compatibility testing Before a recipient receives a transfusion, compatibility testing between donor and recipient blood must be done. The first step before a transfusion is given is to type and screen the recipients blood. Typing of recipients blood determines the ABO and Rh status. The sample is then screened for any alloantibodies that may react with donor blood. It takes about 45 minutes to complete (depending on the method used). The blood bank scientist also checks for special requirements of the patient (e.g. need for washed, irradiated or CMV negative blood) and the history of the patient to see if they have previously identified antibodies and any other serological anomalies. A positive screen warrants an antibody panel/investigation to determine if it is clinically significant. An antibody panel consists of commercially prepared group O red cell suspensions from donors that have been phenotyped for antigens that correspond to commonly encountered and clinically significant alloantibodies. Donor cells may have homozygous (e.g. K+k+), heterozygous (K+k-) expression or no expression of various antigens (K−k−). The phenotypes of all the donor cells being tested are shown in a chart. The patients serum is tested against the various donor cells. Based on the reactions of the patients serum against the donor cells, a pattern will emerge to confirm the presence of one or more antibodies. Not all antibodies are clinically significant (i.e. cause transfusion reactions, HDN, etc.). Once the patient has developed a clinically significant antibody it is vital that the patient receive antigen-negative red blood cells to prevent future transfusion reactions. A direct antiglobulin test (Coombs test) is also performed as part of the antibody investigation.If there is no antibody present, an immediate spin crossmatch or computer-assisted crossmatch is performed where the recipient serum and donor rbc are incubated. In the immediate spin method, two drops of patient serum are tested against a drop of 3–5% suspension of donor cells in a test tube and spun in a serofuge. Agglutination or hemolysis (i.e., positive Coombs test) in the test tube is a positive reaction and the unit should not be transfused. If an antibody is suspected, potential donor units must first be screened for the corresponding antigen by phenotyping them. Antigen negative units are then tested against the patient plasma using an antiglobulin/indirect crossmatch technique at 37 degrees Celsius to enhance reactivity and make the test easier to read. In urgent cases where crossmatching cannot be completed, and the risk of dropping hemoglobin outweighs the risk of transfusing uncrossmatched blood, O-negative blood is used, followed by crossmatch as soon as possible. O-negative is also used for children and women of childbearing age. It is preferable for the laboratory to obtain a pre-transfusion sample in these cases so a type and screen can be performed to determine the actual blood group of the patient and to check for alloantibodies. Compatibility of ABO and Rh system for Red Cell (Erythrocyte) Transfusion This chart shows possible matches in blood transfusion between donor and receiver using ABO and Rh system. Adverse effects In the same way that the safety of pharmaceutical products is overseen by pharmacovigilance, the safety of blood and blood products is overseen by haemovigilance. This is defined by the World Health Organization (WHO) as a system "...to identify and prevent occurrence or recurrence of transfusion related unwanted events, to increase the safety, efficacy and efficiency of blood transfusion, covering all activities of the transfusion chain from donor to recipient." The system should include monitoring, identification, reporting, investigation and analysis of adverse events near-misses and reactions related to transfusion and manufacturing. In the UK this data is collected by an independent organisation called SHOT (Serious Hazards Of Transfusion).Transfusions of blood products are associated with several complications, many of which can be grouped as immunological or infectious. There is controversy on potential quality degradation during storage. Immunologic reaction Acute hemolytic reactions are defined according to Serious Hazards of Transfusion (SHOT) as "fever and other symptoms/signs of haemolysis within 24 hours of transfusion; confirmed by one or more of the following: a fall of Hb, rise in lactate dehydrogenase (LDH), positive direct antiglobulin test (DAT), positive crossmatch" This is due to destruction of donor red blood cells by preformed recipient antibodies. Most often this occurs because of clerical errors or improper ABO blood typing and crossmatching resulting in a mismatch in ABO blood type between the donor and the recipient. Symptoms include fever, chills, chest pain, back pain, hemorrhage, increased heart rate, shortness of breath, and rapid drop in blood pressure. When suspected, transfusion should be stopped immediately, and blood sent for tests to evaluate for presence of hemolysis. Treatment is supportive. Kidney injury may occur because of the effects of the hemolytic reaction (pigment nephropathy). The severity of the transfusion reaction is depended upon amount of donors antigen transfused, nature of the donors antigens, the nature and the amount of recipient antibodies. Delayed hemolytic reactions occur more than 24 hours after a transfusion. They usually occur within 28 days of a transfusion. They can be due to either a low level of antibodies present prior to the start of the transfusion, which are not detectable on pre-transfusion testing; or development of a new antibody against an antigen in the transfused blood. Therefore, delayed haemolytic reaction does not manifest until after 24 hours when enough antibodies are available to cause a reaction. The red blood cells are removed by macrophages from the blood circulation into liver and spleen to be destroyed, which leads to extravascular haemolysis. This process usually mediated by anti-Rh and anti-Kidd antibodies. However, this type of transfusion reaction is less severe when compared to acute haemolytic transfusion reaction. Febrile nonhemolytic reactions are, along with allergic transfusion reactions, the most common type of blood transfusion reaction and occur because of the release of inflammatory chemical signals released by white blood cells in stored donor blood or attack on donors white blood cells by recipients antibodies. This type of reaction occurs in about 7% of transfusions. Fever is generally short lived and is treated with antipyretics, and transfusions may be finished as long as an acute hemolytic reaction is excluded. This is a reason for the now-widespread use of leukoreduction – the filtration of donor white cells from red cell product units. Allergic transfusion reactions are caused by IgE anti-allergen antibodies. When antibodies are bound to its antigens, histamine is released from mast cells and basophils. Either IgE antibodies from the donors or recipients side can cause the allergic reaction. It is more common in patients who have allergic conditions such as hay fever. Patient may feel itchy or having hives but the symptoms are usually mild and can be controlled by stopping the transfusion and giving antihistamines. Anaphylactic reactions are rare life-threatening allergic conditions caused by IgA anti-plasma protein antibodies. For patients who have selective immunoglobulin A deficiency, the reaction is presumed to be caused by IgA antibodies in the donors plasma. The patient may present with symptoms of fever, wheezing, coughing, shortness of breath, and circulatory shock. Urgent treatment with epinephrine is needed. Post-transfusion purpura is an extremely rare complication that occurs after blood product transfusion and is associated with the presence of antibodies in the patients blood directed against both the donors and recipients platelets HPA (human platelet antigen). Recipients who lack this protein develop sensitization to this protein from prior transfusions or previous pregnancies, can develop thrombocytopenia, bleeding into the skin, and can display purplish discolouration of skin which is known as purpura. Intravenous immunoglobulin (IVIG) is treatment of choice. Transfusion-related acute lung injury (TRALI) is a syndrome that is similar to acute respiratory distress syndrome (ARDS), which develops during or within 6 hours of transfusion of a plasma-containing blood product. Fever, hypotension, shortness of breath, and tachycardia often occurs in this type of reaction. For a definitive diagnosis to be made, symptoms must occur within 6 hours of transfusion, hypoxemia must be present, there must be radiographic evidence of bilateral infiltrates and there must be no evidence of left atrial hypertension (fluid overload). It occurs in 15% of the transfused patient with mortality rate of 5 to 10%. Recipient risk factors includes: end-stage liver disease, sepsis, haematological malignancies, sepsis, and ventilated patients. Antibodies to human neutrophil antigens (HNA) and human leukocyte antigens (HLA) have been associated with this type of transfusion reaction. Donors antibodies interacting with antigen positive recipient tissue result in release of inflammatory cytokines, resulting in pulmonary capillary leakage. The treatment is supportive. Transfusion associated circulatory overload (TACO) is a common, yet underdiagnosed, reaction to blood product transfusion consisting of the new onset or exacerbation of three of the following within 6 hours of cessation of transfusion: acute respiratory distress, elevated brain natriuretic peptide (BNP), elevated central venous pressure (CVP), evidence of left heart failure, evidence of positive fluid balance, and/or radiographic evidence of pulmonary edema. Transfusion-associated graft versus host disease frequently occurs in immunodeficient patients where recipients body failed to eliminate donors T cells. Instead, donors T cells attack the recipients cells. It occurs one week after transfusion. Fever, rash, diarrhoea are often associated with this type of transfusion reaction. Mortality rate is high, with 89.7% of the patients dead after 24 days. Immunosuppressive treatment is the most common way of treatment. Irradiation and leukoreduction of blood products is necessary for high risk patients to prevent T cells from attacking recipient cells. Infection The use of greater amount of red blood cells is associated with a high risk of infections. In those who were given red blood only with significant anemia infection rates were 12% while in those who were given red blood at milder levels of anemia infection rates were 17%.On rare occasions, blood products are contaminated with bacteria. This can result in a life-threatening infection known as transfusion-transmitted bacterial infection. The risk of severe bacterial infection is estimated, as of 2002, at about 1 in 50,000 platelet transfusions, and 1 in 500,000 red blood cell transfusions. Blood product contamination, while rare, is still more common than actual infection. The reason platelets are more often contaminated than other blood products is that they are stored at room temperature for short periods of time. Contamination is also more common with longer duration of storage, especially if that means more than 5 days. Sources of contaminants include the donors blood, donors skin, phlebotomists skin, and containers. Contaminating organisms vary greatly, and include skin flora, gut flora, and environmental organisms. There are many strategies in place at blood donation centers and laboratories to reduce the risk of contamination. A definite diagnosis of transfusion-transmitted bacterial infection includes the identification of a positive culture in the recipient (without an alternative diagnosis) as well as the identification of the same organism in the donor blood. Since the advent of HIV testing of donor blood in the mid/later 1980s, ex. 1985s ELISA, the transmission of HIV during transfusion has dropped dramatically. Prior testing of donor blood only included testing for antibodies to HIV. However, because of latent infection (the "window period" in which an individual is infectious, but has not had time to develop antibodies) many cases of HIV seropositive blood were missed. The development of a nucleic acid test for the HIV-1 RNA has dramatically lowered the rate of donor blood seropositivity to about 1 in 3 million units. As transmittance of HIV does not necessarily mean HIV infection, the latter could still occur at an even lower rate. The transmission of hepatitis C via transfusion currently stands at a rate of about 1 in 2 million units. As with HIV, this low rate has been attributed to the ability to screen for both antibodies as well as viral RNA nucleic acid testing in donor blood. Other rare transmissible infections include hepatitis B, syphilis, Chagas disease, cytomegalovirus infections (in immunocompromised recipients), HTLV, and Babesia. Comparison table Inefficacy Transfusion inefficacy or insufficient efficacy of a given unit(s) of blood product, while not itself a "complication" per se, can nonetheless indirectly lead to complications – in addition to causing a transfusion to fully or partly fail to achieve its clinical purpose. This can be especially significant for certain patient groups such as critical-care or neonatals. For red blood cells (RBC), by far the most commonly transfused product, poor transfusion efficacy can result from units damaged by the so-called storage lesion – a range of biochemical and biomechanical changes that occur during storage. With red cells, this can decrease viability and ability for tissue oxygenation. Although some of the biochemical changes are reversible after the blood is transfused, the biomechanical changes are less so, and rejuvenation products are not yet able to adequately reverse this phenomenon. There has been controversy about whether a given product units age is a factor in transfusion efficacy, specifically about whether "older" blood directly or indirectly increases risks of complications. Studies have not been consistent on answering this question, with some showing that older blood is indeed less effective but with others showing no such difference; these developments are being closely followed by hospital blood bankers – who are the physicians, typically pathologists, who collect and manage inventories of transfusable blood units. Certain regulatory measures are in place to minimize RBC storage lesion – including a maximum shelf life (currently 42 days), a maximum auto-hemolysis threshold (currently 1% in the US, 0.8% in Europe), and a minimum level of post-transfusion RBC survival in vivo (currently 75% after 24 hours). However, all of these criteria are applied in a universal manner that does not account for differences among units of product. For example, testing for the post-transfusion RBC survival in vivo is done on a sample of healthy volunteers, and then compliance is presumed for all RBC units based on universal (GMP) processing standards (RBC survival by itself does not guarantee efficacy, but it is a necessary prerequisite for cell function, and hence serves as a regulatory proxy). Opinions vary as to the "best" way to determine transfusion efficacy in a patient in vivo. In general, there are not yet any in vitro tests to assess quality or predict efficacy for specific units of RBC blood product prior to their transfusion, though there is exploration of potentially relevant tests based on RBC membrane properties such as erythrocyte deformability and erythrocyte fragility (mechanical).Physicians have adopted a so-called "restrictive protocol" – whereby transfusion is held to a minimum – in part because of the noted uncertainties surrounding storage lesion, in addition to the very high direct and indirect costs of transfusions. However, the restrictive protocol is not an option with some especially vulnerable patients who may require the best possible efforts to rapidly restore tissue oxygenation. Although transfusions of platelets are far less numerous (relative to RBC), platelet storage lesion and resulting efficacy loss is also a concern. Other A known relationship between intra-operative blood transfusion and cancer recurrence has been established in colorectal cancer. In lung cancer intra-operative blood transfusion has been associated with earlier recurrence of cancer, worse survival rates and poorer outcomes after lung resection. Also studies shown to us, failure of the immune system caused by blood transfusion can be categorized as one of the main factors leading to more than 10 different cancer types that are fully associated with blood transfusion and the innate and adaptive immune system. Allogeneic blood transfusion, through five major mechanisms including the lymphocyte-T set, myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), natural killer cells (NKCs), and dendritic cells (DCs) can help the recipients defense mechanisms. On the other hand, the role for each of the listed items includes activation of the antitumor CD8+ cytotoxic T lymphocytes (CD8+/CTL), temporal inactivation of Tregs, inactivation of the STAT3 signaling pathway, the use of bacteria to enhance the antitumor immune response and cellular Immunotherapy. Transfusion-associated volume overload is a common complication simply because blood products have a certain amount of volume. This is especially the case in recipients with underlying cardiac or kidney disease. Red cell transfusions can lead to volume overload when they must be repeated because of insufficient efficacy (see above). Plasma transfusion is especially prone to causing volume overload because large volumes are usually required to give any therapeutic benefit. It has been proved that blood transfusion produce worse outcomes after cytoreductive surgery and HIPEC. Hypothermia can occur with transfusions with large quantities of blood products which normally are stored at cold temperatures. Core body temperature can go down as low as 32 °C and can produce physiologic disturbances. Prevention should be done with warming the blood to ambient temperature prior to transfusions. Transfusions with large amounts of red blood cells, whether due to severe hemorrhaging and/or transfusion inefficacy (see above), can lead to an inclination for bleeding. The mechanism is thought to be due to disseminated intravascular coagulation, along with dilution of recipient platelets and coagulation factors. Close monitoring and transfusions with platelets and plasma is indicated when necessary. Metabolic alkalosis can occur with massive blood transfusions because of the breakdown of citrate stored in blood into bicarbonate. Hypocalcemia can also occur with massive blood transfusions because of the complex of citrate with serum calcium. Calcium levels below 0.9 mmol/L should be treated. Blood doping is often used by athletes, drug addicts or military personnel for reasons such as to increase physical stamina, to fake a drug detection test or simply to remain active and alert during the duty-times respectively. However a lack of knowledge and insufficient experience can turn a blood transfusion into a sudden death. For example, when individuals run the frozen blood sample directly in their veins this cold blood rapidly reaches the heart, where it disturbs the hearts original pace leading to cardiac arrest and sudden death. Frequency of use Globally around 85 million units of red blood cells are transfused in a given year.In the United States, blood transfusions were performed nearly 3 million times during hospitalizations in 2011, making it the most common procedure performed. The rate of hospitalizations with a blood transfusion nearly doubled from 1997, from a rate of 40 stays to 95 stays per 10,000 population. It was the most common procedure performed for patients 45 years of age and older in 2011, and among the top five most common for patients between the ages of 1 and 44 years.According to the New York Times: "Changes in medicine have eliminated the need for millions of blood transfusions, which is good news for patients getting procedures like coronary bypasses and other procedures that once required a lot of blood." And, "Blood bank revenue is falling, and the decline may reach $1.5 billion a year this year [2014] from a high of $5 billion in 2008." Job losses will reach as high as 12,000 within the next three to five years, roughly a quarter of the total in the industry, according to the Red Cross. History Beginning with William Harveys experiments on the circulation of blood, recorded research into blood transfusion began in the 17th century, with successful experiments in transfusion between animals. However, successive attempts by physicians to transfuse animal blood into humans gave variable, often fatal, results.Pope Innocent VIII is sometimes said to have been given "the worlds first blood transfusion" by his physician Giacomo di San Genesio, who had him drink (by mouth) the blood of three 10-year-old boys. The boys subsequently died. The evidence for this story, however, is unreliable and considered a possible anti-Jewish blood libel. Early attempts The Incas The first reported successful blood transfusions were performed by the Incas as early as the 1500s. Spanish conquistadors witnessed blood transfusions when they arrived in the sixteenth century. The prevalence of type O blood among Indigenous people of the Andean region meant such procedures would have held less risk than blood transfusion attempts among populations with incompatible blood types, which contributed to the failures of early attempts in Europe. Animal blood Working at the Royal Society in the 1660s, the physician Richard Lower began examining the effects of changes in blood volume on circulatory function and developed methods for cross-circulatory study in animals, obviating clotting by closed arteriovenous connections. The new instruments he was able to devise enabled him to perform the first reliably documented successful transfusion of blood in front of his distinguished colleagues from the Royal Society.According to Lowers account, "...towards the end of February 1665 [I] selected one dog of medium size, opened its jugular vein, and drew off blood, until its strength was nearly gone. Then, to make up for the great loss of this dog by the blood of a second, I introduced blood from the cervical artery of a fairly large mastiff, which had been fastened alongside the first, until this latter animal showed ... it was overfilled ... by the inflowing blood." After he "sewed up the jugular veins", the animal recovered "with no sign of discomfort or of displeasure". Lower had performed the first blood transfusion between animals. He was then "requested by the Honorable [Robert] Boyle ... to acquaint the Royal Society with the procedure for the whole experiment", which he did in December 1665 in the Societys Philosophical Transactions.The first blood transfusion from animal to human was administered by Dr. Jean-Baptiste Denys, eminent physician to King Louis XIV of France, on June 15, 1667. He transfused the blood of a sheep into a 15-year-old boy, who survived the transfusion. Denys performed another transfusion into a labourer, who also survived. Both instances were likely due to the small amount of blood that was actually transfused into these people. This allowed them to withstand the allergic reaction. Denyss third patient to undergo a blood transfusion was Swedish Baron Gustaf Bonde. He received two transfusions. After the second transfusion Bonde died. In the winter of 1667, Denys performed several transfusions on Antoine Mauroy with calfs blood. On the third account Mauroy died.Six months later in London, Lower performed the first human transfusion of animal blood in Britain, where he "superintended the introduction in [a patients] arm at various times of some ounces of sheeps blood at a meeting of the Royal Society, and without any inconvenience to him." The recipient was Arthur Coga, "the subject of a harmless form of insanity." Sheeps blood was used because of speculation about the value of blood exchange between species; it had been suggested that blood from a gentle lamb might quiet the tempestuous spirit of an agitated person and that the shy might be made outgoing by blood from more sociable creatures. Coga received 20 shillings (equivalent to £183 in 2021) to participate in the experiment.Lower went on to pioneer new devices for the precise control of blood flow and the transfusion of blood; his designs were substantially the same as modern syringes and catheters. Shortly after, Lower moved to London, where his growing practice soon led him to abandon research.These early experiments with animal blood provoked a heated controversy in Britain and France. Finally, in 1668, the Royal Society and the French government both banned the procedure. The Vatican condemned these experiments in 1670. Blood transfusions fell into obscurity for the next 150 years. Human blood The science of blood transfusion dates to the first decade of the 20th century, with the discovery of distinct blood types leading to the practice of mixing some blood from the donor and the receiver before the transfusion (an early form of cross-matching).In the early 19th century, British obstetrician Dr. James Blundell made efforts to treat hemorrhage by transfusion of human blood using a syringe. In 1818 following experiments with animals, he performed the first successful transfusion of human blood to treat postpartum hemorrhage. Blundell used the patients husband as a donor, and extracted four ounces of blood from his arm to transfuse into his wife. During the years 1825 and 1830, Blundell performed 10 transfusions, five of which were beneficial, and published his results. He also invented a number of instruments for the transfusion of blood. He made a substantial amount of money from this endeavour, roughly $2 million ($50 million real dollars).In 1840, at St Georges Hospital Medical School in London, Samuel Armstrong Lane, aided by Blundell, performed the first successful whole blood transfusion to treat haemophilia.However, early transfusions were risky and many resulted in the death of the patient. By the late 19th century, blood transfusion was regarded as a risky and dubious procedure, and was largely shunned by the medical establishment. Work to emulate James Blundell continued in Edinburgh. In 1845 the Edinburgh Journal described the successful transfusion of blood to a woman with severe uterine bleeding. Subsequent transfusions were successful with patients of Professor James Young Simpson after whom the Simpson Memorial Maternity Pavilion in Edinburgh was named.Various isolated reports of successful transfusions emerged towards the end of the 19th century. The largest series of early successful transfusions took place at the Edinburgh Royal Infirmary between 1885 and 1892. Edinburgh later became the home of the first blood donation and blood transfusion services. 20th century Only in 1901, when the Austrian Karl Landsteiner discovered three human blood groups (O, A, and B), did blood transfusion achieve a scientific basis and become safer.Landsteiner discovered that adverse effects arise from mixing blood from two incompatible individuals. He found that mixing incompatible types triggers an immune response and the red blood-cells clump. The immunological reaction occurs when the receiver of a blood transfusion has antibodies against the donor blood-cells. The destruction of red blood cells releases free hemoglobin into the bloodstream, which can have fatal consequences. Landsteiners work made it possible to determine blood group and allowed blood transfusions to take place much more safely. For his discovery he won the Nobel Prize in Physiology and Medicine in 1930; many other blood groups have been discovered since.George Washington Crile is credited with performing the first surgery using a direct blood transfusion in 1906 at St. Alexis Hospital in Cleveland while a professor of surgery at Case Western Reserve University.Jan Janský also discovered the human blood groups; in 1907 he classified blood into four groups: I, II, III, IV. His nomenclature is still used in Russia and in states of the former USSR, in which blood types O, A, B, and AB are respectively designated I, II, III, and IV. Dr. William Lorenzo Mosss (1876–1957) Moss-blood typing technique of 1910 was widely used until World War II.William Stewart Halsted, M.D. (1852–1922), an American surgeon, performed one of the first blood transfusions in the United States. He had been called to see his sister after she had given birth. He found her moribund from blood loss, and in a bold move withdrew his own blood, transfused his blood into his sister, and then operated on her to save her life. Blood banks in WWI While the first transfusions had to be made directly from donor to receiver before coagulation, it was discovered that by adding anticoagulant and refrigerating the blood it was possible to store it for some days, thus opening the way for the development of blood banks. John Braxton Hicks was the first to experiment with chemical methods to prevent the coagulation of blood at St Marys Hospital, London in the late-19th century. His attempts, using phosphate of soda, however, proved unsuccessful. The Belgian doctor Albert Hustin performed the first non-direct transfusion on March 27, 1914, though this involved a diluted solution of blood. The Argentine doctor Luis Agote used a much less diluted solution in November of the same year. Both used sodium citrate as an anticoagulant.The First World War (1914-1918) acted as a catalyst for the rapid development of blood banks and transfusion techniques. Canadian doctor and Lieutenant Lawrence Bruce Robertson became instrumental in persuading the Royal Army Medical Corps to adopt the use of blood transfusion at the Casualty Clearing Stations for the wounded. In October 1915, Robertson performed his first wartime transfusion with a syringe to a patient who had multiple shrapnel wounds. He followed this up with four subsequent transfusions in the following months, and his success was reported to Sir Walter Morley Fletcher, director of the Medical Research Committee. Robertson published his findings in the British Medical Journal in 1916 and, with the help of a few like-minded individuals (including the eminent physician Edward William Archibald (1872–1945), who introduced the citrate anticoagulant method), was able to persuade the British authorities of the merits of blood transfusion. Robertson went on to establish the first blood-transfusion apparatus at a Casualty Clearing Station on the Western Front in the spring of 1917.Oswald Hope Robertson, a medical researcher and U.S. Army officer, was attached to the RAMC in 1917, where he became instrumental in establishing the first blood banks in preparation for the anticipated Third Battle of Ypres. He used sodium citrate as the anticoagulant; blood was extracted from punctures in the vein and was stored in bottles at British and American Casualty Clearing Stations along the Front. Robertson also experimented with preserving separated red blood cells in iced bottles. Geoffrey Keynes, a British surgeon, developed a portable machine that could store blood to enable transfusions to be carried out more easily. Expansion The secretary of the British Red Cross, Percy Oliver, established the worlds first blood-donor service in 1921. In that year, Oliver was contacted by Kings College Hospital, where they were in urgent need of a blood donor. After providing a donor, Oliver set about organizing a system for the voluntary registration of blood donors at clinics around London, with Sir Geoffrey Keynes appointed as a medical adviser. Volunteers were subjected to a series of physical tests to establish their blood group. The London Blood Transfusion Service was free of charge and expanded rapidly in its first few years of operation. By 1925 it was providing services for almost 500 patients; it was incorporated into the structure of the British Red Cross in 1926. Similar systems developed in other cities, including Sheffield, Manchester and Norwich, and the services work began to attract international attention. France, Germany, Austria, Belgium, Australia and Japan established similar services.Alexander Bogdanov founded an academic institution devoted to the science of blood transfusion in Moscow in 1925. Bogdanov was motivated, at least in part, by a search for eternal youth, and remarked with satisfaction on the improvement of his eyesight, suspension of balding, and other positive symptoms after receiving 11 transfusions of whole blood. Bogdanov died in 1928 as a result of one of his experiments, when the blood of a student with malaria and tuberculosis was given to him in a transfusion. Following Bogdanovs lead, Vladimir Shamov and Sergei Yudin in the USSR pioneered the transfusion of cadaveric blood from recently deceased donors. Yudin performed such a transfusion successfully for the first time on March 23, 1930, and reported his first seven clinical transfusions with cadaveric blood at the Fourth Congress of Ukrainian Surgeons at Kharkiv in September. However, this method was never used widely, even in the Soviet Union. Nevertheless, the Soviet Union was the first to establish a network of facilities to collect and store blood for use in transfusions at hospitals. Frederic Durán-Jordà established one of the earliest blood banks during the Spanish Civil War in 1936. Duran joined the Transfusion Service at the Barcelona Hospital at the start of the conflict, but the hospital was soon overwhelmed by the demand for blood and the paucity of available donors. With support from the Department of Health of the Spanish Republican Army, Duran established a blood bank for the use of wounded soldiers and civilians. The 300–400 mL of extracted blood was mixed with 10% citrate solution in a modified Duran Erlenmeyer flask. The blood was stored in a sterile glass enclosed under pressure at 2 °C. During 30 months of work, the Transfusion Service of Barcelona registered almost 30,000 donors, and processed 9,000 liters of blood.In 1937 Bernard Fantus, director of therapeutics at the Cook County Hospital in Chicago, established the first hospital blood-bank in the United States. In setting up a hospital laboratory that preserved, refrigerated and stored donor blood, Fantus originated the term "blood bank". Within a few years, hospital and community blood-banks were established across the United States.Frederic Durán-Jordà fled to Britain in 1938 and worked with Dr Janet Vaughan at the Royal Postgraduate Medical School at Hammersmith Hospital to establish a system of national blood banks in London. With the outbreak of war appearing imminent in 1938, the War Office created the Army Blood Supply Depot (ABSD) in Bristol, headed by Lionel Whitby and in control of four large blood-depots around the country. British policy through the war was to supply military personnel with blood from centralized depots, in contrast to the approach taken by the Americans and Germans where troops at the front were bled to provide required blood. The British method proved more successful in adequately meeting all requirements, and over 700,000 donors were bled over the course of the war. This system evolved into the National Blood Transfusion Service established in 1946, the first national service to be implemented. Stories tell of Nazis in Eastern Europe during World War II using captive children as repeated involuntary blood-donors. Medical advances A blood-collection program was initiated in the US in 1940 and Edwin Cohn pioneered the process of blood fractionation. He worked out the techniques for isolating the serum albumin fraction of blood plasma, which is essential for maintaining the osmotic pressure in the blood vessels, preventing their collapse. Gordon R. Ward, writing in the correspondence columns of the British Medical Journal, proposed the use of blood plasma as a substitute for whole blood and for transfusion purposes as early as 1918. At the onset of World War II, liquid plasma was used in Britain. A large project, known as "Blood for Britain", began in August 1940 to collect blood in New York City hospitals for the export of plasma to Britain. A dried plasma package was developed, which reduced breakage and made transportation, packaging, and storage much simpler. The resulting dried plasma package came in two tin cans containing 400 mL bottles. One bottle contained enough distilled water to reconstitute the dried plasma contained within the other bottle. In about three minutes, the plasma would be ready to use and could stay fresh for around four hours. Dr. Charles R. Drew was appointed medical supervisor, and he was able to transform the test-tube methods into the first successful technique for mass production. Another important breakthrough came in 1937–40 when Karl Landsteiner (1868–1943), Alex Wiener, Philip Levine, and R.E. Stetson discovered the Rhesus blood group system, which was found to be the cause of the majority of transfusion reactions up to that time. Three years later, the introduction by J.F. Loutit and Patrick L. Mollison of acid–citrate–dextrose (ACD) solution, which reduced the volume of anticoagulant, permitted transfusions of greater volumes of blood and allowed longer-term storage. Carl Walter and W.P. Murphy Jr. introduced the plastic bag for blood collection in 1950. Replacing breakable glass bottles with durable plastic bags made from PVC allowed for the evolution of a collection system capable of safe and easy preparation of multiple blood components from a single unit of whole blood. In the field of cancer surgery, the replacement of massive blood-loss became a major problem. The cardiac-arrest rate was high. In 1963 C. Paul Boyan and William S. Howland discovered that the temperature of the blood and the rate of infusion greatly affected survival rates, and introduced blood warming to surgery.Further extending the shelf-life of stored blood up to 42 days was an anticoagulant preservative, CPDA-1, introduced in 1979, which increased the blood supply and facilitated resource-sharing among blood banks.As of 2006 about 15 million units of blood products were transfused per year in the United States. By 2013 the number had declined to about 11 million units, because of the shift towards laparoscopic surgery and other surgical advances and studies that have shown that many transfusions were unnecessary. For example, the standard of care reduced the amount of blood transfused in one case from 750 to 200 mL. Special populations Neonate To ensure the safety of blood transfusion to pediatric patients, hospitals are taking additional precautions to avoid infection and prefer to use specially tested pediatric blood units that are guaranteed negative for Cytomegalovirus. Most guidelines recommend the provision of CMV-negative blood components and not simply leukoreduced components for newborns or low birthweight infants in whom the immune system is not fully developed. These specific requirements place additional restrictions on blood donors who can donate for neonatal use. Neonatal transfusions typically fall into one of two categories: "Top-up" transfusions, to replace losses due to investigational losses and correction of anemia. Exchange (or partial exchange) transfusions are done for removal of bilirubin, removal of antibodies and replacement of red cells (e.g., for anemia secondary to thalassemias and other hemoglobinopathies). Significant blood loss A massive transfusion protocol is used when significant blood loss is present such as in major trauma, when more than ten units of blood are needed. Packed red blood cells, fresh frozen plasma, and platelets are generally administered. Typically higher ratios of fresh frozen plasma and platelets are given relative to packed red blood cells. Unknown blood type Because blood type O negative is compatible with anyone, it is often overused and in short supply. According to the American Association of Blood Banks, the use of this blood should be restricted to persons with O negative blood, as nothing else is compatible with them, and women who might be pregnant and for whom it would be impossible to do blood group testing before giving them emergency treatment. Whenever possible, the AABB recommends that O negative blood be conserved by using blood type testing to identify a less scarce alternative. Religious objections Jehovahs Witnesses may object to blood transfusions because of their belief that blood is sacred. Research into alternatives Although there are clinical situations where transfusion with red blood cells is the only clinically appropriate option, clinicians look at whether alternatives are feasible. This can be due to several reasons, such as patient safety, economic burden or scarcity of blood. Guidelines recommend blood transfusions should be reserved for patients with or at risk of cardiovascular instability due to the degree of their anaemia. In these cases parenteral iron is recommended. Thus far, there are no available oxygen-carrying blood substitutes, which is the typical objective of a blood (RBC) transfusion; however, there are widely available non-blood volume expanders for cases where only volume restoration is required. These are helping doctors and surgeons avoid the risks of disease transmission and immune suppression, address the chronic blood donor shortage, and address the concerns of Jehovahs Witnesses and others who have religious objections to receiving transfused blood. The research in this area is ongoing. A number of blood substitutes have been explored, but thus far they all have serious limitations. Most attempts to find a suitable alternative to blood thus far have concentrated on cell-free hemoglobin solutions. Blood substitutes could make transfusions more readily available in emergency medicine and in pre-hospital EMS care. If successful, such a blood substitute could save many lives, particularly in trauma where massive blood loss results. Hemopure, a hemoglobin-based therapy, is approved for use in South Africa. Other uses Minor blood transfusions are used by a minority of nyaope drug addicts in South Africa to economically share the high the drug induces in a practice colloquially known as Bluetoothing, named after the wireless technology of the same name. Veterinary use Veterinarians also administer transfusions to other animals. Various species require different levels of testing to ensure a compatible match. For example, cats have 3 known blood types, cattle have 11, dogs have 13, pigs have 16, and horses have 34. However, in many species (especially horses and dogs), cross matching is not required before the first transfusion, as antibodies against non-self cell surface antigens are not expressed constitutively – i.e. the animal has to be sensitized before it will mount an immune response against the transfused blood. The rare and experimental practice of inter-species blood transfusions is a form of xenograft. See also Anemia Arnault Tzanck Blood transfusion in Sri Lanka Blood type (non-human) Xenotransfusion Young blood transfusion, a pseudoscientific practice involving the transfusion of blood taken from young donors to older recipients that is claimed to have health benefits AIDS References Further reading Tucker, Holly (2012). Blood Work: A Tale of Medicine and Murder in the Scientific Revolution. W. W. Norton & Company. ISBN 978-0393342239. "Milk as a Substitute for Blood Transfusion", historical account, Scientific American, 13 July 1878, p. 19 External links Transfusion Evidence Library searchable source of evidence for transfusion medicine. Blood transfusion societies American Association of Blood Banks (AABB) British Blood Transfusion Society (BBTS) International Society of Blood Transfusion (ISBT) Books Blood Groups and Red Cell Antigens Free online book at NCBI Bookshelf ID: NBK2261 Handbook of Transfusion Medicine Free book published in the UK 5th edition Guidelines American Association of Blood Banks Clinical Practice Guidelines Australian National Blood Authority Patient Blood Management Guidelines British Committee for Standards in Haematology National Institute for Health and Care Excellence Blood Transfusion Guidance UK Guidance for transfusion. Canadian Blood Transfusion Guidelines German Medical Association Guidelines (English), published 2014. Patient information Blood Transfusion Leaflets (NHS Blood and Transplant) Blood Transfusion Leaflets (Welsh Blood Service) Blood Transfusion Information (Scotland) Blood Transfusion Information (Australia) Blood Transfusion Information (American Cancer Society)

You are a medical interpreter. Your duty is to translate medical terms into easily digestible information, maintaining accuracy and detail.

I'm encountering the term 'Bells palsy' in medical literature. What's its definition?

Bells palsy is a type of facial paralysis that results in a temporary inability to control the facial muscles on the affected side of the face. In most cases, the weakness is temporary and significantly improves over weeks. Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or, in rare cases, both sides of the face. Other symptoms include drooping of the eyelid, a change in taste, and pain around the ear. Typically symptoms come on over 48 hours. Bells palsy can trigger an increased sensitivity to sound known as hyperacusis.The cause of Bells palsy is unknown and it can occur in any age. Risk factors include diabetes, a recent upper respiratory tract infection, and pregnancy. It results from a dysfunction of cranial nerve VII (the facial nerve). Many believe that this is due to a viral infection that results in swelling. Diagnosis is based on a persons appearance and ruling out other possible causes. Other conditions that can cause facial weakness include brain tumor, stroke, Ramsay Hunt syndrome type 2, myasthenia gravis, and Lyme disease.The condition normally gets better by itself, with most achieving normal or near-normal function. Corticosteroids have been found to improve outcomes, while antiviral medications may be of a small additional benefit. The eye should be protected from drying up with the use of eye drops or an eyepatch. Surgery is generally not recommended. Often signs of improvement begin within 14 days, with complete recovery within six months. A few may not recover completely or have a recurrence of symptoms.Bells palsy is the most common cause of one-sided facial nerve paralysis (70%). It occurs in 1 to 4 per 10,000 people per year. About 1.5% of people are affected at some point in their lives. It most commonly occurs in people between ages 15 and 60. Males and females are affected equally. It is named after Scottish surgeon Charles Bell (1774–1842), who first described the connection of the facial nerve to the condition. Signs and symptoms Bells palsy is characterized by a one-sided facial droop that comes on within 72 hours. In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, through the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bells palsy may present with loss of taste sensation in the anterior 2⁄3 of the tongue on the affected side.Although the facial nerve innervates the stapedius muscle of the middle ear (through the tympanic branch), sound sensitivity, causing normal sounds to be perceived as very loud (hyperacusis), and dysacusis are possible but hardly ever clinically evident.Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bells palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction". Cause The cause of Bells palsy is unknown. Risk factors include diabetes, a recent upper respiratory tract infection, and pregnancy.Some viruses are thought to establish a persistent (or latent) infection without symptoms, e.g., the varicella zoster virus and the Epstein–Barr virus, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggested as a cause of acute Bells palsy. As the facial nerve swells and becomes inflamed in reaction to the infection, it causes pressure within the Fallopian canal, resulting in the restriction of blood and oxygen to the nerve cells. Other viruses and bacteria that have been linked to the development of Bells palsy include HIV, sarcoidosis and Lyme Disease. This new activation could be triggered by trauma, environmental factors, and metabolic or emotional disorders.Familial inheritance has been found in 4–14% of cases. There may also be an association with migraines.In December 2020, the U.S. FDA recommended that recipients of the Pfizer and Moderna COVID-19 vaccines should be monitored for symptoms of Bells palsy after several cases were reported among clinical trial participants, though the data were not sufficient to determine a causal link. Genetics A meta-analysis of genome-wide association study (GWAS) identified the first unequivocal association with Bells palsy. Pathophysiology Bells palsy is the result of a malfunction of the facial nerve (cranial nerve VII), which controls the muscles of the face. Facial palsy is typified by inability to move the muscles of facial expression. The paralysis is of the infranuclear/lower motor neuron type. It is thought that as a result of inflammation of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal (the stylomastoid foramen), blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bells palsy per se. Possible causes of facial paralysis include tumor, meningitis, stroke, diabetes mellitus, head trauma and inflammatory diseases of the cranial nerves (sarcoidosis, brucellosis, etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy. In a few cases, bilateral facial palsy has been associated with acute HIV infection. In some research, the herpes simplex virus type 1 (HSV-1) has been identified in a majority of cases diagnosed as Bells palsy through endoneurial fluid sampling. Other research, however, identified, out of a total of 176 cases diagnosed as Bells palsy, HSV-1 in 31 cases (18%) and herpes zoster in 45 cases (26%).In addition, HSV-1 infection is associated with demyelination of nerves. This nerve damage mechanism is different from the above-mentioned—that edema, swelling and compression of the nerve in the narrow bone canal is responsible for nerve damage. Demyelination may not even be directly caused by the virus, but by an unknown immune response. Diagnosis Bells palsy is a diagnosis of exclusion, meaning it is diagnosed by elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. The degree of nerve damage can be assessed using the House-Brackmann score. One study found that 45% of patients are not referred to a specialist, which suggests that Bells palsy is considered by physicians to be a straightforward diagnosis that is easy to manage.Other conditions that can cause similar symptoms include herpes zoster, Lyme disease, sarcoidosis, stroke, and brain tumors. Differential diagnosis Once the facial paralysis sets in, many people may mistake it as a symptom of a stroke; however, there are a few subtle differences. A stroke will usually cause a few additional symptoms, such as numbness or weakness in the arms and legs. And unlike Bells palsy, a stroke will usually let patients control the upper part of their faces. A person with a stroke will usually have some wrinkling of their forehead.In areas where Lyme disease is common, it accounts for about 25% of cases of facial palsy. In the U.S., Lyme is most common in the New England and Mid-Atlantic states and parts of Wisconsin and Minnesota. The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an expanding rash that may be accompanied by headaches, body aches, fatigue, or fever. In up to 10–15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed as the Lyme rash typically does not itch and is not painful. The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bells palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed, and if it exceeds 10%, empiric therapy with antibiotics should be initiated, without corticosteroids, and reevaluated upon completion of laboratory tests for Lyme disease. Corticosteroids have been found to harm outcomes for facial palsy caused by Lyme disease.One disease that may be difficult to exclude in the differential diagnosis is involvement of the facial nerve in infections with the herpes zoster virus. The major differences in this condition are the presence of small blisters, or vesicles, on the external ear, significant pain in the jaw, ear face, and/or neck and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existing herpes zoster infection leading to facial paralysis in a Bells palsy type pattern is known as Ramsay Hunt syndrome type 2. The prognosis for Bells palsy patients is generally much better than for Ramsay Hunt syndrome type 2 patients. Treatment Steroids have been shown to be effective at improving recovery in Bells palsy while antivirals have not. In those who are unable to close their eyes, eye protective measures are required. Management during pregnancy is similar to management in the non-pregnant. Steroids Corticosteroids such as prednisone improve recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery. Antivirals One review found that antivirals (such as aciclovir) are ineffective in improving recovery from Bells palsy beyond steroids alone in mild to moderate disease. Another review found a benefit when combined with corticosteroids but stated the evidence was not very good to support this conclusion.In severe disease it is also unclear. One 2015 review found no effect regardless of severity. Another review found a small benefit when added to steroids.They are commonly prescribed due to a theoretical link between Bells palsy and the herpes simplex and varicella zoster virus. There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out. Eye protection When Bells palsy affects the blink reflex and stops the eye from closing completely, frequent use of tear-like eye drops or eye ointments is recommended during the day and protecting the eyes with patches or taping them shut is recommended for sleep and rest periods. Physiotherapy Physiotherapy can be beneficial to some individuals with Bells palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve. It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles. To reduce pain, heat can be applied to the affected side of the face. There is no high quality evidence to support the role of electrical stimulation for Bells palsy. Surgery Surgery may be able to improve outcomes in facial nerve palsy that has not recovered. A number of different techniques exist. Smile surgery or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. Adverse effects include hearing loss which occurs in 3–15% of people. A Cochrane review (updated in 2021), after reviewing applicable randomized and quasi-randomized controlled trials was unable to determine if early surgery is beneficial or harmful. As of 2007 the American Academy of Neurology did not recommend surgical decompression. Alternative medicine The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). There is very tentative evidence for hyperbaric oxygen therapy in severe disease. Prognosis Most people with Bells palsy start to regain normal facial function within 3 weeks—even those who do not receive treatment. In a 1982 study, when no treatment was available, of 1,011 patients, 85% showed first signs of recovery within 3 weeks after onset. For the other 15%, recovery occurred 3–6 months later. After a follow-up of at least one year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. Recovery was judged moderate in 12% and poor in only 4% of patients. Another study found that incomplete palsies disappear entirely, nearly always in the course of one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop sequelae. A third study found a better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis.Major possible complications of the condition are chronic loss of taste (ageusia), chronic facial spasm, facial pain and corneal infections. Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections that branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination—but some nerves may sidetrack leading to a condition known as synkinesis. For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily. Around 9% of people have some sort of ongoing problems after Bells palsy, typically the synkinesis already discussed, or spasm, contracture, tinnitus or hearing loss during facial movement or crocodile-tear syndrome. This is also called gustatolacrimal reflex or Bogorads syndrome and results in shedding tears while eating. This is thought to be due to faulty regeneration of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur. Epidemiology The number of new cases of Bells palsy ranges from about one to four cases per 10,000 population per year. The rate increases with age. Bells palsy affects about 40,000 people in the United States every year. It affects approximately 1 person in 65 during a lifetime. A range of annual incidence rates have been reported in the literature: 15, 24, and 25–53 (all rates per 100,000 population per year). Bells palsy is not a reportable disease, and there are no established registries for people with this diagnosis, which complicates precise estimation. Frequency About 40,000 people are affected by Bells Palsy in the United States every year. It can affect anyone of any gender and age, but its incidence seems to be highest in those in the 15- to 45-year-old age group. History The Persian physician Muhammad ibn Zakariya al-Razi (865–925) detailed the first known description of peripheral and central facial palsy.Cornelis Stalpart van der Wiel (1620–1702) in 1683 gave an account of Bells palsy and credited the Persian physician Ibn Sina (980–1037) for describing this condition before him. James Douglas (1675–1742) and Nicolaus Anton Friedreich (1761–1836) also described it. Scottish neurophysiologist Sir Charles Bell read his paper to the Royal Society of London on July 12, 1821, describing the role of the facial nerve. He became the first to detail the neuroanatomical basis of facial paralysis. Since then, idiopathic peripheral facial paralysis has been referred to as Bells palsy, named after him.A notable person with Bells palsy is former Prime Minister of Canada Jean Chrétien. During the 1993 Canadian federal election, Chrétiens first as leader of the Liberal Party of Canada, the opposition Progressive Conservative Party of Canada ran an attack ad in which voice actors criticized him over images that seemed to highlight his abnormal facial expressions. The ad was interpreted as an attack on Chrétiens physical appearance and garnered widespread anger among the public, while Chrétien used the ad to make himself more sympathetic to voters. The ad had the adverse effect of increasing Chrétiens lead in the polls and the subsequent backlash clinched the election for the Liberals, which the party won in a landslide. References External links Bells palsy at Curlie

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

Please help me grasp the concept behind the medical term 'Rheumatoid arthritis.'

Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Pain and stiffness often worsen following rest. Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body. The disease may also affect other parts of the body, including skin, eyes, lungs, heart, nerves and blood. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart. Fever and low energy may also be present. Often, symptoms come on gradually over weeks to months.While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves the bodys immune system attacking the joints. This results in inflammation and thickening of the joint capsule. It also affects the underlying bone and cartilage. The diagnosis is made mostly on the basis of a persons signs and symptoms. X-rays and laboratory testing may support a diagnosis or exclude other diseases with similar symptoms. Other diseases that may present similarly include systemic lupus erythematosus, psoriatic arthritis, and fibromyalgia among others.The goals of treatment are to reduce pain, decrease inflammation, and improve a persons overall functioning. This may be helped by balancing rest and exercise, the use of splints and braces, or the use of assistive devices. Pain medications, steroids, and NSAIDs are frequently used to help with symptoms. Disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the progression of disease. Biological DMARDs may be used when disease does not respond to other treatments. However, they may have a greater rate of adverse effects. Surgery to repair, replace, or fuse joints may help in certain situations.RA affects about 24.5 million people as of 2015. This is between 0.5 and 1% of adults in the developed world with 5 and 50 per 100,000 people newly developing the condition each year. Onset is most frequent during middle age and women are affected 2.5 times as frequently as men. It resulted in 38,000 deaths in 2013, up from 28,000 deaths in 1990. The first recognized description of RA was made in 1800 by Dr. Augustin Jacob Landré-Beauvais (1772–1840) of Paris. The term rheumatoid arthritis is based on the Greek for watery and inflamed joints. Signs and symptoms RA primarily affects joints, but it also affects other organs in more than 15–25% of cases. Associated problems include cardiovascular disease, osteoporosis, interstitial lung disease, infection, cancer, feeling tired, depression, mental difficulties, and trouble working. Joints Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved.: 1098  Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function. The fibroblast-like synoviocytes (FLS), highly specialized mesenchymal cells found in the synovial membrane, have an active and prominent role in these pathogenic processes of the rheumatic joints.RA typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and typically lasts for more than an hour. Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, such as osteoarthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are less prominent. The pain associated with RA is induced at the site of inflammation and classified as nociceptive as opposed to neuropathic. The joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical.: 1098 As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may develop almost any deformity depending on which joints are most involved. Specific deformities, which also occur in osteoarthritis, include ulnar deviation, boutonniere deformity (also "buttonhole deformity", flexion of proximal interphalangeal joint and extension of distal interphalangeal joint of the hand), swan neck deformity (hyperextension at proximal interphalangeal joint and flexion at distal interphalangeal joint) and "Z-thumb." "Z-thumb" or "Z-deformity" consists of hyperextension of the interphalangeal joint, fixed flexion and subluxation of the metacarpophalangeal joint and gives a "Z" appearance to the thumb.: 1098  The hammer toe deformity may be seen. In the worst case, joints are known as arthritis mutilans due to the mutilating nature of the deformities. Skin The rheumatoid nodule, which is sometimes in the skin, is the most common non-joint feature and occurs in 30% of people who have RA. It is a type of inflammatory reaction known to pathologists as a "necrotizing granuloma". The initial pathologic process in nodule formation is unknown but may be essentially the same as the synovitis, since similar structural features occur in both. The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space. Surrounding the necrosis is a layer of palisading macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of connective tissue containing clusters of lymphocytes and plasma cells, corresponding to the subintimal zone in synovitis. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the elbow, the heel, the knuckles, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer, ACPA, and severe erosive arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.Several forms of vasculitis occur in RA, but are mostly seen with long-standing and untreated disease. The most common presentation is due to involvement of small- and medium-sized vessels. Rheumatoid vasculitis can thus commonly present with skin ulceration and vasculitic nerve infarction known as mononeuritis multiplex.Other, rather rare, skin associated symptoms include pyoderma gangrenosum, Sweets syndrome, drug reactions, erythema nodosum, lobe panniculitis, atrophy of finger skin, palmar erythema, and skin fragility (often worsened by corticosteroid use).Diffuse alopecia areata (Diffuse AA) occurs more commonly in people with rheumatoid arthritis. RA is also seen more often in those with relatives who have AA. Lungs Lung fibrosis is a recognized complication of rheumatoid arthritis. It is also a rare but well-recognized consequence of therapy (for example with methotrexate and leflunomide). Caplans syndrome describes lung nodules in individuals with RA and additional exposure to coal dust. Exudative pleural effusions are also associated with RA. Heart and blood vessels People with RA are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly increased. Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis. Many people with RA do not experience the same chest pain that others feel when they have angina or myocardial infarction. To reduce cardiovascular risk, it is crucial to maintain optimal control of the inflammation caused by RA (which may be involved in causing the cardiovascular risk), and to use exercise and medications appropriately to reduce other cardiovascular risk factors such as blood lipids and blood pressure. Doctors who treat people with RA should be sensitive to cardiovascular risk when prescribing anti-inflammatory medications, and may want to consider prescribing routine use of low doses of aspirin if the gastrointestinal effects are tolerable. Blood Anemia is by far the most common abnormality of the blood cells which can be caused by a variety of mechanisms. The chronic inflammation caused by RA leads to raised hepcidin levels, leading to anemia of chronic disease where iron is poorly absorbed and also sequestered into macrophages. The red cells are of normal size and color (normocytic and normochromic). A low white blood cell count usually only occurs in people with Feltys syndrome with an enlarged liver and spleen. The mechanism of neutropenia is complex. An increased platelet count occurs when inflammation is uncontrolled. Other Kidneys Renal amyloidosis can occur as a consequence of untreated chronic inflammation. Treatment with penicillamine or gold salts such as sodium aurothiomalate are recognized causes of membranous nephropathy. Eyes The eye can be directly affected in the form of episcleritis or scleritis, which when severe can very rarely progress to perforating scleromalacia. Rather more common is the indirect effect of keratoconjunctivitis sicca, which is a dryness of eyes and mouth caused by lymphocyte infiltration of lacrimal and salivary glands. When severe, dryness of the cornea can lead to keratitis and loss of vision as well as being painful. Preventive treatment of severe dryness with measures such as nasolacrimal duct blockage is important. Liver Liver problems in people with rheumatoid arthritis may be due to the underlying disease process or as a result of the medications used to treat the disease. A coexisting autoimmune liver disease, such as primary biliary cirrhosis or autoimmune hepatitis may also cause problems. Neurological Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome caused by compression of the median nerve by swelling around the wrist. Rheumatoid disease of the spine can lead to myelopathy. Atlanto-axial subluxation can occur, owing to erosion of the odontoid process and/or transverse ligaments in the cervical spines connection to the skull. Such an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing the spinal cord. Clumsiness is initially experienced, but without due care, this can progress to quadriplegia or even death. Constitutional symptoms Constitutional symptoms including fatigue, low grade fever, malaise, morning stiffness, loss of appetite and loss of weight are common systemic manifestations seen in people with active RA. Bones Local osteoporosis occurs in RA around inflamed joints. It is postulated to be partially caused by inflammatory cytokines. More general osteoporosis is probably contributed to by immobility, systemic cytokine effects, local cytokine release in bone marrow and corticosteroid therapy. Cancer The incidence of lymphoma is increased, although it is uncommon and associated with the chronic inflammation, not the treatment of RA. The risk of non-melanoma skin cancer is increased in people with RA compared to the general population, an association possibly due to the use of immunosuppression agents for treating RA. Teeth Periodontitis and tooth loss are common in people with rheumatoid arthritis. Risk factors RA is a systemic (whole body) autoimmune disease. Some genetic and environmental factors affect the risk for RA. Genetic Worldwide, RA affects approximately 1% of the adult population and occurs one in 1000 children. Studies show RA primarily affects individuals between the ages of 40–60 years and is seen more commonly in females. A family history of RA increases the risk around three to five times; as of 2016, it was estimated that genetics may account for between 40 and 65% of cases of seropositive RA, but only around 20% for seronegative RA. RA is strongly associated with genes of the inherited tissue type major histocompatibility complex (MHC) antigen. HLA-DR4 is the major genetic factor implicated – the relative importance varies across ethnic groups.Genome-wide association studies examining single-nucleotide polymorphisms have found around one hundred alleles associated with RA risk. Risk alleles within the HLA (particularly HLA-DRB1) genes harbor more risk than other loci. The HLA encodes proteins which controls recognition of self versus nonself molecules. Other risk loci include genes affecting co-stimulatory immune pathways, for example CD28 and CD40, cytokine signaling, lymphocyte receptor activation threshold (e.g., PTPN22), and innate immune activation appear to have less influence than HLA mutations. Environmental There are established epigenetic and environmental risk factors for RA. Smoking is an established risk factor for RA in Caucasian populations, increasing the risk three times compared to non-smokers, particularly in men, heavy smokers, and those who are rheumatoid factor positive. Modest alcohol consumption may be protective.Silica exposure has been linked to RA. Vitamin D deficiency There are claims that patients that have lower vitamin D levels by 8-10 ng/mL are at risk for rheumatoid arthritis. Negative findings No infectious agent has been consistently linked with RA and there is no evidence of disease clustering to indicate its infectious cause, but periodontal disease has been consistently associated with RA.The many negative findings suggest that either the trigger varies, or that it might, in fact, be a chance event inherent with the immune response. Pathophysiology RA primarily starts as a state of persistent cellular activation leading to autoimmunity and immune complexes in joints and other organs where it manifests. The clinical manifestations of disease are primarily inflammation of the synovial membrane and joint damage, and the fibroblast-like synoviocytes play a key role in these pathogenic processes. Three phases of progression of RA are an initiation phase (due to non-specific inflammation), an amplification phase (due to T cell activation), and chronic inflammatory phase, with tissue injury resulting from the cytokines, IL–1, TNF-alpha, and IL–6. Non-specific inflammation Factors allowing an abnormal immune response, once initiated, become permanent and chronic. These factors are genetic disorders which change regulation of the adaptive immune response. Genetic factors interact with environmental risk factors for RA, with cigarette smoking as the most clearly defined risk factor.Other environmental and hormonal factors may explain higher risks for women, including onset after childbirth and hormonal medications. A possibility for increased susceptibility is that negative feedback mechanisms – which normally maintain tolerance – are overtaken by positive feedback mechanisms for certain antigens, such as IgG Fc bound by rheumatoid factor and citrullinated fibrinogen bound by antibodies to citrullinated peptides (ACPA - Anti–citrullinated protein antibody). A debate on the relative roles of B-cell produced immune complexes and T cell products in inflammation in RA has continued for 30 years, but neither cell is necessary at the site of inflammation, only autoantibodies to IgGFc, known as rheumatoid factors and ACPA, with ACPA having an 80% specificity for diagnosing RA. As with other autoimmune diseases, people with RA have abnormally glycosylated antibodies, which are believed to promote joint inflammation. Amplification in the synovium Once the generalized abnormal immune response has become established – which may take several years before any symptoms occur – plasma cells derived from B lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in large quantities. These activate macrophages through Fc receptor and complement binding, which is part of the intense inflammation in RA. Binding of an autoreactive antibody to the Fc receptors is mediated through the antibodys N-glycans, which are altered to promote inflammation in people with RA.This contributes to local inflammation in a joint, specifically the synovium with edema, vasodilation and entry of activated T-cells, mainly CD4 in microscopically nodular aggregates and CD8 in microscopically diffuse infiltrates. Synovial macrophages and dendritic cells function as antigen-presenting cells by expressing MHC class II molecules, which establishes the immune reaction in the tissue. Chronic inflammation The disease progresses by forming granulation tissue at the edges of the synovial lining, pannus with extensive angiogenesis and enzymes causing tissue damage. The fibroblast-like synoviocytes have a prominent role in these pathogenic processes. The synovium thickens, cartilage and underlying bone disintegrate, and the joint deteriorates, with raised calprotectin levels serving as a biomarker of these events. Importantly inflammatory events are not limited to synovium but it appear to be systemic, evidence suggest that alterations in T helper profile favoring inflammation such as inflammatory IL-17A producing T helper cells and pathogenic Th17 cells are come from both memory and effector compartment in RA patients peripheral blood.Cytokines and chemokines attract and accumulate immune cells, i.e. activated T- and B cells, monocytes and macrophages from activated fibroblast-like synoviocytes, in the joint space. By signalling through RANKL and RANK, they eventually trigger osteoclast production, which degrades bone tissue. The fibroblast-like synoviocytes that are present in the synovium during rheumatoid arthritis display altered phenotype compared to the cells present in normal tissues. The aggressive phenotype of fibroblast-like synoviocytes in rheumatoid arthritis and the effect these cells have on the microenvironment of the joint can be summarized into hallmarks that distinguish them from healthy fibroblast-like synoviocytes. These hallmark features of fibroblast-like synoviocytes in rheumatoid arthritis are divided into 7 cell-intrinsic hallmarks and 4 cell-extrinsic hallmarks. The cell-intrinsic hallmarks are: reduced apoptosis, impaired contact inhibition, increased migratory invasive potential, changed epigenetic landscape, temporal and spatial heterogeneity, genomic instability and mutations, and reprogrammed cellular metabolism. The cell-extrinsic hallmarks of FLS in RA are: promotes osteoclastogenesis and bone erosion, contributes to cartilage degradation, induces synovial angiogenesis, and recruits and stimulates immune cells. Diagnosis Imaging X-rays of the hands and feet are generally performed when many joints affected. In RA, there may be no changes in the early stages of the disease or the x-ray may show osteopenia near the joint, soft tissue swelling, and a smaller than normal joint space. As the disease advances, there may be bony erosions and subluxation. Other medical imaging techniques such as magnetic resonance imaging (MRI) and ultrasound are also used in RA.Technical advances in ultrasonography like high-frequency transducers (10 MHz or higher) have improved the spatial resolution of ultrasound images depicting 20% more erosions than conventional radiography. Color Doppler and power Doppler ultrasound are useful in assessing the degree of synovial inflammation as they can show vascular signals of active synovitis. This is important, since in the early stages of RA, the synovium is primarily affected, and synovitis seems to be the best predictive marker of future joint damage. Blood tests When RA is clinically suspected, a physician may test for rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPAs measured as anti-CCP antibodies). It is positive in 75–85%, but a negative RF or CCP antibody does not rule out RA, rather, the arthritis is called seronegative, which is in about 15–25% of people with RA. During the first year of illness, rheumatoid factor is more likely to be negative with some individuals becoming seropositive over time. RF is a non-specific antibody and seen in about 10% of healthy people, in many other chronic infections like hepatitis C, and chronic autoimmune diseases such as Sjögrens syndrome and systemic lupus erythematosus. Therefore, the test is not specific for RA.Hence, new serological tests check for anti-citrullinated protein antibodies ACPAs. These tests are again positive in 61–75% of all RA cases, but with a specificity of around 95%. As with RF, ACPAs are many times present before symptoms have started.The by far most common clinical test for ACPAs is the anti-cyclic citrullinated peptide (anti CCP) ELISA. In 2008 a serological point-of-care test for the early detection of RA combined the detection of RF and anti-MCV with a sensitivity of 72% and specificity of 99.7%.To improve the diagnostic capture rate in the early detection of patients with RA and to risk stratify these individuals, the rheumatology field continues to seek complementary markers to both RF and anti-CCP. 14-3-3η (YWHAH) is one such marker that complements RF and anti-CCP, along with other serological measures like c-reactive protein. In a systematic review, 14-3-3η has been described as a welcome addition to the rheumatology field. The authors indicate that the serum based 14-3-η marker is additive to the armamentarium of existing tools available to clinicians, and that there is adequate clinical evidence to support its clinical benefits.Other blood tests are usually done to differentiate from other causes of arthritis, like the erythrocyte sedimentation rate (ESR), C-reactive protein, full blood count, kidney function, liver enzymes and other immunological tests (e.g., antinuclear antibody/ANA) are all performed at this stage. Elevated ferritin levels can reveal hemochromatosis, a mimic of RA, or be a sign of Stills disease, a seronegative, usually juvenile, variant of rheumatoid arthritis. Classification criteria In 2010, the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria were introduced.The new criteria are not diagnostic criteria, but are classification criteria to identify disease with a high likelihood of developing a chronic form. However a score of 6 or greater unequivocally classifies a person with a diagnosis of rheumatoid arthritis.These new classification criteria overruled the "old" ACR criteria of 1987 and are adapted for early RA diagnosis. The "new" classification criteria, jointly published by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) establish a point value between 0 and 10. Four areas are covered in the diagnosis: joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal joints, the interphalangeal joint of the thumb, second through fifth metatarsophalangeal joint and wrist as small joints, and shoulders, elbows, hip joints, knees, and ankles as large joints: Involvement of 1 large joint gives 0 points Involvement of 2–10 large joints gives 1 point Involvement of 1–3 small joints (with or without involvement of large joints) gives 2 points Involvement of 4–10 small joints (with or without involvement of large joints) gives 3 points Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points serological parameters – including the rheumatoid factor as well as ACPA – "ACPA" stands for "anti-citrullinated protein antibody": Negative RF and negative ACPA gives 0 points Low-positive RF or low-positive ACPA gives 2 points High-positive RF or high-positive ACPA gives 3 points acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated CRP value (c-reactive protein) duration of arthritis: 1 point for symptoms lasting six weeks or longerThe new criteria accommodate to the growing understanding of RA and the improvements in diagnosing RA and disease treatment. In the "new" criteria, serology and autoimmune diagnostics carries major weight, as ACPA detection is appropriate to diagnose the disease in an early state, before joints destructions occur. Destruction of the joints viewed in radiological images was a significant point of the ACR criteria from 1987. This criterion no longer is regarded to be relevant, as this is just the type of damage that treatment is meant to avoid. Differential diagnoses Several other medical conditions can resemble RA, and need to be distinguished from it at the time of diagnosis: Crystal induced arthritis (gout, and pseudogout) – usually involves particular joints (knee, MTP1, heels) and can be distinguished with an aspiration of joint fluid if in doubt. Redness, asymmetric distribution of affected joints, pain occurs at night and the starting pain is less than an hour with gout. Osteoarthritis – distinguished with X-rays of the affected joints and blood tests, older age, starting pain less than an hour, asymmetric distribution of affected joints and pain worsens when using joint for longer periods. Systemic lupus erythematosus (SLE) – distinguished by specific clinical symptoms and blood tests (antibodies against double-stranded DNA) One of the several types of psoriatic arthritis resembles RA – nail changes and skin symptoms distinguish between them Lyme disease causes erosive arthritis and may closely resemble RA – it may be distinguished by blood test in endemic areas Reactive arthritis – asymmetrically involves heel, sacroiliac joints and large joints of the leg. It is usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica. Axial spondyloarthritis (including ankylosing spondylitis) – this involves the spine, although an RA-like symmetrical small-joint polyarthritis may occur in the context of this condition. Hepatitis C – RA-like symmetrical small-joint polyarthritis may occur in the context of this condition. Hepatitis C may also induce rheumatoid factor auto-antibodies.Rarer causes which usually behave differently but may cause joint pains: Sarcoidosis, amyloidosis, and Whipples disease can also resemble RA. Hemochromatosis may cause hand joint arthritis. Acute rheumatic fever can be differentiated by a migratory pattern of joint involvement and evidence of antecedent streptococcal infection. Bacterial arthritis (such as by Streptococcus) is usually asymmetric, while RA usually involves both sides of the body symmetrically. Gonococcal arthritis (a bacterial arthritis) is also initially migratory and can involve tendons around the wrists and ankles.Sometimes arthritis is in an undifferentiated stage (i.e. none of the above criteria is positive), even if synovitis is witnessed and assessed with ultrasound imaging. Difficult-to-treat Rheumatoid arthritis (D2T RA) is a specific classification RA by the European League against Rheumatism (EULAR).Signs of illness: Persistence of signs and symptoms Drug resistance Does not respond on two or more biological treatments Does not respond on anti-rheumatic drugs with different mechanism of actionFactors contributing to difficult-to-treat disease: Genetic risk factors Environmental factors (diet, smoking, physical activity) Overweight and obese Genetic factors Genetic factors such as HLA-DR1B1, TRAF1, PSORS1C1 and microRNA 146a are associated with difficult to treat rheumatoid arthritis, other gene polymorphisms seem to be correlated with response to biologic modifying anti-rheumatic drugs (bDMARDs). Next one is FOXO3A gene region been reported as associated with worst disorder. The minor allele at FOXO3A summon a differential response of monocytes in RA patients. FOXO3A can provide an increase of pro-inflammatory cytokines, including TNFα. Possible gene polymorphism: STAT4, PTPN2, PSORS1C1 and TRAF3IP2 genes had been correlated with response to TNF inhibitors. HLA-DR1 and HLA-DRB1 gene The HLA-DRB1 gene is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex is the human version of the major histocompatibility complex (MHC). Currently, have been identified at least 2479 different versions of the HLA-DRB1 gene. The presence of HLA-DRB1 alleles seems to predict radiographic damage, which may be partially mediated by ACPA development, and also elevated sera inflammatory levels and high swollen joint count. HLA-DR1 is encoded by the most risk allele HLA-DRB1 which share a conserved 5-aminoacid sequence that is correlated with the development of anti-citrullinated protein antibodies. HLA-DRB1 gene have more strong correlation with disease development. Susceptibility to and outcome for rheumatoid arthritis (RA) may associate with particular HLA-DR alleles, but these alleles vary among ethnic groups and geographic areas. MicroRNAs MicroRNAs are a factor in the development of that type of disease. MicroRNAs usually operate as a negative regulator of the expression of target proteins and their increased concentration after biologic treatment (bDMARDs) or after anti-rheumatic drugs. Level of miRNA before and after anti-TNFa/DMRADs combination therapy are potential novel biomarkers for predicting and monitoring outcome. For instance, some of them were found significantly upregulated by anti-TNFa/DMRADs combination therapy. For example, miRNA-16-5p, miRNA-23-3p, miRNA125b-5p, miRNA-126-3p, miRNA-146a-5p, miRNA-223-3p. Curious fact is that only responder patients showed an increase in those miRNAs after therapy, and paralleled the reduction of TNFα, interleukin (IL)-6, IL-17, rheumatoid factor (RF), and C-reactive protein (CRP). Monitoring progression Many tools can be used to monitor remission in rheumatoid arthritis. DAS28: Disease Activity Score of 28 joints (DAS28) is widely used as an indicator of RA disease activity and response to treatment. Joints included are (bilaterally): proximal interphalangeal joints (10 joints), metacarpophalangeal joints (10), wrists (2), elbows (2), shoulders (2) and knees (2). When looking at these joints, both the number of joints with tenderness upon touching (TEN28) and swelling (SW28) are counted. The erythrocyte sedimentation rate (ESR) is measured and the affected person makes a subjective assessment (SA) of disease activity during the preceding 7 days on a scale between 0 and 100, where 0 is "no activity" and 100 is "highest activity possible". With these parameters, DAS28 is calculated as: D A S 28 = 0.56 × T E N 28 + 0.28 × S W 28 + 0.70 × ln ⁡ ( E S R ) + 0.014 × S A {\displaystyle DAS28=0.56\times {\sqrt {TEN28}}+0.28\times {\sqrt {SW28}}+0.70\times \ln(ESR)+0.014\times SA} From this, the disease activity of the affected person can be classified as follows: It is not always a reliable indicator of treatment effect. One major limitation is that low-grade synovitis may be missed. Other: Other tools to monitor remission in rheumatoid arthritis are: ACR-EULAR Provisional Definition of Remission of Rheumatoid arthritis, Simplified Disease Activity Index and Clinical Disease Activity Index. Some scores do not require input from a healthcare professional and allow self-monitoring by the person, like HAQ-DI. Prevention There is no known prevention for the condition other than the reduction of risk factors. Supplementation Evidence suggests that increasing vitamin D levels to the range of 40–60 ng/mL could reduce the risk of rheumatoid arthritis. Management There is no cure for RA, but treatments can improve symptoms and slow the progress of the disease. Disease-modifying treatment has the best results when it is started early and aggressively. The results of a recent systematic review found that combination therapy with tumor necrosis factor (TNF) and non-TNF biologics plus methotrexate (MTX) resulted in improved disease control, Disease Activity Score (DAS)-defined remission, and functional capacity compared with a single treatment of either methotrexate or a biologic alone.The goals of treatment are to minimize symptoms such as pain and swelling, to prevent bone deformity (for example, bone erosions visible in X-rays), and to maintain day-to-day functioning. This is primarily addressed with disease-modifying antirheumatic drugs (DMARDs); dosed physical activity; analgesics and physical therapy may be used to help manage pain. RA should generally be treated with at least one specific anti-rheumatic medication. The use of benzodiazepines (such as diazepam) to treat the pain is not recommended as it does not appear to help and is associated with risks. Lifestyle Regular exercise is recommended as both safe and useful to maintain muscle strength and overall physical function. Physical activity is beneficial for people with rheumatoid arthritis who experience fatigue, although there was little to no evidence to suggest that exercise may have an impact on physical function in the long term, a study found that carefully dosed exercise has shown significant improvements in patients with RA. Moderate effects have been found for aerobic exercises and resistance training on cardiovascular fitness and muscle strength in RA. Furthermore, physical activity had no detrimental side effects like increased disease activity in any exercise dimension. It is uncertain if eating or avoiding specific foods or other specific dietary measures help improve symptoms. Occupational therapy has a positive role to play in improving functional ability in people with rheumatoid arthritis. Weak evidence supports the use of wax baths (thermotherapy) to treat arthritis in the hands.Educational approaches that inform people about tools and strategies available to help them cope with rheumatoid arthritis may improve a persons psychological status and level of depression in the shorter-term. The use of extra-depth shoes and molded insoles may reduce pain during weight-bearing activities such as walking. Insoles may also prevent the progression of bunions. Disease-modifying agents Disease-modifying antirheumatic drugs (DMARDs) are the primary treatment for RA. They are a diverse collection of drugs, grouped by use and convention. They have been found to improve symptoms, decrease joint damage, and improve overall functional abilities. DMARDs should be started early in the disease as they result in disease remission in approximately half of people and improved outcomes overall.The following drugs are considered DMARDs: methotrexate, sulfasalazine, leflunomide, hydroxychloroquine, TNF inhibitors (certolizumab, adalimumab, infliximab and etanercept), abatacept, and anakinra. Additionally, rituximab and tocilizumab are monoclonal antibodies and are also DMARDs. Use of tocilizumab is associated with a risk of increased cholesterol levels.The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and leflunomide. Leflunomide is effective when used from 6–12 months, with similar effectiveness to methotrexate when used for 2 years. Sulfasalazine also appears to be most effective in the short-term treatment of rheumatoid arthritis.Hydroxychloroquine, in addition to its low toxicity profile, is considered effective for treatment of moderate RA treatment.Agents may be used in combination, however, people may experience greater side effects. Methotrexate is the most important and useful DMARD and is usually the first treatment. A combined approach with methotrexate and biologics improves ACR50, HAQ scores and RA remission rates. Triple therapy consisting of methotrexate, sulfasalazine and hydroxychloroquine may also effectively control disease activity. Adverse effects should be monitored regularly with toxicity including gastrointestinal, hematologic, pulmonary, and hepatic. Side effects such as nausea, vomiting or abdominal pain can be reduced by taking folic acid.A 2015 Cochrane review found rituximab with methotrexate to be effective in improving symptoms compared to methotrexate alone. Rituximab works by decreasing levels of B-cells (immune cell that is involved in inflammation). People taking rituximab had improved pain, function, reduced disease activity and reduced joint damage based on x-ray images. After 6 months, 21% more people had improvement in their symptoms using rituximab and methotrexate.Biological agents should generally be used only if methotrexate and other conventional agents are not effective after a trial of three months. They are associated with a higher rate of serious infections as compared to other DMARDs. Biological DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha inhibitors (TNF inhibitors) such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, interleukin 6 blockers such as tocilizumab, and T cell co-stimulation blockers such as abatacept. They are often used in combination with either methotrexate or leflunomide. Biologic monotherapy or tofacitinib with methotrexate may improve ACR50, RA remission rates and function. Abatacept should not be used at the same time as other biologics. In those who are well controlled (low disease activity) on TNF inhibitors, decreasing the dose does not appear to affect overall function. Discontinuation of TNF inhibitors (as opposed to gradually lowering the dose) by people with low disease activity may lead to increased disease activity and may affect remission, damage that is visible on an x-ray, and a persons function. People should be screened for latent tuberculosis before starting any TNF inhibitor therapy to avoid reactivation of tuberculosis.TNF inhibitors and methotrexate appear to have similar effectiveness when used alone and better results are obtained when used together. Golimumab is effective when used with methotraxate. TNF inhibitors may have equivalent effectiveness with etanercept appearing to be the safest. Injecting etanercept, in addition to methotrexate twice a week may improve ACR50 and decrease radiographic progression for up to 3 years. Abatacept appears effective for RA with 20% more people improving with treatment than without but long term safety studies are yet unavailable. Adalimumab slows the time for the radiographic progression when used for 52 weeks. However, there is a lack of evidence to distinguish between the biologics available for RA. Issues with the biologics include their high cost and association with infections including tuberculosis. Use of biological agents may reduce fatigue. The mechanism of how biologics reduce fatigue is unclear. Gold (sodium aurothiomalate) and cyclosporin Sodium aurothiomalate (gold) and cyclosporin are less commonly used due to more common adverse effects. However, cyclosporin was found to be effective in the progressive RA when used up to one year. Anti-inflammatory and analgesic agents Glucocorticoids can be used in the short term and at the lowest dose possible for flare-ups and while waiting for slow-onset drugs to take effect. Combination of glucocorticoids and conventional therapy has shown a decrease in rate of erosion of bones. Steroids may be injected into affected joints during the initial period of RA, prior to the use of DMARDs or oral steroids.Non-NSAID drugs to relieve pain, like paracetamol may be used to help relieve the pain symptoms; they do not change the underlying disease. The use of paracetamol may be associated with the risk of developing ulcers.NSAIDs reduce both pain and stiffness in those with RA but do not affect the underlying disease and appear to have no effect on peoples long term disease course and thus are no longer first line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular, or kidney problems. Rofecoxib was withdrawn from the global market as its long-term use was associated to an increased risk of heart attacks and strokes. Use of methotrexate together with NSAIDs is safe, if adequate monitoring is done. COX-2 inhibitors, such as celecoxib, and NSAIDs are equally effective. A 2004 Cochrane review found that people preferred NSAIDs over paracetamol. However, it is yet to be clinically determined whether NSAIDs are more effective than paracetamol.The neuromodulator agents topical capsaicin may be reasonable to use in an attempt to reduce pain. Nefopam by mouth and cannabis are not recommended as of 2012 as the risks of use appear to be greater than the benefits.Limited evidence suggests the use of weak oral opioids but the adverse effects may outweigh the benefits.Alternatively, physical therapy has been tested and shown as an effective aid in reducing pain in patients with RA. As most RA is detected early and treated aggressively, physical therapy plays more of a preventative and compensatory role, aiding in pain management alongside regular rheumatic therapy. Surgery Especially for affected fingers, hands, and wrists, synovectomy may be needed to prevent pain or tendon rupture when drug treatment has failed. Severely affected joints may require joint replacement surgery, such as knee replacement. Postoperatively, physiotherapy is always necessary.: 1080, 1103  There is insufficient evidence to support surgical treatment on arthritic shoulders. Physiotherapy For people with RA, physiotherapy may be used together with medical management. This may include cold and heat application, electronic stimulation, and hydrotherapy. Although medications improve symptoms of RA, muscle function is not regained when disease activity is controlled.Physiotherapy promotes physical activity. In RA, physical activity like exercise in the appropriate dosage (frequency, intensity, time, type, volume, progression) and physical activity promotion is effective in improving cardiovascular fitness, muscle strength, and maintaining a long term active lifestyle. In the short term, resistance exercises, with or without range of motion exercises, improve self-reported hand functions. Physical activity promotion according to the public health recommendations should be an integral part of standard care for people with RA and other arthritic diseases. Additionally, the combination of physical activities and cryotherapy show its efficacy on the disease activity and pain relief. The combination of aerobic activity and cryotherapy may be an innovative therapeutic strategy to improve the aerobic capacity in arthritis patients and consequently reduce their cardiovascular risk while minimizing pain and disease activity. Compression gloves Compression gloves are handwear designed to help prevent the occurrence of various medical disorders relating to blood circulation in the wrists and hands. They can be used to treat the symptoms of arthritis, though the medical benefits may be limited. Alternative medicine In general, there is not enough evidence to support any complementary health approaches for RA, with safety concerns for some of them. Some mind and body practices and dietary supplements may help people with symptoms and therefore may be beneficial additions to conventional treatments, but there is not enough evidence to draw conclusions. A systematic review of CAM modalities (excluding fish oil) found that " The available evidence does not support their current use in the management of RA.". Studies showing beneficial effects in RA on a wide variety of CAM modalities are often affected by publication bias and are generally not high quality evidence such as randomized controlled trials (RCTs).A 2005 Cochrane review states that low level laser therapy can be tried to improve pain and morning stiffness due to rheumatoid arthritis as there are few side-effects.There is limited evidence that Tai Chi might improve the range of motion of a joint in persons with rheumatoid arthritis. The evidence for acupuncture is inconclusive with it appearing to be equivalent to sham acupuncture.A Cochrane review in 2002 showed some benefits of the electrical stimulation as a rehabilitation intervention to improve the power of the hand grip and help to resist fatigue. D‐penicillamine may provide similar benefits as DMARDs but it is also highly toxic. Low-quality evidence suggests the use of therapeutic ultrasound on arthritic hands. Potential benefits include increased grip strength, reduced morning stiffness and number of swollen joints. There is tentative evidence of benefit of transcutaneous electrical nerve stimulation (TENS) in RA. Acupuncture‐like TENS (AL-TENS) may decrease pain intensity and improve muscle power scores.Low-quality evidence suggests people with active RA may benefit from assistive technology. This may include less discomfort and difficulty such as when using an eye drop device. Balance training is of unclear benefits. Dietary supplements Fatty acids There has been a growing interest in the role of long-chain omega-3 polyunsaturated fatty acids to reduce inflammation and alleviate the symptoms of RA. Metabolism of omega-3 polyunsaturated fatty acids produces docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), which inhibits pro-inflammatory eicosanoids and cytokines (TNF-a, IL-1b and IL-6), decreasing both lymphocyte proliferation and reactive oxygen species. These studies showed evidence for significant clinical improvements on RA in inflammatory status and articular index. Gamma-linolenic acid, an omega-6 fatty acid, may reduce pain, tender joint count and stiffness, and is generally safe. For omega-3 polyunsaturated fatty acids (found in fish oil, flax oil and hemp oil), a meta-analysis reported a favorable effect on pain, although confidence in the effect was considered moderate. The same review reported less inflammation but no difference in joint function. A review examined the effect of marine oil omega-3 fatty acids on pro-inflammatory eicosanoid concentrations; leukotriene4 (LTB4) was lowered in people with rheumatoid arthritis but not in those with non-autoimmune chronic diseases. (LTB4) increases vascular permeabiltity and stimulates other inflammatory substances. A third meta-analysis looked at fish consumption. The result was a weak, non-statistically significant inverse association between fish consumption and RA. A fourth review limited inclusion to trials in which people eat ≥2.7 g/day for more than three months. Use of pain relief medication was decreased, but improvements in tender or swollen joints, morning stiffness and physical function were not changed. Collectively, the current evidence is not strong enough to determine that supplementation with omega-3 fatty acids or regular consumption of fish are effective treatments for rheumatoid arthritis. Diets Patients with RA often claim that their symptoms are alleviated by special diets or by simple elimination of certain foods. In contrast, some foods might provoke hypersensitivity responses, which may increase symptoms of RA.The Dong diet has been suggested for a benefit in RA. This diet is rich in oils, seafood, vegetables, and rice which improve symptoms of RA. It eliminates citrus fruits, chocolate, dairy produce, flour products, alcohol, additives, spices, fizzy drinks, and red meat which are implicated in the aggravation of symptoms.The Mediterranean diet is a well‐balanced, nutritionally adequate diet that encompasses all the food groups. This diet is rich in fresh fruits and vegetables, whole grains, seafood, nuts and legumes, and olive oil. In contrast, it limits red meat, sugary foods, and dairy, in small portions of yogurt and cheese. The foods in this category parallel the Dong Diet closely and show evidence of overlap. There is beneficial effect in using a Mediterranean diet and Dong diet for a reduction in the number of tender joints, stiffness, and pain.Vitamins Adequate Vitamin concentrations may provide an important defence against the increased oxidant stress in patients with RA. Here we look at the effects of vitamins E, C and B on the management of RA. In general vitamin E deficiency enhances components of the inflammatory response and suppresses components of the immune response. Molecular studies have demonstrated that the formation of the pro-inflammatory prostaglandin E2 is inhibited 95% by aspirin when combined with vitamin E compared to control. This suggests that vitamin E supplementation reduces the need for high dosage of aspirin needed by patients with RA to relieve joint symptoms. This can offer double benefits because lowering the dose of aspirin can also reduce the gastric irritation side effect for patients. Even though there is no evidence of only taking vitamin E supplementation alone, I believe patients with RA should be encouraged to increase their consumption of vitamin E rich cereals, fruit, and vegetables. Vitamin C is necessary for the growth and development of all body tissues and plays an important role in antioxidant defences. In animal studies biochemical markers of antioxidant defence mechanisms were increased with vitamin C supplementation and infiltration of inflammatory cells into synovial fluid were decreased. From these studies I can conclude that vitamin C supplementation may be more effective for the pain associated with RA however long-term use might aggravate onset of osteoarthritis. Vitamin B6 and B9 play a role in RA management as well. Studies have shown that low plasma levels of pyridoxal-5-phosphate, the metabolically active form of vitamin B6, have been reported in RA patients, which may be associated with the elevated TNF-a production. Folate supplies are also decreased in RA patients who are taking Methotrexate, an anti-rheumatic drug. We see that folate supplementation can reduce the mucosal and gastrointestinal side effects of low dose Methotrexate in patients with RA. This works in a similar pattern to aspirin and vitamin E supplementation. Therefore, RA patients should be advised to consume dietary sources of vitamin B6 and B9 up to the dietary reference value, until further research is undertaken into the toxicity and effectiveness of large dose supplementation. Food containing high source of vitamin E to help treat Rheumatoid Arthritis include almonds, avocados, spinach, sunflower seeds and peanut butter. Vitamin C foods include oranges, orange juice, strawberry, broccoli, brussel sprouts and potatoes. Brown rice, barley, and fish contain sources of vitamin B6 and B9. Lastly, Vitamin D can be included in the diet by incorporating tuna, salmon, orange juice and almond Milk into diet.Minerals Minerals including fluoride, iron, calcium, and zinc have been studied in the role of RA management. The effects of fluoride supplementation in preventing RA-induced bone loss were examined in a randomized control trial. Results suggest that fluoride therapy may increase vertebral bone mass in RA patients.Approximately, one-third of cases of anaemia in RA patients may be caused by depletion of iron stores. A major cause for iron deficiency anaemia is the poor dietary intake. Deferioxamine, an iron-chelating agent, which has possible anti-inflammatory properties, causes haemoglobin and serum iron levels to increases. This shows that iron stores are needed within the body and an adequate dietary intake to meet the recommended intakes should be encouraged, even though there is no evidence for additional routine supplementation for patients with RA. Studies have examined the effect of calcium supplementation on bone mineral density among subjects taking corticosteroids. A study of calcium combined with vitamin D3 in RA patients taking low-dose corticosteroids demonstrated a reduction in bone mineral density loss in both the spine and trochanter, but not the femoral neck. However, no change was seen in BMD with calcium and vitamin D3 supplementation in RA patients not receiving corticosteroids. Therefore, there is little evidence to support calcium and vitamin D supplementation in corticosteroid receiving RA patients. Lastly, low levels of serum zinc have been reported in patients with RA which may be caused by elevated IL-1b levels. However, Zinc supplementations yield contradictory results and at present do not support a therapeutic use of zinc. Food containing high source of fluoride to help treat Rheumatoid Arthritis include tomatoes, oranges, bell peppers and grapefruit, which you should eat in moderation. Iron can be incorporated into the diet by eating seafood, spinach, and peas. Moderate amounts of calcium should be included into the diet by having milk, cheese, dairy products, curly kale, okra, bread and fortified flour products such as cereals. Herbal The American College of Rheumatology states that no herbal medicines have health claims supported by high-quality evidence and thus they do not recommend their use. There is no scientific basis to suggest that herbal supplements advertised as "natural" are safer for use than conventional medications as both are chemicals. Herbal medications, although labelled "natural", may be toxic or fatal if consumed. Due to the false belief that herbal supplements are always safe, there is sometimes a hesitancy to report their use which may increase the risk of adverse reaction.The following are under investigation for treatments for RA, based on preliminary promising results (not recommended for clinical use yet): boswellic acid, curcumin, devils claw, Euonymus alatus, and thunder god vine (Tripterygium wilfordii). NCCIH has noted that, "In particular, the herb thunder god vine (Tripterygium wilfordii) can have serious side effects."There is conflicting evidence on the role of erythropoiesis-stimulating agents for treatment of anemia in persons with rheumatoid arthritis. Pregnancy More than 75% of women with rheumatoid arthritis have symptoms improve during pregnancy but might have symptoms worsen after delivery. Methotrexate and leflunomide are teratogenic (harmful to foetus) and not used in pregnancy. It is recommended women of childbearing age should use contraceptives to avoid pregnancy and to discontinue its use if pregnancy is planned. Low dose of prednisolone, hydroxychloroquine and sulfasalazine are considered safe in pregnant persons with rheumatoid arthritis. Prednisolone should be used with caution as the side effects include infections and fractures. Vaccinations People with RA have an increased risk of infections and mortality and recommended vaccinations can reduce these risks. The inactivated influenza vaccine should be received annually. The pneumococcal vaccine should be administered twice for people under the age 65 and once for those over 65. Lastly, the live-attenuated zoster vaccine should be administered once after the age 60, but is not recommended in people on a tumor necrosis factor alpha blocker. Prognosis The course of the disease varies greatly. Some people have mild short-term symptoms, but in most the disease is progressive for life. Around 25% will have subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor prognosis. Prognostic factors Poor prognostic factors include, Persistent synovitis Early erosive disease Extra-articular findings (including subcutaneous rheumatoid nodules) Positive serum RF findings Positive serum anti-CCP autoantibodies Positive serum 14-3-3η (YWHAH) levels above 0.5 ng/ml Carriership of HLA-DR4 "Shared Epitope" alleles Family history of RA Poor functional status Socioeconomic factors Elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) Increased clinical severity. Mortality RA reduces lifespan on average from three to twelve years. Young age at onset, long disease duration, the presence of other health problems, and characteristics of severe RA—such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints—have been shown to associate with higher mortality. Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that individuals with RA have a doubled risk of heart disease, independent of other risk factors such as diabetes, excessive alcohol use, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor. It is possible that the use of new biologic drug therapies extend the lifespan of people with RA and reduce the risk and progression of atherosclerosis. This is based on cohort and registry studies, and still remains hypothetical. It is still uncertain whether biologics improve vascular function in RA or not. There was an increase in total cholesterol and HDLc levels and no improvement of the atherogenic index. Epidemiology RA affects between 0.5 and 1% of adults in the developed world with between 5 and 50 per 100,000 people newly developing the condition each year. In 2010 it resulted in about 49,000 deaths globally.Onset is uncommon under the age of 15 and from then on the incidence rises with age until the age of 80. Women are affected three to five times as often as men.The age at which the disease most commonly starts is in women between 40 and 50 years of age, and for men somewhat later. RA is a chronic disease, and although rarely, a spontaneous remission may occur, the natural course is almost invariably one of the persistent symptoms, waxing and waning in intensity, and a progressive deterioration of joint structures leading to deformations and disability.There is an association between periodontitis and rheumatoid arthritis (RA), hypothesised to lead to enhanced generation of RA-related autoantibodies. Oral bacteria that invade the blood may also contribute to chronic inflammatory responses and generation of autoantibodies. History The first recognized description of RA in modern medicine was in 1800 by the French physician Dr Augustin Jacob Landré-Beauvais (1772–1840) who was based in the famed Salpêtrière Hospital in Paris. The name "rheumatoid arthritis" itself was coined in 1859 by British rheumatologist Dr Alfred Baring Garrod.The art of Peter Paul Rubens may possibly depict the effects of RA. In his later paintings, his rendered hands show, in the opinion of some physicians, increasing deformity consistent with the symptoms of the disease. RA appears to some to have been depicted in 16th-century paintings. However, it is generally recognized in art historical circles that the painting of hands in the 16th and 17th century followed certain stylized conventions, most clearly seen in the Mannerist movement. It was conventional, for instance, to show the upheld right hand of Christ in what now appears a deformed posture. These conventions are easily misinterpreted as portrayals of disease.Historic (though not necessarily effective) treatments for RA have also included: rest, ice, compression and elevation, apple diet, nutmeg, some light exercise every now and then, nettles, bee venom, copper bracelets, rhubarb diet, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electroconvulsive therapy (ECT). Etymology Rheumatoid arthritis is derived from the Greek word ῥεύμα-rheuma (nom.), ῥεύματος-rheumatos (gen.) ("flow, current"). The suffix -oid ("resembling") gives the translation as joint inflammation that resembles rheumatic fever. Rhuma which means watery discharge might refer to the fact that the joints are swollen or that the disease may be made worse by wet weather. Research Meta-analysis found an association between periodontal disease and RA, but the mechanism of this association remains unclear. Two bacterial species associated with periodontitis are implicated as mediators of protein citrullination in the gums of people with RA.Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population. However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear. One meta-analysis found that vitamin D levels are low in people with rheumatoid arthritis and that vitamin D status correlates inversely with prevalence of rheumatoid arthritis, suggesting that vitamin D deficiency is associated with susceptibility to rheumatoid arthritis.The fibroblast-like synoviocytes have a prominent role in the pathogenic processes of the rheumatic joints, and therapies that target these cells are emerging as promising therapeutic tools, raising hope for future applications in rheumatoid arthritis.Possible links with intestinal barrier dysfunction are investigated. References External links Rheumatoid arthritis at Curlie "Rheumatoid Arthritis". MedlinePlus. U.S. National Library of Medicine.

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I've encountered the term 'Quinapril' while reading about medical topics. What does it refer to exactly?

Quinapril, sold under the brand name Accupril among others, is a medication used to treat high blood pressure (hypertension), heart failure, and diabetic kidney disease. It is a reasonable initial treatment for high blood pressure. It is taken by mouth.Common side effects include headaches, dizziness, feeling tired, and cough. Serious side effects may include liver problems, low blood pressure, angioedema, kidney problems, and high blood potassium. Use in pregnancy and breastfeeding is not recommended. It is an ACE inhibitor and works by decreasing renin-angiotensin-aldosterone system activity.Quinapril was patented in 1980 and came into medical use in 1989. It is available as a generic medication. In 2019, it was the 294th most commonly prescribed medication in the United States, with more than 1 million prescriptions. Medical uses Quinapril is indicated for the treatment of high blood pressure (hypertension) and as adjunctive therapy in the management of heart failure. It may be used for the treatment of hypertension by itself or in combination with thiazide diuretics, and with diuretics and digoxin for heart failure. Contraindications Pregnancy Impaired renal and liver function Patients with a history of angioedema related to previous treatment with an ACE inhibitor Hypersensitivity to quinapril Side effects Side effects of quinapril include dizziness, cough, vomiting, upset stomach, angioedema, and fatigue. Mechanism of action Quinapril inhibits angiotensin converting enzyme, an enzyme which catalyses the formation of angiotensin II from its precursor, angiotensin I. Angiotensin II is a powerful vasoconstrictor and increases blood pressure through a variety of mechanisms. Due to reduced angiotensin production, plasma concentrations of aldosterone are also reduced, resulting in increased excretion of sodium in the urine and increased concentrations of potassium in the blood. Partial Recall In April of 2022, Pfizer voluntarily recalled five batches of the drug because of the presence of a nitrosamine, NNitroso-quinapril. Testing found that the amount of nitrosamines was above the acceptable daily intake level (all humans are exposed to nitrosamines up to a certain daily level by cured and grilled meats, water, dairy products, and vegetables) set by the U.S.s Food and Drug Administration (FDA). Though long-term ingestion of NNitroso-quinapril potentially might cause cancer in some individuals, there is not believed to be an imminent risk of harm. References External links "Quinapril hydrochloride". Drug Information Portal. U.S. National Library of Medicine.

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I've come across the term 'Enasidenib' in a medical context, but I'm not sure what it means. Can you clarify?

Enasidenib (INN; trade name Idhifa) is a medication used to treat relapsed or refractory acute myeloid leukemia in people with specific mutations of the isocitrate dehydrogenase 2 (IDH2) gene, determined by an FDA-approved IDH2 companion diagnostic test. It is an inhibitor of IDH2. It was developed by Agios Pharmaceuticals and is licensed to Celgene for further development. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication. Medical use Enasidenib is used to treat relapsed or refractory acute myeloid leukemia in people with specific mutations of the IDH2 gene, determined by an FDA-approved IDH2 companion diagnostic test. Adverse effects The main serious adverse effect of enasidenib is differentiation syndrome. Pharmacology Isocitrate dehydrogenase is a critical enzyme in the citric acid cycle. Mutated forms of IDH produce high levels of the (R)-enantiomer of 2-hydroxyglutarate (R-2-HG) and can contribute to the growth of tumors. IDH1 catalyzes this reaction in the cytoplasm, while IDH2 catalyzes this reaction in mitochondria. Mutations of IDH2 are more common than IDH1 mutations, 8 to 19% compared to 7 to 14% respectively, in those affected with AML. Enasidenib disrupts this cycle by decreasing total (R)-2-HG levels in the mitochondria. History The U.S. Food and Drug Administration (FDA) granted the application for enasidenib fast track designation and orphan drug designation for acute myeloid leukemia in 2014.Enasidenib was approved by the FDA in August 2017, for relapsed or refractory acute myeloid leukemia (AML) in people with specific mutations of the IDH2 gene, determined by an FDA-approved IDH2 companion diagnostic test. References External links "Enasidenib". Drug Information Portal. U.S. National Library of Medicine. "Enasidenib mesylate". NCI Dictionary of Cancer Terms. National Cancer Institute. "Enasidenib mesylate". National Cancer Institute.

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What does the medical term 'Spastic quadriplegia' encompass?

Spastic quadriplegia, also known as spastic tetraplegia, is a subset of spastic cerebral palsy that affects all four limbs (both arms and legs). Compared to quadriplegia, spastic tetraplegia is defined by spasticity of the limbs as opposed to strict paralysis. It is distinguishable from other forms of cerebral palsy in that those afflicted with the condition display stiff, jerky movements stemming from hypertonia of the muscles.Spastic quadriplegia, while affecting all four limbs more or less equally, can still present parts of the body as stiffer than others, such as one arm being tighter than another arm, and so forth. Spastic triplegia, meanwhile, involves three limbs (such as one arm and two legs, or one leg and two arms, etc.); spastic diplegia affects two limbs (commonly just the legs), spastic hemiplegia affects one or another entire side of the body (left or right); and spastic monoplegia involves a single limb. Symptoms and signs Spastic quadriplegia can be detected by the abnormal development of motor skills in children. Symptoms can present themselves as early as three months but are generally seen before the child reaches two years of age. Some warning signs include: a child of more than two months who has stiff legs that scissor and is unable to control his or her head, and a child of more than twelve months who has not developed the ability to crawl or stand.Spastic quadriplegia also presents a range of symptoms that affect the musculature. Many experience contractures, which are defined as joints that cannot be stretched or moved. Clonus is another symptom that is characterized by alternating, rapid muscle contraction and relaxation. This presents itself as tremors and scissoring of the limbs. Distonia, or lasting muscle contractions and tightness, is also often experienced by those affected by spastic quadriplegia. These involuntary muscle contractions may affect the development of structural muscle around the hip and lead to hip dysplasia and dislocation, making it difficult to sit. The combination of these symptoms often makes it difficult for the patients to walk as well. Although the arms and legs of patients are often stiff, the neck is usually limp due to the lack of voluntary muscle control. Causes Spastic quadriplegia is generally caused by brain damage or disruptions in normal brain development preceding birth. According to the National Institutes of Health, there are four types of brain damage that can cause spastic quadriplegia. These include, damage to the white matter (periventricular leukomalacia), abnormal brain development (cerebral dysgenesis), bleeding in the brain (intracranial hemorrhage), and brain damage due to lack of oxygen (hypoxic-ischemic encephalopathy or intrapartum asphyxia).The white matter of the brain is especially vulnerable between the 26th and 34th weeks of maturation, and damage to the white matter can interfere with the brain’s ability to transmit signals to the rest of the body. Spastic quadriplegia can be caused by a condition known as periventricular leukomalacia which results in the formation of lesions and holes in the white matter of the brain.Prior to the 26th week of maturation, the fetal brain is particularly susceptible to various toxins whose effects can ultimately hinder normal development. Exposure of the brain to infectious agents is especially dangerous because they can trigger immune responses that activate cytokines and lead to inflammation of the brain. Some infections that have been linked to the development of spastic quadriplegia include meningitis, herpes, rubella, and encephalitis. A difference in blood types between the mother and the fetus can also initiate a problematic immune response and cause brain damage. Severe jaundice, can also lead to brain damage and spastic quadriplegia due to a buildup of bilirubin in the blood.Bleeding in the brain caused by fetal strokes, blood clots, weak and malformed blood vessels, or high maternal blood pressure may also lead to brain damage causing spastic quadriplegia. Maternal infection, most specifically pelvic inflammatory disease, has been shown to increase the risk of fetal stroke.Hypoxia, lack of oxygen to the brain, can also cause damage in the cerebral motor cortex and other brain regions. This lack of oxygen can be the result of placenta malfunction, womb rupture, umbilical cord damage, low maternal blood pressure or asphyxia during labor and delivery.Children who experienced many complications during birth, such as, prematurity, insufficient oxygen, low birthweight, aspiration, head injury, or bleeding in the brain have a greater risk of developing spastic quadriplegia. Children whose mothers were ill during the pregnancy or did not receive adequate nutrition are also more likely to develop the disease. Diagnosis Spastic quadriplegia can be diagnosed as early as age one after a noticed delay in development, particularly a delay in rolling, crawling, sitting, or walking. However, depending on the severity, signs may not show up until the age of three. Muscle tone is sometimes used to make the diagnosis for spastic quadriplegia as affected children often appear to be either too stiff or too floppy.Another important diagnostic factor is the persistence of primitive reflexes past the age at which they should have disappeared (6–12 months of age). These reflexes include the rooting reflex, the sucking reflex, and the Moro reflex, among others.Magnetic resonance imaging (MRI) or a computed tomography scan (CT scan) may be used to locate the cause of the symptoms. Ultrasound may be used for the same function in premature babies.Because cerebral palsy refers to a group of disorders, it is important to have a clear and systematic naming system. These disorders must be non-progressive, non-transient, and not due to injury to the spinal cord. Disorders within the group are classified based on two characteristics- the main physiological symptom, and the limbs that are affected. For a disorder to be diagnosed as spastic quadriplegia, an individual must show spastic symptoms (as opposed to athetotic, hypertonic, ataxic, or atonic symptoms) and it must be present in all four limbs (as opposed to hemiplegic, diplegic, or triplegic cases).While a diagnosis may be able to be made shortly after birth based on family history and observation of the infant, it is often postponed until after the child is between 18–24 months old in order to monitor the possible regression or progression of symptoms. Scientific classification The scientific classifications for these types include: Management Research Doublecortin positive cells, similar to stem cells, are extremely adaptable and, when extracted from a brain, cultured and then re-injected in a lesioned area of the same brain, they can help repair and rebuild it. The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials. Notes == External links ==

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I'm trying to understand 'Monteggia fracture' within a medical context. Could you shed some light on it?

The Monteggia fracture is a fracture of the proximal third of the ulna with dislocation of the proximal head of the radius. It is named after Giovanni Battista Monteggia. Causes Mechanisms include: Fall outstretched hand with the forearm in excessive pronation (hyper-pronation injury). The ulna fractures in the proximal one-third of the shaft due to extreme dislocation. Depending on the impact and forces applied in each direction, degree of energy absorption determines pattern, involvement of the radial head and whether or not open soft tissue occurs. Direct blow on back of upper forearm would be a very uncommon cause. In this context, isolated ulnar shaft fractures are most commonly seen in defence against blunt trauma (e.g. nightstick injury). Such an isolated ulnar shaft fracture is not a Monteggia fracture. It is called a nightstick fracture. Diagnosis Classification There are four types (depending upon displacement of the radial head): I - Extension type (60%) - ulna shaft angulates anteriorly (extends) and radial head dislocates anteriorly. II - Flexion type (15%) - ulna shaft angulates posteriorly (flexes) and radial head dislocates posteriorly. III - Lateral type (20%) - ulna shaft angulates laterally (bent to outside) and radial head dislocates to the side. IV - Combined type (5%) - ulna shaft and radial shaft are both fractured and radial head is dislocated, typically anteriorly.These are known as the Bado types. Management Monteggia fractures may be managed conservatively in children with closed reduction (resetting and casting), but due to high risk of displacement causing malunion, open reduction internal fixation is typically performed.Osteosynthesis (open reduction and internal fixation) of the ulnar shaft is considered the standard of care in adults. It promotes stability of the radial head dislocation and allows very early mobilisation to prevent stiffness. The elbow joint is particularly susceptible to loss of motion. Prognosis In children, the results of early treatment are always good, typically normal or nearly so. If diagnosis is delayed, reconstructive surgery is needed and complications are much more common and results poorer. In adults, the healing is slower and results usually not as good.Complications of ORIF surgery for Monteggia fractures can include non-union, malunion, nerve palsy and damage, muscle damage, arthritis, tendonitis, infection, stiffness and loss of range of motion, compartment syndrome, audible popping or snapping, deformity, and chronic pain associated with surgical hardware such as pins, screws, and plates. Several surgeries may be needed to correct this type of fracture as it is almost always a very complex fracture that requires a skilled orthopedic surgeon, usually a specialist familiar with this type of injury. See also Galeazzi fracture Hume fracture Essex-Lopresti fracture References == External links ==

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Can you demystify the medical term '17q12 microdeletion syndrome' for me?

17q12 microdeletion syndrome, also known as 17q12 deletion syndrome, is a rare chromosomal anomaly caused by the deletion of a small amount of material from a region in the long arm of chromosome 17. It is typified by deletion of the HNF1B gene, resulting in kidney abnormalities and renal cysts and diabetes syndrome. It also has neurocognitive effects, and has been implicated as a genetic factor for autism and schizophrenia. 17q12 microdeletion syndrome is not to be confused with 17q12 microduplication syndrome, caused by the addition of genetic material in the same region from which it is removed in the microdeletion, or 17q21.31 microdeletion syndrome, another name for Koolen–De Vries syndrome. Presentation 17q12 microdeletions have a variable phenotype, ranging from few or no symptoms to severe disability. The condition is thought to be underdiagnosed, and cases with milder phenotypes may not reach clinical attention unless they have an affected child themselves. The most characteristic symptom is renal cysts and diabetes syndrome (RCAD), also known as "type 5 diabetes", which is caused by deletion of the associated HNF1B gene in the region. RCAD is associated with kidney abnormalities and a characteristic form of diabetes that causes atrophy of the pancreas. However, some people with 17q12 microdeletions have normal renal function. RCAD is diagnosed in approximately 40% of people with 17q12 microdeletions, usually prior to age 25, while kidney abnormalities more broadly occur in approximately 85-90%.People with 17q12 microdeletions have a characteristic facial phenotype, albeit a subtle one not usually obvious in daily life. Macrocephaly is common, along with high arched eyebrows, flattening of the malar region, and epicanthic folds. Pathological short stature is possible, and a characteristic "short and stocky" body shape occurs in many cases.17q12 microdeletions are associated with neurocognitive and developmental involvement of variable severity. Some have mild to moderate intellectual disability; however, such impairment is not universal. Average intelligence is in the average to low average range. Speech delay is common, regardless of intellectual functioning. The most striking association between 17q12 microdeletions and neurodevelopment is the raised prevalence of autism spectrum disorder, with significant increases in both diagnosis and subclinical autistic traits. 17q12 microdeletions have been implicated as one of the major genetic causes of high-functioning autistic spectrum disorders. Schizophrenia is also a significant psychiatric complication of 17q12 microdeletion syndrome. 17q12 microdeletions are estimated to occur in approximately 1 in 1,600 people with schizophrenia, compared to an estimation of below 1 in 50,000 in the general population. Epilepsy, usually mild, occurs in approximately one-third of cases.Reproductive system anomalies are associated with 17q12 microdeletions, particularly in females. 17q12 microdeletions have been linked to uterine malformations, most frequently Müllerian agenesis, where the uterus and part of the vaginal canal are absent. Causes 17q12 microdeletion syndrome is an autosomal dominant disorder, where one copy of the relevant mutation is enough to cause the condition. Most cases are de novo, or spontaneous mutations that do not occur in the probands parents; approximately 75% are de novo, while 25% are inherited. People with 17q12 microdeletions who have normal fertility have a 50% chance of passing the deletion down to their offspring. Environmental factors have not been implicated in the syndrome. Diagnosis Like other chromosomal microdeletions, 17q12 microdeletion syndrome is diagnosed via fluorescence in situ hybridization. Traditional karyotyping, used to diagnose major chromosomal disorders such as aneuploidy, is rarely sensitive enough to detect microdeletions. Treatment As the underlying 17q12 microdeletion is an innate genetic disorder, it cannot by itself be treated. Rather, treatment is symptomatic and supportive. The high prevalence of kidney disease indicates routine monitoring of renal function, particularly in people taking potentially nephrotoxic medications such as lithium. The comorbities involved in 17q12 microdeletion syndrome require caution in medical treatment; for instance, the increased risk of diabetes requires strict monitoring for post-transplantation diabetes mellitus in kidney transplant patients, as does the risk of weight gain and diabetes from neuroleptic drugs in those with a mental health diagnosis. Epidemiology The prevalence of 17q12 microdeletion syndrome is unknown, and it is likely to be underdiagnosed. 17q12 microdeletions are estimated to occur in approximately 1 in 600 people on the autism spectrum and 1 in 1,600 with schizophrenia, but are far rarer in the general population. General prevalence is estimated to be between 1 in 14,000 and 1 in 62,500.In addition to the increased prevalence in autism and schizophrenia, some other clinical populations have increased prevalence of 17q12 microdeletion syndrome. The condition occurs in approximately 2% of those with congenital kidney abnormalities and 3-6% of women with Müllerian agenesis. It is one of the ten most common microdeletions amongst children with idiopathic developmental delay. Microduplication 17q12 microduplication syndrome is far rarer than the corresponding microdeletion, estimated to occur roughly one-fifth as frequently as 17q12 microdeletion syndrome. Due to its rarity and the overlap between their phenotypes, 17q12 microduplications are usually discussed as an adjunct to microdeletions. Like the microdeletion syndrome, the microduplication syndrome has a broad phenotypic range, ranging from asymptomatic to profound disability; intellectual disability is frequently but not always more severe than the microdeletion, while physical health is often better. Epilepsy is a frequent finding. A case of sex reversal has been reported. While autism comorbid with 17q12 microduplication has been reported, it appears far rarer than in the microdeletion. Physical anomalies associated with 17q12 microduplication syndrome include syndactyly, microcephaly, epicanthic folds, and thick eyebrows or a unibrow. The 17q12 microduplication appears to have a low penetrance, as many cases are inherited from asymptomatic parents. See also Causes of autism Risk factors of schizophrenia References == External links ==

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Can you break down the meaning of the medical term 'Cryptorchidism' for me?

Cryptorchidism is the absence of one or both testes from the scrotum. The word is from Greek κρυπτός (kryptos) hidden and ὄρχις (orchis) testicle. It is the most common birth defect of the male genital tract. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis. However, about 80% of cryptorchid testes descend by the first year of life (the majority within three months), making the true incidence of cryptorchidism around 1% overall. Cryptorchidism may develop after infancy, sometimes as late as young adulthood, but that is exceptional. Cryptorchidism is distinct from monorchism, the condition of having only one testicle. Though the condition may occur on one or both sides, it more commonly affects the right testis.A testis absent from the normal scrotal position may be: Anywhere along the "path of descent" from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring In the inguinal canal Ectopic, having "wandered" from the path of descent, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, or the femoral canal Undeveloped (hypoplastic) or severely abnormal (dysgenetic) Missing (also see anorchia).About two-thirds of cases without other abnormalities are unilateral; most of the other third involve both testes. In 90% of cases, an undescended testis can be felt in the inguinal canal. In a small minority of cases, missing testes may be found in the abdomen or appear to be nonexistent (truly "hidden"). Undescended testes are associated with reduced fertility, increased risk of testicular germ-cell tumors, and psychological problems when fully-grown. Undescended testes are also more susceptible to testicular torsion (and subsequent infarction) and inguinal hernias. Without intervention, an undescended testicle will usually descend during the first year of life, but to reduce these risks, undescended testes can be brought into the scrotum in infancy by a surgical procedure called an orchiopexy.Although cryptorchidism nearly always refers to congenital absence or maldescent, a testis observed in the scrotum in early infancy can occasionally "reascend" (move back up) into the inguinal canal. A testis that can readily move or be moved between the scrotum and canal is referred to as retractile. Cryptorchidism, hypospadias, testicular cancer, and poor semen quality make up the syndrome known as testicular dysgenesis syndrome. Signs and symptoms Infertility Many men who were born with undescended testes have reduced fertility, even after orchiopexy in infancy. The reduction with unilateral cryptorchidism is subtle, with a reported infertility rate of about 10%, compared with about 6% reported by the same study for the general population of adult men. The fertility reduction after orchiopexy for bilateral cryptorchidism is more marked, about 38%, or six times that of the general population. The basis for the universal recommendation for early surgery is research showing degeneration of spermatogenic tissue and reduced spermatogonia counts after the second year of life in undescended testes. The degree to which this is prevented or improved by early orchiopexy is still uncertain. Cancer risk One of the strongest arguments for early orchiopexy is reducing the risk of testicular cancer. About one in 500 men born with one or both testes undescended develops testicular cancer, roughly a four- to 40-fold increased risk. The peak incidence occurs in the third and fourth decades of life. The risk is higher for intra-abdominal testes and somewhat lower for inguinal testes, but even the normally descended testis of a man whose other testis was undescended has about a 20% higher cancer risk than those of other men.The most common type of testicular cancer occurring in undescended testes is seminoma. It is usually treatable if caught early, so urologists often recommend that boys who had orchiopexy as infants be taught testicular self-examination, to recognize testicular masses and seek early medical care for them. Cancer developing in an intra-abdominal testis would be unlikely to be recognized before considerable growth and spread, and one of the advantages of orchiopexy is that a mass developing in a scrotal testis is far easier to recognize than an intra-abdominal mass. Orchidopexy was originally thought to result in easier detection of testicular cancer, but did not lower the risk of actually developing cancer. However, recent data have shown a paradigm shift. The New England Journal of Medicine published in 2007 that orchidopexy performed before puberty resulted in a significantly reduced risk of testicular cancer than if done after puberty.The risk of malignancy in the undescended testis is four to 10 times higher than that in the general population and is about one in 80 with a unilateral undescended testis and one in 40 to one in 50 for bilateral undescended testes. The peak age for this tumor is 15–45 years old. The most common tumor developing in an undescended testis is a seminoma (65%); in contrast, after orchiopexy, seminomas represent only 30% of testicular tumors. Causes In most full-term infant boys with cryptorchidism but no other genital abnormalities, a cause cannot be found, making this a common, sporadic, unexplained (idiopathic) birth defect. A combination of genetics, maternal health, and other environmental factors may disrupt the hormones and physical changes that influence the development of the testicles. Severely premature infants can be born before descent of testes. Low birth weight is also a known factor. A contributing role of environmental chemicals called endocrine disruptors that interfere with normal fetal hormone balance has been proposed. The Mayo Clinic lists "parents exposure to some pesticides" as a known risk factor. Risk factors may include exposure to regular alcohol consumption during pregnancy (five or more drinks per week, associated with a three-fold increase in cryptorchidism when compared to nondrinking mothers. Cigarette smoking is also a known risk factor. Family history of undescended testicles or other problems of genital development Cryptorchidism occurs at a much higher rate in a large number of congenital malformation syndromes. Among the more common are Down syndrome, Prader–Willi syndrome, and Noonan syndrome. In vitro fertilization, use of cosmetics by the mother, and pre-eclampsia have also been recognized as risk factors for development of cryptorchidism.In 2008, a study was published that investigated the possible relationship between cryptorchidism and prenatal exposure to a chemical called phthalate (DEHP), which is used in the manufacture of plastics. The researchers found a significant association between higher levels of DEHP metabolites in pregnant mothers and several sex-related changes, including incomplete descent of the testes in their sons. According to the lead author of the study, a national survey found that 25% of U.S. women had phthalate levels similar to the levels that were found to be associated with sexual abnormalities.A 2010 study examined the prevalence of congenital cryptorchidism among offspring whose mothers had taken mild analgesics, primarily over-the-counter pain medications including ibuprofen (e.g. Advil) and paracetamol (acetaminophen). Combining the results from a survey of pregnant women prior to their due date in correlation with the health of their children and an ex vivo rat model, the study found that pregnant women who had been exposed to mild analgesics had a higher prevalence of baby boys born with congenital cryptorchidism.New insight into the testicular descent mechanism has been hypothesized by the concept of a male programming window derived from animal studies. According to this concept, testicular descent status is "set" during the period from eight to 14 weeks of gestation in humans. Undescended testis is a result of disruption in androgen levels only during this programming window. Mechanism Normal development The testes begin as an immigration of primordial germ cells into testicular cords along the gonadal ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the third to fifth months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-Müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia develops during the third and fourth months of gestation and the fetus continues to grow, develop, and differentiate. The testes remain high in the abdomen until the seventh month of gestation when they move from the abdomen through the inguinal canals into the two sides of the scrotum. Movement has been proposed to occur in two phases, under the control of somewhat different factors. The first phase, movement across the abdomen to the entrance of the inguinal canal, appears controlled (or at least greatly influenced) by anti-Müllerian hormone (AMH). The second phase, in which the testes move through the inguinal canal into the scrotum, is dependent on androgens (most importantly testosterone). In rodents, androgens induce the genitofemoral nerve to release calcitonin gene-related peptide, which produces rhythmic contractions of the gubernaculum, a ligament which connects the testis to the scrotum, but a similar mechanism has not been demonstrated in humans. Maldevelopment of the gubernaculum or deficiency or insensitivity to either AMH or androgen can, therefore, prevent the testes from descending into the scrotum. Some evidence suggests an additional paracrine hormone, referred to as descendin, may be secreted by the testes. In many infants with inguinal testes, further descent of the testes into the scrotum occurs in the first six months of life. This is attributed to the postnatal surge of gonadotropins and testosterone that normally occurs between the first and fourth months of life. Spermatogenesis continues after birth. In the third to fifth months of life, some of the fetal spermatogonia residing along the basement membrane become type A spermatogonia. More gradually, other fetal spermatogonia become type B spermatogonia and primary spermatocytes by the fifth year after birth. Spermatogenesis arrests at this stage until puberty. Most normal-appearing undescended testes are also normal by microscopic examination, but reduced spermatogonia can be found. The tissue in undescended testes becomes more markedly abnormal ("degenerates") in microscopic appearance between two and four years after birth. Some evidence indicates early orchiopexy reduces this degeneration. Pathophysiology At least one contributing mechanism for reduced spermatogenesis in cryptorchid testes is temperature. The temperature of testes in the scrotum is at least a few degrees cooler than in the abdomen. Animal experiments in the middle of the 20th century suggested that raising the temperature could damage fertility. Some circumstantial evidence suggests tight underwear and other practices that raise the testicular temperature for prolonged periods can be associated with lower sperm counts. Nevertheless, research in recent decades suggests that the issue of fertility is more complex than a simple matter of temperature. Subtle or transient hormone deficiencies or other factors that lead to a lack of descent also may impair the development of spermatogenic tissue. The inhibition of spermatogenesis by ordinary intra-abdominal temperature is so potent that continual suspension of normal testes tightly against the inguinal ring at the top of the scrotum by means of special "suspensory briefs" has been researched as a method of male contraception, and was referred to as "artificial cryptorchidism" by one report. An additional factor contributing to infertility is the high rate of anomalies of the epididymis in boys with cryptorchidism (over 90% in some studies). Even after orchiopexy, these may also affect sperm maturation and motility at an older age. Diagnosis The most common diagnostic dilemma in otherwise normal boys is distinguishing a retractile testis from a testis that will not descend spontaneously into the scrotum. Retractile testes are more common than truly undescended testes and do not need to be operated on. In normal males, as the cremaster muscle relaxes or contracts, the testis moves lower or higher ("retracts") in the scrotum. This cremasteric reflex is much more active in infant boys than older men. A retractile testis high in the scrotum can be difficult to distinguish from a position in the lower inguinal canal. Though various maneuvers are used to do so, such as using a cross-legged position, soaping the examiners fingers, or examining in a warm bath, the benefit of surgery in these cases can be a matter of clinical judgment. In the minority of cases with bilaterally nonpalpable testes, further testing to locate the testes, assess their function, and exclude additional problems is often useful. Scrotal ultrasound or magnetic resonance imaging performed and interpreted by a radiologist can often locate the testes while confirming absence of a uterus. At ultrasound, the undescended testis usually appears small, less echogenic than the contralateral normal testis and usually located in the inguinal region. With color Doppler ultrasonography, the vascularity of the undescended testis is poor.A karyotype can confirm or exclude forms of dysgenetic primary hypogonadism, such as Klinefelter syndrome or mixed gonadal dysgenesis. Hormone levels (especially gonadotropins and AMH) can help confirm that hormonally functional testes are worth attempting to rescue, as can stimulation with a few injections of human chorionic gonadotropin to elicit a rise of the testosterone level. Occasionally, these tests reveal an unsuspected and more complicated intersex condition. In the even smaller minority of cryptorchid infants who have other obvious birth defects of the genitalia, further testing is crucial and has a high likelihood of detecting an intersex condition or other anatomic anomalies. Ambiguity can indicate either impaired androgen synthesis or reduced sensitivity. The presence of a uterus by pelvic ultrasound suggests either persistent Müllerian duct syndrome (AMH deficiency or insensitivity) or a severely virilized genetic female with congenital adrenal hyperplasia. An unambiguous micropenis, especially accompanied by hypoglycemia or jaundice, suggests congenital hypopituitarism. Treatment The primary management of cryptorchidism is watchful waiting, due to the high likelihood of self-resolution. Where this fails, orchiopexy is effective if inguinal testes have not descended after 4–6 months. Surgery is often performed by a pediatric urologist or pediatric surgeon, but in many communities still by a general urologist or surgeon. When the undescended testis is in the inguinal canal, hormonal therapy is sometimes attempted and very occasionally successful. The most commonly used hormone therapy is human chorionic gonadotropin (hCG). A series of hCG injections (10 injections over five weeks is common) is given and the status of the testis/testes is reassessed at the end. Although many trials have been published, the reported success rates range widely, from roughly 5% to 50%, probably reflecting the varying criteria for distinguishing retractile testes from low inguinal testes. Hormone treatment does have the occasional incidental benefits of allowing confirmation of Leydig cell responsiveness (proven by a rise of the testosterone by the end of the injections) or inducing additional growth of a small penis (via the testosterone rise). Some surgeons have reported facilitation of surgery, perhaps by enhancing the size, vascularity, or healing of the tissue. A newer hormonal intervention used in Europe is the use of GnRH analogs such as nafarelin or buserelin; the success rates and putative mechanism of action are similar to hCG, but some surgeons have combined the two treatments and reported higher descent rates. Limited evidence suggests that germ cell count is slightly better after hormone treatment; whether this translates into better sperm counts and fertility rates at maturity has not been established. The cost of either type of hormone treatment is less than that of surgery and the chance of complications at appropriate doses is minimal. Nevertheless, despite the potential advantages of a trial of hormonal therapy, many surgeons do not consider the success rates high enough to be worth the trouble, since the surgery itself is usually simple and uncomplicated. In cases where the testes are identified preoperatively in the inguinal canal, orchiopexy is often performed as an outpatient and has a very low complication rate. An incision is made over the inguinal canal. The testis with accompanying cord structure and blood supply is exposed, partially separated from the surrounding tissues ("mobilized"), and brought into the scrotum. It is sutured to the scrotal tissue or enclosed in a "subdartos pouch". The associated passage back into the inguinal canal, an inguinal hernia, is closed to prevent reascent. In patients with intra-abdominal maldescended testis, laparoscopy is useful to see for oneself the pelvic structures, position of the testis and decide upon surgery (single or staged procedure ). Surgery becomes more complicated if the blood supply is not ample and elastic enough to be stretched into the scrotum. In these cases, the supply may be divided, some vessels sacrificed with expectation of adequate collateral circulation. In the worst case, the testis must be "autotransplanted" into the scrotum, with all connecting blood vessels cut and reconnected (anastomosed). When the testis is in the abdomen, the first stage of surgery is exploration to locate it, assess its viability, and determine the safest way to maintain or establish the blood supply. Multistage surgeries, or autotransplantation and anastomosis, are more often necessary in these situations. Just as often, intra-abdominal exploration discovers that the testis is nonexistent ("vanished"), or dysplastic and not salvageable. The principal major complication of all types of orchiopexy is a loss of the blood supply to the testis, resulting in loss of the testis due to ischemic atrophy or fibrosis. Other animals Cryptorchidism is seen in all domestic animals, most commonly in stallions, boars, and canines. The prevalence of this condition can vary depending on species and breed. Evidence of this condition is more likely in companion animals and swine than ruminants. The cause of this condition can vary from a combination of genetics, environment, and epigenetics. Dogs Cryptorchidism is common in male dogs, occurring at a rate up to 10%. This condition is one of the most common congenital defects in purebred dogs (11%), with 14% reported in Siberian Huskies. Although the genetics are not fully understood, it is thought to be a recessive, and probably polygenetic, trait. Some have speculated that it is a sex-limited autosomal recessive trait; however, it is unlikely to be simple recessive. Dog testes usually descend by 10 days of age and it is considered to be cryptorchidism if they do not descend by the age of eight weeks. Cryptorchidism can be either bilateral (causing sterility) or unilateral, and inguinal or abdominal (or both). Because it is an inherited trait, affected dogs should not be bred and should be castrated. The parents should be considered carriers of the defect and a breeder should thoughtfully consider whether to breed the carrier parent or not. Littermates may be normal, carriers, or cryptorchid. Castration of the undescended teste(s) should be considered for cryptorchid dogs due to the high rate of testicular cancer, especially Sertoli cell tumors. The incidence of testicular cancer is 13.6 times higher in dogs with abdominally retained testicles compared with normal dogs. Testicular torsion is also more likely in retained testicles. Surgical correction is by palpation of the retained testicle and subsequent exploration of the inguinal canal or abdomen, but showing altered dogs is against AKC rules, making this correction pointless for breeding stock. Orchiopexy is an option for pet dogs that will not be used for breeding. Commonly affected breeds include: Alaskan Klee Kai Boxer Chihuahua Dachshund (miniature) Bulldog Maltese Miniature Schnauzer Pekingese Pomeranian Poodle (toy and miniature) Pug Shetland Sheepdog Siberian Husky Whippet Yorkshire Terrier Cats Cryptorchidism is rarer in cats than it is in dogs. In one study, 1.9% of intact male cats were cryptorchid. Persians are predisposed. Normally, the testicles are in the scrotum by the age of six to eight weeks. Male cats with one cryptorchid testicle may still be fertile; however, male cats with two cryptorchid testicles are most likely to be sterile. Urine spraying is one indication that a cat with no observable testicles may not be neutered; other signs are the presence of enlarged jowls, thickened facial and neck skin, and spines on the penis (which usually regress within six weeks after castration). Most cryptorchid cats present with an inguinal testicle. Testicular tumors and testicular torsion are rare in cryptorchid cats, but castration is usually performed due to unwanted behavior such as urine spraying. Horses In horses, cryptorchidism is sufficiently common that affected males (ridglings) are routinely gelded. Rarely, cryptorchidism is due to the presence of a congenital testicular tumor such as a teratoma, which has a tendency to grow large. References External links Kidshealth.org: Cryptorchidism

You act as a mediator between medical professionals and the public. Provide comprehensive explanations of medical terms, ensuring they are both precise and easily understood.

Could you offer a clear explanation of the term 'Viral cardiomyopathy' as used in the medical field?

Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19, which has been seen to cause this in persons otherwise thought to have a "low risk" of the viruss effects. COVID-19 Cardiomyopathy Patients with Covid-19 frequently experience heart issues. According to studies, people who have had previous cardiovascular conditions like cardiomyopathy, hypertension, coronary heart disease, or arrhythmia are more likely to become critically ill from SARS-CoV-2 infection. Myocarditis may result from a direct viral infection of the myocardium. Cardiovascular biomarkers like troponin, lactate dehydrogenase, high sensitivity amino-terminal B-type natriuretic peptide, creatinine kinase, and creatinine kinase myocardial band, which indicate myocardial damage, increase in concentration in response to covid-19. Hundreds of studies have reported myocarditis/myopericarditis caused by Covid-19 infection in living patients, with a male predominance (58%), and a median age of 50 years. See also Coxsackievirus-induced cardiomyopathy Myocarditis Pericarditis Vaccine adverse event References External links Myocarditis on emedicine

You act as a mediator between medical professionals and the public. Provide comprehensive explanations of medical terms, ensuring they are both precise and easily understood.

I've encountered the term 'Trachonychia' while reading about medical topics. What does it refer to exactly?

Trachyonychia, is a condition characterized by rough accentuated linear ridges (longitudinal striations) on the nails of the fingers and toes. When the condition occurs on all the twenty nails of the fingers and toes, it is known as twenty-nail dystrophy, most evident in childhood, favoring males.Trachyonychia causes the nails to become opalescent, thin, dull, fragile, and finely longitudinally ridged, and, as a result, distally notched. It can be a manifestation of lichen planus, psoriasis, alopecia areata, immunoglobulin A deficiency, atopic dermatitis, and ichthyosis vulgaris."The longitudinal striations can occur as a normal part of the aging process", and not until the nails start to thin and get a sandpaper look is the condition called trachonychia. The nails are opalescent and frequently are brittle and split at the free margin. There has been evidence of the condition as a cutaneous manifestation of lichen planus. It has also been associated with other diseases such as eczema, psoriasis, alopecia areata, and atopic dermatitis. Trachonychia is often seen in vitiligo patients – suggesting that they are more susceptible to this condition. References == External links ==

You are a medical interpreter. Your duty is to translate medical terms into easily digestible information, maintaining accuracy and detail.

Can you break down the meaning of the medical term 'Nocardiosis' for me?

Nocardiosis is an infectious disease affecting either the lungs (pulmonary nocardiosis) or the whole body (systemic nocardiosis). It is due to infection by a bacterium of the genus Nocardia, most commonly Nocardia asteroides or Nocardia brasiliensis. It is most common in adult males, especially those with a weakened immune system. In patients with brain nocardia infection, mortality exceeds 80%; in other forms, mortality is 50%, even with appropriate therapy.It is one of several conditions that have been called "the great imitator". Cutaneous nocardiosis commonly occurs in immunocompetent hosts and is caused in 80% of cases by Nocardia brasiliensis. Signs and symptoms Pulmonary infection Produces a virulent form of pneumonia (progressive) Night sweats, fever, cough, chest pain Pulmonary nocardiosis is subacute in onset and refractory to treatment with standard antibiotics Symptoms are more severe in immunocompromised individuals Radiologic studies show multiple pulmonary infiltrates, with a tendency to central necrosisNeurological infection Headache, lethargy, confusion, seizures, sudden onset of neurological deficit CT scan shows cerebral abscess Nocardial meningitis is difficult to diagnoseCardiac conditions Nocardia has been highly linked to endocarditis as a main manifestation In recorded cases, it has caused damage to heart valves whether natural or prostheticLymphocutaneous disease Nocardial cellulitis is akin to erysipelas but is less acute Nodular lymphangeitis mimics sporotrichosis with multiple nodules alongside a lymphatic pathway Chronic subcutaneous infection is a rare complication and osteitis may ensue May be misidentified and treated as a staph infection, specifically superficial skin infections Cultures must incubate more than 48 hours to guarantee an accurate testOcular disease Very rarely, nocardiae cause keratitis Generally there is a history of ocular traumaDisseminated nocardiosis Dissemination occurs through the spreading enzymes possessed by the bacteria Disseminated infection can occur in very immunocompromised patients It generally involves both lungs and brain Fever, moderate or very high can be seen Multiple cavitating pulmonary infiltrates develop Cerebral abscesses arise later Cutaneous lesions are very rarely seen If untreated, the prognosis is poor for this form of disease Causes Normally found in soil, these organisms cause occasional sporadic disease in humans and animals throughout the world. Another well publicized find is that of Nocardia as part of the oral microflora. Nocardia spp. have been reported in the normal gingivae and periodontal pockets along with other species such as Actinomyces, Arthromyces and Streptomyces spp.The usual mode of transmission is inhalation of organisms suspended in dust. Another very common method is by traumatic introduction, especially in the jaw. This leads to the entrance of Nocardia into the blood stream and the propagation of its pathogenic effects. Transmission by direct inoculation through puncture wounds or abrasions is less common. Generally, nocardial infection requires some degree of immune suppression.A weakened immune system is a general indicator of a person who is more susceptible to nocardiosis, such as someone who already has a disease that weakens their immune system. Additionally, those with low T-cell counts or other complications involving T-cells can expect to have a higher chance of becoming infected. Besides those with weak immune systems, a local traumatic inoculation can cause nocardiosis, specifically the cutaneous, lymphocutaneous, and subcutaneous forms of the disease. There is no racial pattern in the risk of becoming infected with Nocardiosis. Diagnosis Diagnosis of nocardiosis can be made by a doctor using various techniques. These techniques include, but are not limited to: a chest x-ray to analyze the lungs, a bronchoscopy, a brain/lung/skin biopsy, or a sputum culture. However, diagnosis may be difficult. Nocardiae are gram positive, weakly acid-fast, branching rod-shaped bacteria and can be visualized by a modified Ziehl–Neelsen stain such as the Fite-Faraco method. In the clinical laboratory, routine cultures may be held for insufficient time to grow nocardiae, and referral to a reference laboratory may be needed for species identification. Pulmonary infiltration and pleural effusion are usually detected via x-ray. Treatment Nocardiosis requires at least 6 months of treatment, preferably with trimethoprim/sulfamethoxazole or high doses of sulfonamides. In patients who do not respond to sulfonamide treatment, other drugs, such as ampicillin, erythromycin, or minocycline, may be added.Treatment also includes surgical drainage of abscesses and excision of necrotic tissue. The acute phase requires complete bed rest; as the patient improves, activity can increase.A new combination drug therapy (sulfonamide, ceftriaxone, and amikacin) has also shown promise. Prognosis The prognosis of nocardiosis is highly variable. The state of the hosts health, site, duration, and severity of the infection all play parts in determining the prognosis. Currently, skin and soft tissue infections have a 100% cure rate, and pleuropulmonary infections have a 90% cure rate with appropriate therapy. The cure rate falls to 63% with those infected with disseminated nocardiosis, with only half of patients surviving infections that cause brain abscess. Additionally, 44% of people who are infected in the central nervous system (CNS) die, increasing to 85% if that person has an already weakened immune system. There are no preventative treatments for nocardiosis. The only recommendation is to protect open wounds to limit entrance of the bacterium. Epidemiology Although there are no international data available on worldwide infection rates per year, there are roughly 500–1000 documented cases of nocardiosis per year in the US. Most of these cases occur in men, as there is a 3:1 ratio of male of female cases annually; however, this difference may be due to exposure frequency rather than susceptibility differences. From an age perspective, it is not highly more prevalent in one age group than another. Cutaneous nocardiosis is slightly more common in middle aged men, but as a whole, all age groups are susceptible. There is no racial pattern in the risk of becoming infected with nocardiosis. References External links Webmd article on Nocardiosis

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Could you please explain the term 'Chromosome abnormality' in simple language?

A chromosomal abnormality, chromosomal anomaly, chromosomal aberration, chromosomal mutation, or chromosomal disorder, is a missing, extra, or irregular portion of chromosomal DNA. These can occur in the form of numerical abnormalities, where there is an atypical number of chromosomes, or as structural abnormalities, where one or more individual chromosomes are altered. Chromosome mutation was formerly used in a strict sense to mean a change in a chromosomal segment, involving more than one gene. Chromosome anomalies usually occur when there is an error in cell division following meiosis or mitosis. Chromosome abnormalities may be detected or confirmed by comparing an individuals karyotype, or full set of chromosomes, to a typical karyotype for the species via genetic testing. Numerical abnormality An abnormal number of chromosomes is called aneuploidy, and occurs when an individual is either missing a chromosome from a pair (resulting in monosomy) or has more than two chromosomes of a pair (trisomy, tetrasomy, etc.). Aneuploidy can be full, involving a whole chromosome missing or added, or partial, where only part of a chromosome is missing or added. Aneuploidy can occur with sex chromosomes or autosomes.An example of trisomy in humans is Down syndrome, which is a developmental disorder caused by an extra copy of chromosome 21; the disorder is therefore also called trisomy 21.An example of monosomy in humans is Turner syndrome, where the individual is born with only one sex chromosome, an X. Sperm aneuploidy Exposure of males to certain lifestyle, environmental and/or occupational hazards may increase the risk of aneuploid spermatozoa. In particular, risk of aneuploidy is increased by tobacco smoking, and occupational exposure to benzene, insecticides, and perfluorinated compounds. Increased aneuploidy is often associated with increased DNA damage in spermatozoa. Structural abnormalities When the chromosomes structure is altered, this can take several forms: Deletions: A portion of the chromosome is missing or has been deleted. Known disorders in humans include Wolf–Hirschhorn syndrome, which is caused by partial deletion of the short arm of chromosome 4; and Jacobsen syndrome, also called the terminal 11q deletion disorder. Duplications: A portion of the chromosome has been duplicated, resulting in extra genetic material. Known human disorders include Charcot–Marie–Tooth disease type 1A, which may be caused by duplication of the gene encoding peripheral myelin protein 22 (PMP22) on chromosome 17. Inversions: A portion of the chromosome has broken off, turned upside down, and reattached, therefore the genetic material is inverted. Insertions: A portion of one chromosome has been deleted from its normal place and inserted into another chromosome. Translocations: A portion of one chromosome has been transferred to another chromosome. There are two main types of translocations: Reciprocal translocation: Segments from two different chromosomes have been exchanged. Robertsonian translocation: An entire chromosome has attached to another at the centromere - in humans, these only occur with chromosomes 13, 14, 15, 21, and 22. Rings: A portion of a chromosome has broken off and formed a circle or ring. This can happen with or without the loss of genetic material. Isochromosome: Formed by the mirror image copy of a chromosome segment including the centromere.Chromosome instability syndromes are a group of disorders characterized by chromosomal instability and breakage. They often lead to an increased tendency to develop certain types of malignancies. Inheritance Most chromosome abnormalities occur as an accident in the egg cell or sperm, and therefore the anomaly is present in every cell of the body. Some anomalies, however, can happen after conception, resulting in Mosaicism (where some cells have the anomaly and some do not). Chromosome anomalies can be inherited from a parent or be "de novo". This is why chromosome studies are often performed on parents when a child is found to have an anomaly. If the parents do not possess the abnormality it was not initially inherited; however, it may be transmitted to subsequent generations. Acquired chromosome abnormalities Most cancers, if not all, could cause chromosome abnormalities, with either the formation of hybrid genes and fusion proteins, deregulation of genes and overexpression of proteins, or loss of tumor suppressor genes (see the "Mitelman Database" and the Atlas of Genetics and Cytogenetics in Oncology and Haematology,). Furthermore, certain consistent chromosomal abnormalities can turn normal cells into a leukemic cell such as the translocation of a gene, resulting in its inappropriate expression. DNA damage during spermatogenesis During the mitotic and meiotic cell divisions of mammalian gametogenesis, DNA repair is effective at removing DNA damages. However, in spermatogenesis the ability to repair DNA damages decreases substantially in the latter part of the process as haploid spermatids undergo major nuclear chromatin remodeling into highly compacted sperm nuclei. As reviewed by Marchetti et al., the last few weeks of sperm development before fertilization are highly susceptible to the accumulation of sperm DNA damage. Such sperm DNA damage can be transmitted unrepaired into the egg where it is subject to removal by the maternal repair machinery. However, errors in maternal DNA repair of sperm DNA damage can result in zygotes with chromosomal structural aberrations.Melphalan is a bifunctional alkylating agent frequently used in chemotherapy. Meiotic inter-strand DNA damages caused by melphalan can escape paternal repair and cause chromosomal aberrations in the zygote by maternal misrepair. Thus both pre- and post-fertilization DNA repair appear to be important in avoiding chromosome abnormalities and assuring the genome integrity of the conceptus. Detection Depending on the information one wants to obtain, different techniques and samples are needed. For the prenatal diagnosis of a foetus, amniocentesis, chorionic villus sampling or circulating foetal cells would be collected and analysed in order to detect possible chromosomal abnormalities. For the preimplantational diagnosis of an embryo, a blastocyst biopsy would be performed. For a lymphoma or leukemia screening the technique used would be a bone marrow biopsy. See also Aneuploidy Chromosome segregation Genetic disorder List of genetic disorders Gene therapy Nondisjunction Obstetrical complications References External links Chromosome+disorders at the US National Library of Medicine Medical Subject Headings (MeSH)

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Please help me grasp the concept behind the medical term 'Central serous chorioretinopathy.'

Central serous chorioretinopathy (CSC or CSCR), also known as central serous retinopathy (CSR), is an eye disease that causes visual impairment, often temporary, usually in one eye. When the disorder is active it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.The disease is considered of unknown cause. It mostly affects white males in the age group 20 to 50 (male:female ratio 6:1) and occasionally other groups. The condition is believed to be exacerbated by stress or corticosteroid use. Pathophysiology Recently, central serous chorioretinopathy has been understood to be part of the pachychoroid spectrum. In pachychoroid spectrum disorders, of which CSR represents stage II, the choroid, the highly vascularized layer below the retina, is thickened and congested with increased blood vessel diameter, especially in the deep choroid (the so-called Hallers layer). This results in increased pressure from the deep choroid against the superficial choroid close to the retina, damaging the fine blood vessels (capillaries) needed to supply oxygen and nutrients to the retinal pigment epithelium and retina. Additionally, fluid can leak from these damaged vessels and accumulate under the retina. Different stages of the pachychoroid are defined depending on the amount of cumulative damage. If there are defects in the retinal pigment epithelium without accumulation of fluid below the retina, a pachychoroid pigmentepitheliopathy (PPE) is present. Accumulation of fluid results in central serous chorioretinopathy (CSR). The development of secondary blood vessels, so-called choroidal neovascularization (CNV) leads to pachychoroid neovasculopathy (PNV). If parts of these new vessels bulge outward, so-called aneurysms develop within this CNV, defining pachychoroid aneurysmal type 1 CNV (or, still widely used, polypoidal choroidal vasculopathy (PCV)). Since the individual stages develop one after the other from the respective preliminary stage, pachychoroidal diseases of the macula are divided into 4 stages according to Siedlecki, Schworm and Priglinger: Risk factors CSR is sometimes called idiopathic CSR which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSR. CSR has also been associated with cortisol and corticosteroids. Persons with CSR have higher levels of cortisol. Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSR-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone), commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions, can trigger CSR, aggravate it and cause relapses. In a case report, a young male was using Prednisolone and began to display subretinal fluid indicative of CSR. With the discontinuation of the steroid drop the subretinal fluid resolved and did not show any sign of recurrence. Thus indicating the steroid was the probable cause of the CSR. A study of 60 persons with Cushings syndrome found CSR in 3 (5%). Cushings syndrome is characterized by very high cortisol levels. Certain sympathomimetic drugs have also been associated with causing the disease.Evidence has also implicated helicobacter pylori (see gastritis) as playing a role. It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack. Evidence also shows that people with MPGN type II kidney disease can develop retinal abnormalities including CSR caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys. Diagnosis The diagnosis usually starts with a dilated examination of the retina, followed with confirmation by optical coherence tomography and fluorescein angiography. The angiography test will usually show one or more fluorescent spots with fluid leakage. In 10%-15% of the cases these will appear in a "classic" smokestack shape. Differential diagnosis should be immediately performed to rule out retinal detachment, which is a medical emergency. A clinical record should be taken to keep a timeline of the detachment. The affected eye will sometimes exhibit a refractive spectacle prescription that is more far-sighted than the fellow eye due to the decreased focal length caused by the raising of the retina. Indocyanine green angiography or laser Doppler imaging can be used to reveal the underlying swollen choroidal vessels under the retinal pigment epithelium and assess the health of the retina in the affected area which can be useful in making a treatment decision. Treatment Any ongoing corticosteroid treatment should be tapered and stopped, where possible. It is important to check current medication, including nasal sprays and creams, for ingredients of corticosteroids, if found seek advice from a medical practitioner for an alternative. Most eyes with CSR undergo spontaneous resorption of subretinal fluid within 3–4 months. Recovery of visual acuity usually follows. Treatment should be considered if resorption does not occur within 3–4 months, spontaneously or as the result of counselling. The available evidence suggests that half-dose (or half-fluence) photodynamic therapy is the treatment of choice for CSR with subretinalfluid for longer than 3–4 months.Due to the natural disease course of CSR - in which spontaneous resolution of subretinal fluid may occur - retrospective studies may erroneously report positive treatment outcomes and should, therefore, be evaluated with caution. Laser treatments Full-dose photodynamic therapy (PDT) with verteporfin was first described in CSR in 2003. Later, reduced-settings PDT (half-dose, half-fluence, and half-time) was found to have the same efficacy and a lower chance of complications. Follow-up studies have confirmed the treatments long-term effectiveness including its effectiveness for the chronic variant of the disease. In the PLACE trial, half-dose photodynamic therapy was found to be superior compared to high-density subthreshold micropulse laser, both with regard to anatomical and functional outcomes. Indocyanine green angiography can be used to predict how the patient will respond to PDT.Laser photocoagulation, which effectively burns the leak area shut, may be considered in cases where there is little improvement in a 3- to 4-month duration, and the leakage is confined to a single or a few sources of leakage at a safe distance from the fovea. Laser photocoagulation is not indicated for cases where the leak is very near the central macula or for cases where the leakage is widespread and its source is difficult to identify. Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage. Even so, laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors. Foveal attenuation has been associated with more than 4 months duration of symptoms, however a better long-term outcome has not been demonstrated with laser photocoagulation than without photocoagulation.In chronic cases, transpupillary thermotherapy has been suggested as an alternative to laser photocoagulation where the leak is in the central macula.Yellow micropulse laser has shown promise in very limited retrospective trials. Oral medications Spironolactone is a mineralocorticoid receptor antagonist that may help reduce the fluid associated with CSR. In a retrospective study noted by Acta Ophthalmologica, spironolactone improved visual acuity in CSR patients over the course of 8 weeks.Eplerenone is another mineralocorticoid receptor antagonist that has been thought to reduce the subretinal fluid that is present with CSR. In a study noted in International Journal of Ophthalmology, results showed Epleronone decreased the subretinal fluid both horizontally and vertically over time. However, the most recent and largest randomized controlled trial showed that eplerenone has no significant effect on chronic CSR.Low dosage ibuprofen has been shown to quicken recovery in some cases. Topical treatment Though no topical treatment has been proven to be effective in the treatment of CSR. Some doctors have attempted to use nonsteroidal topical medications to reduce the subretinal fluid associated with CSR. The nonsteroidal topical medications that are sometimes used to treat CSR are, Ketorolac, Diclofenac, or Bromfenac. Lifestyle changes People who have irregular sleep patterns, type A personalities, sleep apnea, or systemic hypertension are more susceptible to CSR, as stated in Medscape. "The pathogenesis here is thought to be elevated circulating cortisol and epinephrine, which affect the autoregulation of the choroidal circulation." With management of these lifestyle patterns and associated cortisol and epinephrine levels, it has been shown that the fluid associated with CSR can spontaneously resolve. Melatonin has been shown to help regulate sleep in people who have irregular sleep patterns (such as 3rd shift workers, or overnight employees), in turn, better regulating cortisol and epinephrine levels to manage CSR. A Cochrane review seeking to compare the effectiveness of various treatment for CSR found low quality evidence that half-dose PDT treatment resulted in improved visual acuity and less recurrence of CSR in patients with acute CSR, compared to patients in the control group. The review also found benefits in micropulse laser treatments, where patients with acute and chronic CSR had improved visual acuity compared to control patients. Prognosis The prognosis for CSR is generally excellent. While immediate vision loss may be as poor as 20/200 in the affected eye, clinically, over 90% of patients regain 20/25 vision or better within 45 days. Once the fluid has resolved, either spontaneously or through treatment, distortion is reduced and visual acuity improves as the eye heals. However, some visual abnormalities can remain even where visual acuity is measured at 20/20. This includes localized reductions in light sensitivity as assessed by visual field testing (microperimetry). Lasting problems include decreased night vision, reduced color discrimination, and localized distortion caused by scarring of the sub-retinal layers.Complications include subretinal neovascularization and pigment epithelial detachment.The disease can re-occur causing progressive vision loss. There is also a chronic form, titled as type II central serous retinopathy, which occurs in approximately 5% of cases. This exhibits diffuse rather than localized abnormality of the pigment epithelium, producing a persistent subretinal fluid. The serous fluid in these cases tends to be shallow rather than dome shaped. The prognosis for this condition is less favorable and continued clinical consultation is advised. See also Diabetic retinopathy Hypertensive retinopathy Macular degeneration Posterior vitreous detachment References == External links ==

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What is the significance of the term 'Anterior interosseous syndrome' in the medical field?

Anterior interosseous syndrome is a medical condition in which damage to the anterior interosseous nerve (AIN), a distal motor and sensory branch of the median nerve, classically with severe weakness of the pincer movement of the thumb and index finger, and can cause transient pain in the wrist (the terminal, sensory branch of the AIN innervates the bones of the carpal tunnel). Most cases of AIN syndrome are now thought to be due to a transient neuritis, although compression of the AIN in the forearm is a risk, such as pressure on the forearm from immobilization after shoulder surgery. Trauma to the median nerve or around the proximal median nerve have also been reported as causes of AIN syndrome. Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome. Although the exact etiology is unknown, there is evidence that it is caused by an immune-mediated response that can follow other illnesses, such as pneumonia or severe viral illness. Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome. While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset. Other retrospective studies have concluded that there is no difference in outcome in surgically versus nonsurgically treated patients. The role of surgery in AIN syndrome remains controversial. Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) or fascial compression, and persistent symptoms beyond 1 year of conservative treatment. Symptoms and signs Patients may experience poorly localised, transient pain in the wrist, i.e. where the sensory branch of the AIN is mapped in the brain. The pain is sometimes referred into the cubital fossa and elbow pain has been reported as being a primary complaint.⁠ The characteristic severe impairment of the pincer movement of the thumb and index finger is most striking. Clinical signs In a pure lesion of the anterior interosseous nerve there is weakness of the long flexor muscle of the thumb (Flexor pollicis longus), the deep flexor muscles of the index and middle fingers (Flexor digitorum profundus I & II), and the pronator quadratus muscle.There is no sensory deficit since the anterior interosseous nerve has no cutaneous branch to skin, but there is a large sensory branch to the volar carpus, and transient wrist pain may be experienced. Causes Injuries of the forearm with compression of the nerve from swelling is the most common cause: examples include supracondylar fractures, often associated with haemorrhage into the deep musculature; injury secondary to open reduction of a forearm fracture; or dislocation of the elbow.⁠⁠Direct trauma from a penetrating injury such as a stab wound is a possible cause for the syndrome.Fibrous bands or Arcuate ligament~arcuate (curved) ligaments may entrap the median as well as the anterior interosseous nerve, in which case a patient may experience hand numbness as well as wrist pain.⁠⁠Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis.⁠Anterior interosseous nerve entrapment or compression injury remains a difficult clinical diagnosis because it is mainly a motor nerve problem, and the syndrome is often mistaken for index finger and/or thumb tendon injury.⁠ Anatomy The anterior interosseous nerve is a branch of the median nerve, with a large sensory branch to the wrist bones, which arises just below the elbow. It passes distally, anteriorly along the interosseous membrane and innervates flexor pollicis longus, flexor digitorum profundus to index and middle finger as well as pronator quadratus, and supplies sensory feedback from the wrist bones, i.e. the carpal tunnel, not skin. Diagnosis Electrophysiologic testing is an essential part of the evaluation of anterior interosseous nerve syndrome. Nerve conduction studies may be normal or show pronator quadratus latency.⁠⁠Electromyography (EMG) is generally most useful and will reveal abnormalities in the flexor pollicis longus, flexor digitorum profundus I and II and pronator quadratus muscles.⁠⁠The role or MRI and ultrasound imaging in the diagnosis of Kiloh-Nevin syndrome is unclear.⁠If asked to make the "OK" sign, patients will make a triangle sign instead. This pinch-test exposes the weakness of the flexor pollicis longus muscle and the flexor digitorum profundus I leading to weakness of the flexion of the distal phalanges of the thumb and index finger. This results in impairment of the pincer movement and the patient will have difficulty picking up a small item, such as a coin, from a flat surface. Ericsons Test Ericsons Test is a clinical maneuver for assessing the strength of the FDP and FPL muscles in anterior interosseous nerve syndrome, and other proximal entrapments of the median nerve. In contrast to the "OK sign," Ericsons test isolates the action of the FDP and FPL while eliminating the contribution of the tenodesis effect and other adaptations that patients may use, usually unconsciously, to augment distal pincer strength. Failing to control for compensatory wrist tenodesis can mask an underlying proximal median nerve weakness in a patient who can otherwise make a normal OK-sign.While facing the patient in what resembles an arm wrestling stance, with elbows planted firmly on a level surface and maintained touching the thorax, the examiner uses one hand to lock the patients wrist in neutral, around which the patient curls his fingers. With the other hand, the examiner then attempts to "peel" back the tips of each individual finger against patient resistance. It is crucial that motion of the upper extremity be restricted to the distal IP joint, and that the MP and PIP joints are in full flexion and wrist neutral or slightly flexed. If the distal flexors of the index finger and thumb are weak, the patient will be unable to resist this motion, and Ericsons test is considered positive for proximal median nerve weakness.Ericsons test is frequently positive for proximal median nerve weakness (of which AIN syndrome is but one subtype) even in the context of normal imaging, EMG, and nerve conduction studies, which highlights the clinical nature of the diagnosis. Overreliance on electrical diagnostic workup unfairly excludes patients who would otherwise benefit from surgical decompression. Treatment Surgical decompression can give excellent results if the clinical picture and the EMG suggest a compression neuropathy. In brachial plexus neuritis, conservative management may be more appropriate. Spontaneous recovery has been reported, but is said to be delayed and incomplete.There may be a role for physiotherapy in some cases, and this should be directed specifically towards the pattern of pain and symptoms. Soft tissue massage, stretches and exercises to directly mobilise the nerve tissue may be used.⁠ History The syndrome was first described by Parsonage and Turner in 1948⁠ and further defined as isolated lesion of the anterior interosseous nerve by Leslie Gordon Kiloh and Samuel Nevin in 1952. References == External links ==

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Could you offer a clear explanation of the term 'Fibroma' as used in the medical field?

Fibromas are benign tumors that are composed of fibrous or connective tissue. They can grow in all organs, arising from mesenchyme tissue. The term "fibroblastic" or "fibromatous" is used to describe tumors of the fibrous connective tissue. When the term fibroma is used without modifier, it is usually considered benign, with the term fibrosarcoma reserved for malignant tumors. Types Hard fibroma The hard fibroma (fibroma durum) consists of many fibres and few cells, e.g. in skin it is called dermatofibroma (fibroma simplex or nodulus cutaneous). A special form is the keloid, which derives from hyperplastic growth of scars. Soft fibroma The soft fibroma (fibroma molle) or fibroma with a shaft (acrochordon, skin tag, fibroma pendulans) consist of many loosely connected cells and less fibroid tissue. It mostly appears at the neck, armpits or groin. The photo shows a soft fibroma of the eyelid. Other types of fibroma The fibroma cavernosum or angiofibroma, consists of many often dilated vessels, it is a vasoactive tumor occurring almost exclusively in adolescent males. The cystic fibroma (fibroma cysticum) has central softening or dilated lymphatic vessels. The myxofibroma (fibroma myxomatodes) is produced by liquefaction of the underlying soft tissue. The cemento-ossifying fibroma is hard and fibrous, most frequently seen in the jaw or mouth, sometimes in connection with a fracture or another type of injury. Other fibromas: chondromyxoid fibroma, desmoplasmic fibroma, nonossifying fibroma, ossifying fibroma, nuchal fibroma, collagenous fibroma, fibroma of tendon sheath, perifollicular fibroma, pleomorphic fibroma, uterine fibroma, Gardner fibroma, etc. The neurofibroma is a benign nerve-sheath tumor in the peripheral nervous system. Ovarian fibroma It appears in the sex cord-stromal tumour group of ovarian neoplasms. Ovary fibromas are most frequent during middle age, and rare in children. Upon gross pathological inspection, ovary fibromas are firm and white or tan. Variants with edema are especially likely to be associated with Meigs syndrome. On microscopic examination, there are intersecting bundles of spindle cells producing collagen. There may be thecomatous areas (fibrothecoma). The presence of an ovarian fibroma can cause ovarian torsion in some cases. Treatment Benign fibromas may, but need not, be removed. Removal is usually a brief outpatient procedure or using cryotherapy in which the lesion is deep frozen (-196 degrees Celsius using liquid nitrogen) and thawed for two or more cycles, with full recovery within 3 to 4 weeks. The cryotherapy treatment needs no anesthetics and is painless. Another simple treatment is snip removal after injecting local anesthetic. See also Acrochordon (skin tags) Fibrous lesions References == External links ==

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I'm looking for a concise explanation of the medical term 'Megaureter.'

Megaureter is a medical anomaly whereby the ureter is abnormally dilated. Congenital megaureter is an uncommon condition which is more common in males, may be bilateral, and is often associated with other congenital anomalies. The cause is thought to be aperistalsis of the distal ureter, leading to dilatation.The cutoff value for megaureter is when it is wider than 6 or 7 mm.A functional obstruction at the lower end of the ureter leads to progressive dilatation and a tendency to infection. The ureteric orifice appears normal and a ureteric catheter passes easily.Definitive surgical treatment involves refashioning the lower end of the affected ureter so that a tunnelled reimplantation into the bladder can be done to prevent reflux. References Bailey and Loves Short Practice of Surgery == External links ==

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Could you please explain the term 'Infantile apnea' in simple language?

Infantile apnea is a rare disease that is characterized by cessation of breathing in an infant for at least 20 seconds or a shorter respiratory pause that is associated with a slow heart rate, bluish discolouration of the skin, extreme paleness, gagging, choking and/or decreased muscle tone. Infantile apnea occurs in children under the age of one and it is more common in premature infants. Symptoms of infantile apnea occur most frequently during the rapid eye movement (REM) stage of sleep. The nature and severity of breathing problems in patients can be detected in a sleep study called a polysomnography which measures the brain waves, heartbeat, body movements and breathing of a patient overnight. Infantile apnea can be caused by developmental problems that result in an immature brainstem or it can be caused other medical conditions. As children grow and develop, infantile apnea usually does not persist. Infantile apnea may be related to some cases of sudden infant death syndrome (SIDS) however, the relationship between infantile apnea and SIDS is not known. Cause √ having a family history of sleep apnea. √ being overweight or obese. ✓ having certain medical conditions (cerebral palsy, Down syndrome, sickle cell disease, abnormalities in the skull or face) ✓ being born with a low birth weight. ✓ having a large tongue. Diagnosis Classification There are three major categories of apnea known as central, obstructive, and mixed apnea. Central Apnea Central apnea is characterized by insufficient responsiveness from respiratory centers such as the medulla, which results in poor coordination of the body systems that are necessary for breathing. Respiratory muscles and nerves to lose the ability to effectively receive and process signals from the brain causing respiratory efforts to cease. Central apnea is quite common and can be found in healthy, full-term infants for short periods of time before breathing patterns in the infant stabilize. In premature infants, central apnea is attributed to an underdeveloped respiratory system which results in decreased response to higher carbon dioxide levels and difficulty breathing. Head trauma may also cause central apnea as it interferes with normal signalling of the central respiratory system, this might be present in infants who suffer from abuse so investigating patient background is an important consideration. Obstructive Apnea Obstructive apnea occurs when the airway passages are obstructed and little to no air exchange occurs, resulting in impaired breathing. In some cases, it occurs when patients are born with a small airway opening. Patients with obstructive apnea often have vigorous inspiratory effort but the efforts are still ineffective. Normally, the muscles at the level of the throat relax and dilate while asleep in order to open up airway however, patients with obstructive apnea may have decreased neuromuscular tone of the muscles responsible for dilating the pharynx during sleep. The inability of the vocal cords to move and the presence of a foreign body may also cause obstructive apnea. Cases of obstructive apnea are rarely found in infants that are healthy. Mixed Apnea Mixed apnea is a combination of both central and obstructive factors. The majority of premature infants with sleep apnea have mixed apnea. Epidemiology When infants have a lower birth weight or younger gestational age, there is a greater risk of infantile apnea. With the advancement of neonatal intensive care units and the greater technology available, there are more successful premature births compared to the past. With the greater number of premature infants being born, there is also a greater number of children with infantile apnea. Approximately 85 percent of infants born with a weight less than 2.2 pounds (1 kg) experience infantile apnea within the first month after birth. This risk decreases to 25 percent for infants weighing less than 5.5 pounds (2.5 kg). Studies have found that almost 2% of the pediatric population experience obstructive sleep apnea. == References ==

You act as a bridge between medical jargon and everyday language. Explain medical terms in a manner that is comprehensive yet approachable for non-experts.

Can you break down the meaning of the medical term 'Epstein syndrome' for me?

Epstein syndrome is a rare genetic disease characterized by a mutation in the MYH9 gene in nonmuscle myosin. This disease affects the patients renal system and can result in kidney failure. Epstein Syndrome was first discovered in 1972 when two families had similar symptoms to Alport syndrome. Epstein syndrome and other Alport-like disorders were seen to be caused by mutations in the MYH9 (myosin heavy chain 9) gene, however, Epstein syndrome differs as it was more specifically linked to a mutation on the R702 codon on the MYH9 gene. Diseases with mutations on the MYH9 gene also include May–Hegglin anomaly, Sebastian syndrome and Fechtner syndrome. Signs and symptoms Initial symptoms are often described as bleeding tendency and thrombocytopenia. Bleeding tendency may be observed in epistaxis and purpura. Other symptoms may include macrothrombocytopenia, proteinuria, nephropathy, sensorineural hearing loss, low platelet count, oral lesions and cataracts. The most common symptoms include macrothrombocytopenia, mild sensorineural hearing loss and nephritis. The symptoms and the severity of these symptoms vary between patients where most patients experience nephritis in childhood and then progress to kidney failure in adolescence. In macrothrombocytopenia platelet sizes can reach to approximately 6.6 um compared to a normal platelet size of 2.5 um where 30% platelets can reach the size of an erythrocytes. This large platelet size can be compared with MYH9 disorders where platelet size can vary between 4.5 um and the 6.6 um that is found in Epstein Syndrome with mutations on the R207 codon. Causes Epstein Syndrome is caused by a mutation in MYH9 gene. This mutation is autosomal dominant and is thereby inherited if one or both parents carry the mutated gene. However, there have been cases where Epstein Syndrome has been sporadic or non-congenital. Mutations are found in the nonmuscle myosin heavy chain IIA and is associated with chromosome 22. The MYH9 gene encodes for tissues including platelets, cochlea, renal cells, neutrophils and eyes. Pathophysiology The main symptom in Epstein Syndrome is thrombocytopaenia. Thrombocytopaenia is generally inherited as an autosomal dominant gene and platelets are found to aggregate with either epinephrine or collagen. Platelets assist in blood clotting and coagulate when there are damages blood vessels. This coagulation attempts to cease bleeding. Thrombocytopaenia means there is low platelet volume in the blood. This means there are less platelets to coagulate in presence of a damaged blood vessel, which can result in bleeding problems. The platelets are large (macrothrombocytopenia) and often consist of neutrophil inclusions. The large size of platelets may be due to excess microtubule coils and tublin. This large size of the platelets also affects their ability to bind to each other to seal damaged blood vessels and stop bleeding.Nephritis involves the inflammation of the kidney and this inflammation results in a reduced ability to filter blood and remove nitrogenous wastes. This excessive accumulation of wastes will result in a continued build-up of wastes including urea which interferes with metabolism.One of the kidneys functions include osmoregulation which involves the regulation of osmotic pressure in the blood by regulating the water content in blood pressure. Through osmosis (water movement from a low solute concentration to an area of high solute concentration) water is reabsorbed back into the blood from nephron tubules in the kidney. This maintenance of water concentration in the blood is essential for maintaining blood pressure and is affected in nephritis. Diagnosis The cardinal symptom in Epstein syndrome is thrombocytopaenia with giant platelets (macrothrombocytopenia). A peripheral blood smear is taken from the patient and a light microscope is used to these identify giant platelets. Leukocyte inclusions are also examined for, because approximately 41.1% of R207 mutations have leukocyte inclusions. These are often abnormal neutrophils with a small size of approximately less than 0.7 um and have an abnormallocation on the non-muscle myosin heavy chain IIA (NMMHC-II). These inclusion bodies have RNA and no DNA. RNA in these inclusion bodies can be located in immunofluorescence analysis with the anti nonmuscle heavy chain IIA antibody.Hematology analysers or a hemocytometer can be used to determine the amount of platelets. A sample of blood is drawn from a patients arm. A small amount of platelets in blood smears compared to the normal range of 150,000 to 450,000 platelets in microliter of blood suggest thrombocytopaenia, which is a common symptom in Epstein syndrome.A urine sample is often collected where a urinalysis can be used to determine the volume of proteins excreted in urine. Abnormal amounts of protein detected means the patient has proteinuria. Patients with Epstein syndrome often have large proteinuria where they excrete above 3.5g of protein in their urine in a day. This is one of the initial signs of renal disease.Easy bruising and abnormal bleeding tendencies are also described in initial diagnosis. This supports the common misdiagnosis for chronic idiopathic thrombocytopaenia purpura in patients with Epstein syndrome. These symptoms are often noticed in early childhood due to the congenital cause of the disease. Treatment Epstein syndrome is regarded as a refractory disease. Treatments include renal transplantation, however, this may become problematic as patients low platelet count (thrombocytopaenia) increase the risks of complications in surgery. Successful Renal transplants can arise from cadavers or from live donors. To minimize the risk of patients losing too much blood during the perioperative period, HLA-matched platelet infusions can be used to maintain satisfactory platelet levels. Nephritis involves the inflammation of the kidney and this inflammation results in a reduced ability to filter blood. In order to ensure the transplanted kidney is recognised as ‘self’ by Major Histocompatibility cells, immunosuppression drugs are used post operation. Immunosuppression medication may include calcineurin inhibitor, antimetabolite and methylprednisolone and assist in suppressing the immune systems response to the transplanted kidney Maintenance As a result of nephritis, a healthy blood pressure becomes difficult to maintain and hence medication including vasopressin may be prescribed to maintain blood pressure. Severe nephritis may mean kidney dialysis is required to ensure the blood is being filtered. This may include either peritoneal dialysis or haemodialysis, however, haemodialysis is most common as Epstein syndrome patients will often eventually have renal transplants. Peritoneal dialysis involves blood being filtered through a membrane in the abdomen (peritoneum). Whereas haemodialysis involves blood being filtered through a dialyser, which consists of a semi-permeable membrane where toxins including urea are removed from the blood. Haemodialysis also filters blood quicker than peritoneal dialysis.Intravenous immunoglobin treatments can be used to support the patients immune system as well as medication with Prednisolone to reduce inflammation.Sensorineural hearing loss is a common symptom in Epstein syndrome and can be treated with cochlea implants. Cochlea implants have four main parts including the electrode array, the transmitter, the receiver/stimulator and the microphone. The microphone is positioned behind the ear and receives sound waves, the processor then converts the sound into electrical signals. These electrical signals are further converted into electrical impulses in the cochlea where the transmitter is located, which in turn sends the signal to the auditory nerve. This results in a nervous impulse sent to the brain where the ‘sound’ is deciphered. Prognosis In most case Epstein syndrome patients will endure early-onset end-stage renal disease (ESRD) at the end of adolescence. Expected kidney failure means patients will need renal transplants in the near future. Notable cases In a study which investigated suitable management for severe Epstein syndrome, four patients were observed. Patient 1 demonstrated a common background and symptoms for Epstein syndrome. Patient 1 was a male who was initially diagnosed with chronic idiopathic thrombocytopaenia purpura in early childhood and then macrothrobocytopaenia. He progressed to kidney failure and began haemodialysis at seventeen years old. Patient 1 was only diagnosed with Epstein syndrome at the age of thirty-three where the mutation in the nonmuscle myosin was noticed. His eldest son also carried the same mutation.An Epstein syndrome patient with oral lesions was recorded to be the first with this symptom. The patient was a twenty-six-year-old female who was diagnosed with thrombocytopaenia with purpura at age four. She was then finally diagnosed with Epstein syndrome at twenty-two years old when she developed symptoms for hearing loss as well as proteinuria and hematuria revealing poor kidney function. After an oral examination, palatal purpua in her mouth was observed.A Japanese male was diagnosed with sporadic Epstein syndrome where both his parents did not have the R702H mutation. He was initially diagnosed with chronic macrothrombocytopaenia at three years old and throughout childhood symptoms for hearing loss and proteinuria were observed. At 24 years old his kidney failure had severely progressed as well as his hearing loss and thrombocytopenia. A genetic test confirmed he had the R702H mutation despite having no familial record of Epstein syndrome. References == External links ==

You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

I'd like to learn more about the medical term 'Homelessness.' Can you provide some details?

Homelessness or houselessness – also known as a state of being unhoused or unsheltered – is the condition of lacking stable, safe, and adequate housing. People can be categorized as homeless if they are: living on the streets, also known as rough sleeping (primary homelessness); moving between temporary shelters, including houses of friends, family, and emergency accommodation (secondary homelessness); and living in private boarding houses without a private bathroom or security of tenure (tertiary homelessness). have no permanent house or place to live safely Internally Displaced Persons, persons compelled to leave their places of domicile, who remain as refugees within their countrys borders.The rights of people experiencing homelessness also varies from country to country. United States government homeless enumeration studies also include people who sleep in a public or private place, which is not designed for use as a regular sleeping accommodation for human beings. Homelessness and poverty are interrelated. There is no methodological consensus on counting homeless people and identifying their needs; therefore, in most cities, only estimated homeless populations are known. In 2005, an estimated 100 million people worldwide were homeless, and as many as one billion people (one in 6.5 at the time) live as squatters, refugees, or in temporary shelter, all lacking adequate housing. Scarce and expensive housing is the main cause of rising homelessness in the United States. United Nations definition In 2004, the United Nations sector of Economic and Social Affairs defined a homeless household as those households without a shelter that would fall within the scope of living quarters due to a lack of a steady income. They carry their few possessions with them, sleeping in the streets, in doorways or on piers, or in another space, on a more or less random basis.In 2009, at the United Nations Economic Commission for Europe Conference of European Statisticians (CES), held in Geneva, Switzerland, the Group of Experts on Population and Housing Censuses defined homelessness as: In its Recommendations for the Censuses of Population and Housing, the CES identifies homeless people under two broad groups: (a) Primary homelessness (or rooflessness). This category includes persons living in the streets without a shelter that would fall within the scope of living quarters; (b) Secondary homelessness. This category may include persons with no place of usual residence who move frequently between various types of accommodations (including dwellings, shelters, and institutions for the homeless or other living quarters). This category includes persons living in private dwellings but reporting no usual address on their census form. The CES acknowledges that the above approach does not provide a full definition of the homeless. Article 25 of the Universal Declaration of Human Rights, adopted 10 December 1948 by the UN General Assembly, contains this text regarding housing and quality of living: Everyone has the right to a standard of living adequate for the health and well-being of himself and of his family, including food, clothing, housing, and medical care and necessary social services, and the right to security in the event of unemployment, sickness, disability, widowhood, old age or other lack of livelihood in circumstances beyond his control. The ETHOS Typology of Homelessness and Housing Exclusion was developed as a means of improving understanding and measurement of homelessness in Europe, and to provide a common "language" for transnational exchanges on homelessness. The ETHOS approach confirms that homelessness is a process (rather than a static phenomenon) that affects many vulnerable households at different points in their lives.The typology was launched in 2005 and is used for different purposes: as a framework for debate, for data collection purposes, for policy purposes, monitoring purposes, and in the media. This typology is an open exercise that makes abstraction of existing legal definitions in the EU member states. It exists in 25 language versions, the translations being provided mainly by volunteer translators. Despite all the international agreements and efforts, many countries and individuals in power do not consider housing as a human right. Former US President, Jimmy Carter, addressed this issue in a 2017 interview. He said, “A lot of people dont look at housing as a human right, but it is.” His view contrasts with many American, especially those in power, that do not believe this right is inline with the US constitution. Other terms Recent homeless enumeration survey documentation utilizes the term unsheltered homeless. The common colloquial term street people does not fully encompass all unsheltered people, in that many such persons do not spend their time in urban street environments. Many shun such locales, because homeless people in urban environments may face the risk of being robbed or assaulted. Some people convert unoccupied or abandoned buildings ("squatting"), or inhabit mountainous areas or, more often, lowland meadows, creek banks, and beaches. Many jurisdictions have developed programs to provide short-term emergency shelter during particularly cold spells, often in churches or other institutional properties. These are referred to as warming centers, and are credited by their advocates as lifesaving. History Early history through the 19th century United Kingdom Following the Peasants Revolt, English constables were authorized under 1383 English Poor Laws statute to collar vagabonds and force them to show support; if they could not, the penalty was gaol. Vagabonds could be sentenced to the stocks for three days and nights; in 1530, whipping was added. The presumption was that vagabonds were unlicensed beggars. In 1547, a bill was passed that subjected vagrants to some of the more extreme provisions of the criminal law, namely two years servitude and branding with a "V" as the penalty for the first offense and death for the second. Large numbers of vagabonds were among the convicts transported to the American colonies in the 18th century. During the 16th century in England, the state first tried to give housing to vagrants instead of punishing them, by introducing bridewells to take vagrants and train them for a profession. In the 17th and 18th centuries, these were replaced by workhouses but these were intended to discourage too much reliance on state help. United States In the Antebellum South, the availability of slave labor made it difficult for poor white people to find work. To prevent poor white people from cooperating with enslaved black people, slaveowners policed poor whites with vagrancy laws.After the American Civil War, a large number of homeless men formed part of a counterculture known as "hobohemia" all over the United States. In smaller towns, hobos temporarily lived near train tracks and hopped onto trains to various destinations.The growing movement toward social concern sparked the development of rescue missions, such as the U.S. first rescue mission, the New York City Rescue Mission, founded in 1872 by Jerry and Maria McAuley. Modern 20th century The Great Depression of the 1930s caused a devastating epidemic of poverty, hunger, and homelessness in the United States. When Franklin D. Roosevelt took over the presidency from Herbert Hoover in 1933, he passed the New Deal, which greatly expanded social welfare, including providing funds to build public housing. This marked the end of the Great Depression.How the Other Half Lives and Jack Londons The People of the Abyss (1903) discussed homelessness and raised public awareness, which caused some changes in building codes and some social conditions. In England, dormitory housing called "spikes" was provided by local boroughs. By the 1930s in England, there were 30,000 people living in these facilities. In 1933, George Orwell wrote about poverty in London and Paris, in his book Down and Out in Paris and London. In general, in most countries, many towns and cities had an area that contained the poor, transients, and afflicted, such as a "skid row". In New York City, for example, there was an area known as "the Bowery", traditionally, where people with an alcohol use disorder were to be found sleeping on the streets, bottle in hand. In the 1960s in the UK, nature and growing problem of homelessness changed in England as public concern grew. The number of people living "rough" in the streets had increased dramatically. However, beginning with the Conservative administrations Rough Sleeper Initiative, the number of people sleeping rough in London fell dramatically. This initiative was supported further by the incoming Labour administration from 2009 onwards with the publication of the Coming in from the Cold strategy published by the Rough Sleepers Unit, which proposed and delivered a massive increase in the number of hostel bed spaces in the capital and an increase in funding for street outreach teams, who work with rough sleepers to enable them to access services.Scotland saw a slightly different picture, with the impact of the right to buy ending in a devastating drop in available social housing, something that has never ever recovered. The 1980s and the 1990s resulted in an ever increasing picture of people becoming homeless, with very few rights to provide access to allow change. 2000s However this picture changed in Scotland from 2001, as the Scottish Parliament came into place. It was agreed by all parties that a ten-year plan to eradicate homelessness by the end of 2012 would be implemented. The minister of housing met with the third sector and Local Authorities every 6 weeks, checking on progress, whilst consultations brought about legislative change, alongside work to prevent homelessness. There was a peak in applications around 2005, but from there onwards figures dropped year on year for the next 8 years. However, with a focus on the broader numbers of people experiencing homelessness, many people with higher levels of need got caught in the system. Work from 2017 started to address this, with a framework currently in place to work towards a day where everyone in Scotland has a home suitable to meet their needs. In 2002, research showed that children and families were the largest growing segment of the homeless population in the United States, and this has presented new challenges to agencies. In the US, the government asked many major cities to come up with a ten-year plan to end homelessness. One of the results of this was a "Housing First" solution. The Housing First program offers homeless people access to housing without having to undergo tests for sobriety and drug usage. The Housing First program seems to benefit homeless people in every aspect except for substance abuse, for which the program offers little accountability. An emerging consensus is that the Housing First program still gives clients a higher chance at retaining their housing once they get it. A few critical voices argue that it misuses resources and does more harm than good; they suggest that it encourages rent-seeking and that there is not yet enough evidence-based research on the effects of this program on the homeless population. Some formerly homeless people, who were finally able to obtain housing and other assets which helped to return to a normal lifestyle, have donated money and volunteer services to the organizations that provided aid to them during their homelessness. Alternatively, some social service entities that help homeless people now employ formerly homeless individuals to assist in the care process. Homelessness has migrated toward rural and suburban areas. The number of homeless people has not changed dramatically but the number of homeless families has increased according to a report of HUD. The United States Congress appropriated $25 million in the McKinney-Vento Homeless Assistance Grants for 2008 to show the effectiveness of Rapid Re-housing programs in reducing family homelessness. In February 2009, President Obama signed the American Recovery and Reinvestment Act of 2009, part of which addressed homelessness prevention, allocating $1.5 billion for a Homeless Prevention Fund. The Emergency Shelter Grant (ESG) programs name was changed to Emergency Solution Grant (ESG) program, and funds were re-allocated to assist with homeless prevention and rapid re-housing for families and individuals. Causes Major reasons for homelessness include: Rent and eviction Gentrification is a process in which a formerly affordable neighborhood becomes popular with wealthier people, raising housing prices and pushing poorer residents out. Gentrification can cause or influence evictions, foreclosures, and rent regulation. Increased wealth disparity and income inequality causes distortions in the housing market that push rent burdens higher, making housing unaffordable.In many countries, people lose their homes by government orders to make way for newer upscale high-rise buildings, roadways, and other governmental needs. The compensation may be minimal, in which case the former occupants cannot find appropriate new housing and become homeless. Mortgage foreclosures where mortgage holders see the best solution to a loan default is to take and sell the house to pay off the debt can leave people homeless. Foreclosures on landlords often lead to the eviction of their tenants. "The Sarasota, Florida, Herald Tribune noted that, by some estimates, more than 311,000 tenants nationwide have been evicted from homes this year after lenders took over the properties."Rent regulation also has a small effect on shelter and street populations. This is largely due to rent control reducing the quality and quantity of housing. For example, a 2019 study found that San Franciscos rent control laws reduced tenant displacement from rent controlled units in the short-term, but resulted in landlords removing 30% of the rent controlled units from the rental market, (by conversion to condos or TICs) which led to a 15% citywide decrease in total rental units, and a 7% increase in citywide rents. Economics A substantial percentage of the US homeless population are individuals who are chronically unemployed, or have trouble managing their expenses. This can lead to poverty. Factors that can lead to economic struggle include neighbourhood gentrification (as previously discussed), drug addiction or gambling addiction, job loss, debt, chronic overspending of money, loss of money and/or assets due to divorce, death of breadwinning spouse, being denied jobs due to discrimination, living off of welfare or disability income, and many others. Poverty Poverty is a significant factor in homelessness. Alleviation of poverty, as a result, plays an essential role in eliminating homelessness. Some non-governmental organizations (NGOs) have studied ‘unconditional cash transfers’ (UCTs) to low-income families and individuals to reduce poverty in developing countries. Despite their initial concern about UTC’s potential negative effects on the recipients, the researchers found promising results. The study in Kenya found that the assisted households increased their consumption and savings. While the families spent more for their food and food security, they did not incur any expenses on unnecessary goods or services. This study shows that a proper approach to poverty could effectively eliminate this factor as part of a solution to homelessness. Providing access to education and employment to low-income families and individuals must also be considered to combat poverty and preventing homelessness. Physical and mental health It is not surprising that many researchers have identified that “Homelessness is closely connected to decline in physical and mental health”. Most people who use homeless shelters on a frequent basis face multiple disadvantages, such as increased prevalence of physical and mental health problems, disabilities, addiction, poverty, and discrimination. Studies have shown that homeless people have a high level of morbidity and mortality. Moreover, they suffer from a wide range of health problems, including contracting sever infectious diseases (such as tuberculosis, HIV/AIDs, and STDs), addictions, and mental illnesses. Notably, the lack of access to healthcare for homeless people adversely affects the healthcare system as well. Homeless people often obtain their care in emergency departments, partly due to their lack of adequate health insurance, especially for medications. Statistics demonstrate that they are admitted to hospital five times more than the public and stay under care much longer. Their prolonged healthcare imposes a significant cost to the healthcare system and deprives others from receiving their timely healthcare. Studies show that preventive and primary care (which homeless people are not receiving) substantially lower the overall healthcare costs. Unfortunately, in terms of providing adequate treatment to homeless people with respect to their mental illness, the healthcare system’s performance has not been promising, either. It is apparent that a comprehensive solution to homelessness must include an effective approach to providing healthcare to homeless people. Disabilities, especially where disability services are non-existent, inconvenient, or poorly performing can impact a persons ability to support house payments, mortgages, or rent, especially if they are unable to work. Traumatic brain injury is one main disability that can account for homelessness. According to a Canadian survey, traumatic brain injury is widespread among homeless people and, for around 70% of respondents, can be attributed to a time "before the onset of homelessness"Being afflicted with a mental disorder, including substance use disorders, where mental health services are unavailable or difficult to access can also drive homelessness for the same reasons as disabilities. A United States federal survey done in 2005 indicated that at least one-third of homeless men and women have serious psychiatric disorders or problems. Autism spectrum disorders and schizophrenia are the top two common mental disabilities among the U.S. homeless. Personality disorders are also very prevalent, especially Cluster A. Substance abuse can also cause homelessness from behavioral patterns associated with addiction, that alienate an addicted individuals family and friends, who could otherwise provide support during difficult economic times. Discrimination A history of experiencing domestic violence can also attribute to homelessness. Compared to housed women, homeless women were more likely to report childhood histories of abuse, as well as more current physical abuse by male partners.Gender disparities also influence the demographics of homelessness. The experiences of homeless women and women in poverty are often overlooked, however, they experience specific gender-based victimization. As individuals with little to no physical or material capital, homeless women are particularly targeted by male law enforcement, and men living on the street. It has been found that "street-based homelessness dominates mainstream understanding of homelessness and it is indeed an environment in which males have far greater power (OGrady and Gaietz, 2004)." Women on the street are often motivated to gain capital through affiliation and relationships with men, rather than facing homelessness alone. Within these relationships, women are still likely to be physically and sexually abused.Social exclusion related to sexual orientation, gender identity or expression, or sex characteristics can also attribute to homelessness based on discrimination. Relationship breakdown, particularly in relation to young people and their parents, such as disownment due to sexuality or gender identity is one example.Former imprisonment status and a criminal history can also affect securing housing. Human and natural disasters Natural disasters, including but not limited to earthquakes, hurricanes, tsunamis, tornadoes, and volcanic eruptions can cause homelessness. An example is the 1999 Athens earthquake in Greece, in which many middle class people became homeless, with some of them living in containers, especially in the Nea Ionia earthquake survivors container city provided by the government; in most cases, their only property that survived the quake was their car. Such people are known in Greece as seismopathis, meaning earthquake-struck.War or armed conflict can create refugees fleeing the violence. Whether they be either domestic or foreign to the country, the number of migrants can outstrip the supply of affordable housing, leaving some section of this population to be homeless. Foster care Transitions from foster care and other public systems can also impact homelessness; specifically, youth who have been involved in, or are a part of the foster care system, are more likely to become homeless. Most leaving the system have no support and no income, making it nearly impossible to break the cycle, and forcing them to live on the streets. There is also a lack of shelter beds for youth; various shelters have strict and stringent admissions policies. Choice Although uncommon, some choose to be homeless as a personal lifestyle choice. There are different reasons why someone would choose to become homeless. They may not want to contribute to a capitalist society, which includes having a job, spending and owing money, and paying taxes to the government. The main aspect of freeganism is anti-consumerism, and avoiding spending excessive amounts of money at all costs. Some see homelessness as more free than living in a house or apartment, and prefer being in nature, as well as away from other people. Some may have had a traumatic experience in a house or apartment, such as a fire, and feel safer outside, being able to survey their surroundings. Challenges The basic problem of homelessness is the need for personal shelter, warmth, and safety. Other difficulties include: Hygiene and sanitary facilities Hostility from the public and laws against urban vagrancy Cleaning and drying of clothes Obtaining, preparing, and storing food Keeping contact with friends, family, and government service providers without a permanent location or mailing address Medical problems, including issues caused by an individuals homeless state (e.g., hypothermia or frostbite from sleeping outside in cold weather), or issues which are exacerbated by homelessness due to lack of access to treatment (e.g., mental health and the individual not having a place to store prescription drugs) Personal security, quiet, and privacy, especially for sleeping, bathing, and other hygiene activities Safekeeping of bedding, clothing, and possessions, which may have to be carried at all timesPeople experiencing homelessness face many problems beyond the lack of a safe and suitable home. They are often faced with reduced access to private and public services and vital necessities: General rejection or discrimination from other people Increased risk of suffering violence and abuse Limited access to education Loss of usual relationships with the mainstream Not being seen as suitable for employment Reduced access to banking services Reduced access to communications technology Reduced access to healthcare and dental services Targeting by municipalities to exclude from public space Implication of hostile architecture Difficulty forming trust in relation to services, systems, and other people; exacerbating pre-existing difficulty accessing aid and escaping homelessness, particularly present in the chronically homeless. Statistics from the past twenty years, in Scotland, demonstrate that the biggest cause of homelessness is varying forms of relationship breakdown.There is sometimes corruption and theft by the employees of a shelter, as evidenced by a 2011 investigative report by FOX 25 TV in Boston, wherein a number of Boston public shelter employees were found stealing large amounts of food over a period of time from the shelters kitchen for their private use and catering. Homeless people are often obliged to adopt various strategies of self-presentation in order to maintain a sense of dignity, which constrains their interaction with passers-by, and leads to suspicion and stigmatization by the mainstream public.Homelessness is also a risk factor for depression caused by prejudice. When someone is prejudiced against people who are homeless, and then becomes homeless themselves, their anti-homelessness prejudice turns inward, causing depression. "Mental disorders, physical disability, homelessness, and having a sexually transmitted infection are all stigmatized statuses someone can gain despite having negative stereotypes about those groups." Difficulties can compound exponentially. A study found that in the city of Hong Kong over half of the homeless people in the city (56%) had some degree of mental illness. Only 13% of the 56% were receiving treatment for their condition leaving a huge portion of homeless untreated for their mental illness.The issue of anti-homeless architecture came to light in 2014, after a photo displayed hostile features (spikes on the floor) in London, and took social media by storm. The photo of an anti-homeless structure was a classic example of hostile architecture, in an attempt to discourage people from attempting to access or use public space in irregular ways. However, although this has only recently came to light, hostile architecture has been around for a long time in many places.: 68  An example of this is a low overpass that was put in place between New York City and Long Island. Robert Moses, an urban planner, designed it this way in an attempt to prevent public buses from being able to pass through it. Healthcare Health care for homeless people is a major public health challenge. When compared to the general population, people who are homeless experience higher rates of adverse physical and mental health outcomes. Chronic disease severity, respiratory conditions, rates of mental health illnesses and substance use are all often greater in homeless populations than the general population. Homelessness is also associated with a high risk of suicide attempts. Homeless people are more likely to suffer injuries and medical problems from their lifestyle on the street, which includes poor nutrition, exposure to the severe elements of weather, and a higher exposure to violence. Yet at the same time, they have reduced access to public medical services or clinics, in part because they often lack identification or registration for public healthcare services. There are significant challenges in treating homeless people who have psychiatric disorders because clinical appointments may not be kept, their continuing whereabouts are unknown, their medicines may not be taken as prescribed, medical and psychiatric histories are not accurate, and other reasons. Because many homeless people have mental illnesses, this has presented a crisis in care.The conditions affecting homeless people are somewhat specialized, and have opened a new area of medicine tailored to this population. Skin conditions, including scabies, are common, because homeless people are exposed to extreme cold in the winter, and have little access to bathing facilities. They have problems caring for their feet, and have more severe dental problems than the general population. Diabetes, especially untreated, is widespread in the homeless population. Specialized medical textbooks have been written to address this for providers.Due to the demand for free medical services by homeless people, it might take months to get a minimal dental appointment in a free-care clinic. Communicable diseases are of great concern, especially tuberculosis, which spreads more easily in crowded homeless shelters in high-density urban settings. There has been ongoing concern and studies about the health and wellness of the older homeless population, typically ages 50 to 64 and older, as to whether they are significantly more sickly than their younger counterparts, and if they are under-served.A 2011 study led by Dr. Rebecca T. Brown in Boston, conducted by the Institute for Aging Research (an affiliate of Harvard Medical School), Beth Israel Deaconess Medical Center, and the Boston Health Care for the Homeless Program found the elderly homeless population had "higher rates of geriatric syndromes, including functional decline, falls, frailty, and depression than seniors in the general population, and that many of these conditions may be easily treated if detected". The report was published in the Journal of Geriatric Internal Medicine. There are government avenues which provide resources for the development of healthcare for homeless people. In the United States, the Bureau of Primary Health Care has a program that provides grants to fund the delivery of healthcare to homeless people. According to 2011 UDS, data community health centers were able to provide service to 1,087,431 homeless individuals. There are also many nonprofit and religious organizations which provide healthcare services to homeless people. These organizations help meet the large need which exists for expanding healthcare for homeless people. There have been significant numbers of unsheltered persons dying of hypothermia, adding impetus to the trend of establishing warming centers, as well as extending enumeration surveys with vulnerability indexes. Effect on life expectancy In 1999, Dr. Susan Barrow of the Columbia University Center for Homelessness Prevention Studies reported in a study that the "age-adjusted death rates of homeless men and women were four times those of the general U.S. population and two to three times those of the general population of New York City". A report commissioned by homeless charity Crisis in 2011 found that on average, homeless people in the UK have a life expectancy of 47 years, 30 years younger than the rest of the population. Health impacts of extreme weather events People experiencing homelessness are at a significant increased risk to the effects of extreme weather events. Such weather events include extreme heat and cold, floods, storm surges, heavy rain, and droughts. While there are many contributing factors to these events, climate change is driving an increasing frequency and intensity of these events. The homeless population is considerably more vulnerable to these weather events, due to their higher rates of chronic disease, and lower socioeconomic status. Despite having a minimal carbon footprint, homeless people unfortunately experience a disproportionate burden of the effects of climate change.Homeless persons have increased vulnerability to extreme weather events for many reasons. They are disadvantaged in most social determinants of health, including lack of housing and access to adequate food and water, reduced access to health care, and difficulty in maintaining health care. They have significantly higher rates of chronic disease including respiratory disease and infections, gastrointestinal disease, musculoskeletal problems and mental health disease. In fact, self-reported rates of respiratory diseases (including asthma, chronic bronchitis and emphysema) are double that of the general population.The homeless population often live in higher risk urban areas, with increased exposure and little protection from the elements. They also have limited access to clean drinking water, and other methods of cooling down. The built environment in urban areas also contributes to the "heat island effect", the phenomenon whereby cities experience higher temperatures due to the predominance of dark, paved surfaces, and lack of vegetation. Homeless populations are often excluded from disaster planning efforts, further increasing their vulnerability when these events occur. Without the means to escape extreme temperatures and seek proper shelter, and cooling or warming resources, homeless people are often left to suffer the brunt of the extreme weather. The health effects that result from extreme weather include exacerbation of chronic diseases and acute illnesses. Pre-existing conditions can be greatly exacerbated by extreme heat and cold, including cardiovascular, respiratory, skin and renal disease, often resulting in higher morbidity and mortality during extreme weather. Acute conditions such as sunburn, dehydration, heat stroke, and allergic reactions are also common. In addition, a rise in insect bites can lead to vector-borne infections. Mental health conditions can also be impacted by extreme weather events as a result of lack of sleep, increased alcohol consumption, reduced access to resources and reduced ability to adjust to the environmental changes. In fact, pre-existing psychiatric illness has been shown to triple the risk of death from extreme heat. Overall, extreme weather events appear to have a "magnifying effect" in exacerbating the underlying prevalent mental and physical health conditions of homeless populations. Case study: Hurricane Katrina In 2005, Hurricane Katrina, a category 5 hurricane, made landfall on Florida and Louisiana. It particularly affected the city of New Orleans and the surrounding areas. Hurricane Katrina was the deadliest hurricane in the US in seven decades, with more than 1,600 confirmed deaths, and more than 1,000 people missing. The hurricane disproportionately affected marginalized individuals, and individuals with lower socioeconomic status (i.e., 93% of shelter residents were African–American, 32% had household incomes below $10,000/year and 54% were uninsured). The storm nearly doubled the number of homeless people in New Orleans. While in most cities, homeless people account for 1% of the population, in New Orleans, the homeless account for 4% of the population. In addition to its devastating effects on infrastructure and the economy, the estimated prevalence of mental illness and the incidence of West Nile Virus more than doubled after Hurricane Katrina in the hurricane-affected regions. Legal documentation Homeless people may find it difficult to document their date of birth or their address. Due to the fact that homeless people usually have no place to store possessions, they often lose their belongings, including identification and other documents, or find them destroyed by police or others. Without a photo ID, homeless persons cannot get a job or access many social services, including healthcare. They can be denied access to even the most basic assistance: clothing closets, food pantries, certain public benefits, and in some cases, emergency shelters. Obtaining replacement identification is difficult. Without an address, birth certificates cannot be mailed. Fees may be cost-prohibitive for impoverished persons. And some states will not issue birth certificates unless the person has photo identification, creating a Catch-22. This problem is far less acute in countries that provide free-at-use health care, such as the UK, where hospitals are open-access day and night and make no charges for treatment. In the U.S., free-care clinics for homeless people and other people do exist in major cities, but often attract more demand than they can meet. Victimization by violent crimes Homeless people are often the victims of violent crime. A 2007 study found that the rate of violent crimes against homeless people in the United States is increasing. A study of women veterans found that homelessness is associated with domestic violence, both directly, as the result of leaving an abusive partner, and indirectly, due to trauma, mental health conditions, and substance abuse. Stigma Conditions such as alcoholism and mental illness are often associated with homelessness. Many people fear homeless people, due to the stigma surrounding the homeless community. Surveys have revealed that before spending time with the homeless, most people fear them, but after spending time with homeless people, that fear is lessened, or is no longer there. Another effect of this stigma is isolation.The stigmas of homelessness can thus be divided into three major categories in general: (1) attributing homelessness to personal incompetency and health conditions (e.g., unemployment, mental health issues, substance abuse, etc.); (2) seeing homeless people as posing threats to ones personal safety; and (3) de-sanitizing homeless people (i.e., seeing them as pathogens). Past research has shown that those types of stigmas are being reinforced through the fact that one is homeless and have a negative impact on effective public policymaking in terms of reducing homelessness. When a person lives on a street, many aspects of their personal situations, such as mental health issues and alcoholism, are more likely to be exposed to the public as compared to people who are not homeless and have access to resources that will help improve their personal crises. Such lack of privacy inevitably reinforces stigma by increasing observations of stereotypes for the public. Furthermore, media often attributes those personal crises to the direct cause of crimes, further leading the public to believe that homeless people are a threat to their personal safety. Many also believe that contacts with homeless people increase their chance of contracting diseases given that they lack access to stable, sanitary living conditions. Those types of stigmas are intertwined with each other when shaping public opinions on policies related to the homeless population, resulting in many ineffective policies that do not reduce homelessness at all. An example of such ineffective but somewhat popular policies is imposing bans on sleeping on the streets.Relying on the famous contact hypothesis, researchers argue that increasing contact between the homeless population and non-homeless population is likely to change public opinions on this out-group and make the public more well-informed when it comes to policymaking. While some believe that the contact hypothesis is only valid on the condition that the context and type of contact are specified, in the case of reducing discrimination against the homelessness population, some survey data indicate that the context (e.g., the proportion of the homeless population in ones city) and type of contact (e.g., TV shows about the homelessness population or interpersonal conversations about homelessness) do not produce much variation as they all increase positive attitudes towards homeless people and public policies that aid this group. Given that the restrictions of contexts and types of contact to reduce stigma are minimal, this finding is informative and significant to the government when it comes to making policies to offer institutional support for reducing discrimination in a country and for gauging public opinions on their proposed policies to reduce homelessness. Global statistics Demographics In western countries such as the United States, the typical homeless person is male and single, with the Netherlands reporting 80% of homeless people aged 18–65 to be men. Some cities have particularly high percentages of males in homeless populations, with men comprising eighty-five percent of the homeless in Dublin. Non-white people are also overrepresented in homeless populations, with such groups two and one-half times more likely to be homeless in the U.S. The median age of homeless people is approximately 35. Statistics for developed countries In 2005, an estimated 100 million people worldwide were homeless. The following statistics indicate the approximate average number of homeless people at any one time. Each country has a different approach to counting homeless people, and estimates of homelessness made by different organizations vary wildly, so comparisons should be made with caution. European Union: 3,000,000 (UN-HABITAT 2004) England: 11,580 single households were assessed as rough sleeping at the point of approach in 2021, up 39% from 2019–20, with 119,400 households owed a prevention duty in 2020–21 Scotland: 27,571 households were assessed as homeless in 2020/21, a decrease of 13% compared to 2019/20 Canada: 150,000 Australia: On census night in 2006 there were 105,000 people homeless across Australia, an increase from the 99,900 Australians who were counted as homeless in the 2001 census United States: The HUD 2018 Annual Homeless Assessment Report (AHAR) to Congress reports that in a single night, roughly 553,000 people were experiencing homelessness in the United States. According to HUDs July 2010 fifth Homeless Assessment Report to Congress, in a single night in January 2010, single-point analysis reported to HUD showed 649,917 people experiencing homelessness. This number had increased from January 2009s 643,067. The unsheltered count increased by 2.8 percent while the sheltered count remained the same. Also, HUD reported the number of chronically homeless people (persons with severe disabilities and long homeless histories) decreased one percent between 2009 and 2010, from 110,917 to 109,812. Since 2007 this number had decreased by 11 percent. This was mostly due to the expansion of permanent supportive housing programs.The change in numbers has occurred due to the prevalence of homelessness in local communities rather than other changes. According to HUDs July 2010 Homeless Assessment Report to Congress, more than 1.59 million people spent at least one night in an emergency shelter or transitional housing program during the 2010 reporting period, a 2.2 percent increase from 2009. Most users of homeless shelters used only an emergency shelter, while 17 percent used only transitional housing, and less than 5 percent used both during the reporting period. Since 2007, the annual number of those using homeless shelters in cities has decreased from 1.22 million to 1.02 million, a 17 percent decrease. The number of persons using homeless shelters in suburban and rural areas increased 57 percent, from 367,000 to 576,000. In the U.S., the federal governments HUD agency has required federally-funded organizations to use a computer tracking system for homeless people and their statistics, called HMIS (Homeless Management Information System). There has been some opposition to this kind of tracking by privacy advocacy groups, such as EPIC.However, HUD considers its reporting techniques to be reasonably accurate for homeless in shelters and programs in its Annual Homeless Assessment Report to Congress. Actually determining and counting the number of homeless is very difficult in general due to their lifestyle habits. There are so-called "hidden homeless" out of sight of the normal population and perhaps staying on private property. Various countries, states, and cities have come up with differing means and techniques to calculate an approximate count. For example, a one night "homeless census count", called a point-in-time (PIT) count, usually held in early winter for the year, is a technique used by a number of American cities, such as Boston. Los Angeles uses a mixed set of techniques for counting, including the PIT street count.In 2003, The United States Department of Housing and Urban Development (HUD) had begun requiring a PIT count in all "Continuum of Care" communities which required them to report a count of people, housing status, and geographic locations of individuals counted. Some communities provide sub-population information to the PIT, such as information on veterans, youth, and elderly individuals, as done in Boston.Japan: 20,000–100,000 (some figures put it at 200,000–400,000). Reports show that homelessness is on the rise in Japan since the mid-1990s. There are more homeless men than homeless women in Japan because it is usually easier for women to get a job and they are less isolated than men. Also Japanese families usually provide more support for women than they do for men. Developing and undeveloped countries The number of homeless people worldwide grew steadily in 2005. In some developing countries such as Nigeria and South Africa, homelessness is rampant, with millions of children living and working on the streets. Homelessness has become a problem in the countries of China, India, Thailand, Indonesia, and the Philippines despite their growing prosperity, partly due to migrant workers who have trouble finding permanent homes.Determining the true number of homeless people worldwide varies between 100 million and 1 billion people based on the exact definition used. Refugees, asylum-seekers, and internally displaced persons can also be considered homeless in that they, too, experience "marginalization, minority status, socioeconomic disadvantage, poor physical health, collapse of social supports, psychological distress, and difficulty adapting to host cultures" such as the domestic homeless.In the past twenty years, scholars such as Tipple and Speak have begun to refer to homelessness as the "antithesis or absence of home" rather than rooflessness or the "lack of physical shelter." This complication in the homelessness debate further delineates the idea that home actually consists of an adequate shelter, an experienced and dynamic place that serves as a "base" for nurturing human relationships and the "free development of individuals" and their identity. Thus, the home is perceived to be an extension of ones self and identity. In contrast, the homeless experience, according to Moore, constitutes more as a "lack of belonging" and a loss of identity that leads to individuals or communities feeling "out of place" once they can no longer call a place of their own home.This new perspective on homelessness sheds light on the plight of refugees, a population of stateless people who are not normally included in the mainstream definition of homelessness. It has also created problems for researchers because the nature of "counting" homeless people across the globe relies heavily on who is considered a homeless person. Homeless individuals, and by extension refugees, can be seen as lacking lack the "crucible of our modern society" and lacking a way of actively belonging to and engaging with their respective communities or cultures. As Casavant demonstrates, a spectrum of definitions for homelessness, called the "continuum of homelessness", should refer to refugees as homeless individuals because they not only lose their home, but they are also afflicted with a myriad of problems that parallel those affecting the domestic homeless, such as "[a lack of] stable, safe and healthy housing, an extremely low income, adverse discrimination in access to services, with problems of mental health, alcohol, and drug abuse or social disorganization". Refugees, like the domestic homeless, lose their source of identity and way of connecting with their culture for an indefinite period of time. Thus, the current definition of homelessness unfortunately allows people to simplistically assume that homeless people, including refugees, are merely "without a place to live" when that is not the case. As numerous studies show, forced migration and displacement brings with it another host of problems including socioeconomic instability, "increased stress, isolation, and new responsibilities" in a completely new environment.For people in Russia, especially the youth, alcohol and substance use is a major cause and reason for becoming and continuing to be homeless. The United Nations Centre for Human Settlements (UN-Habitat) wrote in its Global Report on Human Settlements in 1995: "Homelessness is a problem in developed as well as in developing countries. In London, for example, life expectancy among homeless people is more than 25 years lower than the national average." Poor urban housing conditions are a global problem, but conditions are worst in developing countries. Habitat says that today 600 million people live in life- and health-threatening homes in Africa, Asia, and Latin America. For example, more than three in four young people had insufficient means of shelter and sanitation in some African countries like Malawi. "The threat of mass homelessness is greatest in those regions because that is where population is growing fastest. By 2015, the 10 largest cities in the world will be in Asia, Latin America, and Africa. Nine of them will be in developing countries: Mumbai, India – 27.4 million; Lagos, Nigeria – 24.4; Shanghai, China – 23.4; Jakarta, Indonesia – 21.2; São Paulo, Brazil – 20.8; Karachi, Pakistan – 20.6; Beijing, China – 19.4; Dhaka, Bangladesh – 19; Mexico City, Mexico – 18.8. The only city in a developed country that will be in the top ten is Tokyo, Japan – 28.7 million."In 2008, Dr. Anna Tibaijuka, executive director of UN-HABITAT, referring to the recent report "State of the Worlds Cities Report 2008/2009", said that the world economic crisis we are in should be viewed as a "housing finance crisis" in which the poorest of poor were left to fend for themselves. Refuges and alternative accommodation There are various places where a homeless person might seek refuge: 24-hour Internet cafes are now used by over 5,000 Japanese "Net cafe refugees". An estimated 75% of Japans 3,200 all-night internet cafes cater to regular overnight guests, who in some cases have become their main source of income. 24-hour McDonalds restaurants are used by "McRefugees" in Japan, China and Hong Kong. There are about 250 McRefugees in Hong Kong. Couch surfing: temporary sleeping arrangements in dwellings of friends or family members ("couch surfing"). This can also include housing in exchange for labor or sex. Couch surfers may be harder to recognize than street homeless people and are often omitted from housing counts. Homeless shelters: including emergency cold-weather shelters opened by churches or community agencies, which may consist of cots in a heated warehouse, or temporary Christmas Shelters. More elaborate homeless shelters such as Pinellas Hope in Florida provide residents with a recreation tent, a dining tent, laundry facilities, outdoor tents, casitas, and shuttle services that help inhabitants get to their jobs each day. Inexpensive boarding houses: have also been called flophouses. They offer cheap, low-quality temporary lodging. Inexpensive motels offer cheap, low-quality temporary lodging. However, some who can afford housing live in a motel by choice. For example, David and Jean Davidson spent 22 years at various UK Travelodges. Public places: Parks, bus or train stations, public libraries, airports, public transportation vehicles (by continual riding where unlimited passes are available), hospital lobbies or waiting areas, college campuses, and 24-hour businesses such as coffee shops. Many public places use security guards or police to prevent people from loitering or sleeping at these locations for a variety of reasons, including image, safety, and comfort of patrons. Shantytowns: ad hoc dwelling sites of improvised shelters and shacks, usually near rail yards, interstates and high transportation veins. Some shantytowns have interstitial tenting areas, but the predominant feature consists of hard structures. Each pad or site tends to accumulate roofing, sheathing, plywood, and nailed two by fours. Single room occupancy (more commonly abbreviated to SRO):a form of housing that is typically aimed at residents with low or minimal incomes who rent small, furnished single rooms with a bed, chair, and sometimes a small desk. SRO units are rented out as permanent residence or primary residence to individuals, within a multi-tenant building where tenants share a kitchen, toilets or bathrooms. In the 2010s, some SRO units may have a small refrigerator, microwave and sink. (also called a "residential hotel"). Squatting in an unoccupied structure where a homeless person may live without payment and without the owners knowledge or permission. Often these buildings are long abandoned and not safe to occupy. Tent cities: ad hoc campsites of tents and improvised shelters consisting of tarpaulins and blankets, often near industrial and institutionally zoned real estate such as rail yards, highways and high transportation veins. A few more elaborate tent cities, such as Dignity Village, are hybrids of tent cities and shantytowns. Tent cities frequently consist only of tents and fabric improvised structures, with no semi-permanent structures at all. Outdoors: on the ground or in a sleeping bag, tent, or improvised shelter, such as a large cardboard box, under a bridge, in an urban doorway, in a park or a vacant lot. Tunnels such as abandoned subway, maintenance, or train tunnels are popular among the long-term or permanent homeless. The inhabitants of such refuges are called in some places, like New York City, "Mole People". Natural caves beneath urban centers allow for places where people can congregate. Leaking water pipes, electric wires, and steam pipes allow for some of the essentials of living. Vehicles: cars or trucks used as temporary or sometimes long-term living quarters, for example by those recently evicted from a home. Some people live in recreational vehicles (RVs), school buses, vans, sport utility vehicles, covered pickup trucks, station wagons, sedans, or hatchbacks. The vehicular homeless, according to homeless advocates and researchers, comprise the fastest-growing segment of the homeless population. Many cities have safe parking programs in which lawful sites are permitted at churches or in other out-of-the-way locations. For example, because it is illegal to park on the street in Santa Barbara, the New Beginnings Counseling Center worked with the city to make designated parking lots available to homeless people. Other housing options Transitional housingTransitional housing provides temporary housing for certain segments of the homeless population, including the working homeless, and is meant to transition residents into permanent, affordable housing. This is usually a room or apartment in a residence with support services. The transitional time can be relatively short, for example, one or two years, and in that time the person must file for and obtain permanent housing along with gainful employment or income, even if Social Security or assistance. Sometimes transitional housing programs charge a room and board fee, maybe 30% of an individuals income, which is sometimes partially or fully refunded after the person procures a permanent residence. In the U.S., federal funding for transitional housing programs was originally allocated in the McKinney–Vento Homeless Assistance Act of 1986.FoyersFoyers are a specific type of transitional housing designed for homeless or at-risk teens. Foyers are generally institutions that provide affordable accommodation as well as support and training services for residents. They were pioneered in the 1990s in the United Kingdom, but have been adopted in areas in Australia and the United States as well. Supportive housingSupportive housing is a combination of housing and services intended as a cost-effective way to help people live more stable, productive lives. Supportive housing works well for those who face the most complex challenges – individuals and families confronted with homelessness who also have very low incomes or serious, persistent issues such as substance use disorder, addictions, alcohol use disorder, mental illness, HIV/AIDS, or other serious challenges. A 2021 systematic review of 28 interventions, mostly in North America, showed that interventions with highest levels of support led to improved outcomes for both housing stability, and health outcomes.Government initiatives In South Australia, the state government of Premier Mike Rann (2002–2011) committed substantial funding to a series of initiatives designed to combat homelessness. Advised by Social Inclusion Commissioner David Cappo and the founder of New Yorks Common Ground program, Rosanne Haggerty, the Rann government established Common Ground Adelaide, building high-quality inner city apartments (combined with intensive support) for "rough sleeping" homeless people. The government also funded the Street to Home program and a hospital liaison service designed to assist homeless people admitted to the emergency departments of Adelaides major public hospitals. Rather than being released back into homelessness, patients identified as rough sleepers were found accommodation backed by professional support. Common Ground and Street to Home now operate across Australia in other States. Assistance and resources Most countries provide a variety of services to assist homeless people. Provisions of food, shelter, and clothing and may be organized and run by community organizations, often with the help of volunteers, or by government departments. Assistance programs may be supported by government, charities, churches, and individual donors. However, not all homeless people can access these resources. In 1998, a study by Koegel and Schoeni of a homeless population in Los Angeles, California, found that a significant minority of homeless did not participate in government assistance programs, with high transaction costs being a likely contributing factor. Social supports While some homeless people are known to have a community with one another, providing each other various types of support, people who are not homeless also may provide them friendship, relational care, and other forms of assistance. Such social supports may occur through a formal process, such as under the auspices of a non-governmental organization, religious organization, or homeless ministry, or may be done on an individual basis. Income Employment The United States Department of Labor has sought to address one of the main causes of homelessness, a lack of meaningful and sustainable employment, through targeted training programs and increased access to employment opportunities that can help homeless people develop sustainable lifestyles. This has included the development of the United States Interagency Council on Homelessness, which addresses homelessness on the federal level in addition to connecting homeless individuals to resources at the state level. All individuals who are in need of assistance are able, in theory, to access employment and training services under the Workforce Investment Act (WIA), although this is contingent upon funding and program support by the government. Income sources outside of regular employment Waste management Homeless people can also use waste management services to earn money. Some homeless people find returnable bottles and cans and bring them to recycling centers to earn money. They can sort out organic trash from other trash or separate out trash made of the same material (for example, different types of plastics, and different types of metal). In addition, rather than picking waste at landfills, they can also collect litter found on/beside the road to earn an income. Street newspapers Street newspapers are newspapers or magazines sold by homeless or poor individuals and produced mainly to support these populations. Most such newspapers primarily provide coverage about homelessness and poverty-related issues and seek to strengthen social networks within homeless communities, making them a tool for allowing homeless individuals to work. Medicine The 2010 passage of the Patient Protection and Affordable Care Act could provide new healthcare options for homeless people in the United States, particularly through the optional expansion of Medicaid. A 2013 Yale study indicated that a substantial proportion of the chronically homeless population in America would be able to obtain Medicaid coverage if states expanded Medicaid under the Affordable Care Act.In 1985, the Boston Health Care for the Homeless Program was founded to assist the growing numbers of homeless living on the streets and in shelters in Boston and who were suffering from a lack of effective medical services. In 2004, Boston Health Care for the Homeless in conjunction with the National Health Care for the Homeless Council published a medical manual called The Health Care of Homeless Persons, edited by James J. OConnell, M.D., specifically for the treatment of the homeless population. In June 2008 in Boston, the Jean Yawkey Place, a four-story, 7,214.2-square-metre (77,653 sq ft) building, was opened by the Boston Health Care for the Homeless Program. It is an entire full-service building on the Boston Medical Center campus dedicated to providing healthcare for homeless people. It also contains a long-term care facility, the Barbara McInnis House, which expanded to 104 beds and is the first and largest medical respite program for homeless people in the United States.In Los Angeles, a collaboration between the Ostrow School of Dentistry of the University of Southern California and the Union Rescue Mission shelter offer homeless people in the Skid Row area free dental services.Studies on the effects of intensive mental health interventions have demonstrated some improvements in housing stability and to be economically beneficial on cost-analysis. Housing Permanent supportive housing (PSH) interventions appear to have improvements in housing stability for people living with homelessness even in long-term. Savings from housing homeless in the US In 2013, a Central Florida Commission on Homelessness study indicated that the region spends $31,000 a year per homeless person to cover "salaries of law enforcement officers to arrest and transport homeless individuals – largely for nonviolent offenses such as trespassing, public intoxication or sleeping in parks – as well as the cost of jail stays, emergency room visits and hospitalization for medical and psychiatric issues. This did not include "money spent by nonprofit agencies to feed, clothe and sometimes shelter these individuals". In contrast, the report estimated the cost of permanent supportive housing at "$10,051 per person per year" and concluded that "[h]ousing even half of the regions chronically homeless population would save taxpayers $149 million over the next decade – even allowing for 10 percent to end up back on the streets again." This particular study followed 107 long-term-homeless residents living in Orange, Osceola or Seminole Counties. There are similar studies showing large financial savings in Charlotte and Southeastern Colorado from focusing on simply housing the homeless."In general, housing interventions had mixed economic results on cost-analysis studies. Innovative solutions Los Angeles conducted a competition promoted by Mayor Eric Garcetti soliciting ideas from developers to use bond money more efficiently in building housing for the citys homeless population. The top five winners were announced on 1 February 2019 and the concepts included using assembly-ready molded polymer panels that can be put together with basic tools, prefabricated 5-story stack-able houses, erecting privately financed modular buildings on properties that do not require City Council approval, using bond money to convert residential garages into small apartments which are then dedicated to homeless rentals, and the redeveloping of Bungalow-court units, the small low-income iconic buildings that housed 7% of the citys population in the 1920s.In the neighborhood of Westlake, Los Angeles, the city is funding the first transitionally homeless housing building using "Cargotecture", or "architecture built from repurposed shipping containers." The Hope on Alvarado micro-apartment building will consist of 4-stories of 84 containers stacked together like Lego bricks on top of a traditionally constructed ground floor. Completion is anticipated by the end of 2019. Political action Voting for elected officials is important for the homeless population to have a voice in the democratic process.There are also many community organizations and social movements around the world which are taking action to reduce homelessness. They have sought to counteract the causes and reduce the consequences by starting initiatives that help homeless people transition to self-sufficiency. Social movements and initiatives tend to follow a grassroots, community-based model of organization – generally characterized by a loose, informal and decentralized structure, with an emphasis on radical protest politics. By contrast, an interest group aims to influence government policies by relying on more of a formal organizational structure. These groups share a common element: they are both made up of and run by a mix of allies of the homeless population and former or current members of the homeless population. Both grassroots groups and interest groups aim to break stereotyped images of homeless people as being weak and hapless, or defiant criminals and drug addicts, and to ensure that the voice of homeless people and their representatives is clearly heard by policymakers. Organizing in homeless shelters Homeless shelters can become grounds for community organization and the recruitment of homeless individuals into social movements for their own cause. Cooperation between the shelter and an elected representative from the homeless community at each shelter can serve as the backbone of this type of initiative. The representative presents and forwards problems raises concerns and provides new ideas to the director and staff of the shelters. Examples of possible problems are ways to deal with substance use disorders by certain shelter users, and resolution of interpersonal conflicts. SAND, the Danish National Organization for Homeless People, is one example of an organization that uses this empowerment approach. Issues reported at the homeless shelters are then addressed by SAND at the regional or national level. To open further dialogue, SAND organizes regional discussion forums where staff and leaders from the shelters, homeless representatives, and local authorities meet to discuss issues and good practices at the shelters. Veteran specific There are a number of homeless organizations that support homeless veterans, an issue most commonly seen in the United States.Non-governmental organizations house or redirect homeless veterans to care facilities. Social Security Income/Social Security Disability Income, Access, Outreach, Recovery Program (SOAR) is a national project funded by the Substance Abuse and Mental Health Services Administration. It is designed to increase access to SSI/SSDI for eligible adults who are homeless or at risk of becoming homeless and have a mental illness or a co-occurring substance use disorder. Using a three-pronged approach of Strategic Planning, Training, and Technical Assistance (TA), the SOAR TA Center coordinates this effort at the state and community level.The United States Department of Housing and Urban Development and Veterans Administration have a special Section 8 housing voucher program called VASH (Veterans Administration Supported Housing), or HUD-VASH, which gives out a certain number of Section 8 subsidized housing vouchers to eligible homeless and otherwise vulnerable US armed forces veterans. The HUD-VASH program has shown success in housing many homeless veterans. The support available to homeless veterans varies internationally, however. For example, in England, where there is a national right to housing, veterans are only prioritized by local authority homelessness teams if they are found to be vulnerable due to having served in the Armed Forces.Under the Department of Labor, the Veterans Employment and Training Service (VETS) offers a variety of programs targeted at ending homelessness among veterans. The Homeless Veterans Reintegration Program (HVRP) is the only national program that is exclusively focused on assisting veterans as they reenter the workforce. The VETS program also has an Incarcerated Veterans Transition Program, as well as services that are unique to female Veterans. Mainstream programs initiated by the Department of Labor have included the Workforce Investment Act, One-Stop Career Centers, and a Community Voice Mail system that helps to connect homeless individuals around the United States with local resources. Targeted labor programs have included the Homeless Veterans Reintegration Project, the Disability Program Navigator Initiative, efforts to end chronic homelessness through providing employment and housing projects, Job Corps, and the Veterans Workforce Investment Program (VWIP). By location Africa Egypt Homelessness in Egypt is a significant social issue affecting some 12 million people in the country. Egypt has over 1,200 areas designated for irregular dwellings that do not conform to standard building laws, allowing homeless people to build shacks and other shelters for themselves.Reportedly, in Egypt, homelessness is defined to include those living in marginal housing. Some scholars have stated that there is no agreed upon definition of homelessness in Egypt due to the difficulties government would face if an official definition were accepted.According to UNICEF, there are 1 million children living on the streets in Egypt. Other researchers estimate the number to be some 3 million. Homelessness NGOs assisting street children include those such as Hope Village Society, and NAFAS. Other NGOs, such as Plan International Egypt, work to reintegrate street children back into their families. South Africa Homelessness in South Africa dates back to the apartheid period. Increasing unemployment, lack of affordable housing, social disintegration, and social and economic policies have all been identified as contributing factors to the issue. Some scholars argue that solutions to homelessness in South Africa lie more within the private sphere than in the legal and political spheres.There is no national census on homeless people in South Africa, researchers instead rely on individual studies of homeless persons in particular cities. The South African homeless population has been estimated at 200,000 people from a diverse range of backgrounds. Most South African municipalities primarily view homelessness as a social dependency issue, responding with social interventions. One study found that three out of four South African metropolitan municipalities viewed homelessness primarily as a social dependency issue, responding with social interventions. At the same time, homeless South Africans indicated that the most important thing the municipality could assist them with was employment and well-located affordable housing. Asia China In 2011, there were approximately 2.41 million homeless adults and 179,000 homeless children living in the country. However, one publication estimated that there were one million homeless children in China in 2012.Housing in China is highly regulated by the Hukou system. This gives rise to a large number of migrant workers, numbering at 290.77 million in 2019. These migrant workers have rural Hukou, but they move to the cities in order to find better jobs, though due to their rural Hukou they are entitled to fewer privileges than those with urban Hukou. According to Huili et al., these migrant workers "live in overcrowded and unsanitary conditions" and are always at risk of displacement to make way for new real estate developments. In 2017, the government responded to a deadly fire in a crowded building in Beijing by cracking down on dense illegal shared accommodations and evicting the residents, leaving many migrant laborers homeless. This comes in the context of larger attempts by the government to limit the population increase in Beijing, often targeting migrant laborers. However, according to official government statistics, migrant workers in China have an average of 20.4 square metres (220 sq ft) of living space per capita, and the vast majority of migrant workers have basic living facilities such as heating, bathing, refrigerators, and washing machines. Several natural disasters have led to homelessness in China. The 2000 Yunnan earthquake left 92,479 homeless and destroyed over 41,000 homes.Homelessness among people with mental health problems is much less common in China than in high-income countries, due to stronger family ties, but is increasing due to migration within families and as a result of the one-child policy. A study in Xiangtan found at least 2439 schizophrenic people that have been homeless on a total population of 2.8 million. It was found that "homelessness was more common in individuals from rural communities (where social support services are limited), among those who wander away from their communities (i.e., those not from Xiangtan municipality), and among those with limited education (who are less able to mobilize social supports). Homelessness was also associated with greater age; [the cause] may be that older patients have burned their bridges with relatives and, thus, end up on the streets."During the Cultural Revolution a large part of child welfare homes were closed down, leaving their inhabitants homeless. By the late 1990s, many new homes were set up to accommodate abandoned children. In 1999, the Ministry of Civil Affairs estimated the number of abandoned children in welfare homes to be 66,000.According to the Ministry of Civil Affairs, China had approximately 2,000 shelters and 20,000 social workers to aid approximately 3 million homeless people in 2014.From 2017 to 2019, the government of Guangdong Province assisted 5,388 homeless people in reuniting with relatives elsewhere in China. The Guangdong government assisted more than 150,000 people over a three-year period.In 2020, in the wake of the COVID-19 pandemic, the Chinese Ministry of Civil Affairs announced several actions of the Central Committee in response to homelessness, including increasing support services and reuniting homeless people with their families. In Wuhan, the situation for homeless people was particularly bad, as the lockdown made it impossible for homeless migrants to return to other parts of the country. The Wuhan Civil Affairs Bureau set up 69 shelters in the city to house 4,843 people. India The Universal Declaration of Human Rights defines homeless as those who do not live in a regular residence due to lack of adequate housing, safety, and availability. The United Nations Economic and Social Council Statement has a broader definition for homelessness; it defines homelessness as follows: When we are talking about housing, we are not just talking about four walls and a roof. The right to adequate housing is about security of tenure, affordability, access to services and cultural adequacy. It is about protection from forced eviction and displacement, fighting homelessness, poverty and exclusion. India defines homeless as those who do not live in census houses, but rather stay on pavements, roadsides, railway platforms, staircases, temples, streets, in pipes, or other open spaces. There are 1.77 million homeless people in India, or 0.15% of the countrys total population, according to the 2011 census consisting of single men, women, mothers, the elderly, and the disabled. However, it is argued that the numbers are far greater than accounted by the point in time method. For example, while the Census of 2011 counted 46.724 homeless individuals in Delhi, the Indo-Global Social Service Society counted them to be 88,410, and another organization called the Delhi Development Authority counted them to be 150,000. Furthermore, there is a high proportion of mentally ill and street children in the homeless population. There are 18 million street children in India, the largest number of any country in the world, with 11 million being urban. Finally, more than three million men and women are homeless in Indias capital city of New Delhi; the same population in Canada would make up approximately 30 electoral districts. A family of four members has an average of five homeless generations in India.There is a shortage of 18.78 million houses in the country. Total number of houses has increased from 52.06 million to 78.48 million (as per 2011 census). However, the country still ranks as the 124th wealthiest country in the world as of 2003. More than 90 million people in India make less than US$1 per day, thus setting them below the global poverty threshold. The ability of the Government of India to tackle urban homelessness and poverty may be affected in the future by both external and internal factors. The number of people living in slums in India has more than doubled in the past two decades and now exceeds the entire population of Britain, the Indian Government has announced. About 78 million people in India live in slums and tenements. 17% of the worlds slum dwellers reside in India. Subsequent to the release of Slumdog Millionaire in 2008, Mumbai was a slum tourist destination for slumming where homeless people and slum dwellers alike could be openly viewed by tourists. Israel Homelessness in Israel is a phenomenon that mostly developed after the mid-1980s.Homelessness increased following the wave of Soviet immigration in 1991. As many as 70 percent of homeless people in Tel Aviv are immigrants from the former Soviet Union, nearly all of them men. According to homeless shelter founder Gilad Harish, "when the recession hit Israel in the early 90s, the principle of last in, first out kicked in, and many Russian immigrants lost their jobs. Being new to the country, they didnt have a strong family support system to fall back on like other Israelis do. Some ended up on the street with nowhere to go."The number of homeless people in Israel grew in the 2000s, and the Association for Civil Rights in Israel claimed that the authorities were ignoring the issue.Some 2,000 families in Israel lose their homes every year after defaulting on their mortgage loans. However, a law amendment passed in 2009 protects the rights of mortgage debtors and ensures that they are not evicted after failing to meet mortgage payments. The amendment is part of a wider reform in the law in the wake of a lengthy battle by the Association for Civil Rights in Israel and other human rights groups.In 2007, the number of homeless youth was on the rise. More than 25% of all homeless youth in 2007 were girls, compared to 15% in 2004. A report by Elem, a non-profit organization that helps youth at risk, pointed to a 5% rise in the number of youths either homeless or wandering the streets late at night while their parents worked or due to strained relations at home. The organization estimated that in 2007 it provided programs or temporary shelter to roughly 32,000 youths in some 30 locations countrywide.In 2014, the number of homeless individuals in Israel was estimated at 1,831, about 600 of whom were living on the streets of Tel Aviv. This makes up 0.02% of the countrys population, a low figure compared to other developed nations. In July 2015, the Welfare Ministry estimated the number of homeless to be between 800 and 900, including 450 receiving services and treatment from their municipalities but continuing to live on the streets. Elem claimed the true figure was much higher. In December 2015, a large study by the Welfare Ministry found that 2,300 people in Israel were homeless.Homeless people in Israel are entitled to a monthly government stipend of NIS 1,000. In addition, there are both state-run homeless shelters operated by the Welfare Ministry and privately run shelters. Adi Nes, an Israeli photographer, has brought public attention to the issue by taking pictures of Israels homeless. Japan Homelessness in Japan (ホームレス, 浮浪者)) is a social issue primarily affecting middle-aged and elderly males. Homelessness is thought to have peaked in the 1990s as a consequence of the collapse of the Japanese asset price bubble and has largely fallen since then. According to the "Special Act in regards to Supporting the Autonomy of the Homeless Population" (Japanese: ホームレスの自立の支援等に関する特別措置法)), the term "homeless" is defined as "those who utilize city parks, river banks, roads, train stations, and other facilities as their place of stay in order to live their daily lives".Names for the homeless in Japan include hōmuresu (ホームレス, from the English "homeless"), furousha (浮浪者, meaning "wandering person"), kojiki (乞食, meaning beggar), and runpen (ルンペン, from German [[wikt:Lumpen|Lumpen]]). More recently, nojukusha (野宿者, "person who sleeps outside") and nojuku roudousha (野宿労働者, "laborer who sleeps outside") have been used to avoid negative connotations associated with the word "homeless". Philippines There are approximately 4.5 million homeless people in the Philippines, about 3 million of them in Manila. Europe One fifth of the total population of the European Union – totalling 91.4 million people – are still at risk of poverty or social exclusion, and access to housing remains difficult for many Europeans. According to a Eurostat survey, three-in-100 people say they have already had to live with relatives on a temporary basis while one-in-100 people say they have already lived on the street, in emergency or temporary accommodation or in a place not suitable for housing. Homelessness in Denmark (6,431) Homelessness in Finland (4,300) Homelessness in France (300,000) Homelessness in Germany (678,000) Homelessness in Greece (40,000) Homelessness in Hungary (30,000) Homelessness in Ireland (8,313) Homelessness in the Netherlands (39,300) Homelessness in Portugal (8,209) Homelessness in Spain (40,000) Homelessness in Sweden (34,000) Switzerland Homelessness in Switzerland is a known social issue, however, there are few estimates as to the number of Swiss people affected. Homelessness is less visible in Switzerland than in many other Western countries. The majority of homeless people in Geneva are Swiss or French, with a minority from other countries.One Swiss study found that 1.6 percent of all patients admitted to psychiatric wards were homeless. The study reported that social factors and psychopathology are independently contributing to the risk of homelessness.In 2014, Swiss authorities reportedly began allowing homeless people to sleep in fallout shelters built during the Cold War.There are a number of centers for providing food for the homeless, including the Suneboge community center. United Kingdom Homelessness across the UK is a devolved matter, resulting in different legislation, frameworks, and even definitions, from country to country. Since the late 1990s, housing policy has been a devolved matter, and state support for homeless people, together with legal rights in housing, have therefore diverged to a certain degree. A national service, called Streetlink, was established in 2012 to help members of the public obtain near-immediate assistance for specific rough sleepers, with the support of the Government (as housing is a devolved matter, the service currently only extends to England). The annual number of homeless households in England peaked in 2003–04 at 135,420 before falling to a low of 40,020 in 2009–10. In 2017–18, there were 56,600 homeless households, which was 60 per cent below the 2003–04 peak, and 40 per cent higher than the 2009–10 low. The UK has more than 120,000 children in temporary accommodation, a number which has increased from 69,050 children in 2010.In 2007 the official figures for England were that an average of 498 people slept rough each night, with 248 of those in London.Homelessness in England since 2010 has been rising. By 2016 it is estimated the numbers sleeping rough had more than doubled since 2010. The National Audit Office say in relation to homelessness in England 2010–17 there has been a 60% rise in households living in temporary accommodation and a rise of 134% in rough sleepers. It is estimated 4,751 people bedded down outside overnight in England in 2017, up 15% on previous year. The housing charity Shelter used data from four sets of official 2016 statistics and calculated 254,514 people in England were homeless.The Homelessness Reduction Act 2017 places a new duty on local authorities in England to assist people threatened with homelessness within 56 days and to assess, prevent and relieve homelessness for all eligible applicants including single homeless people from April 2018. Before the 2017 HRA, homeless households were defined and measured as those who were owed a main homelessness duty by local authorities. But since 2018, the definition of homeless households has broadened as households are owed a new relief duty and a prevention duty. The main homelessness duty definition has not been changed by the 2017 HRA. However, these households are now only owed a main duty if their homelessness has not been successfully prevented or relieved. In 2019–20, 288,470 households were owed the new prevention or relief duties, which is four times the number of households owed the main duty in 2017–18 prior to implementation of the Homelessness Reduction Act.The picture in Scotland is considerably different, with law that entitles everyone to a roof over their head if they are homeless. This accommodation is often in the form of somewhere temporary, until something permanent becomes available. Though across the course of 2022 this will change, reducing the use of temporary accommodation, in line with the Homeless and Rough Sleeping Action Group (HARSAG) recommendations. Currently people are spending an average of 199 days(April 2020 to March 2021)in temporary accommodation before being housed in somewhere permanent.Most recently updated in October 2020, Scotland is working to eradicate homelessness through the Ending Homelessness Together action plan. It is anticipated that with this, alongside a focus on prevention, and Local Authorities working with the third sector on plans known as Rapid Rehousing Transition Plans, that people will no longer be homeless for any length of time. In terms of figures, in 2020/21, there were 42,149 people in homeless households – 30,345 adults and 11,804 children in Scotland. This was a drop of 9% from the previous year, though it is unclear if this was partly due to statistics being collected differently during the start of the pandemic. North America Canada United States After Franklin D. Roosevelt took over the presidency from Herbert Hoover in 1933, he oversaw passage of the New Deal, which greatly expanded social welfare, including providing funds to build public housing. This marked the end of the Great Depression. However, the number of homeless people grew in the 1980s, when Ronald Reagan decimated the public housing budget in the 1980s, including the federally funded affordable housing production put in place by the New Deal. By the mid-1980s, there was a dramatic increase in family homelessness. Tied into this was an increasing number of impoverished and runaway children, teenagers, and young adults, which created a new substratum of the homeless population (street children or street youth).In 2015, the United States reported that there were 564,708 homeless people within its borders, one of the higher reported figures worldwide.Housing First is an initiative to help homeless people reintegrate into society, and out of homeless shelters. It was initiated by the federal governments Interagency Council on Homelessness. It asks cities to come up with a plan to end chronic homelessness. In this direction, there is the belief that if homeless people are given independent housing to start, with some proper social supports, then there would be no need for emergency homeless shelters, which it considers a good outcome. However this is a controversial position.There is evidence that the Housing First program works more efficiently than Treatment First programs. Studies show that having the stability of housing through the Housing First program will encourage homeless people to focus on other struggles they are facing, such as substance abuse. Meanwhile, Treatment First programs promote an "all or nothing" approach which require clients to participate in programs applicable to their struggles as a condition for housing assistance. Treatment First utilizes a less individualistic approach than Housing First and solutions are created under one standard rather than fit to each clients specific needs. In 2009 it was estimated that one out of 50 children or 1.5 million children in the United States would experience some form of homelessness each year.In 2010 in New York City, where there were over 36,000 homeless people in 2009, there was a mobile video exhibit in the streets showing a homeless person on a screen and asking onlookers and passersby to text with their cellphones a message for him, and they also could donate money by cellphones to the organization Pathways to Housing. In September 2010, it was reported that the Housing First Initiative had significantly reduced the chronic homeless single person population in Boston, Massachusetts, although homeless families were still increasing in number. Some shelters were reducing the number of beds due to lowered numbers of homeless, and some emergency shelter facilities were closing, especially the emergency Boston Night Center. In 2011, the Department of Veterans Affairs Supportive Services for Veterans Families Initiative, SSVF, began funding private non-profit organizations and consumer cooperatives to provide supportive services to very low-income veteran families living in or transitioning to permanent housing.In 2019, in an interview with CBS News, scholar Sara Goldrick-Rab said that her study on college student homelessness found that "[n]early one in ten college students said they were homeless in the last year, meaning they had at least one night where they did not know where they were going to sleep." Puerto Rico According to the count by the Puerto Rico Department of Family, in January 2017 there were 3,501 homeless persons in the territory. The study shows that 26% of this population live in the capital, San Juan. Other municipalities percentage of this population was Ponce with 6.3%, Arecibo with 6%, Caguas with 5.3%, and Mayagüez with 4.7%. Results from the study determined that 76% of the homeless population were men and 24% were women and that both men and women populations, were on average age, 40 years old. This steadily increasing population, might have increased more drastically as a result of Hurricane María which caused over 90 billion dollars in damage to the island of Puerto Rico.Data provided by the Department of Community Social Development of San Juan, indicates that in 1988 the number of homeless in the municipality was of 368, while in 2017 there are about 877 persons without a home. While the average age for the overall homeless population is 40 years old for both women and men, in San Juan the median is 48 years for men and 43 years for women. Other data obtained showed that more than 50% have university level education. Also it revealed that 35% of men and 25% of women have relapsed more than four times after unsuccessful attempts to reinsert themselves socially. Reasons given to wander are varied with the most common causes being drug abuse (30.6%), family problems (22.4%), financial or economic problems (15.0%), and others such as unemployment, mental health problems, domestic violence, evictions, or lack of support when released from prison. Oceania Australia In Australia the Supported Accommodation Assistance Program (SAAP) is a joint Commonwealth and state government program which provides funding for more than 1,200 organizations which are aimed to assist homeless people or those in danger of becoming homeless, as well as women and children escaping domestic violence. They provide accommodation such as refuges, shelters, and half-way houses, and offer a range of supported services. The Commonwealth has assigned over $800 million between 2000 and 2005 for the continuation of SAAP. The current program, governed by the Supported Assistance Act 1994, specifies that "the overall aim of SAAP is to provide transitional supported accommodation and related support services, in order to help people who are homeless to achieve the maximum possible degree of self-reliance and independence. This legislation has been established to help the homeless people of the nation and help rebuild the lives of those in need. The cooperation of the states also helps enhance the meaning of the legislation and demonstrates their desire to improve the nation as best they can." In 2011, the Specialist Homelessness Services (SHS) program replaced the SAAP program. Indonesia Homelessness in Indonesia refers to the issue of homelessness, a condition wherein people lack a stable and appropriate place of housing. The number of homeless people in Indonesia is estimated to be up to 3 million people in the country, over 28,000 in Jakarta alone. A number of terms are used to describe homeless people in Indonesia, including tunawisma, which is used by the government, and gelandangan, meaning "tramp".Squatters and street homeless people are often targeted by police raids who say that homeless people "disturb the attractiveness of the city".One cause of homelessness in Indonesia is forced evictions. According to researchers, between the years 2000 and 2005 over 92,000 people were forcefully evicted from their homes. New Zealand Homelessness in New Zealand has been linked to the general issue of lack of suitable housing. The homeless population is generally measured through the countrys census and by universities and other academic centres. In 2009, urban homelessness (rough sleepers or improvised dwellings) were estimated at less than 300, while rural homelessness (improvised dwellings) was estimated between 500 and 1000. An additional 8,000–20,000 live in "temporary accommodation unsuited for long-term habitation (caravans, campgrounds, substandard housing and boarding houses)." Homelessness in New Zealand has traditionally been reduced by the provision of state housing, similar to Germany and other developed countries.Statistical authorities in New Zealand have expanded their definition of homelessness to include people living in improvised shelters, people staying in camping grounds/motor camps and people sharing accommodation with someone elses household.The issue is believed to have become increasingly visible in recent years. Media in New Zealand have published an accusatory account of the presence of homeless people in public spaces, positioning homeless men as disruptive threats. Though community members have shown support though writing opinion pieces.In late January 2019, the New York Times reported rising housing prices to be a major factor in the increasing homelessness in New Zealand so that "smaller markets like Tauranga, a coastal city on the North Island with a population of 128,000, had seen an influx of people who had left Auckland in search of more affordable housing. Average property values in Tauranga had risen to $497,000 from $304,000 in the last five years, and Demographia now rated it among the 10 least affordable cities in the world — along with famously expensive locales such as Hong Kong, San Francisco, Sydney and Vancouver, British Columbia."In mid August 2019, the Associate Housing Minister Kris Faafoi and Social Development Minister Carmel Sepuloni announced that the Government would be launching a NZ$54 million program to tackle homelessness in New Zealand. This includes investing $31 million over the next four years for 67 intensive case managers and navigators to work with homeless people and a further $16 million for the Sustaining Tenancies Programme. This funding complements the Governments Housing First programme. Russia and the USSR After the abolition of serfdom in Russia in 1861, major cities experienced a large influx of former peasants who sought jobs as industrial workers in rapidly developing Russian industry. These people often lived in harsh conditions, sometimes renting a room shared between several families. There also was a large number of shelterless homeless. Immediately after the October Revolution a special program of "compression" (уплотнение) was enabled: people who had no shelter were settled in flats of those who had large (4, 5, or 6-room) flats with only one room left to previous owners. The flat was declared state property. This led to a large number of shared flats where several families lived simultaneously. Nevertheless, the problem of complete homelessness was mostly solved as anybody could apply for a room or a place in dormitory (the number of shared flats steadily decreased after large-scale residential building program was implemented starting in the 1960s). By 1922 there were at least 7 million homeless children in Russia as a result of nearly a decade of devastation from World War I and the Russian Civil War. This led to the creation of a large number of orphanages. By the 1930s the USSR declared the abolition of homelessness and any citizen was obliged to have a propiska – a place of permanent residency. Nobody could be stripped of propiska without substitution or refuse it without a confirmed permission (called "order") to register in another place. If someone wanted to move to another city or expand their living area, he had to find a partner who wanted to mutually exchange the flats. The right for shelter was secured in the Soviet constitution. Not having permanent residency was legally considered a crime. After the breakup of the USSR, the problem of homelessness sharpened dramatically, partially because of the legal vacuum of the early 1990s with some laws contradicting each other and partially because of a high rate of frauds in the realty market. In 1991 articles 198 and 209 of Russian criminal code which instituted a criminal penalty for not having permanent residence were abolished. In Moscow, the first overnight shelter for homeless was opened in 1992. In the late 1990s, certain amendments in law were implemented to reduce the rise in homelessness, such as the prohibition of selling last flat with registered children. In 2002, there were 300,000 homeless people in Moscow.Nevertheless, the state is still obliged to give permanent shelter for free to anybody who needs better living conditions or has no permanent registration, because the right to shelter is still included in the constitution. Several projects of special cheap social flats for those who failed to repay mortgages were proposed to facilitate mortgage market.In 2022, it was reported that Russian authorities were targeting homeless people to conscript them into the war in Ukraine. Popular culture Homelessness in popular culture is depicted in various works. Films Modern Times, 1936 film, shows negative effects of vagrancy laws. Cathy Come Home, 1966, shows the effects of homelessness on parenthood. God Bless the Child, 1988, made-for-TV movie about a single mother (Mare Winningham) living on the streets of New York City with her young daughter. Homeless Sam & Sally, a 2020 dark comedy film and a television series with the same name released in 2019, is about a story regarding a mother named Sally Silver and her mentally ill son Sam Silver who comes up with ways to live normal lives while being homeless in Koreatown, Los Angeles. Dark Days, 2000, 81 minutes, documentary by Marc Singer, who followed the lives of people living in the Freedom Tunnel, an Amtrak tunnel in New York City. Homeless to Harvard: The Liz Murray Story, 2003 film about a homeless girl, Liz Murray, who works her way up to admission to Harvard University. 66 Months, a 2011 British documentary film about a homeless man who makes it on his own for 6 years without any government programs helping him. The Pursuit of Happyness, a 2006 biographical film where a father and son struggle to get a job and end up homeless after an eviction and later a tax garnishment. After several weeks living from place to place in 1981 San Francisco, he lands a permanent position in a brokerage firm after successfully completing an unpaid internship. Same Kind of Different as Me, 2017 American film about a successful art dealer, his wife and an initially violent member of a homeless shelter community. It is based on the 2006 book of the same name. Curly Sue, a 1991 comedy drama film that focuses on a homeless con artist and his friend who gets lucky with a roof over their heads by tricking a wealthy attorney. Life Stinks, a 1991 comedy film about a wealthy businessman who bets a corporate rival that he can live his life as a homeless man but finds out later on in the story that being homeless isnt easy or fun. The Saint of Fort Washington, a 1993 drama film where a homeless disabled man gets guidance from a friendly veteran as they cope with the realities of being on the streets. See also Ghost town repopulation Grave dwellers Homeless Jesus, a bronze sculpture by Canadian sculptor Timothy Schmalz depicting Jesus as a homeless person sleeping on a park bench, which since 2013 has been installed in many places across the world Hunter-gatherers Internally displaced person Nomads Right to housing References Further reading External links Homeless of New York – Article + Video Archived 26 March 2020 at the Wayback Machine – The Uncommon Magazine, by Avery Kim, 6 July 2016 Homeless Statistics for Australia, Canada, United Kingdom and the United States, all data from around the year 2001. PBS, "Home at Last?", NOW series program, first aired on 2 February 2007. The topic was what will most help homeless people reenter the fabric of society. Homelessness at Curlie Homelessness in Europe FEANTSA is the European Federation of National Organisations Working with the Homeless is an umbrella of not-for-profit organizations which participate in or contribute to the fight against homelessness in Europe. About | Policy Scotland | Edinburgh PolicyScotland.org work with organisations across the country to input to policy changes and implement good practice Report Card on Child Homelessness by the American Institutes for Research. Summarized in Child homelessness on the rise in US Archived 29 November 2014 at the Wayback Machine (November 2014), Palm Beach Post Utah found a brilliantly effective solution for homelessness (February 2015), Natasha Bertrand, Business Insider

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I need a basic explanation for the medical term 'Arachnophobia.'

Arachnophobia is a specific phobia brought about by the irrational fear of spiders and other arachnids such as scorpions. Signs and symptoms People with arachnophobia tend to feel uneasy in any area they believe could harbour spiders or that has visible signs of their presence, such as webs. If arachnophobes see a spider, they may not enter the general vicinity until they have overcome the panic attack that is often associated with their phobia. Some people scream, cry, have emotional outbursts, experience trouble breathing, sweat and experience increased heart rates when they come in contact with an area near spiders or their webs. In some extreme cases, even a picture, a toy, or a realistic drawing of a spider can trigger intense fear. Reasons Arachnophobia may be an exaggerated form of an instinctive response that helped early humans to survive or a cultural phenomenon that is most common in predominantly European societies. Evolutionary An evolutionary reason for the phobia remains unresolved. One view, especially held in evolutionary psychology, is that the presence of venomous spiders led to the evolution of a fear of spiders, or made acquisition of a fear of spiders especially easy. Like all traits, there is variability in the intensity of fear of spiders, and those with more intense fears are classified as phobic. Being relatively small, spiders do not fit the usual criterion for a threat in the animal kingdom where size is a factor, but they can have medically significant venom and/or cause skin irritation with their setae. However, a phobia is an irrational fear as opposed to a rational fear.By ensuring that their surroundings were free from spiders, arachnophobes would have had a reduced risk of being bitten in ancestral environments, giving them a slight advantage over non-arachnophobes in terms of survival. However, having a disproportionate fear of spiders in comparison to other, potentially dangerous creatures present during Homo sapiens environment of evolutionary adaptiveness may have had drawbacks.In The Handbook of the Emotions (1993), psychologist Arne Öhman studied pairing an unconditioned stimulus with evolutionarily-relevant fear-response neutral stimuli (snakes and spiders) versus evolutionarily-irrelevant fear-response neutral stimuli (mushrooms, flowers, physical representation of polyhedra, firearms, and electrical outlets) on human subjects and found that ophidiophobia (fear of snakes) and arachnophobia required only one pairing to develop a conditioned response while mycophobia, anthophobia, phobias of physical representations of polyhedra, firearms, and electrical outlets required multiple pairings and went extinct without continued conditioning while the conditioned ophidiophobia and arachnophobia were permanent.Psychiatrist Randolph M. Nesse notes that while conditioned fear responses to evolutionarily novel dangerous objects such as electrical outlets is possible, the conditioning is slower because such cues have no prewired connection to fear, noting further that despite the emphasis of the risks of speeding and drunk driving in drivers education, it alone does not provide reliable protection against traffic collisions and that nearly one-quarter of all deaths in 2014 of people aged 15 to 24 in the United States were in traffic collisions. Nesse, psychiatrist Isaac Marks, and evolutionary biologist George C. Williams have noted that people with systematically deficient responses to various adaptive phobias (e.g. arachnophobia, ophidiophobia, basophobia) are more temperamentally careless and more likely to receive unintentional injuries that are potentially fatal and have proposed that such deficient phobia should be classified as "hypophobia" due to its selfish genetic consequences.A 2001 study found that people could detect images of spiders among images of flowers and mushrooms more quickly than they could detect images of flowers or mushrooms among images of spiders. The researchers suggested that this was because fast response to spiders was more relevant to human evolution. Cultural An alternative view is that the dangers, such as from spiders, are overrated and not sufficient to influence evolution. Instead, inheriting phobias would have restrictive and debilitating effects upon survival, rather than being an aid. For some communities such as in Papua New Guinea and Cambodia spiders are included in traditional foods. This suggests arachnophobia may, at least in part, be a cultural, rather than genetic trait.Stories about spiders in the media often contain errors and use sensationalistic vocabulary, which could contribute to the fear of spiders. Treatments The fear of spiders can be treated by any of the general techniques suggested for specific phobias. The first line of treatment is systematic desensitization – also known as exposure therapy. Before engaging in systematic desensitization, it is common to train the individual with arachnophobia in relaxation techniques, which will help keep the patient calm. Systematic desensitization can be done in vivo (with live spiders) or by getting the individual to imagine situations involving spiders, then modelling interaction with spiders for the person affected and eventually interacting with real spiders. This technique can be effective in just one session, although it generally takes more time.Recent advances in technology have enabled the use of virtual or augmented reality spiders for use in therapy. These techniques have proven to be effective. It has been suggested that exposure to short clips from the Spider-Man movies may help to reduce an individuals arachnophobia. Epidemiology Arachnophobia affects 3.5 to 6.1 percent of the global population. See also Apiphobia, fear of bees Entomophobia, fear of insects Myrmecophobia, fear of ants References External links Stiemerling, D. (1973). "Analysis of a spider and monster phobia". Z Psychosom Med Psychoanal (in German). 19 (4): 327–45. PMID 4129447. National Geographic: "Fear of Snakes, Spiders Rooted in Evolution, Study Finds"

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm trying to understand 'Suxamethonium chloride' within a medical context. Could you shed some light on it?

Suxamethonium chloride, also known as suxamethonium or succinylcholine, or simply sux by medical abbreviation, is a medication used to cause short-term paralysis as part of general anesthesia. This is done to help with tracheal intubation or electroconvulsive therapy. It is administered by injection, either into a vein or into a muscle. When used in a vein, onset of action is generally within one minute and effects last for up to 10 minutes.Common side effects include low blood pressure, increased saliva production, muscle pain, and rash. Serious side effects include malignant hyperthermia and allergic reactions. It is not recommended in people who are at risk of high blood potassium or a history of myopathy. Use during pregnancy appears to be safe for the baby. Suxamethonium is in the neuromuscular blocker family of medications and is of the depolarizing type. It works by blocking the action of acetylcholine on skeletal muscles. Side effects of succinylcholine chloride injection include anaphylaxis, hyperkalemia, and malignant hyperthermia.Suxamethonium was described as early as 1906 and came into medical use in 1951. It is on the World Health Organizations List of Essential Medicines. Suxamethonium is available as a generic medication. It may colloquially be referred to as "sux". Medical uses Succinylcholine chloride injection is indicated, in addition to general anesthesia, to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.Its medical uses are limited to short-term muscle relaxation in anesthesia and intensive care, usually for facilitation of endotracheal intubation. It is popular in emergency medicine due to its rapid onset and brief duration of action. The former is a major point of consideration in the context of trauma care, where endotracheal intubation may need to be completed very quickly. The latter means that, should attempts at endotracheal intubation fail and the person cannot be ventilated, there is a prospect for neuromuscular recovery and the onset of spontaneous breathing before low blood oxygen levels occurs. It may be better than rocuronium in people without contraindications due to its faster onset of action and shorter duration of action.Suxamethonium is also commonly used as the sole muscle relaxant during electroconvulsive therapy, favoured for its short duration of action.Suxamethonium is quickly degraded by plasma butyrylcholinesterase and the duration of effect is usually in the range of a few minutes. When plasma levels of butyrylcholinesterase are greatly diminished or an atypical form is present (an otherwise harmless inherited disorder), paralysis may last much longer, as is the case in liver failure or in neonates.It is recommended that the vials be stored at a temperature between 2°-8 °C. The multi-dose vials are stable for up to 14 days at room temperature without significant loss of potency. Unless otherwise indicated in the prescribing information, room temperature for storage of medications is 15°-25 °C (59°-77 °F). Side effects Side effects include malignant hyperthermia, muscle pains, acute rhabdomyolysis with high blood levels of potassium, transient ocular hypertension, constipation and changes in cardiac rhythm, including slow heart rate, and cardiac arrest. In people with neuromuscular disease or burns, an injection of suxamethonium can lead to a large release of potassium from skeletal muscles, potentially resulting in cardiac arrest. Conditions having susceptibility to suxamethonium-induced high blood potassium are burns, closed head injury, acidosis, Guillain–Barré syndrome, cerebral stroke, drowning, severe intra-abdominal sepsis, massive trauma, myopathy, and tetanus. Suxamethonium does not produce unconsciousness or anesthesia, and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. Therefore, administration of the drug to a conscious patient is contraindicated. Hyperkalemia The side effect of high blood potassium may occur because the acetylcholine receptor is propped open, allowing continued flow of potassium ions into the extracellular fluid. A typical increase of potassium ion serum concentration on administration of suxamethonium is 0.5 mmol per liter. The increase is transient in otherwise healthy patients. The normal range of potassium is 3.5 to 5 mEq per liter. High blood potassium does not generally result in adverse effects below a concentration of 6.5 to 7 mEq per liter. Therefore, the increase in serum potassium level is usually not catastrophic in otherwise healthy patients. Severely high blood levels of potassium can cause changes in cardiac electrophysiology, which, if severe, can result in arrhythmias and even cardiac arrest. Malignant hyperthermia Malignant hyperthermia (MH) from suxamethonium administration can result in a drastic and uncontrolled increase in skeletal muscle oxidative metabolism. This overwhelms the bodys capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly. Susceptibility to malignant hyperthermia is often inherited as an autosomal dominant disorder, for which there are at least six genetic loci of interest, the most prominent being the ryanodine receptor gene (RYR1). MH susceptibility is phenotype and genetically related to central core disease (CCD), an autosomal dominant disorder characterized both by MH symptoms and by myopathy. MH is usually unmasked by anesthesia, or when a family member develops the symptoms. There is no simple, straightforward test to diagnose the condition. When MH develops during a procedure, treatment with dantrolene sodium is usually initiated; dantrolene and the avoidance of suxamethonium administration in susceptible people have markedly reduced the mortality from this condition. Apnea The normal short duration of action of suxamethonium is due to the rapid metabolism of the drug by non-specific plasma cholinesterases. However plasma cholinesterase activity is reduced in some people due to either genetic variation or acquired conditions, which results in a prolonged duration of neuromuscular block. Genetically, ninety six percent of the population have a normal (Eu:Eu) genotype and block duration; however, some people have atypical genes (Ea, Es, Ef) which can be found in varying combinations with the Eu gene, or other atypical genes (see Pseudocholinesterase deficiency). Such genes will result in a longer duration of action of the drug, ranging from 20 minutes up to several hours. Acquired factors that affect plasma cholinesterase activity include pregnancy, liver disease, kidney failure, heart failure, thyrotoxicosis, and cancer, as well as a number of other drugs.If unrecognized by a clinician it could lead to awareness if anesthesia is discontinued whilst still paralyzed or hypoxemia (and potentially fatal consequences) if artificial ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed.Mivacurium, a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity.Deliberate induction of conscious apnea using this drug led to its use as a form of aversion therapy in the 1960s and 1970s in some prison and institutional settings. This use was discontinued after negative publicity concerning the terrifying effects on subjects of this treatment and ethical questions about the punitive use of painful aversion. Mechanism of action There are two phases to the blocking effect of suxamethonium. Phase 1 block Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptors monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum. In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by acetylcholinesterase. The muscle cell is then ready for the next signal. Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization. Calcium is removed from the muscle cell cytoplasm independent of repolarization (depolarization signaling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculations. The results are membrane depolarization and transient fasciculations, followed by paralysis. Phase 2 block While this phase is not abnormal and is a part of its mechanism of action, it is undesirable during surgery, due to the inability to depolarize the cell again. Often, patients must be on a ventilator for hours if Phase 2 block occurs. It is caused by the blood concentration of suxamethonium exceeding the therapeutic window. Desensitization occurs at the nerve terminal, and the myocyte becomes less sensitive to acetylcholine; the membrane repolarizes and cannot be depolarized again. Chemistry Suxamethonium is an odorless, white crystalline substance. Aqueous solutions have a pH of about 4. The dihydrate melts at 160 °C, whereas the anhydrous melts at 190 °C. It is highly soluble in water (1 gram in about 1 mL), soluble in ethyl alcohol (1 gram in about 350 mL), slightly soluble in chloroform, and practically insoluble in ether. Suxamethonium is a hygroscopic compound. The compound consists of two acetylcholine molecules that are linked by their acetyl groups. It can also be viewed as a central moiety of succinic acid with two choline moieties, one on each end. History Suxamethonium was first discovered in 1906 by Reid Hunt and René de M. Taveau. When studying the drug, animals were given curare and thus they missed the neuromuscular blocking properties of suxamethonium. Instead in 1949 an Italian group led by Daniel Bovet was first to describe succinylcholine induced paralysis. The clinical introduction of suxamethonium was described in 1951 by several groups. Papers published by Stephen Thesleff and Otto von Dardel in Sweden are important but also to be mentioned is work by Bruck, Mayrhofer and Hassfurther in Austria, Scurr and Bourne in UK, and Foldes in America. Abuse Dubai authorities deem that the murder of Hamas operative Mahmoud al-Mabhouh was carried out on their soil by Mossad agents with the use of suxamethonium chloride injection. Entering Dubai under false passports in 2010, the Mossad agents found al-Mabhouh at a hotel, immobilized him with the drug, electrocuted him, then suffocated him by pillow in an assassination. A high concentration of suxamethonium chloride was found in al-Mabhouhs body post-mortem. The incident triggered significant diplomatic crises in the Middle East, Europe, and Australia.It was used by serial killer Efren Saldivar (1988-1998), and in the murder of Kathy Augustine (2006). Brand names It is available in German-speaking countries under the trade name Lysthenon among others. Other animals It is sometimes used in combination with pain medications and sedatives for euthanasia and immobilization of horses. References External links "Suxamethonium Chloride". Drug Information Portal. U.S. National Library of Medicine.

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I'm seeking clarification on the medical term 'Congenital amegakaryocytic thrombocytopenia.' Could you explain it?

Congenital amegakaryocytic thrombocytopenia (CAMT) is a rare inherited disorder. Presentation The primary manifestations are thrombocytopenia and megakaryocytopenia, or low numbers of platelets and megakaryocytes. There is an absence of megakaryocytes in the bone marrow with no associated physical abnormalities. Cause The cause for this disorder appears to be a mutation in the gene for the TPO receptor, c-mpl, despite high levels of serum TPO. In addition, there may be abnormalities with the central nervous system including the cerebrum and cerebellum which could cause symptoms. Diagnosis Treatment The primary treatment for CAMT is bone marrow transplantation.Bone Marrow/Stem Cell Transplant is the only thing that ultimately cures this genetic disease. Frequent platelet transfusions are required to ensure that platelet levels do not fall to dangerous levels, although this is not always the case. It is known for patients to continue to create very small numbers of platelets over time. See also Thrombopoietin Myeloproliferative leukemia virus oncogene References External links Amegakaryocytic Thrombocytopenia research study of Inherited Bone Marrow Failure Syndromes (IBMFS)

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I've encountered the term 'Citrullinemia' while reading about medical topics. What does it refer to exactly?

Citrullinemia is an autosomal recessive urea cycle disorder that causes ammonia and other toxic substances to accumulate in the blood.Two forms of citrullinemia have been described, both having different signs and symptoms, and are caused by mutations in different genes. Citrullinemia belongs to a class of genetic diseases called urea cycle disorders. The urea cycle is a sequence of chemical reactions taking place in the liver. These reactions process excess nitrogen, generated when protein is used for energy by the body, to make urea, which is excreted by the kidneys. Diagnosis Type I Type I citrullinemia (Online Mendelian Inheritance in Man (OMIM): 215700, also known as classic citrullinemia) usually becomes evident in the first few days of life. Affected infants typically appear normal at birth, but as ammonia builds up in the body, they develop a lack of energy (lethargy), poor feeding, vomiting, seizures, and loss of consciousness. These medical problems can be life-threatening in many cases. A milder form of type I citrullinemia is less common in childhood or adulthood. Some people with gene mutations that cause type I citrullinemia never experience signs and symptoms of the disorder. Investigation for diagnosis of citrullinemia type l elevated citrulline .Type I citrullinemia is the most common form of the disorder, affecting about one in 57,000 births worldwide. Mutations in the ASS gene cause type I citrullinemia. The enzyme made by this gene, argininosuccinate synthetase (EC 6.3.4.5), is responsible for one step of the urea cycle. Mutations in the ASS gene reduce the activity of the enzyme, which disrupts the urea cycle and prevents the body from processing nitrogen effectively. Excess nitrogen, in the form of ammonia, and other byproducts of the urea cycle, accumulate in the bloodstream, leading to the characteristic features of type I citrullinemia. Type II The symptoms of type II citrullinemia (Online Mendelian Inheritance in Man (OMIM): 605814 and Online Mendelian Inheritance in Man (OMIM): 603471) usually appear during adulthood and mainly affect the central nervous system. Characteristic features include confusion, abnormal behaviors (such as aggression, irritability, and hyperactivity), seizures, and coma. Specific investigation like decrease citrulline level , increase ammonium ion . These symptoms can be life-threatening, and are known to be triggered by certain medications, infections, and alcohol intake in people with this type.Type II citrullinemia may also develop in people who had a liver disorder called neonatal cholestasis during infancy. This condition blocks the flow of bile and prevents the body from processing certain nutrients properly. In many cases, the symptoms resolve within a year. Years or even decades later, however, some of these people develop the characteristic features of adult type II citrullinemia.Type II citrullinemia is primarily found in the Japanese population, where it occurs in an estimated one in 100,000 to 230,000 individuals. Type II has also been reported in people from East Asian and Middle Eastern populations. Mutations in the SLC25A13 gene are responsible for type II citrullinemia. This gene makes a protein called citrin, which normally shuttles certain molecules in and out of mitochondria. These molecules are essential for the urea cycle and are also involved in making proteins and nucleotides. Mutations in SLC25A13 typically prevent the production of any functional citrin, which inhibits the urea cycle and disrupts the production of proteins and nucleotides. The resulting buildup of ammonia and other toxic substances leads to the symptoms of type II citrullinemia. Researchers have found many infants with neonatal intrahepatic cholestasis have the same mutations in the SLC25A13 gene as adults with type II citrullinemia. Treatment There are multiple treatment methods. Low protein diets, are intended to minimize production of ammonia. Arginine, sodium benzoate and sodium phenylacetate help to remove ammonia from the blood. Dialysis may be used to remove ammonia from the blood when it reaches critical levels. In some cases, liver transplant has been successful. See also Hyperammonemia Citrullinemia type I References Further reading GeneReviews/NCBI/NIH/UW entry on Argininosuccinate Synthetase Deficiency; ASS Deficiency; Argininosuccinic Acid Synthetase Deficiency; CTLN1; Citrullinemia, Classic GeneReviews/NIH/UW entry on Citrin deficiency and Citrullinemia Type II The U.S. National Library of Medicine == External links ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

I'm seeking clarification on the medical term 'Eliglustat.' Could you explain it?

Eliglustat, sold under the brand name Cerdelga, is a medication used for the treatment of Gauchers disease. It was discovered at the University of Michigan, developed by Genzyme Corp, and was approved by the FDA in August 2014. Commonly used as the tartrate salt, the compound is believed to work by inhibition of glucosylceramide synthase. According to an article in Journal of the American Medical Association the oral substrate reduction therapy resulted in "significant improvements in spleen volume, hemoglobin level, liver volume, and platelet count" in untreated adults with Gaucher disease Type 1. History Norman Radin began exploring the possibility of inhibiting the synthesis of lipid substrates involved in Gauchers disease as early as 1982, and, in collaboration with the laboratory of Jim Shayman, found several candidate inhibitors in the mid-1990s. Genzyme initially rejected the candidates developed by Radin and Shayman, but after a news broke of a competitor developing a new treatment for Gauchers disease, licensed the Radin/Shayman patents in 2000. Eliglustat did not receive FDA approval for another 14 years, a delay that Shayman speculated was due to some company leaders not being fully committed to developing a drug that would compete with imiglucerase (brand name Cerezyme), Genzymes flagship treatment for Gauchers disease. Society and culture Economics In 2014, the annual cost of eliglustat taken orally twice a day was $310,250. Cerezyme cost about $300,000 for the intravenous medication if taken twice a month. Manufacturing costs for eliglustat are slightly lower than for imiglucerase. Genzyme maintains higher prices for orphan drugs—most often paid for by insurers—in order to remain financially sustainable. References External links "Eliglustat". Drug Information Portal. U.S. National Library of Medicine.

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I'd like to learn more about the medical term 'Hyoscyamine.' Can you provide some details?

Hyoscyamine (also known as daturine or duboisine) is a naturally occurring tropane alkaloid and plant toxin. It is a secondary metabolite found in certain plants of the family Solanaceae, including henbane, mandrake, angels trumpets, jimsonweed, tomato, the sorcerers tree, and deadly nightshade. It is the levorotary isomer of atropine (third of the three major nightshade alkaloids) and thus sometimes known as levo-atropine.Brand names for hyoscyamine include Symax, HyoMax, Anaspaz, Egazil, Buwecon, Cystospaz, Levsin, Levbid, Levsinex, Donnamar, NuLev, Spacol T/S, and Neoquess. Uses Hyoscyamine is used to provide symptomatic relief of spasms caused by various lower abdominal and bladder disorders including peptic ulcers, irritable bowel syndrome, diverticulitis, pancreatitis, colic, and interstitial cystitis. It has also been used to relieve some heart problems, control some of the symptoms of Parkinsons disease, as well as for control of abnormal respiratory symptoms and "hyper-mucus secretions" in patients with lung disease.It is also useful in pain control for neuropathic pain, chronic pain and palliative care – "comfort care" – for those with intractable pain from treatment resistant, untreatable, and incurable diseases. When combined with opioids it increases the level of analgesia (pain relief) obtained. Several mechanisms are thought to contribute to this effect. The closely related drugs atropine and hyoscine and other members of the anticholinergic drug group like cyclobenzaprine, trihexyphenidyl, and orphenadrine are also used for this purpose. When hyoscyamine is used along with opioids or other anti-peristaltic agents, measures to prevent constipation are especially important given the risk of paralytic ileus. Adverse effects Side effects include dry mouth and throat, increased appetite leading to weight gain, eye pain, blurred vision, restlessness, dizziness, arrhythmia, flushing, and faintness. An overdose will cause headache, nausea, vomiting, and central nervous system symptoms including disorientation, hallucinations, euphoria, sexual arousal, short-term memory loss, and possible coma in extreme cases. The euphoric and sexual effects are stronger than those of atropine but weaker than those of Hyoscine, as well as dicycloverine, orphenadrine, cyclobenzaprine, trihexyphenidyl, and ethanolamine antihistamines like phenyltoloxamine. Pharmacology Hyoscyamine is an antimuscarinic; i.e., an antagonist of muscarinic acetylcholine receptors. It blocks the action of acetylcholine at parasympathetic sites in sweat glands, salivary glands, stomach secretions, heart muscle, sinoatrial node, smooth muscle in the gastrointestinal tract, and the central nervous system. It increases cardiac output and heart rate, lowers blood pressure and dries secretions. It may antagonize serotonin. At comparable doses, hyoscyamine has 98 per cent of the anticholinergic power of atropine. The other major belladonna-derived drug hyoscine (known in the United States as Scopolamine) has 92 per cent of the antimuscarinic potency of atropine. Biosynthesis in plants Hyoscyamine can be extracted from plants of the family Solanaceae, notably Datura stramonium. As hyoscyamine is a direct precursor in the plant biosynthesis of hyoscine, it is produced via the same metabolic pathway.The biosynthesis of hyoscine begins with the decarboxylation of L-ornithine to putrescine by ornithine decarboxylase (EC 4.1.1.17). Putrescine is methylated to N-methylputrescine by putrescine N-methyltransferase (EC 2.1.1.53).A putrescine oxidase (EC 1.4.3.10) that specifically recognizes methylated putrescine catalyzes the deamination of this compound to 4-methylaminobutanal which then undergoes a spontaneous ring formation to N-methylpyrrolium cation. In the next step, the pyrrolium cation condenses with acetoacetic acid yielding hygrine. No enzymatic activity could be demonstrated that catalyzes this reaction. Hygrine further rearranges to tropinone.Subsequently, tropinone reductase I (EC 1.1.1.206) converts tropinone to tropine which condenses with phenylalanine-derived phenyllactate to littorine. A cytochrome P450 classified as Cyp80F1 oxidizes and rearranges littorine to hyoscyamine aldehyde. Bush medicine basis A bush medicine developed by Aboriginal peoples of the eastern states of Australia from the soft corkwood tree, or Duboisia myoporoides, was used by the Allies in World War II to stop soldiers getting seasick when they sailed across the English Channel during the Invasion of Normandy. Later, it was found that the same substance could be used in the production of scopolamine and hyoscyamine, which are used in eye surgery, and a multi-million dollar industry was built in Queensland based on this substance. == References ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

Could you offer a clear explanation of the term 'Blind loop syndrome' as used in the medical field?

Blind loop syndrome (BLS), also known as stagnant loop syndrome, is a state that occurs when the normal bacterial flora of the small intestine proliferates to numbers that cause significant derangement to the normal physiological processes of digestion and absorption. In some cases of blind loop syndrome, overgrowth of pathogenic non-commensal bacteria has also been noted. It has long been understood that from birth, and throughout life, large amounts of bacteria reside symbiotically within animal gastrointestinal tracts such as the human gastrointestinal tract. The understanding of this gut flora has even led to novel treatments for bowel irregularity that utilize so called "probiotics" or good bacteria that aid in normal digestion. The problem of BLS arises when the bacterial colonies residing in the upper gastrointestinal tract begin to grow out of control or are altered in their makeup thereby creating a burden on the normal physiological processes occurring in the small intestine. This results in problems, among others, of: vitamin B12 deficiency, fat malabsorption and steatorrhea, fat-soluble vitamin deficiencies and intestinal wall injury. Symptoms and signs Most of the symptoms of BLS are non specific but nevertheless warrant the utmost attention. These include: Loss of appetite Nausea Flatulence Diarrhea Fullness after a meal Fatty stools (steatorrhea) Unintentional weight loss Generalised weaknessAs a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with BLS patients with advanced cases should be investigated for: Vitamin B12 deficiency Folate deficiency Iron deficiency Vitamin E deficiency Causes Blind loop syndrome is a complication of surgical operations of the abdomen, as well as inflammatory bowel disease or scleroderma. Another cause is jejunoileal diverticula. Pathophysiology The overgrowth of bacteria in the small intestine is prevented by various mechanical and chemical factors which include the constant peristaltic movement of contents along the length of the gastrointestinal tract and the antibacterial properties of gastric secretions, pancreatic secretions and bile.It follows that a disruption of any of these factors could lead to bacterial overgrowth and indeed BLS has been found to occur in persons with anatomical anomalies that result in stagnation. BLS has also been associated with achlorhydria, dysmotility, fistulae, and strictures. Chronic or high dose opioid therapy may contribute to BLS by reducing gastric motility.Due to the disruption of digestive processes by the overgrowth of intestinal bacteria; malabsorption of bile salts, fat and fat-soluble vitamins, protein and carbohydrates results in damage to the mucosal lining of the intestine by bacteria or via the production of toxic metabolites. Diagnosis A physical examination may reveal a mass or distention of the abdomen.Tests which may be useful for diagnosis include: Abdominal x-ray Abdominal CT scan Contrast enema study Treatment The treatment of BLS follows two basic principles. When a patient presents with symptoms of BLS, the treating physician basically has two recognized options for management: Test-and-treat Treat empirically Test-and-treat method Although it would seem to be the better way to go in terms of management, there has been recent criticism on the need for such testing because of reliability issues. However, it must be stated that there are options such as the glucose breath test and jejunal aspiration the explanations of which are beyond the scope of this current article. Treating empirically The "treat empirically" route also has its difficulties, which have all come under wide debate and study. Recommendations are varied but seem to find some common ground around the notion that treatment should be individualized to the specific circumstances under which a patient has developed BLS since these circumstances affect the complex microbial make up of the affected bowel.Tetracyclines have been the mainstay of treatment for BLS, but recent studies have concluded Rifaximin to be very effective in the treatment of BLS. One study by Di Stefano et al., however, concluded Metronidazole to be more effective than Rifaximin in the treatment of BLS. Surgical management Surgical management is reserved for fixing anatomical causes of bowel obstruction that interfere with normal function once they are amenable to such intervention. These conditions include: Strictures Fistulae Diverticula References == External links ==

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Can you demystify the medical term 'Malabsorption' for me?

Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and a variety of anaemias.Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult in one day includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required sodium, potassium, chloride, calcium, vitamins, and other elements. Salivary, gastric, intestinal, hepatic, and pancreatic secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each of Na+, K+, Cl–, HCO3–, Ca2+, or Mg2+. If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinal malabsorption may ensue. If the abnormality involves a single step in the absorptive process, as in primary lactase deficiency, or if the disease process is limited to the very proximal small intestine, then selective malabsorption of only a single nutrient may occur. However, generalized malabsorption of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs in coeliac disease with extensive involvement of the small intestine. Signs and symptoms Gastrointestinal manifestations Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with a primary or secondary disaccharidase deficiency, such as lactose intolerance or sucrose intolerance. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohns disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption. Extraintestinal manifestations Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic, macrocytic, or dimorphic anemia may reflect impaired iron, folate, or vitamin B12 absorption. Purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of steatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids. Presentation Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can be intestinal or extra-intestinal - the former predominates in severe malabsorption. Diarrhoea, often steatorrhoea, is the most common feature. Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption. It is due to impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed fatty acid. The latter also results in bloating, flatulence and abdominal discomfort. Cramping pain usually suggests obstructive intestinal segment e.g. in Crohns disease, especially if it persists after defecation. Weight loss can be significant despite increased oral intake of nutrients. Growth retardation, failure to thrive, delayed puberty in children Swelling or oedema from loss of protein Anaemias, commonly from vitamin B12, folic acid and iron deficiency presenting as fatigue and weakness. Decreased mental abilities, poor reflexes, and abnormal sensations due to vitamin B12 deficiency. Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis Bleeding tendencies from vitamin K and other coagulation factor deficiencies. Causes Pathophysiology The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, protein, micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells.Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.Intestinal malabsorption can be due to: Congenital or acquired reduction in absorptive surface Defects of ion transport Defects of specific hydrolysis Impaired enterohepatic circulation Mucosal damage (enteropathy) Pancreatic insufficiency Diagnosis There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by symptoms and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption). Classification Some prefer to classify malabsorption clinically into three basic categories: selective, as seen in lactose malabsorption. partial, as observed in abetalipoproteinaemia. total, as in exceptional cases of coeliac disease. Blood tests Routine blood tests may reveal anaemia, high CRP or low albumin; which shows a high correlation for the presence of an organic disease. In this setting, microcytic anaemia usually implies iron deficiency and macrocytosis can be caused by impaired folic acid or B12 absorption or both. Low cholesterol or triglyceride may give a clue toward fat malabsorption. Low calcium and phosphate may give a clue toward osteomalacia from low vitamin D. Specific vitamins like vitamin D or micronutrient like zinc levels can be checked. Fat soluble vitamins (A, D, E and K) are affected in fat malabsorption. Prolonged prothrombin time can be caused by vitamin K deficiency. Serological studies. Specific tests are carried out to determine the underlying cause.IgA Anti-transglutaminase antibodies or IgA Anti-endomysial antibodies for Coeliac disease (gluten sensitive enteropathy). Stool studies Microscopy is particularly useful in diarrhoea, may show protozoa like Giardia, ova, cyst and other infective agents. Fecal fat study to diagnose steatorrhoea is rarely performed nowadays. Low fecal pancreatic elastase is indicative of pancreatic insufficiency. Chymotrypsin and pancreolauryl can be assessed as well Radiological studies Barium follow through is useful in delineating small intestinal anatomy. Barium enema may be undertaken to see colonic or ileal lesions. CT abdomen is useful in ruling out structural abnormality, done in pancreatic protocol when visualising pancreas. Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP. Interventional studies OGD to detect duodenal pathology and obtain D2 biopsy (for coeliac disease, tropical sprue, Whipples disease, abetalipoproteinaemia etc.) Enteroscopy for enteropathy and jejunal aspirate and culture for bacterial overgrowth Capsule Endoscopy is able to visualise the whole small intestine and is occasionally useful. Colonoscopy is necessary in colonic and ileal disease. ERCP will show pancreatic and biliary structural abnormalities. Other investigations 75SeHCAT test to diagnose bile acid malabsorption in ileal disease or primary bile acid diarrhea. Glucose hydrogen breath test for bacterial overgrowth Lactose hydrogen breath test for lactose intolerance Sugar probes or 51Cr-EDTA to determine intestinal permeability. Obsolete tests no longer used clinically D-xylose absorption test for mucosal disease or bacterial overgrowth. Normal in pancreatic insufficiency. Bile salt breath test (14C-glycocholate) to determine bile salt malabsorption. Schilling test to establish cause of B12 deficiency. Management Treatment is directed largely towards management of underlying cause: Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency, hospital admission may be required for nutritional support and detailed advice from dietitians. Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy. In patients whose intestinal absorptive surface is severely limited from disease or surgery, long term total parenteral nutrition may be needed. Pancreatic enzymes are supplemented orally in pancreatic insufficiency. Dietary modification is important in some conditions: Gluten-free diet in coeliac disease. Lactose avoidance in lactose intolerance. Antibiotic therapy to treat Small Bowel Bacterial overgrowth. Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption. See also Fructose malabsorption Protein losing enteropathy References == External links ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I'd like to learn more about the medical term 'Mantle cell lymphoma.' Can you provide some details?

Mantle cell lymphoma (MCL) is a type of non-Hodgkins lymphoma (NHL), comprising about 6% of NHL cases. There are only about 15,000 patients presently in the United States with mantle cell lymphoma. It is named for the mantle zone of the lymph nodes. MCL is a subtype of B-cell lymphoma, due to CD5 positive antigen-naive pregerminal center B-cell within the mantle zone that surrounds normal germinal center follicles. MCL cells generally over-express cyclin D1 due to the t(11:14) translocation, a chromosomal translocation in the DNA. Signs and symptoms At diagnosis, patients typically are in their 60s and present to their physician with advanced disease. About half have B symptoms such as fever, night sweats, or unexplained weight loss (over 10% of body weight). Enlarged lymph nodes (for example, a "bump" on the neck, armpits or groin) or enlargement of the spleen are usually present. Bone marrow, liver and gastrointestinal tract involvement occurs relatively early in the course of the disease. Mantle cell lymphoma has been reported in rare cases to be associated with severe allergic reactions to mosquito bites. These reactions involve extensive allergic reactions to mosquito bites which range from greatly enlarged bite sites that may be painful and involve necrosis to systemic symptoms (e.g. fever, swollen lymph nodes, abdominal pain, and diarrhea), or, in extremely rare cases, to life-threatening anaphylaxis. In several of these cases, the mosquito bite allergy (MBA) reaction occurred prior to the diagnosis of MCL suggesting that MBA can be a manifestation of early-developing mantle cell lymphoma. Pathogenesis MCL, like most cancers, results from the acquisition of a combination of (non-inherited) genetic mutations in somatic cells. This leads to a clonal expansion of malignant B lymphocytes. The factors that initiate the genetic alterations are typically not identifiable, and usually occur in people with no particular risk factors for lymphoma development. Because it is an acquired genetic disorder, MCL is neither communicable nor inheritable.A defining characteristic of MCL is mutation and overexpression of cyclin D1, a cell cycle gene, that contributes to the abnormal proliferation of the malignant cells. MCL cells may also be resistant to drug-induced apoptosis, making them harder to cure with chemotherapy or radiation. Cells affected by MCL proliferate in a nodular or diffuse pattern with two main cytologic variants, typical or blastic. Typical cases are small to intermediate-sized cells with irregular nuclei. Blastic (aka blastoid) variants have intermediate to large-sized cells with finely dispersed chromatin, and are more aggressive in nature. The tumor cells accumulate in the lymphoid system, including lymph nodes and the spleen, with non-useful cells eventually rendering the system dysfunctional. MCL may also replace normal cells in the bone marrow, which impairs normal blood cell production. Diagnosis Diagnosis generally requires stained slides of a surgically removed part of a lymph node. Other methods are also commonly used, including cytogenetics and fluorescence in situ hybridization (FISH). Polymerase chain reaction (PCR) and CER3 clonotypic primers are additional methods, but are less often used.The immunophenotype profile consists of CD5+ (in about 80% of cases), CD10-/+, and it is usually CD5+ and CD10-. CD20+, CD23-/+ (though plus in rare cases). Generally, cyclin D1 is expressed. Cyclin D1-negative mantle cell lymphoma can be diagnosed by detecting the SOX11 marker. The workup for mantle cell lymphoma is similar to the workup for many indolent lymphomas and certain aggressive lymphomas. Mantle cell lymphoma is a systemic disease with frequent involvement of the bone marrow and gastrointestinal tract (generally showing polyposis in the lining). There is also a not-uncommon leukemic phase, marked by its presence in the blood. For this reason, both the peripheral blood and bone marrow are evaluated for the presence of malignant cells. Chest, abdominal, and pelvic CT scans are routinely performed.Since mantle cell lymphoma may present a lymphomatous polyposis coli and colon involvement is common, colonoscopy is considered a routine part of the evaluation. Upper endoscopy and neck CT scan may be helpful in selected cases. In some patients with the blastic variant, lumbar puncture is done to evaluate the spinal fluid for involvement.CT scanPET scan Treatments There are no proven standards of treatment for MCL, and there is no consensus among specialists on how to treat it optimally. Many regimens are available and often get good response rates, but patients almost always get disease progression after chemotherapy. Each relapse is typically more difficult to treat, and relapse is generally faster. Regimens are available that treat relapses, and new approaches are under test. Because of the aforementioned factors, many MCL patients enroll in clinical trials to get the latest treatments.There are four classes of treatments in general use: chemotherapy, immunotherapy, radioimmunotherapy and biologic agents. The phases of treatment are generally: frontline, following diagnosis, consolidation, after frontline response (to prolong remissions), and relapse. Relapse is usually experienced multiple times. Chemotherapy Chemotherapy is widely used as frontline treatment, and often is not repeated in relapse due to side effects. Alternate chemotherapy is sometimes used at first relapse. For frontline treatment, CHOP with rituximab is the most common chemotherapy, and often given as outpatient by IV. A stronger chemotherapy with greater side effects (mostly hematologic) is HyperCVAD, often given in the hospital setting, with rituximab and generally to fitter patients (some of which are over 65). HyperCVAD is becoming popular and showing promising results, especially with rituximab. It can be used on some elderly (over 65) patients, but seems only beneficial when the baseline Beta-2-MG blood test was normal. It is showing better complete remissions (CR) and progression-free survival (PFS) than CHOP regimens. A less intensive option is bendamustine with rituximab.Second line treatment may include fludarabine, combined with cyclophosphamide and/or mitoxantrone, usually with rituximab. Cladribine and clofarabine are two other medications being investigated in MCL. A relatively new regimen that uses old medications is PEP-C, which includes relatively small, daily doses of prednisone, etoposide, procarbazine, and cyclophosphamide, taken orally, has proven effective for relapsed patients. According to Dr. John Leonard, PEP-C may have anti-angiogenetic properties, something that he and his colleagues are testing through an ongoing drug trial.Another approach involves using very high doses of chemotherapy, sometimes combined with total body irradiation (TBI), in an attempt to destroy all evidence of the disease. The downside to this is the destruction of the patients entire immune system as well, requiring rescue by transplantation of a new immune system (hematopoietic stem cell transplantation), using either autologous stem cell transplantation, or those from a matched donor (an allogeneic stem cell transplant). A presentation at the December 2007 American Society of Hematology (ASH) conference by Christian Geisler, chairman of the Nordic Lymphoma Group claimed that according to trial results, mantle cell lymphoma is potentially curable with very intensive chemo-immunotherapy followed by a stem cell transplant, when treated upon first presentation of the disease.These results seem to be confirmed by a large trial of the European Mantle Cell Lymphoma Network indicating that induction regimens containing monoclonal antibodies and high dose ARA-C (Cytarabine) followed by ASCT should become the new standard of care of MCL patients up to approximately 65 years.A study released in April 2013 showed that patients with previously untreated indolent lymphoma, bendamustine plus rituximab can be considered as a preferred first-line treatment approach to R-CHOP because of increased progression-free survival and fewer toxic effects. Immunotherapy Immune-based therapy is dominated by the use of the rituximab monoclonal antibody, sold under the trade name Rituxan (or as Mabthera in Europe and Australia). Rituximab may have good activity against MCL as a single agent, but it is typically given in combination with chemotherapies, which prolongs response duration. There are newer variations on monoclonal antibodies combined with radioactive molecules known as radioimmunotherapy (RIT). These include Zevalin and Bexxar. Rituximab has also been used in small numbers of patients in combination with thalidomide with some effect. In contrast to these antibody-based passive immunotherapies, the field of active immunotherapy tries to activate a patients immune system to specifically eliminate their own tumor cells. Examples of active immunotherapy include cancer vaccines, adoptive cell transfer, and immunotransplant, which combines vaccination and autologous stem cell transplant. Though no active immunotherapies are currently a standard of care, numerous clinical trials are ongoing. Targeted therapy Two Bruton tyrosine kinase inhibitors (BTKi), one In November 2013, ibrutinib (trade name Imbruvica, Pharmacyclics LLC) and in October 2017, acalabrutinib (trade name Calquence, AstraZeneca Pharmaceuticals LP) were approved in the United States for treating MCL. Other targeted agents include the proteasome inhibitor bortezomib, mTOR inhibitors such as temsirolimus, and the P110δ inhibitor GS-1101.In November 2019, zanubrutinib (Brukinsa) was approved in the United States with an indication for the treatment of adults with mantle cell lymphoma who have received at least one prior therapy. Gene therapy Brexucabtagene autoleucel (Tecartus) was approved for medical use in the United States in July 2020, with an indication for the treatment of adults with relapsed or refractory mantle cell lymphoma. It was approved for medical use in the European Union in December 2020.Each dose of brexucabtagene autoleucel is a customized treatment created using the recipients own immune system to help fight the lymphoma. The recipients T cells, a type of white blood cell, are collected and genetically modified to include a new gene that facilitates the targeting and killing of the lymphoma cells. These modified T cells are then infused back into the recipient. Prognosis Recent clinical advances in mantle cell lymphoma (MCL) have seen standard‐of‐care treatment algorithms transformed. Frontline rituximab combination therapy, high dose cytarabine‐based induction in younger patients and, more recently, Bruton Tyrosine Kinase (BTK) inhibitors in the relapse setting have all demonstrated survival advantage in clinical trials (Wang et al., 2013; Eskelund et al., 2016; Rule et al., 2016). Over the last 15 years these practices have gradually become embedded in clinical practice and real‐world data has observed corresponding improvements in patient survival (Abrahamsson et al., 2014; Leux et al., 2014).The overall 5-year survival rate for MCL is generally 50% (advanced stage MCL) to 70% (for limited-stage MCL). Prognosis for individuals with MCL is problematic and indexes do not work as well due to patients presenting with advanced stage disease. Staging is used but is not very informative, since the malignant B-cells can travel freely though the lymphatic system and therefore most patients are at stage III or IV at diagnosis. Prognosis is not strongly affected by staging in MCL and the concept of metastasis does not really apply.The Mantle Cell Lymphoma International Prognostic Index (MIPI) was derived from a data set of 455 advanced stage MCL patients treated in series of clinical trials in Germany/Europe. Of the evaluable population, approximately 18% were treated with high-dose therapy and stem cell transplantation in first remission. The MIPI is able to classify patients into three risk groups: low risk (median survival not reached after median 32 months follow-up and 5-year OS rate of 60%), intermediate risk (median survival 51 months) and high risk (median survival 29 months). In addition to the 4 independent prognostic factors included in the model, the cell proliferation index (Ki-67) was also shown to have additional prognostic relevance. When the Ki67 is available, a biologic MIPI can be calculated.MCL is one of the few NHLs that can cross the boundary into the brain, yet it can be treated in that event.There are a number of prognostic indicators that have been studied. There is not universal agreement on their importance or usefulness in prognosis.Ki-67 is an indicator of how fast cells mature and is expressed in a range from about 10% to 90%. The lower the percentage, the lower the speed of maturity, and the more indolent the disease. Katzenberger et al. Blood 2006;107:3407 graphs survival versus time for subsets of patients with varying Ki-67 indices. He shows median survival times of about one year for 61-90% Ki-67 and nearly 4 years for 5-20% Ki-67 index. MCL cell types can aid in prognosis in a subjective way. Blastic is a larger cell type. Diffuse is spread through the node. Nodular are small groups of collected cells spread through the node. Diffuse and nodular are similar in behavior. Blastic is faster growing and it is harder to get long remissions. Some thought is that given a long time, some non-blastic MCL transforms to blastic. Although survival of most blastic patients is shorter, some data shows that 25% of blastic MCL patients survive to 5 years. That is longer than diffuse type and almost as long as nodular (almost 7 yrs).Beta-2 microglobulin is another risk factor in MCL used primarily for transplant patients. Values less than three have yielded 95% overall survival to six years for auto SCT where over three yields a median of 44 most overall survival for auto SCT (Khouri 03). This is not yet fully validated.Testing for high levels of Lactate dehydrogenase (LDH) in NHL patients is useful because LDH is released when body tissues break down for any reason. While it cannot be used as a sole means of diagnosing NHL, it is a surrogate for tracking tumor burden in those diagnosed by other means. The normal range is approximately 100–190. Epidemiology 6% of non-Hodgkin lymphoma cases are mantle cell lymphoma. As of 2015, the ratio of males to females affected is about 4:1. See also In situ mantle cell lymphoma List of hematologic conditions References Further reading Cohen JB, Zain JM, Kahl BS (2017). "Current Approaches to Mantle Cell Lymphoma: Diagnosis, Prognosis, and Therapies". Am Soc Clin Oncol Educ Book. 37 (37): 512–25. doi:10.1200/EDBK_175448. PMID 28561694. Dreyling M, Ferrero S, Hermine O (November 2014). "How to manage mantle cell lymphoma". Leukemia. 28 (11): 2117–30. doi:10.1038/leu.2014.171. PMID 24854989. S2CID 22105743. Schieber M, Gordon LI, Karmali R (2018). "Current overview and treatment of mantle cell lymphoma". F1000Res. 7: 1136. doi:10.12688/f1000research.14122.1. PMC 6069726. PMID 30109020. == External links ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

I'm seeking clarification on the medical term 'Open bite malocclusion.' Could you explain it?

Open bite is a type of orthodontic malocclusion which has been estimated to occur in 0.6% of the people in the United States. This type of malocclusion has no vertical overlap or contact between the anterior incisors. The term "open bite" was coined by Carevelli in 1842. Causes Open bite malocclusion can happen due to several reasons. It may be genetic in nature, leading to a skeletal open bite or can be caused by functional habits which may lead to dental open bite. In the earlier age, open bite may occur due to a transitional change from primary to the permanent dentition. Some factors that may cause an open bite are: Tongue thrusting Thumb sucking Long-term usage of Pacifier Macroglossia Airway obstruction Adenoid hypertrophy Nasal concha Hypertrophy Types Anterior open bite An anterior open bite occurs in humans when the front teeth fail to touch and there is no overlap between upper incisors and lower incisors. Anterior open can be caused by functional habits such as digit sucking, tongue thrust or long-term pacifier use. When digit sucking habit is present in the late primary to early mixed dentition stages, it can lead to different side-effects such as upper teeth flaring out, lower teeth flaring in, increase in the open bite and the overjet. A posterior crossbite in these children along with decrease in intercanine and intermolar width is also found. The more intense (longer) the habit, the worse the malocclusion may be.Pacifier use has also shown to cause anterior open bites in children. Pacifier use which lasts longer than 18 months, may cause this malocclusion. It is shown that as long as the sucking habit stops before the eruption of permanent teeth, the open bite self-corrects. In some cases, behavior modification may be necessary to eliminate the dental habits. If all else fails, then a tongue crib can be used. Posterior open bite Posterior open bite is caused when posterior teeth such as molars or premolars fail to touch their counterpart tooth. This is more likely to occur in segments where there may be unilateral open bite or open bite related to one or more teeth. Failure of eruption of teeth either due to primary failure or mechanical obstruction during eruption phase can cause the open bite. Sometimes lateral tongue thrust may also prevent the eruption of the posterior teeth, thus eliminating this habit maybe key to eruption in those instances. Skeletal open bite Patient with skeletal open bites that accompany dental open bites may have Adenoid faces or Long face syndrome. They are said to have what is known as Hyperdivergent Growth Pattern which includes characteristics such as: Increased Lower Anterior Facial Height Occlusal plane diverges after the 1st molar contact May accompany dental open bite Narrow nostrils with upturned nose Dolicofacial or Leptoprosopic face pattern Constricted maxillary arch Bilateral Posterior Crossbite High and narrow palatal vault Presence of crowding in teeth Mentalis muscle strain upon forcibly closing of lips Possible gummy smile with increased interlabial gapCephalometric analysis features of skeletal open bite may include: Increased Frankfurt-Mandibular Plane angle Steep Occlusal Plane Angle Increased SN-MP Angle Short Mandibular ramus Increased mandibular body length Downward and backward position of mandible Increased gonial angle Proclined upper incisors, retroclined or upright lower incisors Posterior part of maxilla is tipped downwards Posterior facial height equals 1/2 of anterior facial height Increased hard tissue Lower Anterior Facial Height Increased total anterior facial height Short mandibular ramusViken Sassouni developed Sassouni analysis which indicates that patients with long face syndrome have 4 of their bony planes (mandibular plane, occlusal plane, palatal plane, SN plane) steep to each other. Dental open bite Dental open bite occurs in patients where the anterior teeth fail to touch. However, this is not accompanied by the skeletal tendency of having an open bite. Thus this type of open bite may happen in patients who have horizontal or hypodivergent growth pattern. These patients have normal jaw growth and do not have the long face syndrome. The anterior open bite in these patients may be caused by Macroglossia, Tongue thrusting habit or digit sucking habits. Some of the characteristics of a dental open bite include: Normal lower anterior facial height Horizontal/Hypodivergent growth pattern Occlusal plane diverges after the premolar contact Under-eruption of the anterior incisors Over-eruption of the posterior molars Proclined upper and lower incisors No vertical maxillary excess or gummy smile Presence of habits such as thumb sucking, tongue thrusting Spacing between anterior incisors due to their proclination Open bite correction Primary/mixed dentition Behavior modification Behavior therapy is important especially when children are in their primary dentition in the pre-adolescent age. Improving habits at this time may lead to self-correction of open bite in many cases. Sometimes presence of infantile swallowing into early childhood may lead to an anterior open bite. Habit control through appliances such as Tongue crib or Tongue spurs may be used in adolescents if behavior modification fails to stop the habit. Tongue crib therapy A tongue crib is a removable appliance placed in the maxillary arch to stop the tongue thrusting habit. This appliance may be used in patients with mixed dentition or permanent dentition. The tongue crib is attached through a bar to two bands placed on the upper 1st molars. The crib is shaped like a horseshoe with metal bars that prevent thrusting. The tongue crib eliminates the habit in approximately 90% of patients. . Huang et al. published a study in 1990 which stated that patients who achieved a positive overbite during their tongue crib therapy had a good chance of maintaining that overbite after their orthodontic treatment. They credited this change to a change in the posterior positioning of the tongue due to the crib therapy.Some of the side-effects of using a tongue-crib therapy is that this appliance may trap food, causing inflammation around the appliance. Repeated contact of the tongue with the appliance may lead to an imprint on the tongue which will self-resolve when the appliance is removed. It is important to note that this type of therapy will only work in patients who do not have a skeletal open bite tendency. A skeletal open bite tendency may be addressed via surgery or other treatment. Blue Grass appliance Its a type of appliance which is similar to Nance appliance, but instead of acrylic pad that rests on the anterior palate, this appliance has a plastic roller that patient can use their tongue to break their habit. This appliance is banded to the upper 1st molars and bars extend the appliance to anterior palate where the plastic roller is placed. Vertical pull chin cup Hakan Iscan and others used vertical pull chin cup in 17 patients for 9 months where they applied 400g of force on each side. Compared to controls, they found that patients included in the experimental group had increased eruption of the mandibular incisors, decrease of the ramal inclination, decrease of the mandibular plane, increase of the overbite, decrease of the gonial angle and increase of the mandibular corpus inclination were found. They stated that vertical chin cup maybe effective in treating skeletal open bite patients. However, Pedrin et al. used removable plate with palatal crib and combined it with a high-pull chin cup in 30 patients for 12 months and compared it to 30 patients who were followed with no treatment. They found that no positive skeletal influence on the vertical facial pattern of patients treated for open bite in the mixed dentition by their stated protocol. Another study stated that there is no positive effect of vertical pull chin cup in controlling the vertical facial height and that close of an anterior open bite was mostly done by dentoalveolar changes. Permanent dentition Correction of open bite in permanent dentition may involve extrusion of the anterior teeth or intrusion of the posterior teeth. This decision depends on the incisor show on smiling for a patient. If a patient has normal incisor show at rest smile, than molar intrusion may be done in these type of faces. Extrusion of anterior teeth in these patients will lead to excessive gummy smile which in some cases is not desirable. If a patient does not have a normal incisor show at rest and smile, then anterior extrusion may be done in these patients. High-Pull Headgear This appliance can be used with patients who are growing and in permanent dentition. This appliance has been advocated to be used mainly for controlling the vertical dimension by applying force to intrude molars. Elastics Elastics have been used to correct anterior dental open bite. These elastics can be in configuration of triangular or anterior vertical elastics. Bite blocks R. Kuster and B. Ingerval in 1992, used two types of bite blocks to evaluate their effect on skeletal open bite patients. One group of patients had spring-loaded bite block for one year and other group had repelling magnets as bite blocks for 3 months. Both type of bite blocks exerted intrusive force on both upper and lower posterior teeth. They saw 3mm improvement in overbite with magnet group and 1.3mm improvement in overbite with spring-loaded group. They concluded that this effect resulted due to counter-clockwise rotation of mandible which was caused by intrusion of posterior teeth and increased eruption of incisors. Glossectomy There are not systematic reviews or randomized clinical control trials related to correction of open bite with partial tongue glossectomy but several case reports have been published indicating successful treatment of open bite with this surgical approach. Macroglossia has been reported to cause open bite and bimaxillary protrusion and is also known to be make orthodontic treatment unstable after its completion. Orthognathic surgery An orthognathic surgical approach can be taken to correct an open bite once vertical growth has finished in male and female patients. At that time, a Le-Fort I osteotomy to impact the maxilla is usually done. According to Proffit et al., surgical movement that involves maxillary impaction is the most stable surgical movement in the hierarchy they established. A two jaw surgery can also be performed where Bilateral Sagittal Split Osteotomy can be done to correct any Antero-Posterior changes of the mandible. However, with two jaw surgery a relapse leading to bite opening may happen due to condylar remodeling and resorption. Stability and relapse Surgery vs. non-surgery Geoffrey Greenlee and others published a meta-analysis in 2011 which concluded that patients with orthognathic surgical correction of open bite had 82% stability in comparison to non-surgical correction of open bite which had 75% of stability after 1or more year of treatment. Both the groups started with 2–3 mm of open bite initially. Molar intrusion Man-Suk Baek and others evaluated long-term stability of anterior open bite by intrusion of maxillary posterior teeth. Their results showed that the molars were intruded by 2.39 mm during treatment and relapsed back by 0.45 mm or 22.8%. The incisal overbite increased by 5.56 mm during treatment and relapsed back by 1.20 mm or 17%. They concluded that majority of the relapse occurred during first year of treatment. See also Cephalometric analysis Intrusion (orthodontics) Long face syndrome MEAW Technique Malocclusion == References ==

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

I need a basic explanation for the medical term 'Necrolytic acral erythema.'

Necrolytic acral erythema is a cutaneous condition that is a manifestation of hepatitis C viral infection or zinc deficiency.It is a papulosquamous and sometimes vesiculobullous eruption bearing clinical and histologic similarity to other necrolytic erythemas such as necrolytic migratory erythema, pseudoglucagonoma and nutritional deficiency syndromes. See also List of cutaneous conditions References == External links ==

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I'm trying to understand 'Aromatase excess syndrome' within a medical context. Could you shed some light on it?

Aromatase excess syndrome (AES or AEXS) is a rare genetic and endocrine syndrome which is characterized by an overexpression of aromatase, the enzyme responsible for the biosynthesis of the estrogen sex hormones from the androgens, in turn resulting in excessive levels of circulating estrogens and, accordingly, symptoms of hyperestrogenism. It affects both sexes, manifesting itself in males as marked or complete phenotypical feminization (with the exception of the genitalia; i.e., no pseudohermaphroditism) and in females as hyperfeminization.To date, 30 males and 8 females with AEXS among 15 and 7 families, respectively, have been described in the medical literature. Signs and symptoms Observed physiological abnormalities of the condition include a dramatic overexpression of aromatase and, accordingly, excessive levels of estrogens including estrone and estradiol and a very high rate of peripheral conversion of androgens to estrogens. In one study, cellular aromatase mRNA expression was found to be at least 10 times higher in a female patient compared to the control, and the estradiol/testosterone ratio after an injection of testosterone in a male patient was found to be 100 times greater than the control. Additionally, in another study, androstenedione, testosterone, and dihydrotestosterone (DHT) were found to be either low or normal in males, and follicle-stimulating hormone (FSH) levels were very low (likely due to suppression by estrogen, which has antigonadotropic effects as a form of negative feedback inhibition on sex steroid production in sufficiently high amounts), whereas luteinizing hormone (LH) levels were normal.According to a recent review, estrone levels have been elevated in 17 of 18 patients (94%), while estradiol levels have been elevated only in 13 of 27 patients (48%). As such, estrone is the main estrogen elevated in the condition. In more than half of patients, circulating androstenedione and testosterone levels are low to subnormal. The ratio of circulating estradiol to testosterone is >10 in 75% of cases. FSH levels are said to be consistently low in the condition, while LH levels are in the low to normal range.It is notable that gynecomastia has been observed in patients in whom estradiol levels are within the normal range. This has been suggested to be due to in situ conversion of adrenal androgens into estrone and then estradiol (via local 17β-HSD) in breast tissue (where aromatase activity may be particularly high).The symptoms of AEXS, in males, include heterosexual precocity (precocious puberty with phenotypically-inappropriate secondary sexual characteristics; i.e., a fully or mostly feminized appearance), severe prepubertal or peripubertal gynecomastia (development of breasts in males before or around puberty), high-pitched voice, sparse facial hair, hypogonadism (dysfunctional gonads), oligozoospermia (low sperm count), small testes, micropenis (an unusually small penis), advanced bone maturation, an earlier peak height velocity (an accelerated rate of growth in regards to height), and short final stature due to early epiphyseal closure. The incidence of gynecomastia appears to be 100%, with 20 of 30 male cases opting for mastectomy according to a review.In females, symptoms of AEXS include isosexual precocity (precocious puberty with phenotypically-appropriate secondary sexual characteristics), macromastia (excessively large breasts), an enlarged uterus, menstrual irregularities, and, similarly to males, accelerated bone maturation and short final height. Of seven females described in one report, three (43%) had macromastia. Pubertal breast hypertrophy in association with AEXS has been described in two young girls.Fertility, though usually affected to one degree or another—especially in males—is not always impaired significantly enough to prevent sexual reproduction, as evidenced by vertical transmission of the condition by both sexes. Cause The root cause of AEXS is not entirely clear, but it has been elucidated that inheritable, autosomal dominant genetic mutations affecting CYP19A1, the gene which encodes aromatase, are involved in its etiology. Different mutations are associated with differential severity of symptoms, such as mild to severe gynecomastia. For example, duplications result in relatively mild gynecomastia, while deletions, resulting in chimeric genes, cause moderate or severe gynecomastia. Diagnosis Genetic tests are now available to identify the variants in CYP19A1 associated with AEXS. The National Institutes of Health maintains a list. Treatment Several treatments have been found to be effective in managing AEXS, including aromatase inhibitors and gonadotropin-releasing hormone analogues in both sexes, androgen replacement therapy with non-aromatizable androgens such as DHT in males, and progestogens (which, by virtue of their antigonadotropic properties at high doses, suppress estrogen levels) in females. In addition, male patients often seek bilateral mastectomy, whereas females may opt for breast reduction if warranted.Medical treatment of AEXS is not absolutely necessary, but it is recommended as the condition, if left untreated, may lead to excessively large breasts (which may necessitate surgical reduction), problems with fertility, and an increased risk of endometriosis and estrogen-dependent cancers such as breast and endometrial cancers later in life. At least one case of male breast cancer has been reported. Society and culture Names AEXS has also been referred to as familial hyperestrogenism, familial gynecomastia, and familial adrenal feminization. Notable cases It has been hypothesized that the Pharaoh Akhenaten (husband of Queen Nefertiti) and other members of the 18th Dynasty of ancient Egypt may have had AEXS. Akhenaten and his relatives, including men and young girls, many of whom were the product of inbreeding, are described as having breasts and wide hips, and Akhenaten was described as having a "beautiful and feminine voice," unusual physical features that could be explained by AEXS or another form of hereditary hyperestrogenism. However, numerous other physical abnormalities were also present in the Akhenaten family, and a variety of other conditions have been proposed to explain the observations instead. Most recently, Loeys–Dietz syndrome was proposed as a probable cause, with gynecomastia and feminization possibly being caused by liver cirrhosis-induced hyperestrogenism. See also Androgen insensitivity syndrome Aromatase deficiency Congenital estrogen deficiency Disorders of sex development Estrogen insensitivity syndrome Hyperestrogenism Inborn errors of steroid metabolism Intersex References == External links ==

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I'm trying to understand 'Tiagabine' within a medical context. Could you shed some light on it?

Tiagabine (trade name Gabitril) is an anticonvulsant medication produced by Cephalon that is used in the treatment of epilepsy. The drug is also used off-label in the treatment of anxiety disorders and panic disorder. Medical uses Tiagabine is approved by U.S. Food and Drug Administration (FDA) as an adjunctive treatment for partial seizures in individuals of age 12 and up. It may also be prescribed off-label by physicians to treat anxiety disorders and panic disorder as well as neuropathic pain (including fibromyalgia). For anxiety and neuropathic pain, tiagabine is used primarily to augment other treatments. Tiagabine may be used alongside selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, or benzodiazepines for anxiety, or antidepressants, gabapentin, other anticonvulsants, or opioids for neuropathic pain. It is effective as monotherapy and combination therapy with other antiepileptic drugs in the treatment of partial seizure.The American Academy of Sleep Medicines 2017 clinical practice guidelines recommended against the use of tiagabine in the treatment of insomnia due to poor effectiveness and very low quality of evidence. Side effects Side effects of tiagabine are dose related. The most common side effect of tiagabine is dizziness. Other side effects that have been observed with a rate of statistical significance relative to placebo include asthenia, somnolence, nervousness, memory impairment, tremor, headache, diarrhea, and depression. Adverse effects such as confusion, aphasia (difficulty speaking clearly)/stuttering, and paresthesia (a tingling sensation in the bodys extremities, particularly the hands and fingers) may occur at higher dosages of the drug (e.g., over 8 mg/day). Tiagabine may induce seizures in those without epilepsy, particularly if they are taking another drug which lowers the seizure threshold. There may be an increased risk of psychosis with tiagabine treatment, although data is mixed and inconclusive. Tiagabine can also reportedly interfere with visual color perception. Warning CNS depression Dermatologic reactions Generalized weakness Ophthalmic effects Suicidal ideation Overdose Tiagabine overdose can produce neurological symptoms such as lethargy, single or multiple seizures, status epilepticus, coma, confusion, agitation, tremors, dizziness, dystonias/abnormal posturing, and hallucinations, as well as respiratory depression, tachycardia, hypertension, and hypotension. Overdose may be fatal especially if the victim presents with severe respiratory depression and/or unresponsiveness. Pharmacology Tiagabine increases the level of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system, by blocking the GABA transporter 1 (GAT-1), and hence is classified as a GABA reuptake inhibitor (GRI). Pharmacodynamics Tiagabine is primarily used as an anticonvulsant in the treatment of epilepsy as a supplement. Although the exact mechanism by which Tiagabine exerts its antiseizure effect is unknown, it is thought to be related to its ability to increase the activity of gamma aminobutyric acid (GABA), the central nervous systems major inhibitory neurotransmitter. Tiagabine attaches to the GABA uptake carriers recognition sites. Tiagabine is thought to block GABA uptake into presynaptic neurons as a result of this action, allowing more GABA to be available for receptor binding on the surfaces of post-synaptic cells. Monitoring Parameters Seizure frequency, liver function tests , suicidality History Tiagabine was discovered at Novo Nordisk in Denmark in 1988 by a team of medicinal chemists and pharmacologists under the general direction of Claus Bræstrup. The drug was co-developed with Abbott Laboratories, in a 40/60 cost sharing deal, with Abbott paying a premium for licensing the IP from the Danish company.U.S. patents on tiagabine listed in the Orange Book expired in April 2016. See also CI-966 Deramciclane Nipecotic acid SKF-89976A References External links Gabitril(manufacturers website)

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I'm not familiar with the medical term 'Hydrogen peroxide - urea.' Could you provide some insights?

Hydrogen peroxide - urea (also called Hyperol, artizone, urea hydrogen peroxide, and UHP) is a solid composed of equal amounts of hydrogen peroxide and urea. This compound is a white crystalline solid which dissolves in water to give free hydrogen peroxide. Hydrogen peroxide - urea contains solid and water-free hydrogen peroxide, which offers a higher stability and better controllability than liquid hydrogen peroxide when used as an oxidizing agent. Often called carbamide peroxide in the dental office, it is used as a source of hydrogen peroxide for bleaching, disinfection, and oxidation. Production For the preparation of the complex, urea is dissolved in 30% hydrogen peroxide (molar ratio 2:3) at temperatures below 60 °C. upon cooling this solution, hydrogen peroxide - urea precipitates in the form of small platelets.Determination of the hydrogen peroxide content by titration with potassium permanganate solution gives a value of 35.4% which corresponds to 97.8% of the theoretical maximum value. The remaining impurity consists of urea. Akin to water of crystallization, hydrogen peroxide cocrystallizes with urea with the stoichiometry of 1:1. The compound is simply produced (on a scale of several hundred tonnes a year) by the dissolution of urea in excess concentrated hydrogen peroxide solution, followed by crystallization. The laboratory synthesis is analogous. Structure and properties The solid state structure of this adduct has been determined by neutron diffraction.Hydrogen peroxide-urea is a readily water-soluble, odorless, crystalline solid, which is available as white powder or colorless needles or platelets. Upon dissolving in various solvents, the 1:1 complex dissociates back to urea and hydrogen peroxide. So just like hydrogen peroxide, the (erroneously) so-called adduct is an oxidizer but the release at room temperature in the presence of catalysts proceeds in a controlled manner. Thus the compound is suitable as a safe substitute for the unstable aqueous solution of hydrogen peroxide. Because of the tendency for thermal decomposition, which accelerates at temperatures above 82 °C, it should not be heated above 60 °C, particularly in pure form. The solubility of commercial samples varies from 0.05 g/mL to more than 0.6 g/mL. Applications Disinfectant and bleaching agent Hydrogen peroxide - urea is mainly used as a disinfecting and bleaching agent in cosmetics and pharmaceuticals. As a drug, this compound is used in some preparations for the whitening of teeth. It is also used to relieve minor inflammation of gums, oral mucosal surfaces and lips including canker sores and dental irritation, and to emulsify and disperse earwax.Carbamide peroxide is also suitable as a disinfectant, e.g. for germ reduction on contact lens surfaces or as an antiseptic for mouthwashes, ear drops or for superficial wounds and ulcers. Reagent in organic synthesis In the laboratory, it is used as a more easily handled replacement for hydrogen peroxide. It has proven to be a stable, easy-to-handle and effective oxidizing agent which is readily controllable by a suitable choice of the reaction conditions. It delivers oxidation products in an environmentally friendly manner and often in high yields especially in the presence of organic catalysts such as cis-butenedioic anhydride or inorganic catalysts such as sodium tungstate. It converts thiols selectively to disulfides, secondary alcohols to ketones, sulfides to sulfoxides and sulfones, nitriles to amides, and N-heterocycles to amine oxides. Hydroxybenzaldehydes are converted to dihydroxybenzenes (Dakin reaction) and give, under suitable conditions, the corresponding benzoic acids. It oxidizes ketones to esters, in particular cyclic ketones, such as substituted cyclohexanones or cyclobutanones to give lactones (Baeyer-Villiger oxidation). The epoxidation of various alkenes in the presence of benzonitrile yields oxiranes in yields of 79 to 96%. The oxygen atom transferred to the alkene originates from the peroxoimide acid formed intermediately from benzonitrile. The resulting imidic acid tautomerizes to the benzamide. Safety The compound acts as a strong oxidizing agent and can cause skin irritation and severe eye damage. See also Sodium percarbonate References External links "Hydrogen peroxide urea adduct, UHP". Organic Chemistry Portal. "Carbamide Peroxide Monograph". Drugs.com.

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I'm trying to expand my medical knowledge. Can you elucidate the term 'Piezogenic papules'?

Painful fat herniation is foot pain caused by the herniation of fat through the thin fascial layers of the weight-bearing parts of the heel. The herniation results in small bumps called piezogenic pedal papules or piezogenic papules. Though piezogenic papules are most commonly found on the heel, they can also be found on the wrist and palm.Piezogenic papules are relatively common; in one population-based study, the prevalence was found to be 76%. They occur more frequently in runners, triathletes, and individuals exposed to long periods of standing. They are also common in individuals with connective tissue disorders, especially Ehlers–Danlos syndrome. However, due to their preponderance in the general population, the presence of piezogenic papules alone does not automatically indicate the presence of Ehlers–Danlos syndrome. In most cases, piezogenic papules are of little clinical significance. See also Skin lesion Tennis toe List of cutaneous conditions References == External links ==

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I'd like to learn more about the medical term 'Convex.' Can you provide some details?

Convex or convexity may refer to: Science and technology Convex lens, in optics Mathematics Convex set, containing the whole line segment that joins points Convex polygon, a polygon which encloses a convex set of points Convex polytope, a polytope with a convex set of points Convex metric space, a generalization of the convexity notion in abstract metric spaces Convex function, when the line segment between any two points on the graph of the function lies above or on the graph Convex conjugate, of a function Convexity (algebraic geometry), a restrictive technical condition for algebraic varieties originally introduced to analyze Kontsevich moduli spaces Economics and finance Convexity (finance), second derivatives in financial modeling generally Convexity in economics Bond convexity, a measure of the sensitivity of the duration of a bond to changes in interest rates Convex preferences, an individuals ordering of various outcomes Other uses Convex Computer, a former company that produced supercomputers See also List of convexity topics Non-convexity (economics), violations of the convexity assumptions of elementary economics Obtuse angle All pages with titles beginning with Convex

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Can you break down the meaning of the medical term 'Adverse drug reaction' for me?

An adverse drug reaction (ADR) is a harmful, unintended result caused by taking medication. ADRs may occur following a single dose or prolonged administration of a drug or result from the combination of two or more drugs. The meaning of this term differs from the term "side effect" because side effects can be beneficial as well as detrimental. The study of ADRs is the concern of the field known as pharmacovigilance. An adverse drug event (ADE) refers to any unexpected and inappropriate occurrence at the time a drug is used, whether or not associated with the administration of the drug. An ADR is a special type of ADE in which a causative relationship can be shown. ADRs are only one type of medication-related harm, as harm can also be caused by omitting to take indicated medications. Classification ADRs may be classified by e.g. cause and severity. Cause Type A: Augmented pharmacologic effects - dose dependent and predictableType A reactions, which constitute approximately 80% of adverse drug reactions, are usually a consequence of the drugs primary pharmacological effect (e.g. bleeding when using the anticoagulant warfarin) or a low therapeutic index of the drug (e.g. nausea from digoxin), and they are therefore predictable. They are dose-related and usually mild, although they may be serious or even fatal (e.g. intracranial bleeding from warfarin). Such reactions are usually due to inappropriate dosage, especially when drug elimination is impaired. The term side effects is often applied to minor type A reactions.Type B: IdiosyncraticTypes A and B were proposed in the 1970s, and the other types were proposed subsequently when the first two proved insufficient to classify ADRs. Seriousness The U.S Food and Drug Administration defines a serious adverse event as one when the patient outcome is one of the following: Death Life-threatening Hospitalization (initial or prolonged) Disability - significant, persistent, or permanent change, impairment, damage or disruption in the patients body function/structure, physical activities or quality of life. Congenital abnormality Requires intervention to prevent permanent impairment or damageSeverity is a point on an arbitrary scale of intensity of the adverse event in question. The terms "severe" and "serious", when applied to adverse events, are technically very different. They are easily confused but can not be used interchangeably, requiring care in usage. A headache is severe if it causes intense pain. There are scales like "visual analog scale" that help clinicians assess the severity. On the other hand, a headache is not usually serious (but may be in case of subarachnoid haemorrhage, subdural bleed, even a migraine may temporally fit criteria), unless it also satisfies the criteria for seriousness listed above. Location Adverse effects may be local, i.e. limited to a certain location, or systemic, where medication has caused adverse effects throughout the systemic circulation. For instance, some ocular antihypertensives cause systemic effects, although they are administered locally as eye drops, since a fraction escapes to the systemic circulation. Mechanisms As research better explains the biochemistry of drug use, fewer ADRs are Type B and more are Type A. Common mechanisms are: Abnormal pharmacokinetics due to genetic factors comorbid disease states Synergistic effects between either a drug and a disease two drugs Antagonism effects between either a drug and a disease two drugs Abnormal pharmacokinetics Comorbid disease states Various diseases, especially those that cause renal or hepatic insufficiency, may alter drug metabolism. Resources are available that report changes in a drugs metabolism due to disease states.The Medication Appropriateness Tool for Comorbid Health Conditions in Dementia (MATCH-D) criteria warns that people with dementia are more likely to experience adverse effects, and that they are less likely to be able to reliably report symptoms. Genetic factors Abnormal drug metabolism may be due to inherited factors of either Phase I oxidation or Phase II conjugation. Pharmacogenomics is the study of the inherited basis for abnormal drug reactions. Phase I reactions Inheriting abnormal alleles of cytochrome P450 can alter drug metabolism. Tables are available to check for drug interactions due to P450 interactions.Inheriting abnormal butyrylcholinesterase (pseudocholinesterase) may affect metabolism of drugs such as succinylcholine Phase II reactions Inheriting abnormal N-acetyltransferase which conjugated some drugs to facilitate excretion may affect the metabolism of drugs such as isoniazid, hydralazine, and procainamide.Inheriting abnormal thiopurine S-methyltransferase may affect the metabolism of the thiopurine drugs mercaptopurine and azathioprine. Interactions with other drugs The risk of drug interactions is increased with polypharmacy. Protein binding These interactions are usually transient and mild until a new steady state is achieved. These are mainly for drugs without much first-pass liver metabolism. The principal plasma proteins for drug binding are: albumin α1-acid glycoprotein lipoproteinsSome drug interactions with warfarin are due to changes in protein binding. Cytochrome P450 Patients have abnormal metabolism by cytochrome P450 due to either inheriting abnormal alleles or due to drug interactions. Tables are available to check for drug interactions due to P450 interactions. Synergistic effects An example of synergism is two drugs that both prolong the QT interval. Assessing causality Causality assessment is used to determine the likelihood that a drug caused a suspected ADR. There are a number of different methods used to judge causation, including the Naranjo algorithm, the Venulet algorithm and the WHO causality term assessment criteria. Each have pros and cons associated with their use and most require some level of expert judgement to apply. An ADR should not be labeled as certain unless the ADR abates with a challenge-dechallenge-rechallenge protocol (stopping and starting the agent in question). The chronology of the onset of the suspected ADR is important, as another substance or factor may be implicated as a cause; co-prescribed medications and underlying psychiatric conditions may be factors in the ADR.Assigning causality to a specific agent often proves difficult, unless the event is found during a clinical study or large databases are used. Both methods have difficulties and can be fraught with error. Even in clinical studies some ADRs may be missed as large numbers of test individuals are required to find that adverse drug reaction. Psychiatric ADRs are often missed as they are grouped together in the questionnaires used to assess the population. Monitoring bodies Many countries have official bodies that monitor drug safety and reactions. On an international level, the WHO runs the Uppsala Monitoring Centre, and the European Union runs the European Medicines Agency (EMA). In the United States, the Food and Drug Administration (FDA) is responsible for monitoring post-marketing studies. In Canada, the Marketed Health Products Directorate of Health Canada is responsible for the surveillance of marketed health products. In Australia, the Therapeutic Goods Administration (TGA) conducts postmarket monitoring of therapeutic products. In the UK the Yellow Card Scheme was established in 1963. Epidemiology A study by the Agency for Healthcare Research and Quality (AHRQ) found that in 2011, sedatives and hypnotics were a leading source for adverse drug events seen in the hospital setting. Approximately 2.8% of all ADEs present on admission and 4.4% of ADEs that originated during a hospital stay were caused by a sedative or hypnotic drug. A second study by AHRQ found that in 2011, the most common specifically identified causes of adverse drug events that originated during hospital stays in the U.S. were steroids, antibiotics, opiates/narcotics, and anticoagulants. Patients treated in urban teaching hospitals had higher rates of ADEs involving antibiotics and opiates/narcotics compared to those treated in urban nonteaching hospitals. Those treated in private, nonprofit hospitals had higher rates of most ADE causes compared to patients treated in public or private, for-profit hospitals.MRH is common after hospital discharge in older adults, but methodological inconsistencies between studies and a paucity of data on risk factors limits clear understanding of the epidemiology. There was a wide range in incidence, from 0.4% to 51.2% of participants, and 35% to 59% of harm was preventable. Medication related harm incidence within 30 days after discharge ranged from 167 to 500 events per 1,000 individuals discharged (17–51% of individuals).In the U.S., females had a higher rate of ADEs involving opiates and narcotics than males in 2011, while male patients had a higher rate of anticoagulant ADEs. Nearly 8 in 1,000 adults aged 65 years or older experienced one of the four most common ADEs (steroids, antibiotics, opiates/narcotics, and anticoagulants) during hospitalization. A study showed that 48% of patients had an adverse drug reaction to at least one drug, and pharmacist involvement helps to pick up adverse drug reactions.In 2012, McKinsey & Company concluded that the cost of the 50-100 million preventable error-related adverse drug events would be between US$18–115 billion. See also References Further reading Incidence of adverse drug reactions in human immune deficiency virus-positive patients using highly active antiretroviral therapy PMC 3312730 == External links ==

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What is the significance of the term 'Miltefosine' in the medical field?

Miltefosine, sold under the trade name Impavido among others, is a medication mainly used to treat leishmaniasis and free-living amoeba infections such as Naegleria fowleri and Balamuthia mandrillaris. This includes the three forms of leishmaniasis: cutaneous, visceral and mucosal. It may be used with liposomal amphotericin B or paromomycin. It is taken by mouth.Common side effects include vomiting, abdominal pain, fever, headaches, and decreased kidney function. More severe side effects may include Stevens–Johnson syndrome or low blood platelets. Use during pregnancy appears to cause harm to the baby and use during breastfeeding is not recommended. How it works is not entirely clear.Miltefosine was first made in the early 1980s and studied as a treatment for cancer. A few years later it was found to be useful for leishmaniasis and was approved for this use in 2002 in India. It is on the World Health Organizations List of Essential Medicines. Medical uses Leishmaniasis Miltefosine is primarily used for the treatment of visceral and New World cutaneous leishmaniasis, and is undergoing clinical trials for this use in several countries. This drug is now listed as a core medication for the treatment of leishmaniasis under the WHO Model List of Essential Medicines. Several medical agents have some efficacy against visceral or cutaneous leishmaniasis, however, a 2005 survey concluded that miltefosine is the only effective oral treatment for both forms of leishmaniasis. Amoeba infections Miltefosine has been used successfully in some cases of the very rare, but highly lethal, brain infection by the amoeba, Naegleria fowleri, acquired through water entering the nose during a plunge in contaminated water. It has orphan drug status in the United States for acanthamoeba keratitis and primary amebic meningoencephalitis (PAM). Pregnancy and breastfeeding Miltefosine is listed as pregnancy category D by the FDA. This means there is evidence-based adverse reaction data from investigational or marketing experience or studies in humans of harm to the human fetus. Despite this evidence, the potential benefits of miltefosine may warrant use of the drug in pregnant women despite potential risks. A pregnancy test should be done prior to starting treatment. Effective birth control should be used while on miltefosine and 5 months after discontinuation of treatment. Its use during breast feeding is most likely unsafe. Contraindications Miltefosine is contraindicated in individuals who have a hypersensitivity to this medication, pregnant women, and people who have the Sjögren-Larsson syndrome. It is embryotoxic and fetotoxic in rats and rabbits, and teratogenic in rats but not in rabbits. It is therefore contraindicated for use during pregnancy, and contraception is required beyond the end of treatment in women of child-bearing age. Side effects Common side effects from miltefosine treatment are nausea and vomiting, which occur in 60% of people. Other common side effects are dizziness, headache, and daytime sleepiness.Serious side effects include rash, diarrhea, and arthritis. The side effects are more severe in women and young children. The overall effects are quite mild and easily reversed. Mechanism of action Miltefosine primarily acts on Leishmania by affecting the speciess promastigote and amastigote stages. Miltefosine exerts its activity by interacting with lipids, inhibiting cytochrome c oxidase and causing apoptosis-like cell death. This may affect membrane integrity and mitochondrial function of the parasite. History Cancer While initially studied as a cancer medication, due to side effects it was never used for this purpose.Phospholipid group alkylphosphocholine were known since the early 1980s, particularly in terms of their binding affinity with cobra venom. In 1987 the phospholipids were found to be potent toxins on leukemic cell culture. Initial in vivo investigation on the antineoplastic activity showed positive result, but then only at high dosage and at high toxicity. At the same time in Germany, Hansjörg Eibl, at the Max Planck Institute for Biophysical Chemistry, and Clemens Unger, at the University of Göttingen, demonstrated that the antineoplastic activity of the phospholipid analogue miltefosine (at the time known as hexadecylphosphocholine) was indeed tumour-specific. It was highly effective against methylnitrosourea-induced mammary carcinoma, but less so on transplantable mammary carcinomas and autochthonous benzo(a)pyrene-induced sarcomas, and relatively inactive on Walker 256 carcinosarcoma and autochthonous acetoxymethylmethylnitrosamine-induced colonic tumors of rats. It was subsequently found that miltefosine was structurally unique among lipids having anticancer property in that it lacks the glycerol group, is highly selective on cell types and acts through different mechanism. Leishmaniasis In the same year as the discovery of the anticancer property, miltefosine was reported by S. L. Croft and his team at the London School of Hygiene and Tropical Medicine as having antileishmanial effect as well. The compound was effective against Leishmania donovani amastigotes in cultured mouse peritoneal macrophages at a dose of 12.8 mg/kg/day in a five-day course. However, priority was given to the development of the compound for cutaneous metastases of breast cancer. In 1992 a new research was reported in which the compound was highly effective in mouse against different life cycle stages of different Leishmania species, and in fact, more potent than the conventional sodium stibogluconate therapy by a factor of more than 600. Results of the first clinical trial in humans were reported from Indian patients with chronic leishmaniasis with high degree of success and safety. This promising development promulgated a unique public–private partnership collaboration between ASTA Medica (later Zentaris GmbH), the World Health Organization (WHO) Special Programme for Research and Training in Tropical Diseases, and the Government of India. Eventually, several successful Phase II and III trials led to the approval of miltefosine in 2002 as the first and only oral drug for leishmaniasis. Naegleria fowleri and Acanthamoeba In 2013, the US Centers for Disease Control and Prevention recommended miltefosine for the treatment of free-living amoeba infections such as granulomatous amoebic encephalitis and primary amoebic meningoencephalitis, two fatal protozoal diseases. Historically, only four survivors have been recorded out of 138 confirmed infections in North America. One American survived the infection in 1978 and one individual from Mexico in 2003. In 2013, two children survived and recovered from primary amoebic meningoencephalitis after treatment with miltefosine. In 2016 after treatment that included miltefosine, another child became the fourth person in the United States to survive Naegleria fowleri infection. Society and culture Availability Since 2017 Miltefosine is commercially available in the United States through Profounda. Previously one could only get it from the CDC for emergency use under an expanded access IND protocol for treatment of free-living amoeba (FLA) infections: primary amoebic meningoencephalitis caused by Naegleria fowleri and granulomatous amoebic encephalitis caused by Balamuthia mandrillaris and Acanthamoeba species. Miltefosine is almost exclusively produced by Profounda, a private pharmaceutical company. Economics In the developing world a course of treatment costs US$65 to $150. In the developed world treatment may be 10 to 50 times greater. Further research It is active against some bacteria and fungi, as well as human trematode Schistosoma mansoni and the snail that spreads it Biomphalaria alexandrina. Antiprotozoal and antifungal activities Miltefosine is being investigated by researchers interested in finding treatments for infections which have become resistant to existing drugs. Animal and in vitro studies suggest it may have broad anti-protozoal and anti-fungal properties: Animal studies suggest miltefosine may also be effective against Trypanosoma cruzi, the parasite responsible for Chagas disease. Several studies have found the drug to be effective against types of fungus: Cryptococcus neoformans, Candida, Aspergillus and Fusarium. A 2006 in vitro study found that miltefosine is effective against metronidazole-resistant variants of Trichomonas vaginalis, a sexually transmitted protozoal disease. Cetrimonium bromide, a compound related to miltefosine, was demonstrated in 2007 to exhibit potent in vitro activity against Plasmodium falciparum. An in vitro test in 2006 showed that miltefosine is effective against the deadly protozoan pathogens, Naegleria fowleri, Balamuthia mandrillaris, and Acanthamoeba. However, later studies showed that it is not as potent as other drugs, such as chlorpromazine and diminazene aceturate (Berenil). In 2013, there were reports of failure of miltefosine in the treatment of leishmaniasis. Although drug resistance was suspected, studies in 2014 reported that miltefosine is not so effective in children, most probably related to a lack of drug exposure in children. Moverover, males appeared to have a higher probability of relapse as well. A 2012 in vitro study found that miltefosine had promising activity against Candida albicans biofilms. Anti-HIV activity Miltefosine targets HIV infected macrophages, which play a role in vivo as long-lived HIV-1 reservoirs. The HIV protein Tat activates pro-survival PI3K/Akt pathway in primary human macrophages. Miltefosine acts by inhibiting the PI3K/Akt pathway, thus removing the infected macrophages from circulation, without affecting healthy cells. It significantly reduces replication of HIV-1 in cocultures of human dendritic cells (DCs) and CD4+ T cells, which is due to a rapid secretion of soluble factors and is associated with induction of type-I interferon (IFN) in the human cells. References External links "Miltefosine". Drug Information Portal. U.S. National Library of Medicine. Max Planck Innovation FDA Panel Endorses Miltefosine for Leishmaniasis Med India Drugs.com

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

I've encountered the term 'Ranula' while reading about medical topics. What does it refer to exactly?

A ranula is a mucus extravasation cyst involving a sublingual gland and is a type of mucocele found on the floor of the mouth. Ranulae present as a swelling of connective tissue consisting of collected mucin from a ruptured salivary gland caused by local trauma. If small and asymptomatic further treatment may not be needed, otherwise minor oral surgery may be indicated. Signs and symptoms A ranula usually presents as a translucent, blue, dome-shaped, fluctuant swelling in the tissues of the floor of the mouth. If the lesion is deeper, then there is a greater thickness of tissue separating from the oral cavity and the blue translucent appearance may not be a feature. A ranula can develop into a large lesion many centimeters in diameter, with resultant elevation of the tongue and possibly interfering with swallowing (dysphagia). The swelling is not fixed, may not show blanching, and is non-painful unless it becomes secondarily infected. The usual location is lateral to the midline, which may be used to help distinguish it from a midline dermoid cyst. A cervical ranula presents as a swelling in the neck, with or without a swelling in the mouth. In common with other mucoceles, ranulae may rupture and then cause recurrent swelling. Ranulae may be asymptomatic, although they can fluctuate rapidly in size, shrinking and swelling, making them difficult to detect. Complications Infection Repeated trauma Bursting and reformation Dysphagia (in the case of a large ranula) Causes Minor trauma to the floor of the mouth is thought to damage the delicate ducts that drain saliva from the sublingual gland into the oral cavity. The lesion is a mucous extravasation cyst (mucocele) of the floor of mouth, although a ranula is often larger than other mucoceles (mainly because the overlying mucosa is thicker). They can grow so large that they fill the mouth. The most usual source of the mucin spillage is the sublingual salivary gland, but ranulae may also arise from the submandibular duct or the minor salivary glands in the floor of the mouth. A cervical ranula occurs when the spilled mucin dissects its way through the mylohyoid muscle, which separates the sublingual space from the submandibular space, and creates a swelling in the neck. It may occur following rupture of a simple ranula. Rarely, ranulae may extend backwards into the parapharyngeal space. Mechanism The fluid within a ranula has the viscous, jellylike consistency of egg white. Diagnosis The histologic appearance is similar to mucoceles from other locations. The spilled mucin causes a granulation tissue to form, which usually contains foamy histiocytes. Ultrasound and magnetic resonance imaging may be useful to image the lesion. A small squamous cell carcinoma obstructing the Wharton duct may require clinical examination to be distinguished from a ranula. Criteria Mostly seen in young children and adolescents, both sexes are equally affected. Swelling in floor of mouth, which may be painful. Mostly unilateral, on one side of frenulum. Shape is spherical Size varies from 1 – 5 cm in diameter Color is pale blue with characteristics semi transparent appearance. Surface is smooth and mucous membrane is mobile over the swelling. Tenderness is absent Fluctuation test is positive Transillumination test is positive Cervical lymph nodes are not enlarged. May or may not have prolongation in the neck. Classification A ranula is a type of mucocele, and therefore could be classified as a disorder of the salivary glands. Usually a ranula is confined to the floor of the mouth (termed a "simple ranula"). An unusual variant is the cervical ranula (also called a plunging or diving ranula), where the swelling is in the neck rather than the floor of the mouth. The term ranula is also sometimes used to refer to other similar swellings of the floor of mouth such as true salivary duct cysts, dermoid cysts and cystic hygromas. The Latin word rana means "frog" (ranula = "little frog"). Treatment Treatment of ranulae usually involves removal of the sublingual gland. Surgery may not be required if the ranula is small and asymptomatic. Marsupialization may sometimes be used, where the intra-oral lesion is opened to the oral cavity with the aim of allowing the sublingual gland to re-establish connection with the oral cavity. Epidemiology The lesion is usually present in children. Ranulae are the most common pathologic lesion associated with the sublingual glands. Other animals References Kahn, Michael A. Basic Oral and Maxillofacial Pathology. Volume 1. 2001. External links DermAtlas 259163774

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I'm not familiar with the medical term 'Leukocoria.' Could you provide some insights?

Leukocoria (also white pupillary reflex) is an abnormal white reflection from the retina of the eye. Leukocoria resembles eyeshine, but leukocoria can also occur in animals that lack eyeshine because their retina lacks a tapetum lucidum. Leukocoria is a medical sign for a number of conditions, including Coats disease, congenital cataract, corneal scarring, melanoma of the ciliary body, Norrie disease, ocular toxocariasis, persistence of the tunica vasculosa lentis (PFV/PHPV), retinoblastoma, and retrolental fibroplasia. Because of the potentially life-threatening nature of retinoblastoma, a cancer, that condition is usually considered in the evaluation of leukocoria. In some rare cases (1%) the leukocoria is caused by Coats disease (leaking retinal vessels). Diagnosis On photographs taken using a flash, instead of the familiar red-eye effect, leukocoria can cause a bright white reflection in an affected eye. Leukocoria may appear also in low indirect light, similar to eyeshine. Leukocoria can be detected by a routine eye exam (see Ophthalmoscopy). For screening purposes, the red reflex test is used. In this test, when a light is shone briefly through the pupil, an orange red reflection is normal. A white reflection is leukocoria. Society The fictional serial killer known as "The Collector", the main antagonist of the films The Collector (2009) and The Collection (2012), had the condition in both eyes. (confirmed by first movie actor Juan Fernández de Alarcon) References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

I'm encountering the term 'Dental abscess' in medical literature. What's its definition?

A dental abscess is a localized collection of pus associated with a tooth. The most common type of dental abscess is a periapical abscess, and the second most common is a periodontal abscess. In a periapical abscess, usually the origin is a bacterial infection that has accumulated in the soft, often dead, pulp of the tooth. This can be caused by tooth decay, broken teeth or extensive periodontal disease (or combinations of these factors). A failed root canal treatment may also create a similar abscess. A dental abscess is a type of odontogenic infection, although commonly the latter term is applied to an infection which has spread outside the local region around the causative tooth. Classification The main types of dental abscess are: Periapical abscess: The result of a chronic, localized infection located at the tip, or apex, of the root of a tooth. Periodontal abscess: begins in a periodontal pocket (see: periodontal abscess) Gingival abscess: involving only the gum tissue, without affecting either the tooth or the periodontal ligament (see: periodontal abscess) Pericoronal abscess: involving the soft tissues surrounding the crown of a tooth (see: Pericoronitis) Combined periodontic-endodontic abscess: a situation in which a periapical abscess and a periodontal abscess have combined (see: Combined periodontic-endodontic lesions). Signs and symptoms The pain is continuous and may be described as extreme, growing, sharp, shooting, or throbbing. Putting pressure or warmth on the tooth may induce extreme pain. The area may be sensitive to touch and possibly swollen as well. This swelling may be present at either the base of the tooth, the gum, and/or the cheek, and sometimes can be reduced by applying ice packs. An acute abscess may be painless but still have a swelling present on the gum. It is important to get anything that presents like this checked by a dental professional as it may become chronic later. In some cases, a tooth abscess may perforate bone and start draining into the surrounding tissues creating local facial swelling. In some cases, the lymph glands in the neck will become swollen and tender in response to the infection. It may even feel like a migraine as the pain can transfer from the infected area. The pain does not normally transfer across the face, only upwards or downwards as the nerves that serve each side of the face are separate. Severe aching and discomfort on the side of the face where the tooth is infected is also fairly common, with the tooth itself becoming unbearable to touch due to extreme amounts of pain. Complications If left untreated, a severe tooth abscess may become large enough to perforate bone and extend into the soft tissue eventually becoming osteomyelitis and cellulitis respectively. From there it follows the path of least resistance and may spread either internally or externally. The path of the infection is influenced by such things as the location of the infected tooth and the thickness of the bone, muscle and fascia attachments. External drainage may begin as a boil which bursts allowing pus drainage from the abscess, intraorally (usually through the gum) or extraorally. Chronic drainage will allow an epithelial lining to form in this communication to form a pus draining canal (fistula). Sometimes this type of drainage will immediately relieve some of the painful symptoms associated with the pressure. Internal drainage is of more concern as growing infection makes space within the tissues surrounding the infection. Severe complications requiring immediate hospitalization include Ludwigs angina, which is a combination of growing infection and cellulitis which closes the airway space causing suffocation in extreme cases. Also infection can spread down the tissue spaces to the mediastinum which has significant consequences on the vital organs such as the heart. Another complication, usually from upper teeth, is a risk of sepsis traveling through pathways to which it can possibly lead to endocarditis, brain abscess (extremely rare), or meningitis (also rare). Depending on the severity of the infection, the sufferer may feel only mildly ill, or may in extreme cases require hospital care. Diagnostic A periodontal abscess may be difficult to distinguish from a periapical abscess. Indeed, sometimes they can occur together. Since the management of a periodontal abscess is different from that of a periapical abscess, this differentiation is important to make. If the swelling is over the area of the root apex, it is more likely to be a periapical abscess; if it is closer to the gingival margin, it is more likely to be a periodontal abscess. Similarly, in a periodontal abscess pus most likely discharges via the periodontal pocket, whereas a periapical abscess generally drains via a parulis nearer to the apex of the involved tooth. If the tooth has pre-existing periodontal disease, with pockets and loss of alveolar bone height, it is more likely to be a periodontal abscess; whereas if the tooth has relatively healthy periodontal condition, it is more likely to be a periapical abscess. In periodontal abscesses, the swelling usually precedes the pain, and in periapical abscesses, the pain usually precedes the swelling. A history of toothache with sensitivity to hot and cold suggests previous pulpitis, and indicates that a periapical abscess is more likely. If the tooth gives normal results on pulp sensibility testing, is free of dental caries and has no large restorations; it is more likely to be a periodontal abscess. A dental radiograph is of little help in the early stages of a dental abscess, but later usually the position of the abscess, and hence indication of endodontal/periodontal etiology can be determined. If there is a sinus, a gutta percha point is sometimes inserted before the x-ray in the hope that it will point to the origin of the infection. Generally, periodontal abscesses will be more tender to lateral percussion than to vertical, and periapical abscesses will be more tender to apical percussion. Treatment Successful treatment of a dental abscess centers on the reduction and elimination of the offending organisms. This can include treatment with antibiotics and drainage, however, it has become widely recommended that dentists should improve the antibiotic prescribing practices, by limiting the prescriptions to the acute cases that suffer from the severe signs of spreading infection, in an attempt to overcome the development of antibiotic-resistant bacterial strains in the population. A 2018 Cochrane review has found insufficient evidence to rule out if patients with acute dental abscesses can benefit from antibiotic prescriptions.If the tooth can be restored, root canal therapy can be performed. Non-restorable teeth must be extracted, followed by curettage of all apical soft tissue. Unless they are symptomatic, teeth treated with root canal therapy should be evaluated at 1- and 2-year intervals after the root canal therapy to rule out possible lesional enlargement and to ensure appropriate healing. Abscesses may fail to heal for several reasons: Cyst formation Inadequate root canal therapy Vertical root fractures Foreign material in the lesion Associated periodontal disease Penetration of the maxillary sinusFollowing conventional, adequate root canal therapy, abscesses that do not heal or enlarge are often treated with surgery and filling the root tips; and will require a biopsy to evaluate the diagnosis. See also Barodontalgia Focal infection theory Intraoral dental sinus References == External links ==

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

Please help me grasp the concept behind the medical term 'Normal pressure hydrocephalus.'

Normal-pressure hydrocephalus (NPH), also called malresorptive hydrocephalus, is a form of communicating hydrocephalus in which excess cerebrospinal fluid (CSF) occurs in the ventricles, and with normal or slightly elevated cerebrospinal fluid pressure. As the fluid builds up, it causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications. The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problens/gait deviations (note: this diagnosis method is obsolete). The disease was first described by Salomón Hakim and Adams in 1965.The treatment is surgical placement of a ventriculoperitoneal shunt to drain excess CSF into the lining of the abdomen where the CSF will eventually be absorbed. NPH is often misdiagnosed as other conditions including Parkinsons disease (due to gait) or Alzheimers disease (due to cognitive dysfunction). Signs and symptoms NPH exhibits a classic triad of clinical findings (known as the Adams triad or Hakims triad). The triad consists of walking difficulty, reduced attention span, and urinary frequency or incontinence. The triad is considered obsolete for diagnosis purposes and newer guidelines are available.Gait deviations are present in nearly all patients and usually the first symptom. This is caused by expansion of the lateral ventricles to impinge on the corticospinal tract motor fibers. The typical gait abnormality in NPH is a broad-based, slow, short-stepped, "stuck to the floor", or "magnetic" movement. The gait abnormalities in NPH may bear resemblance to a gait associated with Parkinsons disease. The gait deviation can be classified as mild, marked, or severe: "marked" is when the patient has difficulty walking because of considerable instability; "severe" is when it is not possible for the patient to walk without aids (such as a cane or a wheeled walker).Dementia presents as progressive cognitive impairment which is present in 60% of patients at time of treatment. This is caused by distortions predominantly at the frontal lobe and the subcortex. Initial deficits involve planning, organization, attention, and concentration. Further deficits include difficulty managing finances, taking medications, driving, keeping track of appointments, daytime sleeping, short-term memory impairments, and psychomotor slowing. Late stage features include apathy, reduced drive, slowed thinking, and reduced speech. Urinary incontinence appears late in the illness, and is present in 50% of patients at time of treatment. Urinary dysfunction begins as increased frequency often at night, and progresses to urge incontinence and permanent incontinence. Pathogenesis Every day, the body makes roughly 600–700 ml of CSF, and about the same amount is reabsorbed into the bloodstream. Hydrocephalus is due to an imbalance between the amount of fluid produced and its absorption rate. Enlarged ventricles put increased pressure on the adjacent cortical tissue and cause myriad effects in the patient, including distortion of the fibers in the corona radiata. This leads to an increase in intracranial pressure (ICP). The ICP gradually falls, but still remains slightly elevated, and the CSF pressure reaches a high normal level of 150 to 200 mm H2O. Measurements of ICP, therefore, are not usually elevated. Because of this, patients do not exhibit the classic signs that accompany increased intracranial pressure such as headache, nausea, vomiting, or altered consciousness, although some studies have shown pressure elevations to occur intermittently.The exact pathogenesis is unknown, but consensus on some mechanisms include: An imbalance exists between production and resorption of CSF. The resistance to CSF outflow is often elevated. The disease is not caused by overproduction of CSF or obstruction of CSF flow at the ventricles.The syndrome is often divided into two groups, primary (also called idiopathic) and secondary, based on cause. The underlying etiology of primary NPH has not yet been identified. Primary NPH affects adults age 40 years or older, most commonly affecting the elderly. Secondary NPH can affect persons of any age and occurs due to conditions such as subarachnoid hemorrhage, meningitis, brain surgery, brain radiation, or traumatic brain injury. Diagnosis Patients with suspected NPH should have typical symptoms in addition to ventricular enlargement on neuroimaging. The international evidenced-based diagnostic criteria for primary NPH are: Gradual onset after age 40 years, symptoms duration of ≥ 3–6 months, clinical evidence of gait or balance impairment, and impairment of cognition or urinary incontinence Imaging from magnetic resonance imaging (MRI) or computed tomography (CT) is needed to demonstrate enlarged ventricles and no macroscopic obstruction to cerebrospinal fluid flow. Imaging should show an enlargement to at least one of the temporal horns of lateral ventricles, and impingement against the falx cerebri resulting in a callosal angle ≤ 90° on the coronal view, showing evidence of altered brain water content, or normal active flow (which is referred to as "flow void") at the cerebral aqueduct and fourth ventricle.MRI scans are the preferred imaging. The distinction between normal and enlarged ventricular size by cerebral atrophy is difficult to ascertain. Up to 80% of cases are unrecognized and untreated due to difficulty of diagnosis. Imaging should also reveal the absence of any cerebral mass lesions or any signs of obstructions. Although all patients with NPH have enlarged ventricles, not all elderly patients with enlarged ventricles have primary NPH. Cerebral atrophy can cause enlarged ventricles, as well, and is referred to as hydrocephalus ex vacuo. The Miller Fisher test involves a high-volume lumbar puncture (LP) with removal of 30–50 ml of CSF. Gait and cognitive function are typically tested just before and within 2–3 hours after the LP to assess for signs of symptomatic improvement. The CSF infusion test and the lumbar test are similar tests to Miller Fisher test. The tests have a positive predictive value over 90%, but a negative predictive value less than 50%. The LP should show normal or mildly elevated CSF pressure. CSF should have normal cell contents, glucose levels, and protein levels. Treatment Ventriculoperitoneal shunts For suspected cases of NPH, CSF shunting is the first-line treatment. The most common type used to treat NPH is ventriculoperitoneal (VP) shunts, which drain CSF fluid to the peritoneal cavity. Adjustable valves allow fine-tuning of CSF drainage. NPH symptoms reportedly improve in 70–90% of patients with CSF shunt. Risk-benefit analyses have shown beyond any doubt that surgery for NPH is far better than conservative treatment or the natural course.Gait symptoms improve in ≥ 85% patients. Cognitive symptoms improve in up to 80% of patients when surgery is performed early in the disease course. Urgency and incontinence improves in up to 80% of patients, but only in ≤ 50–60% of patients with shunt implanted late in disease course. The most likely patients to show improvement are those who show only gait deviation, mild or no incontinence, and mild dementia. The risk of adverse events related to shunt placement is 11%, including shunt failure, infections such as ventriculitis, shunt obstruction, over- or under-drainage, and development of a subdural hematoma. Medications No medications are effective for primary NPH. Acetazolamide and other diuretics are not recommended except for limited use in patients who are not candidates for placement of a shunt. Epidemiology The majority of cases are primary NPH. Incidence is estimated to 0.3–3% in patients older than 60 years and raising with older age Its prevalence is reported to be less than 1% in persons under the age of 65, and up to 3% for persons aged 65 or older. No difference in incidence is seen between men and women. Among individuals with dementia, the incidence of NPH is thought to be between 2 and 6%. See also Low pressure hydrocephalus References External links The Normal Pressure Hydrocephalus Center at Johns Hopkins Bayview Medical Center Normal Pressure Hydrocephalus at Cleveland Clinic normal_pressure_hydrocephalus at NINDS When it really is NPH at Likvor Hydrocephalus in Adults at Spina Bifida Resource Center

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Can you break down the meaning of the medical term 'Ganglioneuroblastoma' for me?

Ganglioneuroblastoma is a variant of neuroblastoma that is surrounded by ganglion cells. It can be difficult to diagnose.Nodular ganglioneuroblastoma can be divided by prognosis. Neuroblastic tumors It is contained within the neuroblastic tumors group, which includes: Ganglioneuroma (benign) Ganglioneuroblastoma (intermediate). Neuroblastoma (aggressive) See also Neuroblastoma References == External links ==

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Can you break down the meaning of the medical term 'Hydrochlorothiazide' for me?

Hydrochlorothiazide is a diuretic medication often used to treat high blood pressure and swelling due to fluid build up. Other uses include treating diabetes insipidus and renal tubular acidosis and to decrease the risk of kidney stones in those with a high calcium level in the urine. Hydrochlorothiazide is less effective than chlortalidone for prevention of heart attack or stroke. Hydrochlorothiazide is taken by mouth and may be combined with other blood pressure medications as a single pill to increase effectiveness.Potential side effects include poor kidney function; electrolyte imbalances, including low blood potassium, and, less commonly, low blood sodium, gout, high blood sugar, and feeling lightheaded with standing. While allergies to hydrochlorothiazide are reported to occur more often in those with allergies to sulfa drugs, this association is not well supported. It may be used during pregnancy, but it is not a first-line medication in this group.It is in the thiazide medication class and acts by decreasing the kidneys ability to retain water. This initially reduces blood volume, decreasing blood return to the heart and thus cardiac output. It is believed to lower peripheral vascular resistance in the long run.Two companies, Merck and Ciba, state they discovered the medication which became commercially available in 1959. It is on the World Health Organizations List of Essential Medicines. It is available as a generic drug and is relatively affordable. In 2020, it was the eleventh most commonly prescribed medication in the United States, with more than 41 million prescriptions. Medical uses Hydrochlorothiazide is used for the treatment of hypertension, congestive heart failure, symptomatic edema, diabetes insipidus, renal tubular acidosis. It is also used for the prevention of kidney stones in those who have high levels of calcium in their urine.Multiple studies suggest hydrochlorothiazide could be used as initial monotherapy in people with primary hypertension; however, the decision should be weighed against the consequence of long-term adverse metabolic abnormalities. A review of randomised trials showed varying efficacy in cardiovascular outcomes on age, ethnicity and existing cardiovascular risks. A systematic, multinational, large-scale analysis by Suchard et al. supported equivalence between drug classes for initiating monotherapy in hypertension, however thiazide or thiazide-like diuretics showed better primary effectiveness and safety profiles than angiotensin-converting enzyme inhibitors and non-dihydropyridine calcium channel blockers.Hydrochlorothiazide is less potent but not necessarily less effective than chlorthalidone in reducing blood pressure. More robust studies are required to confirm which drug is superior in reducing cardiovascular events. Side effect profile for both drugs appear similar and are dose dependant.Hydrochlorothiazide is also sometimes used to prevent osteopenia and for treatment of hypoparathyroidism, hypercalciuria, Dents disease, and Ménières disease. For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and increasing the urine osmolality.A low level of evidence, predominantly from observational studies, suggests that thiazide diuretics have a modest beneficial effect on bone mineral density and are associated with a decreased fracture risk when compared with people not taking thiazides. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation.The combination of fixed-dose preparation such as losartan/hydrochlorothiazide has added advantages of a more potent antihypertensive effect with additional antihypertensive efficacy at the dose of 100 mg/25 mg when compared to monotherapy. Adverse effects Hypokalemia, or low blood levels of potassium are an occasional side effect. It can be usually prevented by potassium supplements or by combining hydrochlorothiazide with a potassium-sparing diuretic Other disturbances in the levels of serum electrolytes, including hypomagnesemia (low magnesium), hyponatremia (low sodium), and hypercalcemia (high calcium) Hyperuricemia (high levels of uric acid in the blood). All thiazide diuretics including hydrochlorothiazide can inhibit excretion of uric acid by the kidneys, thereby increasing serum concentrations of uric acid.This may increase the incidence of gout in doses of ≥ 25 mg per day and in more susceptible patients such as male gender of <60 years old. Hyperglycemia, high blood sugar Hyperlipidemia, high cholesterol and triglycerides Headache Nausea/vomiting Photosensitivity Weight gain PancreatitisPackage inserts contain vague and inconsistent data surrounding the use of thiazide diuretics in patients with allergies to sulfa drugs, with little evidence to support these statements. A retrospective cohort study conducted by Strom et al. concluded that there is an increased risk of an allergic reaction occurring in patients with a predisposition to allergic reactions in general rather than cross reactivity from structural components of the sulfonamide-based drug. Prescribers should examine the evidence carefully and assess each patient individually, paying particular attention to their prior history of sulfonamide hypersensitivity rather than relying on drug monograph information.There is an increased risk of non-melanoma skin cancer. In August 2020, the Australian Therapeutic Goods Administration required the Product Information (PI) and Consumer Medicine Information (CMI) for medicines containing hydrochlorothiazide to be updated to include details about an increased risk of non-melanoma skin cancer. In August 2020, the U.S. Food and Drug Administration (FDA) updated the drug label about an increased risk of non-melanoma skin cancer (basal cell skin cancer or squamous cell skin cancer). Mechanism of action Hydrochlorothiazide belongs to the thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na+) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral NaCl co-transporter by competing for the chloride site on the transporter. By impairing Na+ transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss. Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Additionally, by other mechanisms, hydrochlorothiazide is believed to lower peripheral vascular resistance. Dosage In a double-blind, randomized study, the effects of 25 mg/day vs. 50 mg/day of hydrochlorothiazide were evaluated in geriatric patients (n = 51) with isolated systolic hypertension. Both dosages were associated with similar reductions in blood pressure; however, the higher dose (50 mg/day) caused a greater decline in serum potassium concentration. Society and culture Brand names Hydrochlorothiazide is available as a generic drug under a large number of brand names, including Apo-Hydro, Aquazide, BPZide, Dichlotride, Esidrex, Hydrochlorot, Hydrodiuril, HydroSaluric, Hypothiazid, Microzide, Oretic and many others.To reduce pill burden and in order to reduce side effects, hydrochlorothiazide is often used in fixed-dose combinations with many other classes of antihypertensive drugs such as: ACE inhibitors — e.g. Prinzide or Zestoretic (with lisinopril), Co-Renitec (with enalapril), Capozide (with captopril), Accuretic (with quinapril), Monopril HCT (with fosinopril), Lotensin HCT (with benazepril), etc. Angiotensin receptor blockers — e.g. Hyzaar (with losartan), Co-Diovan or Diovan HCT (with valsartan), Teveten Plus (with eprosartan), Avalide or CoAprovel (with irbesartan), Atacand HCT or Atacand Plus (with candesartan), etc. Beta blockers — e.g. Ziac or Lodoz (with bisoprolol), Nebilet Plus or Nebilet HCT (with nebivolol), Dutoprol or Lopressor HCT (with metoprolol), etc. Direct renin inhibitors — e.g. Co-Rasilez or Tekturna HCT (with aliskiren) Potassium sparing diuretics: Dyazide and Maxzide triamterene Sport Use of hydrochlorothiazide is prohibited by the World Anti-Doping Agency for its ability to mask the use of performance-enhancing drugs. References External links "Hydrochlorothiazide". Drug Information Portal. U.S. National Library of Medicine.

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

Could you provide a brief overview of 'Idiopathic pneumonia syndrome' in a medical context?

Idiopathic pneumonia syndrome is a set of pneumonia-like symptoms that occur with no sign of infection in the lung. Idiopathic pneumonia syndrome is a serious condition that can occur after a stem cell transplant. It occurs between 2.2 and 15 percent of hematopoietic stem cell transplants. The incubation period ranges between 4 and 106 days, but mostly is about 22 days from transplant. Symptoms The symptoms are like pneumonia, and include fever, chills, coughing, and breathing problems. Lack of oxygen may also occur. Risk factors Risk factors for IPS can be old age, graft vs host disease, multi organ failure, and multiple organ failure. Diagnosis Treatment Treatment is only supportive, with steroids showing no effect. The need for mechanical ventilation is indicative of a poor prognosis. Steroids are often used, though often without effect. References Idiopathic pneumonia syndrome entry in the public domain NCI Dictionary of Cancer Terms This article incorporates public domain material from the U.S. National Cancer Institute document: "Dictionary of Cancer Terms".

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

Could you offer a clear explanation of the term 'Hypertrophic osteoarthropathy' as used in the medical field?

Hypertrophic osteoarthropathy is a medical condition combining clubbing and periostitis of the small hand joints, especially the distal interphalangeal joints and the metacarpophalangeal joints. Distal expansion of the long bones as well as painful, swollen joints and synovial villous proliferation are often seen. The condition may occur alone (primary), or it may be secondary to diseases like lung cancer. Among patients with lung cancer, it is most associated with adenocarcinoma and least associated with small cell lung cancer. These patients often get clubbing and increased bone deposition on long bones. Their presenting signs and symptoms are sometimes only clubbing and painful ankles. Cause Hypertrophic osteoarthropathy is one of many distant effect disorders due to cancer, with lung cancer being the most common cause but also occurring with ovarian or adrenal malignancies. A distant effect disorder, or a paraneoplastic syndrome, affects distant areas and thus is not related to local compression or obstruction effects from the tumor. Other paraneoplastic syndromes include hypercalcemia, SIADH, Cushings syndrome and a variety of neurological disorders. Thought to be due to fibrovascular proliferation caused by accumulation of megakaryocytes in the digital vessels which are normally filtered by the lungs. Diagnosis People with hypertrophic osteoarthropathy may have bone scans showing parallel lines of activity along the cortex of the shafts and ends of tibiae, femurs and radii; especially around the knees, ankles and wrists. This activity may decrease after treatment of the underlying cause. Treatment Non-steroidal anti-inflammatory drugs (NSAIDs) can give significant relief of the symptoms. Treatment of lung cancer or other causes of hypertrophic osteoarthropathy results in regression of symptoms for some patients. Etymology The eponymous Bamberger–Marie syndrome is named for Austrian internist Eugen von Bamberger and French neurologist Pierre Marie. See also Periosteal reaction Hypertrophic osteopathy References == External links ==

You serve as a guide in the medical field. Explain medical terms thoroughly, ensuring the information is both insightful and comprehensible.

What does the medical term 'Breast' encompass?

The breast is one of two prominences located on the upper ventral region of a primates torso. Both females and males develop breasts from the same embryological tissues. In females, it serves as the mammary gland, which produces and secretes milk to feed infants. Subcutaneous fat covers and envelops a network of ducts that converge on the nipple, and these tissues give the breast its size and shape. At the ends of the ducts are lobules, or clusters of alveoli, where milk is produced and stored in response to hormonal signals. During pregnancy, the breast responds to a complex interaction of hormones, including estrogens, progesterone, and prolactin, that mediate the completion of its development, namely lobuloalveolar maturation, in preparation of lactation and breastfeeding. Humans are the only animals with permanent breasts. At puberty, estrogens, in conjunction with growth hormone, cause permanent breast growth in female humans. This happens only to a much lesser extent in other primates—breast development in other primates generally only occurs with pregnancy. Along with their major function in providing nutrition for infants, female breasts have social and sexual characteristics. Breasts have been featured in ancient and modern sculpture, art, and photography. They can figure prominently in the perception of a womans body and sexual attractiveness. A number of cultures associate breasts with sexuality and tend to regard bare breasts in public as immodest or indecent. Breasts, especially the nipples, are an erogenous zone. Etymology and terminology The English word breast derives from the Old English word brēost (breast, bosom) from Proto-Germanic *breustam (breast), from the Proto-Indo-European base bhreus– (to swell, to sprout). The breast spelling conforms to the Scottish and North English dialectal pronunciations. The Merriam-Webster Dictionary states that "Middle English brest, [comes] from Old English brēost; akin to Old High German brust..., Old Irish brú [belly], [and] Russian bryukho"; the first known usage of the term was before the 12th century.A large number of colloquial terms for breasts are used in English, ranging from fairly polite terms to vulgar or slang. Some vulgar slang expressions may be considered to be derogatory or sexist to women. Evolutionary development Humans are the only mammals whose breasts become permanently enlarged after sexual maturity (known in humans as puberty). The reason for this evolutionary change was unknown. Several hypotheses have been put forward: A link has been proposed to processes for synthesizing the endogenous steroid hormone precursor dehydroepiandrosterone which takes place in fat rich regions of the body like the buttocks and breasts. These contributed to human brain development and played a part in increasing brain size. Breast enlargement may for this purpose may have occurred as early as Homo ergaster (1.7-1.4 MYA). Other breast formation hypotheses may have then taken over as principal drivers.It has been suggested by zoologists Avishag and Amotz Zahavi that the size of the human breasts can be explained by the handicap theory of sexual dimorphism. This would see the explanation for larger breasts as them being an honest display of the womens health and ability to grow and carry them in her life. Prospective mates can then evaluate the genes of a potential mate for their ability to sustain her health even with the additional energy demanding burden she is carrying.The zoologist Desmond Morris describes a sociobiological approach in his popular science book The Naked Ape. He suggests, by making comparisons with the other primates, that breasts evolved to replace swelling buttocks as a sex signal, of ovulation. He notes how humans have, relatively speaking, large penises as well as large breasts. Furthermore, early humans adopted bipedalism and face-to-face coitus. He therefore suggested enlarged sexual signals helped maintain the bond between a mated male and female even though they performed different duties and therefore were separated for lengths of time.The study The Evolution of the Human Breast (2001) proposed that the rounded shape of a womans breast evolved to prevent the sucking infant offspring from suffocating while feeding at the teat; that is, because of the human infants small jaw, which did not project from the face to reach the nipple, he or she might block the nostrils against the mothers breast if it were of a flatter form (cf. common chimpanzee). Theoretically, as the human jaw receded into the face, the womans body compensated with round breasts.Ashley Montague (1965) proposed that breasts came about as an adaptation for infant feeding for a different reason as early human ancestors adopted bipedalism and the loss of body hair. Human upright stance meant infants must be carried at the hip or shoulder instead of on the back as in the apes. This gives the infant less opportunity to find the nipple or the purchase to cling on to the mothers body hair. The mobility of the nipple on a large breast in most human females gives the infant more ability to find grasp it and feed.Other suggestions include simply that permanent breasts attracted mates, that "pendulous" breasts gave infants something to cling to, or that permanent breasts shared the function of a camels hump, to store fat as an energy reserve. Anatomy In women, the breasts overlie the pectoralis major muscles and extend on average from the level of the second rib to the level of the sixth rib in the front of the rib cage; thus, the breasts cover much of the chest area and the chest walls. At the front of the chest, the breast tissue can extend from the clavicle (collarbone) to the middle of the sternum (breastbone). At the sides of the chest, the breast tissue can extend into the axilla (armpit), and can reach as far to the back as the latissimus dorsi muscle, extending from the lower back to the humerus bone (the bone of the upper arm). As a mammary gland, the breast is composed of differing layers of tissue, predominantly two types: adipose tissue; and glandular tissue, which affects the lactation functions of the breasts.: 115 Morphologically the breast is tear-shaped. The superficial tissue layer (superficial fascia) is separated from the skin by 0.5–2.5 cm of subcutaneous fat (adipose tissue). The suspensory Coopers ligaments are fibrous-tissue prolongations that radiate from the superficial fascia to the skin envelope. The female adult breast contains 14–18 irregular lactiferous lobes that converge at the nipple. The 2.0–4.5 mm milk ducts are immediately surrounded with dense connective tissue that support the glands. Milk exits the breast through the nipple, which is surrounded by a pigmented area of skin called the areola. The size of the areola can vary widely among women. The areola contains modified sweat glands known as Montgomerys glands. These glands secrete oily fluid that lubricate and protect the nipple during breastfeeding. Volatile compounds in these secretions may also serve as an olfactory stimulus for the newborns appetite.The dimensions and weight of the breast vary widely among women. A small-to-medium-sized breast weighs 500 grams (1.1 pounds) or less, and a large breast can weigh approximately 750 to 1,000 grams (1.7 to 2.2 pounds) or more. The tissue composition ratios of the breast also vary among women. Some womens breasts have a higher proportion of glandular tissue than of adipose or connective tissues. The fat-to-connective-tissue ratio determines the density or firmness of the breast. During a womans life, her breasts change size, shape, and weight due to hormonal changes during puberty, the menstrual cycle, pregnancy, breastfeeding, and menopause. Glandular structure The breast is an apocrine gland that produces the milk used to feed an infant. The nipple of the breast is surrounded by the areola (nipple-areola complex). The areola has many sebaceous glands, and the skin color varies from pink to dark brown. The basic units of the breast are the terminal duct lobular units (TDLUs), which produce the fatty breast milk. They give the breast its offspring-feeding functions as a mammary gland. They are distributed throughout the body of the breast. Approximately two-thirds of the lactiferous tissue is within 30 mm of the base of the nipple. The terminal lactiferous ducts drain the milk from TDLUs into 4–18 lactiferous ducts, which drain to the nipple. The milk-glands-to-fat ratio is 2:1 in a lactating woman, and 1:1 in a non-lactating woman. In addition to the milk glands, the breast is also composed of connective tissues (collagen, elastin), white fat, and the suspensory Coopers ligaments. Sensation in the breast is provided by the peripheral nervous system innervation by means of the front (anterior) and side (lateral) cutaneous branches of the fourth-, fifth-, and sixth intercostal nerves. The T-4 nerve (Thoracic spinal nerve 4), which innervates the dermatomic area, supplies sensation to the nipple-areola complex. Lymphatic drainage Approximately 75% of the lymph from the breast travels to the axillary lymph nodes on the same side of the body, whilst 25% of the lymph travels to the parasternal nodes (beside the sternum bone).: 116  A small amount of remaining lymph travels to the other breast and to the abdominal lymph nodes. The subareolar region has a lymphatic plexus known as the "subareolar plexus of Sappey". The axillary lymph nodes include the pectoral (chest), subscapular (under the scapula), and humeral (humerus-bone area) lymph-node groups, which drain to the central axillary lymph nodes and to the apical axillary lymph nodes. The lymphatic drainage of the breasts is especially relevant to oncology because breast cancer is common to the mammary gland, and cancer cells can metastasize (break away) from a tumour and be dispersed to other parts of the body by means of the lymphatic system. Shape, texture, and support The morphologic variations in the size, shape, volume, tissue density, pectoral locale, and spacing of the breasts determine their natural shape, appearance, and position on a womans chest. Breast size and other characteristics do not predict the fat-to-milk-gland ratio or the potential for the woman to nurse an infant. The size and the shape of the breasts are influenced by normal-life hormonal changes (thelarche, menstruation, pregnancy, menopause) and medical conditions (e.g. virginal breast hypertrophy). The shape of the breasts is naturally determined by the support of the suspensory Coopers ligaments, the underlying muscle and bone structures of the chest, and by the skin envelope. The suspensory ligaments sustain the breast from the clavicle (collarbone) and the clavico-pectoral fascia (collarbone and chest) by traversing and encompassing the fat and milk-gland tissues. The breast is positioned, affixed to, and supported upon the chest wall, while its shape is established and maintained by the skin envelope. In most women, one breast is slightly larger than the other. More obvious and persistent asymmetry in breast size occurs in up to 25% of women.While it is a common belief that breastfeeding causes breasts to sag, researchers have found that a womans breasts sag due to four key factors: cigarette smoking, number of pregnancies, gravity, and weight loss or gain.The base of each breast is attached to the chest by the deep fascia over the pectoralis major muscles. The space between the breast and the pectoralis major muscle, called retromammary space, gives mobility to the breast. The chest (thoracic cavity) progressively slopes outwards from the thoracic inlet (atop the breastbone) and above to the lowest ribs that support the breasts. The inframammary fold, where the lower portion of the breast meets the chest, is an anatomic feature created by the adherence of the breast skin and the underlying connective tissues of the chest; the IMF is the lower-most extent of the anatomic breast. Normal breast tissue typically has a texture that feels nodular or granular, to an extent that varies considerably from woman to woman. Development The breasts are principally composed of adipose, glandular, and connective tissues. Because these tissues have hormone receptors, their sizes and volumes fluctuate according to the hormonal changes particular to thelarche (sprouting of breasts), menstruation (egg production), pregnancy (reproduction), lactation (feeding of offspring), and menopause (end of menstruation). Puberty The morphological structure of the human breast is identical in males and females until puberty. For pubescent girls in thelarche (the breast-development stage), the female sex hormones (principally estrogens) in conjunction with growth hormone promote the sprouting, growth, and development of the breasts. During this time, the mammary glands grow in size and volume and begin resting on the chest. These development stages of secondary sex characteristics (breasts, pubic hair, etc.) are illustrated in the five-stage Tanner Scale.During thelarche the developing breasts are sometimes of unequal size, and usually the left breast is slightly larger. This condition of asymmetry is transitory and statistically normal in female physical and sexual development. Medical conditions can cause overdevelopment (e.g., virginal breast hypertrophy, macromastia) or underdevelopment (e.g., tuberous breast deformity, micromastia) in girls and women. Approximately two years after the onset of puberty (a girls first menstrual cycle), estrogen and growth hormone stimulate the development and growth of the glandular fat and suspensory tissues that compose the breast. This continues for approximately four years until the final shape of the breast (size, volume, density) is established at about the age of 21. Mammoplasia (breast enlargement) in girls begins at puberty, unlike all other primates in which breasts enlarge only during lactation. Changes during the menstrual cycle During the menstrual cycle, the breasts are enlarged by premenstrual water retention and temporary growth. Pregnancy and breastfeeding The breasts reach full maturity only when a womans first pregnancy occurs. Changes to the breasts are among the first signs of pregnancy. The breasts become larger, the nipple-areola complex becomes larger and darker, the Montgomerys glands enlarge, and veins sometimes become more visible. Breast tenderness during pregnancy is common, especially during the first trimester. By mid-pregnancy, the breast is physiologically capable of lactation and some women can express colostrum, a form of breast milk.Pregnancy causes elevated levels of the hormone prolactin, which has a key role in the production of milk. However, milk production is blocked by the hormones progesterone and estrogen until after delivery, when progesterone and estrogen levels plummet. Menopause At menopause, breast atrophy occurs. The breasts can decrease in size when the levels of circulating estrogen decline. The adipose tissue and milk glands also begin to wither. The breasts can also become enlarged from adverse side effects of combined oral contraceptive pills. The size of the breasts can also increase and decrease in response to weight fluctuations. Physical changes to the breasts are often recorded in the stretch marks of the skin envelope; they can serve as historical indicators of the increments and the decrements of the size and volume of a womans breasts throughout the course of her life. Breastfeeding The primary function of the breasts, as mammary glands, is the nourishing of an infant with breast milk. Milk is produced in milk-secreting cells in the alveoli. When the breasts are stimulated by the suckling of her baby, the mothers brain secretes oxytocin. High levels of oxytocin trigger the contraction of muscle cells surrounding the alveoli, causing milk to flow along the ducts that connect the alveoli to the nipple.Full-term newborns have an instinct and a need to suck on a nipple, and breastfed babies nurse for both nutrition and for comfort. Breast milk provides all necessary nutrients for the first six months of life, and then remains an important source of nutrition, alongside solid foods, until at least one or two years of age. Clinical significance The breast is susceptible to numerous benign and malignant conditions. The most frequent benign conditions are puerperal mastitis, fibrocystic breast changes and mastalgia. Lactation unrelated to pregnancy is known as galactorrhea. It can be caused by certain drugs (such as antipsychotic medications), extreme physical stress, or endocrine disorders. Lactation in newborns is caused by hormones from the mother that crossed into the babys bloodstream during pregnancy. Breast cancer Breast cancer is the most common cause of cancer death among women and it is one of the leading causes of death among women. Factors that appear to be implicated in decreasing the risk of breast cancer are regular breast examinations by health care professionals, regular mammograms, self-examination of breasts, healthy diet, and exercise to decrease excess body fat, and breastfeeding. Male breasts Both females and males develop breasts from the same embryological tissues. Normally, males produce lower levels of estrogens and higher levels of androgens, namely testosterone, which suppress the effects of estrogens in developing excessive breast tissue. In boys and men, abnormal breast development is manifested as gynecomastia, the consequence of a biochemical imbalance between the normal levels of estrogen and testosterone in the male body. Around 70% of boys temporarily develop breast tissue during adolescence. The condition usually resolves by itself within two years. When male lactation occurs, it is considered a symptom of a disorder of the pituitary gland. Plastic surgery Plastic surgery can be performed to augment or reduce the size of breasts, or reconstruct the breast in cases of deformative disease, such as breast cancer. Breast augmentation and breast lift (mastopexy) procedures are done only for cosmetic reasons, whereas breast reduction is sometimes medically indicated. In cases where a womans breasts are severely asymmetrical, surgery can be performed to either enlarge the smaller breast, reduce the size of the larger breast, or both.Breast augmentation surgery generally does not interfere with future ability to breastfeed. Breast reduction surgery more frequently leads to decreased sensation in the nipple-areola complex, and to low milk supply in women who choose to breastfeed. Implants can interfere with mammography (breast x-rays images). Society and culture General In Christian iconography, some works of art depict women with their breasts in their hands or on a platter, signifying that they died as a martyr by having their breasts severed; one example of this is Saint Agatha of Sicily. Femen is a feminist activist group which uses topless protests as part of their campaigns against sex tourism religious institutions, sexism, and homophobia. Femen activists have been regularly detained by police in response to their protests.There is a long history of female breasts being used by comedians as a subject for comedy fodder (e.g., British comic Benny Hills burlesque/slapstick routines). Art history In European pre-historic societies, sculptures of female figures with pronounced or highly exaggerated breasts were common. A typical example is the so-called Venus of Willendorf, one of many Paleolithic Venus figurines with ample hips and bosom. Artifacts such as bowls, rock carvings and sacred statues with breasts have been recorded from 15,000 BC up to late antiquity all across Europe, North Africa and the Middle East. Many female deities representing love and fertility were associated with breasts and breast milk. Figures of the Phoenician goddess Astarte were represented as pillars studded with breasts. Isis, an Egyptian goddess who represented, among many other things, ideal motherhood, was often portrayed as suckling pharaohs, thereby confirming their divine status as rulers. Even certain male deities representing regeneration and fertility were occasionally depicted with breast-like appendices, such as the river god Hapy who was considered to be responsible for the annual overflowing of the Nile. Female breasts were also prominent in Minoan art in the form of the famous Snake Goddess statuettes, and a few other pieces, though most female breasts are covered. In Ancient Greece there were several cults worshipping the "Kourotrophos", the suckling mother, represented by goddesses such as Gaia, Hera and Artemis. The worship of deities symbolized by the female breast in Greece became less common during the first millennium. The popular adoration of female goddesses decreased significantly during the rise of the Greek city states, a legacy which was passed on to the later Roman Empire.During the middle of the first millennium BC, Greek culture experienced a gradual change in the perception of female breasts. Women in art were covered in clothing from the neck down, including female goddesses like Athena, the patron of Athens who represented heroic endeavor. There were exceptions: Aphrodite, the goddess of love, was more frequently portrayed fully nude, though in postures that were intended to portray shyness or modesty, a portrayal that has been compared to modern pin ups by historian Marilyn Yalom. Although nude men were depicted standing upright, most depictions of female nudity in Greek art occurred "usually with drapery near at hand and with a forward-bending, self-protecting posture". A popular legend at the time was of the Amazons, a tribe of fierce female warriors who socialized with men only for procreation and even removed one breast to become better warriors (the idea being that the right breast would interfere with the operation of a bow and arrow). The legend was a popular motif in art during Greek and Roman antiquity and served as an antithetical cautionary tale. Body image Many women regard their breasts as important to their sexual attractiveness, as a sign of femininity that is important to their sense of self. A woman with smaller breasts may regard her breasts as less attractive. Clothing Because breasts are mostly fatty tissue, their shape can—within limits—be molded by clothing, such as foundation garments. Bras are commonly worn by about 90% of Western women, and are often worn for support. The social norm in most Western cultures is to cover breasts in public, though the extent of coverage varies depending on the social context. Some religions ascribe a special status to the female breast, either in formal teachings or through symbolism. Islam forbids free women from exposing their breasts in public. Many cultures, including Western cultures in North America, associate breasts with sexuality and tend to regard bare breasts as immodest or indecent. In some cultures, like the Himba in northern Namibia, bare-breasted women are normal. In some African cultures, for example, the thigh is regarded as highly sexualised and never exposed in public, but breast exposure is not taboo. In a few Western countries and regions female toplessness at a beach is acceptable, although it may not be acceptable in the town center.Social attitudes and laws regarding breastfeeding in public vary widely. In many countries, breastfeeding in public is common, legally protected, and generally not regarded as an issue. However, even though the practice may be legal or socially accepted, some mothers may nevertheless be reluctant to expose a breast in public to breastfeed due to actual or potential objections by other people, negative comments, or harassment. It is estimated that around 63% of mothers across the world have publicly breast-fed. Bare-breasted women are legal and culturally acceptable at public beaches in Australia and much of Europe. Filmmaker Lina Esco made a film entitled Free the Nipple, which is about "...laws against female toplessness or restrictions on images of female, but not male, nipples", which Esco states is an example of sexism in society. Sexual characteristic In some cultures, breasts play a role in human sexual activity. In Western culture, breasts have a "...hallowed sexual status, arguably more fetishized than either sexs genitalia". Breasts and especially the nipples are among the various human erogenous zones. They are sensitive to the touch as they have many nerve endings; and it is common to press or massage them with hands or orally before or during sexual activity. During sexual arousal, breast size increases, venous patterns across the breasts become more visible, and nipples harden. Compared to other primates, human breasts are proportionately large throughout adult females lives. Some writers have suggested that they may have evolved as a visual signal of sexual maturity and fertility.Many people regard bare female breasts to be aesthetically pleasing or erotic, and they can elicit heightened sexual desires in men in many cultures. In the ancient Indian work the Kama Sutra, light scratching of the breasts with nails and biting with teeth are considered erotic. Some people show a sexual interest in female breasts distinct from that of the person, which may be regarded as a breast fetish. A number of Western fashions include clothing which accentuate the breasts, such as the use of push-up bras and decollete (plunging neckline) gowns and blouses which show cleavage. While U.S. culture prefers breasts that are youthful and upright, some cultures venerate women with drooping breasts, indicating mothering and the wisdom of experience.Research conducted at the Victoria University of Wellington showed that breasts are often the first thing men look at, and for a longer time than other body parts. The writers of the study had initially speculated that the reason for this is due to endocrinology with larger breasts indicating higher levels of estrogen and a sign of greater fertility, but the researchers said that "Men may be looking more often at the breasts because they are simply aesthetically pleasing, regardless of the size."Some women report achieving an orgasm from nipple stimulation, but this is rare. Research suggests that the orgasms are genital orgasms, and may also be directly linked to "the genital area of the brain". In these cases, it seems that sensation from the nipples travels to the same part of the brain as sensations from the vagina, clitoris and cervix. Nipple stimulation may trigger uterine contractions, which then produce a sensation in the genital area of the brain. Anthropomorphic geography There are many mountains named after the breast because they resemble it in appearance and so are objects of religious and ancestral veneration as a fertility symbol and of well-being. In Asia, there was "Breast Mountain", which had a cave where the Buddhist monk Bodhidharma (Da Mo) spent much time in meditation. Other such breast mountains are Mount Elgon on the Uganda–Kenya border; Beinn Chìochan and the Maiden Paps in Scotland; the Bundok ng Susong Dalaga (Maidens breast mountains) in Talim Island, Philippines, the twin hills known as the Paps of Anu (Dá Chích Anann or the breasts of Anu), near Killarney in Ireland; the 2,086 m high Tetica de Bacares or La Tetica in the Sierra de Los Filabres, Spain; Khao Nom Sao in Thailand, Cerro Las Tetas in Puerto Rico; and the Breasts of Aphrodite in Mykonos, among many others. In the United States, the Teton Range is named after the French word for nipple. See also Medicine portal Human sexuality portal Udder References Bibliography Hollander, Anne (1993). Seeing through clothes. Berkeley: University of California Press. ISBN 978-0-520-08231-1. Morris, Desmond The Naked Ape: a zoologists study of the human animal Bantam Books, Canada. 1967 Yalom, Marilyn (1998). A history of the breast. London: Pandora. ISBN 978-0-86358-400-8. Venes, Donald (2013). Tabers cyclopedic medical dictionary. Philadelphia: F.A. Davis. ISBN 978-0-8036-2977-6. Lawrence, Ruth (2016). Breastfeeding : a guide for the medical profession, 8th edition. Philadelphia, PA: Elsevier. ISBN 978-0-323-35776-0. External links "Are Women Evolutionary Sex Objects?: Why Women Have Breasts". Archived from the original on 2 December 2011.

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I'm not familiar with the medical term 'Aortoiliac occlusive disease.' Could you provide some insights?

In medicine, aortoiliac occlusive disease is a form of central artery disease involving the blockage of the abdominal aorta as it transitions into the common iliac arteries. Signs and symptoms Classically, it is described in male patients as a triad of the following signs and symptoms: claudication of the buttocks and thighs absent or decreased femoral pulses erectile dysfunctionThis combination is known as Leriche syndrome. However, any number of symptoms may present, depending on the distribution and severity of the disease, such as muscle atrophy, slow wound healing in the legs, and critical limb ischemia. Diagnosis The physical examination usually shows weakened femoral pulses and a reduced ankle-brachial index. The diagnosis can be verified by color duplex scanning, which reveals either a peak systolic velocity ratio ≥2.5 at the site of stenosis and/or a monophasic waveform. MRA and multidetector CTA are often used to determine the extent and type of obstruction. Another technique is digital subtraction angiography which allows verification of the diagnosis and endovascular treatment in a single session. Angiography provides important information regarding the perfusion and patency of distal arteries (e.g. femoral artery). The presence of collateral arteries in the pelvic and groin area is important in maintaining crucial blood flow and lower limb viability. However, angiography should only be used if symptoms warrant surgical intervention. Treatment Treatment involves revascularization typically using either angioplasty or a type of vascular bypass Kissing balloon angioplasty +/- stent, so named because the two common iliac stents touch each other in the distal aorta. Aorto-iliac bypass graft Axillary-bi-femoral and femoral-femoral bypass (sometimes abbreviated "ax-fem fem-fem") History The condition was first described by Robert Graham in 1914, but the condition with its triad of symptoms was ascribed to René Leriche. Leriche, a French surgeon, linked the pathophysiology with the anatomy of the condition. John Hunters dissections of atherosclerotic aortic bifurcations from the late 18th century are preserved at the Hunterian Museum, but Leriche was first to publish on the subject based on a patient he treated with the condition at the age of 30. Following treatment the 30-year-old was able to walk without pain and maintain an erection. See also Claudication Peripheral arterial disease References == External links ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

Can you break down the meaning of the medical term 'Alopecia areata' for me?

Alopecia areata, also known as spot baldness, is a condition in which hair is lost from some or all areas of the body. Often, it results in a few bald spots on the scalp, each about the size of a coin. Psychological stress and illness are possible factors in bringing on alopecia areata in individuals at risk, but in most cases there is no obvious trigger. People are generally otherwise healthy. In a few cases, all the hair on the scalp is lost (alopecia totalis), or all body hair is lost (alopecia universalis). Hair loss can be permanent, or temporary. It is distinctive from pattern hair loss, which is common among males. Alopecia areata is believed to be an autoimmune disease resulting from a breach in the immune privilege of the hair follicles. Risk factors include a family history of the condition. Among identical twins, if one is affected, the other has about a 50% chance of also being affected. The underlying mechanism involves failure by the body to recognize its own cells, with subsequent immune-mediated destruction of the hair follicle.No cure for the condition is known. Efforts may be used to try to speed hair regrowth, such as cortisone injections. Sunscreen, head coverings to protect from cold and sun, and glasses, if the eyelashes are missing, are recommended. In some cases, the hair regrows, and the condition does not reoccur. In others, hair loss and regrowth occurs over years. Among those in whom all body hair is lost, fewer than 10% recover.About 0.15% of people are affected at any one time, and 2% of people are affected at some point in time. Onset is usually in childhood. Females are affected at higher rates than males. Signs and symptoms Typical first symptoms of alopecia areata are small bald patches. The underlying skin is unscarred and looks superficially normal. Although these patches can take many shapes, they are usually round or oval. Alopecia areata most often affects the scalp and beard, but may occur on any part of the body with hair. Different areas of the skin may exhibit hair loss and regrowth at the same time. The disease may also go into remission for a time, or may be permanent. It is common in children.The area of hair loss may tingle or be mildly painful. The hair tends to fall out over a short period of time, with the loss commonly occurring more on one side of the scalp than the other.Exclamation point hairs, narrower along the length of the strand closer to the base, producing a characteristic "exclamation point" appearance, are often present. These hairs are very short (3–4 mm), and can be seen surrounding the bald patches.When healthy hair is pulled out, at most a few should come out, and ripped hair should not be distributed evenly across the tugged portion of the scalp. In cases of alopecia areata, hair tends to pull out more easily along the edge of the patch where the follicles are already being attacked by the bodys immune system than away from the patch where they are still healthy.Nails may have pitting or trachyonychia. Causes Alopecia areata is thought to be a systemic autoimmune disorder in which the body attacks its own anagen hair follicles and suppresses or stops hair growth. For example, T cell lymphocytes cluster around affected follicles, causing inflammation and subsequent hair loss. Hair follicles in a normal state are thought to be kept secure from the immune system, a phenomenon called immune privilege. A breach in this immune privilege state is considered as the cause of alopecia areata. A few cases of babies being born with congenital alopecia areata have been reported.Alopecia areata is not contagious. It occurs more frequently in people who have affected family members, suggesting heredity may be a factor. Strong evidence of genetic association with increased risk for alopecia areata was found by studying families with two or more affected members. This study identified at least four regions in the genome that are likely to contain these genes. In addition, alopecia areata shares genetic risk factors with other autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and celiac disease. It may be the only manifestation of celiac disease.Endogenous retinoids metabolic defect is a key part of the pathogenesis of the alopecia areata.In 2010, a genome-wide association study was completed that identified 129 single nucleotide polymorphisms that were associated with alopecia areata. The genes that were identified include those involved in controlling the activation and proliferation of regulatory T cells, cytotoxic T lymphocyte-associated antigen 4, interleukin-2, interleukin-2 receptor A, and Eos (also known as Ikaros family zinc finger 4), as well as the human leukocyte antigen. The study also identified two genes, PRDX5 and STX17, that are expressed in the hair follicle. Diagnosis Alopecia areata is usually diagnosed based on clinical features. Trichoscopy may aid in establishing the diagnosis. In alopecia areata, trichoscopy shows regularly distributed "yellow dots" (hyperkeratotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening).Oftentimes, however, discrete areas of hair loss surrounded by exclamation mark hairs is sufficient for clinical diagnosis of alopecia areata. Sometimes, reddening of the skin, erythema, may also be present in the balding area.A biopsy is rarely needed to make the diagnosis or aid in the management of alopecia areata. Histologic findings may include peribulbar lymphocytic infiltration resembling a "swarm of bees", a shift in the anagen-to-telogen ratio towards telogen, and dilated follicular infundibulae. Other helpful findings can include pigment incontinence in the hair bulb and follicular stelae. Occasionally, in inactive alopecia areata, no inflammatory infiltrates are found. Classification Commonly, alopecia areata involves hair loss in one or more round spots on the scalp. Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata. Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head. Alopecia areata multilocularis refers to multiple areas of hair loss. Ophiasis refers to hair loss in the shape of a wave at the circumference of the head. The disease may be limited only to the beard, in which case it is called alopecia areata barbae. If the person loses all the hair on the scalp, the disease is then called alopecia areata totalis. If all body hair, including pubic hair, is lost, the diagnosis then becomes alopecia areata universalis.Alopecia areata totalis and universalis are rare. Treatment The objective assessment of treatment efficacy is very difficult and spontaneous remission is unpredictable, but if the affected area is patched, the hair may regrow spontaneously in many cases. None of the existing therapeutic options are curative or preventive.In cases of severe hair loss, limited success has been achieved by using the corticosteroid medications clobetasol or fluocinonide, corticosteroid injections, or cream. Application of corticosteroid creams to the affected skin is less effective and takes longer to produce results. Steroid injections are commonly used in sites where the areas of hair loss on the head are small or especially where eyebrow hair has been lost. Whether they are effective is uncertain. Some other medications that have been used are minoxidil, Elocon (mometasone) ointment (steroid cream), irritants (anthralin or topical coal tar), and topical immunotherapy ciclosporin, sometimes in different combinations. Topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target, and small lesions typically also regrow spontaneously. Oral corticosteroids may decrease the hair loss, but only for the period during which they are taken, and these medications can cause serious side effects. No one treatment is effective in all cases, and some individuals may show no response to any treatment. Few treatments have been well evaluated. A 2008 meta-analysis of oral and topical corticosteroids, topical ciclosporin, photodynamic therapy, and topical minoxidil showed no benefit of hair growth compared with placebo, especially with regard to long-term benefits. For more severe cases, recent studies have shown promising results with the individual use of the immunosuppressant Methotrexate or adjunct use with corticosteroids. However, as relapse of the condition may occur long-term treatment is recommended.When alopecia areata is associated with celiac disease, treatment with a gluten-free diet allows for complete and permanent regrowth of scalp and other body hair in many people, but in others, remissions and recurrences are seen. This improvement is probably due to the normalization of the immune response as a result of gluten withdrawal from the diet.In June 2022, the U.S. Food and Drug Administration (FDA) authorized baricitinib for the treatment of severe alopecia areata. Prognosis In most cases that begin with a small number of patches of hair loss, hair grows back after a few months to a year. In cases with a greater number of patches, hair can either grow back or progress to alopecia areata totalis or, in rare cases, alopecia areata universalis.No loss of body function occurs, and the effects of alopecia areata are psychological (loss of self-image due to hair loss), although these can be severe. Loss of hair also means the scalp burns more easily in the sun. Patients may also have aberrant nail formation because keratin forms both hair and nails.Hair may grow back and then fall out again later. This may not indicate a recurrence of the condition, but rather a natural cycle of growth-and-shedding from a relatively synchronised start; such a pattern will fade over time. Episodes of alopecia areata before puberty predispose to chronic recurrence of the condition.Alopecia can be the cause of psychological stress. Because hair loss can lead to significant changes in appearance, individuals with it may experience social phobia, anxiety, and depression. Epidemiology The condition affects 0.1%–0.2% of the population, with a lifetime risk of 1%-2%. and is more common in females.Alopecia areata occurs in people who are otherwise healthy and have no other skin disorders. Initial presentation most commonly occurs in the early childhood, late teenage years, or young adulthood, but can happen at any ages. Patients also tend to have a slightly higher incidence of conditions related to the immune system, such as asthma, allergies, atopic dermatitis, and hypothyroidism. Research Many medications are being studied. Some of these medications are approved for other diseases, others are not available outside of studies. In 2014, preliminary findings showing that oral ruxolitinib, a drug approved by the US Food and Drug Administration (FDA) for bone marrow disorder myelofibrosis, restored hair growth in three individuals with long-standing and severe disease. The medicine costs almost US$10,000 a month. History Alopecia areata and alopecia barbae have been identified by some as the biblical nethek condition that is part of the greater tzaraath family of skin disorders; the said disorders are purported to being discussed in the Book of Leviticus, chapter 13. Notable people Actor Anthony Carrigan, athlete of American Ninja Warrior fame Kevin Bull, Australian politician Peter Dutton, Australian actor Alan Fletcher, Congresswoman Ayanna Pressley, K-pop singer Peniel Shin of BtoB, and actresses Jada Pinkett Smith, and May Calamawy all have some form of alopecia areata. See also Noncicatricial alopecia Trichotillomania References External links National Institute of Arthritis and Musculoskeletal and Skin Diseases at NIH DermAtlas 42

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

I'm seeking clarification on the medical term 'Lethal midline granuloma.' Could you explain it?

Lethal midline granuloma (LMG) is an historical term for a condition in which necrotic and highly destructive lesions develop progressively in the middle of the face, principally the nose and palate. Many cases presented with ulcerations in or perforations of the palate. LMG was thought to be a manifestation of three or four different diseases: the well-characterized disease of granulomatosis with polyangiitis, the ill-defined disorders of polymorphic reticulosis or mid-line malignant reticulosis, and an incompletely defined form of non-Hodgkins lymphoma. Subsequent studies found that the cells infiltrating the midline tissues in cases of lethal midline granuloma that were not clearly diagnosed as granulomatosis with polyangiitis were: a) infected by the Epstein-Barr virus and b) consisted of malignant lymphocytes, usually NK cells or, rarely, cytotoxic T cells. The disease is therefore now regarded as a NK/T cell malignancy, is grouped with other Epstein-Barr virus-associated lymphoproliferative diseases and is classified by the World Health Organization (2017 update) as a manifestation of the well-defined disease, extranodal NK/T-cell lymphoma, nasal type (ENKTCL-NT). ENKTCL-NT is a rare type of lymphoma that commonly involves the nasal cavity, oral cavity, and/or pharynx but less commonly can also involve the eye, larynx, lung, gastrointestinal tract, skin, and various other tissues. Patients presenting with highly localized midline facial disease fit the historical definition of lethal midline granuloma. These cases, unlike other cases ENKTCL-NT that have more widespread disease, often show no or relatively little progression of their disease over long periods of time. Since cases of LMG that were manifestations of granulomatosis with polyangiitis, a vascular inflammatory but not malignant disease, the term lethal midline granuloma is considered confusing and obsolete. References == External links ==

You act as a bridge between medical jargon and everyday language. Explain medical terms in a manner that is comprehensive yet approachable for non-experts.

I've come across the term 'Epiretinal membrane' in a medical context, but I'm not sure what it means. Can you clarify?

Epiretinal membrane or macular pucker is a disease of the eye in response to changes in the vitreous humor or more rarely, diabetes. Sometimes, as a result of immune system response to protect the retina, cells converge in the macular area as the vitreous ages and pulls away in posterior vitreous detachment (PVD). PVD can create minor damage to the retina, stimulating exudate, inflammation, and leucocyte response. These cells can form a transparent layer gradually and, like all scar tissue, tighten to create tension on the retina which may bulge and pucker, or even cause swelling or macular edema. Often this results in distortions of vision that are clearly visible as bowing and blurring when looking at lines on chart paper (or an Amsler grid) within the macular area, or central 1.0 degree of visual arc. Usually it occurs in one eye first, and may cause binocular diplopia or double vision if the image from one eye is too different from the image of the other eye. The distortions can make objects look different in size (usually larger = macropsia), especially in the central portion of the visual field, creating a localized or field dependent aniseikonia that cannot be fully corrected optically with glasses. Partial correction often improves the binocular vision considerably though. In the young (under 50 years of age), these cells occasionally pull free and disintegrate on their own; but in the majority of those affected (over 60 years of age) the condition is permanent. The underlying photoreceptor cells, rod cells and cone cells, are usually not damaged unless the membrane becomes quite thick and hard; so usually there is no macular degeneration. Cause The source of the cells in epiretinal membranes (ERM) has been found to comprise glial cells, retinal pigment epithelial (RPE) cells, macrophages, fibrocytes, and collagen cells. These cells are found in varying proportions. Those from retinal breaks, previous retinal detachments, or cryopexy are composed mainly of dispersed RPE cells, while cells of glial origin predominate in idiopathic pathology. Laminocytes are the fundamental cell type in idiopathic ERMs. These cells are frequently found in small and dispersed numbers in eyes containing a PVD. The presence of retinal pigment cells invariably indicates proliferative retinopathy and is only seen in association with a retinal detachment or tear. The incidence of associated PVD range from 75 to 93%, and PVD is present in virtually all eyes with retinal breaks or retinal detachments and subsequent ERM formation. PVD can lead to retinal breaks that may liberate RPE cells that initiate membrane formation. Small breaks in the internal limiting membrane (ILM) after PVD also may provide retinal astrocytes access to the vitreous cavity, where they may subsequently proliferate. Many ERM also have ILM fragments that may be peeled separately. Finally, vitreous hemorrhage, inflammation, or both associated with a PVD also may stimulate ERM formation. Both sexes appear to be affected equally frequently. Diagnosis Epiretinal membrane is typically diagnosed by appearance with optical coherence tomography (OCT) of the macula. Features include a thickening of the nerve fiber layer, a serrated appearance to the surface of the retina just beneath a thickened layer of glial tissue at the retinal-vitreous interface. Prevention There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. It has been estimated that Posterior vitreous detachment (PVD) occurs in over 75 percent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms. Treatment Surgeons can remove or peel the membrane through the sclera and improve vision by 2 or more Snellen lines. Usually the vitreous is replaced at the same time with clear (BSS) fluid, in a vitrectomy. Surgery is not usually recommended unless the distortions are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment. More common complications are high intraocular pressure, bleeding in the eye, and cataracts, which are the most frequent complication of vitrectomy surgery. Many patients will develop a cataract within the first few years after surgery. In fact, the visual distortions and diplopia created by cataracts may sometimes be confused with epiretinal membrane. Epidemiology This ocular pathology was first described by Iwanoff in 1865, and it has been shown to occur in about 7% of the population. It can occur more frequently in the older population with postmortem studies showing it in 2% of those aged 50 years and 20% in those aged 75 years. Culture In 1996, Spalding Gray (June 5, 1941 – ca. January 10, 2004), an American actor, screenwriter and playwright, released Grays Anatomy, a film monologue describing his experiences dealing with a macular pucker and his decision to undergo surgery. In the 2011 film Paul, Ruth had Epiretinal membrane complicated by macular edema in her left vitreous cavity. See also Eye surgery References Additional references de Wit GC (2007). "Retinally-induced aniseikonia". Binocul Vis Strabismus Q. 22 (2): 96–101. PMID 17688418. Benson WE, Brown GC, Tasman W, McNamara JA (1988). "Complications of vitrectomy for non-clearing vitreous hemorrhage in diabetic patients". Ophthalmic Surg. 19 (12): 862–4. PMID 3231410. Suami M, Mizota A, Hotta Y, Tanaka M (2007). "Pattern VEPs before and after idiopathic epiretinal membrane removal". Doc Ophthalmol. 114 (2): 67–73. doi:10.1007/s10633-006-9039-4. PMID 17216518. S2CID 22039065. Dev S, Mieler WF, Pulido JS, Mittra RA (1999). "Visual outcomes after pars plana vitrectomy for epiretinal membranes associated with pars planitis". Ophthalmology. 106 (6): 1086–90. doi:10.1016/S0161-6420(99)90247-6. PMID 10366075. Johnson MW (2005). "Perifoveal vitreous detachment and its macular complications". Trans Am Ophthalmol Soc. 103: 537–67. PMC 1447588. PMID 17057817. External links Macular Pucker Resource Guide from the National Eye Institute (NEI).

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

The term 'Angiostrongyliasis' keeps coming up in medical discussions. What does it stand for?

Angiostrongyliasis is an infection by a roundworm of the Angiostrongylus type. Symptoms may vary from none, to mild, to meningitis.Infection with Angiostrongylus cantonensis (rat lungworm) can occur after ingestion of raw or undercooked snails or slugs, and less likely unwashed fruits and vegetables. In humans, A. cantonensis is the most common cause of eosinophilic meningitis or meningoencephalitis. Frequently the infection will resolve without treatment or serious consequences, but in cases with a heavy load of parasites the infection can be so severe it can cause permanent damage to the central nervous system or death. Symptoms Infection first presents with severe abdominal pain, nausea, vomiting, and weakness, which gradually lessens and progresses to fever, and then to central nervous system (CNS) symptoms and severe headache and stiffness of the neck. CNS infection CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a very severe form often progress to unconsciousness. Patients may present with neuropathic pain early in the infection. Eventually, severe infection will lead to ascending weakness, quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7 and 8, and rarely larvae will enter ocular structures. Even with treatment, damage to the CNS may be permanent and result in a variety of negative outcomes depending on the location of the infection, and the patient may experience chronic pain as a result of infection. Eye invasion Symptoms of eye invasion include visual impairment, pain, keratitis, and retinal edema. Worms usually appear in the anterior chamber and vitreous and can sometimes be removed surgically. Incubation period The incubation period in humans is usually from 1 week to 1 month after infection, and can be as long as 47 days. This interval varies, since humans are accidental hosts and the life cycle does not continue predictably as it would in a rat. Cause Transmission Transmission of the parasite is usually from eating raw or undercooked snails or other vectors. Infection is also frequent from ingestion of contaminated water or unwashed salad that may contain small snails and slugs, or have been contaminated by them. Reservoirs Rats are the definitive host and the main reservoir for A. cantonensis, though other small mammals may also become infected. While Angiostrongylus can infect humans, humans do not act as reservoirs since the worm cannot reproduce in humans and therefore humans cannot contribute to their life cycle. Vectors Angiostrongylus cantonensis has many vectors among invertebrates, with the most common being several species of snails, including the giant African land snail (Achatina) in the Pacific islands and apple snails of the genus Pila in Thailand and Malaysia. The golden apple snail, Pomacea canaliculata, is the most important vector in areas of China. Freshwater prawns, crabs, or other paratenic, or transport, hosts can also act as vectors. Organism Morphology A. cantonensis is a nematode roundworm with 3 outer protective collagen layers, and a simple stomal opening or mouth with no lips or buccal cavity leading to a fully developed gastrointestinal tract. Males have a small copulatory bursa at the posterior. Females have a "barber pole" shape down the middle of the body, which is created by the twisting together of the intestine and uterine tubules. The worms are long and slender - males are 15.9–19 mm in length, and females are 21–25 mm in length. Life cycle The adult form of A. cantonensis resides in the pulmonary arteries of rodents, where it reproduces. After the eggs hatch in the arteries, larvae migrate up the pharynx and are then swallowed again by the rodent and passed in the stool. These first stage larvae then penetrate or are swallowed by snail intermediate hosts, where they transform into second stage larvae and then into third stage infective larvae. Humans and rats acquire the infection when they ingest contaminated snails or paratenic (transport) hosts including prawns, crabs, and frogs, or raw vegetables containing material from these intermediate and paratenic hosts. After passing through the gastrointestinal tract, the worms enter circulation. In rats, the larvae then migrate to the meninges and develop for about a month before migrating to the pulmonary arteries, where they fully develop into adults.Humans are incidental hosts; the larvae cannot reproduce in humans and therefore humans do not contribute to the A. cantonensis life cycle. In humans, the circulating larvae migrate to the meninges, but do not move on to the lungs. Sometimes the larvae will develop into the adult form in the brain and CSF, but they quickly die, inciting the inflammatory reaction that causes symptoms of infection. Diagnosis Diagnosis of Angiostrongyliasis is complicated due to the difficulty of presenting the angiostrongylus larvae themselves, and will usually be made based on the presence of eosinophilic meningitis and history of exposure to snail hosts. Eosinophilic meningitis is generally characterized as a meningitis with >10 eosinophils/μL in the CSF or at least 10% eosinophils in the total CSF leukocyte count. Occasionally worms found in the cerebrospinal fluid or surgically removed from the eye can be identified in order to diagnose Angiostrongyliasis. Lumbar puncture Lumbar puncture should always be done in cases of suspected meningitis. In cases of eosinophilc meningitis it will rarely produce worms even when they are present in the CSF, because they tend to cling to the end of nerves. Larvae are present in the CSF in only 1.9-10% of cases. However, as a case of eosinophilic meningitis progresses, intracranial pressure and eosinophil counts should rise. Increased levels of eosinophils in the CSF is a hallmark of the eosinophilic meningitis. Brain imaging Brain lesions, with invasion of both gray and white matter, can be seen on a CT or MRI. However MRI findings tend to be inconclusive, and usually include nonspecific lesions and ventricular enlargement. Sometimes a hemorrhage, probably produced by migrating worms, is present and of diagnostic value. Serology In patients with elevated eosinophils, serology can be used to confirm a diagnosis of angiostrongyliasis rather than infection with another parasite. There are a number of immunoassays that can aid in diagnosis, however serologic testing is available in few labs in the endemic area, and is frequently too non-specific. Some cross reactivity has been reported between A. cantonensis and trichinosis, making diagnosis less specific. The most definitive diagnosis always arises from the identification of larvae found in the CSF or eye, however due to this rarity a clinical diagnosis based on the above tests is most likely. Prevention There are public health strategies that can limit the transmission of A. cantonensis by limiting contact with infected vectors. Vector control may be possible, but has not been very successful in the past. Education to prevent the introduction of rats or snail vectors outside endemic areas is important to limit the spread of the disease. There are no vaccines in development for angiostrongyliasis. Recommendations for individuals To avoid infection when in endemic areas, travelers should: Avoid consumption of uncooked vectors, such as snails and freshwater prawns Avoid drinking water from open sources, which may have been contaminated by vectors Prevent young children from playing with or eating live snails Treatment Treatment of angiostrongyliasis is not well defined, but most strategies include a combination of anti-parasitics to kill the worms, steroids to limit inflammation as the worms die, and pain medication to manage the symptoms of meningitis. Anthelmintics Anthelmintics are often used to kill off the worms, however in some cases this may cause patients to worsen due to toxins released by the dying worms. Albendazole, ivermectin, mebendazole, and pyrantel are all commonly used, though albendazole is usually the drug of choice. Studies have shown that anthelmintic drugs may shorten the course of the disease and relieve symptoms. Therefore, anthelmintics are generally recommended, but should be administered gradually so as to limit the inflammatory reaction. Anti-inflammatories Anthelmintics should generally be paired with corticosteroids in severe infections to limit the inflammatory reaction to the dying parasites. Studies suggest that a two-week regimen of a combination of mebendazole and prednisolone significantly shortened the course of the disease and length of associated headaches without observed harmful side effects. Other studies suggest that albendazole may be more favorable, because it may be less like to incite an inflammatory reaction. Symptomatic treatment Symptomatic treatment is indicated for symptoms such as nausea, vomiting, headache, and in some cases, chronic pain due to nerve damage or muscle atrophy. Epidemiology A. cantonensis and its vectors are endemic to Southeast Asia and the Pacific Basin. The infection is becoming increasingly important as globalization allows it to spread to more locations, and as more travelers encounter the parasites. The parasites probably travel effectively through rats traveling as stowaways on ships, and through the introduction of snail vectors outside endemic areas.Although mostly found in Asia and the Pacific where asymptomatic infection can be as high as 88%, human cases have been reported in the Caribbean, where as much as 25% of the population may be infected. In the United States, cases have been reported in Hawaii, which is in the endemic area. The infection is now endemic in wildlife and a few human cases have also been reported in areas where the parasite was not originally endemic, such as New Orleans and Egypt. The disease has also arrived in Brazil, where there were 34 confirmed cases from 2006 to 2014, including one death. The giant African land snail, which can be a vector of the parasite, has been introduced to Brazil as an invasive species and is spreading the disease. There may be more undiagnosed cases, as Brazilian physicians are not familiar with the eosinophilic meningitis associated to angiostrongyliasis and misdiagnose it as bacterial or viral.The parasite is rarely seen outside of endemic areas, and in these cases patients generally have a history of travel to an endemic area. See also Schistosomiasis, a parasitic disease also spread by snails List of unusual deaths – lists Australian man Sam Ballard as dying from Angiostrongyliasis in 2018, as a result of eating a garden slug eight years earlier on a dare References Further reading "Parasites - Angiostrongyliasis (also known as Angiostrongylus Infection)". CDC. 2015-12-28. Retrieved 2017-04-04. "DPDx - Angiostrongyliasis". CDC. 2016-10-17. Retrieved 2017-04-04. Tabs for Parasite Biology, Image Gallery, Laboratory Diagnosis, and Treatment Information. == External links ==

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

Could you please explain the term 'Sodoku' in simple language?

Sodoku (鼠毒) is a bacterial zoonotic disease. It is caused by the Gram-negative rod Spirillum minus (also known as Spirillum minor). It is a form of rat-bite fever (RBF). Signs and symptoms The initial scratch or wound caused by a bite from a carrier rodent results in mild inflammatory reactions and ulcerations. The wounds may heal initially, but reappear with the onset of symptoms. The symptoms include recurring fever, with body temperature 101–104°F (38–40°C). The fever lasts for 2–4 days, but recurs generally at 4–8 weeks. This cycle may continue for months or years. The other symptoms include regional lymphadenitis, malaise, and headache. The complications include myocarditis, endocarditis, hepatitis, splenomegaly, and meningitis. Causes The infections are acquired through rat bites or scratches. It can occur as nosocomial infections (i.e., acquired from hospitals), or due to exposure or close associations with animals preying on rats, mice, squirrels, etc. Sodoku is mostly seen in Asia and Africa. Local transmission has been reported in US. The incubation period is 4 to 28 days. Prognosis Mortality is 6–10%. References == External links ==

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

What is the significance of the term 'Susacs syndrome' in the medical field?

Susacs syndrome (retinocochleocerebral vasculopathy) is a very rare form of microangiopathy characterized by encephalopathy, branch retinal artery occlusions and hearing loss. The cause is unknown but it is theorized that antibodies are produced against endothelial cells in tiny arteries which leads to damage and the symptoms related to the illness. Despite this being an extremely rare disease, there are 4 registries collecting data on the illness; two are the United States, one in Germany, and one in Portugal. Presentation Susacs syndrome is named for Dr. John Susac (1940–2012), of Winter Haven, Florida, who first described it in 1979. Susacs syndrome is a very rare disease, of unknown cause, and many persons who experience it do not display the bizarre symptoms named here. Their speech can be affected, such as the case of a female of late teens who suffered speech issues and hearing problems, and many experience unrelenting and intense headaches and migraines, some form of hearing loss, and impaired vision. The problem usually corrects itself, but this can take up to five years. In some cases, subjects can become confused. The syndrome usually affects women around the age of 18 years, with female to male ratio of cases of 2:1. William F. Hoyt was the first to call the syndrome "Susac syndrome" and later Robert Daroff asked Dr. Susac to write an editorial in Neurology about the disorder and to use the eponym of Susac syndrome in the title, forever linking this disease with him. Pathogenesis In the March 1979 report in Neurology, Drs. Susac, Hardman and Selhorst reported two patients with the triad of encephalopathy, hearing loss and microangiopathy of the retina. The first patient underwent brain biopsy, which revealed sclerosis of the media and adventitia of small pial and cortical vessels, suggestive of a healed angiitis. Both patients underwent fluorescein retinal angiography that demonstrated multifocal retinal artery occlusions without evidence of embolic disease. Though the exact pathogenesis of this disorder is unknown, the retinal and brain biopsy findings suggest a small vessel vasculopathy leading to arteriolar occlusion and microinfarction of cerebral, retinal and cochlear tissue. Demyelination is not a typical feature of Susacs syndrome. Muscle biopsies from such patients are usually normal, but some have also shown nonspecific signs of inflammation such as dense hyaline material surrounding endomysial capillaries. This suggests a possible systemic component of this disease, despite the predominance of central nervous system features. The latest thinking is that an antibody directed against endothelial cells is the pathogenic mechanism in this disease which causes the microscopic strokes in the brain, retina, and inner ear. Diagnosis Patients typically present with low frequency hearing loss detectable via an audiogram. Headaches are frequently present in addition to roaring tinnitus and often some degree of paranoia. Partial vision loss is often present and caused by branch retinal artery occlusions. The presence of refractile or non-refractile yellow Gass plaques in the retinal arterioles is near pathognomonic for the disease. Fluorescein angiography may demonstrate leakage in areas remote from the retinal infarctions. Radiographic appearance In a recent analysis (Susac et al., 2003), MRI images from 27 patients fulfilling the diagnostic criteria of Susacs syndrome were reviewed. Multifocal supratentorial lesions were present in all patients. Most lesions were small (3 to 7 mm), though some were larger than 7 mm. All 27 patients had corpus callosum lesions. These all had a punched-out appearance on follow up MRI. Though most commonly involving white matter, many patients also had lesions in deep grey matter structures, as well as leptomeningeal enhancement. Multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM) can mimic the MRI changes seen in patients with Susacs syndrome. However, the callosal lesions in Susacs syndrome are centrally located. In comparison, patients with MS and ADEM typically have lesions involving the undersurface of the corpus callosum. Deep gray matter involvement commonly occurs in ADEM but is very rare in MS. Leptomeningeal involvement is not typical of either MS or ADEM. What this means is that if 10 lesions are found in the brain of an MS patient, a lesion may be found in the corpus callosum. If you have 10 lesions in a Susac patient, more than half will be in the corpus callosum. A concern about this illness is that it mimics multiple sclerosis when looking at the vision loss and brain lesions. If close attention is not paid to the retina of a patient with vision loss and brain lesions, their symptoms may be mistaken for MS instead of Susacs syndrome. This may account for the low prevalence of the illness. There is also a pathological similarity between the endotheliopathy in Susacs syndrome with that seen in juvenile dermatomyositis. Treatment Early and aggressive treatment is important to prevent irreversible neurological damage, hearing loss, or vision loss. Medications used include immunosuppressive agents and corticosteroids such a prednisone, or intravenous immunoglobulins (IVIG). Other drugs that have been used are mycophenolate mofetil (Cellcept), azathioprine (Imuran), cyclophosphamide, rituximab, and anti-TNF therapies.Hearing aids or cochlear implants may be necessary in the event of hearing loss. References Egan RA, Nguyen TH, Gass JDM, Rizzo JF, Tivnan J, Susac JO. Retinal Artery Wall Plaques in Susac Syndrome. American Journal of Ophthalmology 135: 483-6; 2003 Susac JO, Murtagh FR, Egan RA, Berger JR, Fox RJ, Galetta S, Costello F, Lee AG, Bakshi R, Lincoff N, Clark J, Daroff R. MRI Findings in Susac Syndrome. Neurology 61: 1783-1787; 2003 Egan RA, Hills WL, Susac JO. Gass Plaques and Fluorescein Leakage in Susac Syndrome. Journal of Neurological Sciences 299(1-2): 97-100; 2010 Susac JO, Rennebohm RM, Egan RA, Daroff RB. Susac’s Syndrome – Update. Journal of Neurological Sciences 299(1-2): 86-91; 2010 Susac JO. Susac Syndrome: the triad of microangiopathy of the brain and retina with hearing loss in young women. Neurology 44(4): 591-3; 1994 Dörr J, Krautwald S, Wildemann B, Jarius S, Ringelstein M, Duning T, Aktas O, Ringelstein EB, Paul F, Kleffner I. Characteristics of Susac Syndrome: a review of all reported cases. Nat Rev Neurol 9(6): 307-16; 2013 Groh S, One of three hundred - My Life with Susac Syndrome. ISBN 9783752679120 == External links ==

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

I need a basic explanation for the medical term 'Cerebrospinal fluid leak.'

A cerebrospinal fluid leak (CSF leak or CSFL) is a medical condition where the cerebrospinal fluid (CSF) surrounding the brain or spinal cord leaks out of one or more holes or tears in the dura mater. A cerebrospinal fluid leak can be either cranial or spinal, and these are two different disorders. A spinal CSF leak can be caused by one or more meningeal diverticula or CSF-venous fistulas not associated with an epidural leak.A CSF leak is either caused by trauma including that arising from medical interventions or spontaneously sometimes in those with predisposing conditions (known as a spontaneous cerebrospinal fluid leak or sCSF leak). Traumatic causes include a lumbar puncture noted by a post-dural-puncture headache, or a fall or other accident. Spontaneous CSF leaks are associated with heritable connective tissue disorders including Marfan syndrome and Ehlers–Danlos syndromes.A loss of CSF greater than its rate of production leads to a decreased volume inside the skull known as intracranial hypotension. Any CSF leak is most often characterized by orthostatic headaches, which worsen when standing, and improve when lying down. Other symptoms can include neck pain or stiffness, nausea, vomiting, dizziness, fatigue, and a metallic taste in the mouth. A CT myelography scan can identify the site of a cerebrospinal fluid leakage. Once identified, the leak can often be repaired by an epidural blood patch, an injection of the patients own blood at the site of the leak, a fibrin glue injection, or surgery. The set of symptoms associated with a sCSF leak is referred to as a spontaneous cerebrospinal fluid leak syndrome (SCSFLS). A sCSF leak is uncommon but not rare, affecting at least one in 20,000 people and many more who go undiagnosed every year. On average, the condition develops at age 42, and women are twice as likely to be affected. Some people with a sCSF leak have a chronic leak of cerebrospinal fluid despite repeated patching attempts, leading to long-term disability due to pain and being unable to be upright, and surgery is often needed. SCSFLS was first described by German neurologist Georg Schaltenbrand in 1938 and by American neurologist Henry Woltman of the Mayo Clinic in the 1950s. Classification Spontaneous cerebrospinal fluid leaks are classified into two main types: cranial leaks, and spinal leaks. The vast majority of leaks are spinal. Cranial leaks occur in the head, and in some of these cases, CSF can leak from the nose, or from the ear. Spinal leaks occur when one or more holes form in the dura along the spinal cord. Both cranial and spinal spontaneous CSF leaks cause neurological symptoms as well as spontaneous intracranial hypotension, diminished volume, and pressure of the cranium. While this symptom can be referred to as intracranial hypotension, the intracranial pressure may be normal, with the underlying issue instead being low CSF volume. For this reason, a SCSFL is referred to as CSF hypovolemia as opposed to CSF hypotension.Spontaneous intracranial hypotension, a subtype of CSF leak, refers to lower than normal than CSF volume due to an initially unknown or insidious cause. This differentiates it from CSF leaks of known causes such as cranial or spinal trauma, surgery or lumbar puncture or spinal anesthesia (most common cause of CSF leak). The International Classification of Headache Disorders (ICHD) Third Edition diagnostic criteria for spontaneous intracranial hypotension includes any headache attributed to low CSF pressure (low CSF opening pressure) or CSF leakage (evidence of CSF leakage on imaging). Further, the headache must have a temporal relation to the low CSF pressure or leakage and the headache cannot be better explained by another ICHD diagnosis. The final criteria is that in the rare cases of spontaneous intracranial hypotension with no headache present, the neurologic symptoms that are present must be attributable to low CSF or explained by the diagnosis of spontaneous intracranial hypotension. Signs and symptoms The most common symptom of a CSF leak is a fast-onset, extremely painful orthostatic headache or thunderclap headache. This headache is usually made worse by standing and typically becomes prominent throughout the day, with the pain becoming less severe when lying down. Orthostatic headaches can become chronic and disabling to the point of incapacitation. Some patients with a SCSFL will develop headaches that begin in the afternoon. This is known as second-half-of-the-day headache. This may be an initial presentation of a spontaneous CSF leak or appear after treatment such as an epidural patch, and likely indicates a slow CSF leak. While high CSF pressure can make lying down unbearable, low CSF pressure due to a leak can be relieved by lying flat on the back.About 50% of people with a CSFL experience neck pain or stiffness, nausea, and vomiting.Other symptoms of a CSF leak include photophobia, dizziness and vertigo, gait disturbances, tinnitus, facial numbness or weakness, visual disturbances, brain fog or difficulties with concentration, neuralgia, fatigue, fluid dripping from the nose or ears,Aural symptoms are also present in many cases of intracranial hypotension due to CSF leak; including muffled hearing, pulsatile tinnitus, hearing loss. Less common symptoms include double vision (due to cranial nerve 6 palsy) or tremor.Movement disorders are uncommon in spontaneous CSF leaks but occasionally can be one of the major components of the clinical presentation.Some cases of chronic intracranial hypotension due to CSF leak may present as personality changes, altered behaviors and impairment of executive functions, similar to behavioral-variant frontotemporal dementia as the frontal and temporal lobes are affected by downward sagging due to reduced intra-cranial pressures.An untreated CSF leak can result in coma or death as late stage findings as the brainstem herniates through the skull base or foramen magnum . Causes A spontaneous CSF leak is termed so as it has previously been thought to be idiopathic, meaning the cause is unknown. The evidence of the last decade suggests however, that these leaks result from either a discogenic pathology, such as microspur, osteophyte or intra-dural disc herniation that pierces the dura like a knife, connective tissue disorder (which can often lead to discogenic pathology), or spinal drainage problems.A cerebrospinal fluid leak can be a rare complication of an anterior cervical discectomy and fusion (ACDF). One study suggested a CSF leak to follow from 0.5% of operations. Another study suggests a CSF leak to follow from 1% of operations. In most of these cases repair is successful. Discogenic causes The most common cause of an intractable "sCSF" leak is discogenic, either from an intra-dural disc herniation, osteophyte or microspur on the disc or vertebral body. "Recent radiological and microsurgical investigations revealed that a calcified, degenerative bony microspur is often the culprit lesion in cases of intractable CSF leaks. Arising from the level of the intervertebrate disk space, these microspurs pierce the ventral dura and produce a slit-like defect a few millimeters in length. These microspurs and the associated CSF leak have to be localized exactly, and then they are amenable to surgical treatment." Connective tissue theory Various scientists and physicians have suggested that SCSFLs may be the result of an underlying connective tissue disorder affecting the spinal dura. It may also run in families and be associated with aortic aneurysms and joint hypermobility.Up to two thirds of those affected demonstrate some type of generalized connective tissue disorder. Marfan syndrome, Ehlers–Danlos syndrome, and autosomal dominant polycystic kidney disease are the three most common connective tissue disorders associated with SCSFLs. Roughly 20% of patients with a SCSFL exhibit features of Marfan syndrome, including tall stature, hollowed chest (pectus excavatum), joint hypermobility and arched palate. However, no other Marfan syndrome presentations are shown. Spinal drainage theory Some studies have proposed that issues with the spinal venous drainage system may cause a CSF leak. According to this theory, dural holes and intracranial hypotension are symptoms caused by low venous pressure in the epidural space. When inferior limb muscles pump blood towards the heart and pressure in the inferior vena cava vein becomes negative, the network of epidural veins is overdrained, causing CSF to be aspirated into the epidural space. True leaks can form at weak points in the spinal meninges. Therefore, the observed CSF hypotension is a result of CSF hypovolemia and reduced epidural venous pressure. Other causes Cranial CSF leaks result from intracranial hypertension in a vast majority of cases. The increased pressure causes a rupture of the cranial dura mater, leading to CSF leak and intracranial hypotension. Patients with a nude nerve root, where the root sleeve is absent, are at increased risk for developing recurrent CSF leaks. Lumbar disc herniation has been reported to cause CSF leaks in at least one case. Degenerative spinal disc diseases cause a disc to pierce the dura mater, leading to a CSF leak.CSF leaks can result from a lumbar puncture procedure. Complications Several complications can occur as a result of SCSFLS including decreased cranial pressure, brain herniation, infection, blood pressure problems, transient paralysis, and coma. The primary and most serious complication of SCSFLS is spontaneous intracranial hypotension, where pressure in the brain is severely decreased. This complication leads to the hallmark symptom of severe orthostatic headaches.People with cranial CSF leaks, the rarer form, have a 10% risk of developing meningitis per year. If cranial leaks last more than seven days, the chances of developing meningitis are significantly higher. Spinal CSF leaks cannot result in meningitis due to the sterile conditions of the leak site. When a CSF leak occurs at the temporal bone, surgery becomes necessary in order to prevent infection and repair the leak. Orthostatic hypotension is another complication that occurs due to autonomic dysfunction when blood pressure drops significantly. The autonomic dysfunction is caused by compression of the brainstem, which controls breathing and circulation.Low CSF volume can cause the cerebellar tonsil position to descend, which can be mistaken for Chiari malformation; however when the CSF leak is repaired the tonsil position often returns to normal (as seen in upright MRI) in this "pseudo-Chiari" condition. A further, albeit rare, complication of CSF leak is transient quadriplegia due to a sudden and significant loss of CSF. This loss results in hindbrain herniation and causes major compression of the upper cervical spinal cord. The quadriplegia dissipates once the patient lies supine. An extremely rare complication of SCSFLS is third nerve palsy, where the ability to move ones eyes becomes difficult and interrupted due to compression of the third cranial nerve.There are documented cases of reversible frontotemporal dementia and coma. Coma due to a CSF leak has been successfully treated by using blood patches and/or fibrin glue and placing the person in the Trendelenburg position. Empty sella syndrome, a bony structure that surround the pituitary gland, occurs in CSF leak patients. Pathophysiology Cerebrospinal fluid is produced by the choroid plexus in the ventricles of the brain and contained by the dura and arachnoid layers of the meninges. The brain floats in CSF, which also transports nutrients to the brain and spinal cord. As holes form in the spinal dura mater, CSF leaks out into the surrounding space. The CSF is then absorbed into the spinal epidural venous plexus or soft tissues around the spine. Due to the sterile conditions of the soft tissues around the spine, there is no risk of meningitis.Lack of CSF pressure and volume can allow the brain to sag and descend through the foramen magnum (large opening) of the occipital bone, at the base of the skull. The lower portion of the brain is believed to stretch or impact one or more cranial nerve complexes, thereby causing a variety of sensory symptoms. Nerves that can be affected and their related symptoms are detailed in the table at right. Diagnosis Diagnosis of CSF leakage can be done by various imaging techniques, chemical tests of bodily fluid discharged from a head orifice, or clinical examination. The use of CT, MRI, and assays are the most common types of CSF leak instrumental tests. Many CSF leaks do not show up on imaging and chemical assays, thus such diagnostic tools are not definitive to rule out CSF leaks. A clinician may often depend upon patient history and exam to diagnose, for example: discharge of excessive amount of clear fluid from the nose upon bending over, the increase in headache following a Valsalva maneuver or the reduction of headache when the patient takes a prone position are positive indicators. A clinical exam is often used as a means to diagnose CSF leaks. Improved patient response to conservative treatment may further define a positive diagnosis. The lack of clinician awareness of the signs -symptoms and ailments- of a CSF leak is the greatest challenge to proper diagnosis and treatment, in particular: the loss of the orthostatic characteristic of headache and that every chronic CSF leaker will have a unique symptom set that as a whole contributes to the underlying condition, and diagnosis of, a CSF leak. The primary place of first complaint to a physician is a hospital emergency room. Up to 94% of those with SCSFLS are initially misdiagnosed. Incorrect diagnoses include migraines, meningitis, Chiari malformation, and psychiatric disorders. The average time from onset of symptoms until definitive diagnosis is 13 months. A 2007 study found a 0% success rate for proper diagnosis in the emergency department. CT Diagnosis of a cerebrospinal fluid leak is performed through a combination of measurement of the CSF pressure and a computed tomography myelogram (CTM) scan of the spinal column for fluid leaks. The opening fluid pressure in the spinal canal is obtained by performing a lumbar puncture, also known as a spinal tap. Once the pressure is measured, a radiocontrast agent is injected into the spinal fluid. The contrast then diffuses out through the dura sac before leaking through dural holes. This allows for a CTM with fluoroscopy to locate and image any sites of dura rupture via contrast seen outside the dura sac in the imagery. MRI There is disagreement over whether MRI should be the diagnostic tool of choice. Magnetic resonance imaging is less effective than CT at directly imaging sites of CSF leak. MRI studies may show pachymeningeal enhancement (when the dura mater looks thick and inflamed), sagging of the brain, pituitary enlargement, subdural hygromas, engorgement of cerebral venous sinuses, and other abnormalities. For 20% of patients, MRIs present as completely normal. MRIs performed with the patient seated upright (vs. laying supine) are not better for diagnosing CSF leaks, but are more than twice as effective at diagnosing cerebellar tonsillar ectopia, also known as Chiari malformation. Cerebellar tonsillar ectopia shares many of the same symptoms as CSF leak, but originates either congenitally or from trauma, including whiplash strain to the dura.An alternate method of locating the site of a CSF leak is to use heavily T2-weighted MR myelography. This has been effective in identifying the sites of a CSF leak without the need for a CT scan, lumbar puncture, and contrast and at locating fluid collections such as CSF pooling. Another highly successful method of locating a CSF leak is intrathecal contrast and MR Myelography.Contrast-enhanced brain MRI with sagittal reformats can assess for the following: Subdural fluid collections Enhancement of the meninges Engorgement of venous structures Pituitary swelling Sagging of the brainFor suspected spinal CSF leaks, spine imaging can be used to guide treatment. Assay Fluid dripping from the nose (CSF rhinorrhoea) or ears (CSF otorrhea) should be collected and tested for the protein Beta-2 transferrin which would be highly accurate in identifying CS fluid and diagnosing a cranial CSF leak. CSF analysis Patients with CSF leaks have been noted to have very low or even negative opening pressures during lumbar puncture. However, patients with confirmed CSF leaks may also demonstrate completely normal opening pressures. In 18–46% of cases, the CSF pressure is measured within the normal range. Analysis of spinal fluid may demonstrate lymphocytic pleocytosis and elevated protein content or xanthochromia. This is hypothesized to be due to increased permeability of dilated meningeal blood vessels and a decrease of CSF flow in the lumbar subarachnoid space. Myelography A myelogram can be used to more precisely identify the location of a CSF leak by injecting a dye to further enhance the imaging. However, CSF leaks are frequently not visible on imaging.For patients with recalcitrant spontaneous intracranial hypotension and no leak found on conventional spinal imaging, digital subtraction myelography, CT myelography and dynamic myelography (a modified conventional myelography technique) should be considered to rule out a CSF-venous fistula. In addition, presence of a hyperdense paraspinal vein should be investigated in imaging as it is highly suggestive of a CSF venous fistula. Treatment Symptomatic treatment usually involves analgesics for both cranial and spinal CSF leaks. Initial measures can include rest, caffeine intake (via coffee or intravenous infusion), and hydration. Corticosteroids may provide transient relief for some patients. An abdominal binder, which increases intracranial pressure by compressing the abdomen, can temporarily relieve symptoms for some people. Sometimes a CSF leak will heal on its own. Otherwise, symptoms may last months or even years. Epidural blood patch The treatment of choice for this condition is the surgical application of epidural blood patches, which has a higher success rate than conservative treatments of bed rest and hydration. Through the injection of a persons own blood into the area of the hole in the dura, an epidural blood patch uses bloods clotting factors to clot the sites of holes. The volume of autologous blood and number of patch attempts for patients is highly variable. One-quarter to one-third of SCSFLS patients do not have relief of symptoms from epidural blood patching. Finding the location of a cerebrospinal fluid leak is not required prior to using an epidural blood patch as initial lumbar epidural blood patches often provide relief of symptoms and resolve the leak without further intervention. Fibrin glue sealant If blood patches alone do not succeed in closing the dural tears, placement of percutaneous fibrin glue can be used in place of blood patching, raising the effectiveness of forming a clot and arresting CSF leakage. Surgical drain technique In extreme cases of intractable CSF leak, a surgical lumbar drain has been used. This procedure is believed to decrease spinal CSF volume while increasing intracranial CSF pressure and volume. This procedure restores normal intracranial CSF volume and pressure while promoting the healing of dural tears by lowering the pressure and volume in the dura. This procedure has led to positive results leading to relief of symptoms for up to one year. Neurosurgical repair Surgery to treat a CSF-venous fistula in CSF leak patients is highly effective. Neurosurgery is available to directly repair leaking meningeal diverticula. The areas of dura leak can be tied together in a process called ligation and then a metal clip can be placed in order to hold the ligation closed. Alternatively, a small compress called a pledget can be placed over the dura leak and then sealed with gel foam and fibrin glue. Primary suturing is rarely able to repair a CSF leak, and in some patients exploration of the dura may be required to properly locate all sites of CSF leak. Adjunct measures The use of antibiotics to prevent meningitis in those with a CSF leak due to a skull fracture is of unclear benefit. Prognosis Long-term outcomes for people with SCSFLS remain poorly studied. Symptoms may resolve in as little as two weeks, or persist for months. Less commonly, patients may have unremitting symptoms for many years. People with chronic SCSFLS may be disabled and unable to work. Recurrent CSF leak at an alternate site after recent repair is common. Epidemiology A 1994 community-based study indicated that two out of every 100,000 people with SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study, women were found to be twice as likely to be affected as men.Studies have shown that SCSFLS runs in families. It is suspected that genetic similarity in families includes weakness in the dura mater which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely. History Spontaneous CSF leaks have been described by notable physicians and reported in medical journals dating back to the early 1900s. German neurologist Georg Schaltenbrand reported in 1938 and 1953 what he termed "aliquorrhea", a condition marked by very low, unobtainable, or even negative CSF pressures. The symptoms included orthostatic headaches and other features that are now recognized as spontaneous intracranial hypotension. A few decades earlier, the same syndrome had been described in French literature as "hypotension of spinal fluid" and "ventricular collapse". In 1940, Henry Woltman of the Mayo Clinic wrote about "headaches associated with decreased intracranial pressure". The full clinical manifestations of intracranial hypotension and CSF leaks were described in several publications reported between the 1960s and early 1990s. Modern reports of spontaneous CSF leak have been reported to medical journals since the late 1980s. Research Tetracosactide is a corticosteroid that causes the brain to produce additional spinal fluid to replace the volume of the lost CSF and alleviate symptoms, and has been given intravenously to treat CSF leaks.In three small studies of 1-2 patients with recurrent CSF leaks where repeated blood patches failed to form clots and relieve symptoms, the patients received temporary but complete resolution of symptoms with an epidural saline infusion. The saline infusion temporarily restores the volume necessary for a patient to avoid SIH until the leak can be repaired properly. Intrathecal saline infusion is used in urgent cases such as intractable pain or decreased consciousness.The gene TGFBR2 has been implicated in several connective tissue disorders including Marfan syndrome, arterial tortuosity, and thoracic aortic aneurysm. A study of patients with SCSFLS demonstrated no mutations in this gene. Minor features of Marfan syndrome have been found in 20% of CSF leak patients. Abnormal findings of fibrillin-1 have been documented in these CSF leak patients, but only one patient demonstrated a fibrillin-1 defect consistent with Marfan syndrome. See also Subdural effusion References External links CFS leak info Spinal CSF leak Spinal CSF leak Canada

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I'm trying to expand my medical knowledge. Can you elucidate the term 'Polyarteritis nodosa'?

Polyarteritis nodosa (PAN) is a systemic necrotizing inflammation of blood vessels (vasculitis) affecting medium-sized muscular arteries, typically involving the arteries of the kidneys and other internal organs but generally sparing the lungs circulation. Small aneurysms are strung like the beads of a rosary, therefore making this "rosary sign" an important diagnostic feature of the vasculitis. PAN is sometimes associated with infection by the hepatitis B or hepatitis C virus. The condition may be present in infants.PAN is a rare disease. With treatment, five-year survival is 80%; without treatment, five-year survival is 13%. Death is often a consequence of kidney failure, myocardial infarction, or stroke. Signs and symptoms PAN may affect nearly every organ system and thus can present with a broad array of signs and symptoms. These manifestations result from ischemic damage to affected organs, often the skin, heart, kidneys, and nervous system. Constitutional symptoms are seen in up to 90% of affected individuals and include fever, fatigue, weakness, loss of appetite, and unintentional weight loss.Skin: The skin may show rashes, swelling, necrotic ulcers, and subcutaneous nodules (lumps). Skin manifestations of PAN include palpable purpura and livedo reticularis in some individuals.Neurologic system: Nerve involvement may cause sensory changes with numbness, pain, burning, and weakness (peripheral neuropathy). Peripheral nerves are often affected, and this most commonly presents as mononeuritis multiplex, which is the most common neurologic sign of PAN. Mononeuritis multiplex develops in more than 70% of patients with polyarteritis nodosa because of damage to arteries supplying large peripheral nerves. Most cases are marked by asymmetric polyneuropathy, but progressive disease can lead to symmetric nerve involvement. Central nervous system involvement may cause strokes or seizures.Renal system: Kidney involvement is common and often leads to death of parts of the kidney. Involvement of the renal artery, which supplies the kidneys with highly oxygenated blood, often leads to high blood pressure in about one-third of cases. deposition of protein or blood in the urine may also be seen. Almost all patients with PAN have renal insufficiency caused by renal artery narrowing, thrombosis, and infarctions. Cardiovascular system: Involvement of the arteries of the heart may cause a heart attack, heart failure, and inflammation of the sac around the heart (pericarditis).Gastrointestinal system: Damage to mesenteric arteries can cause abdominal pain, mesenteric ischemia, and bowel perforation. Abdominal pain may also be seen. Musculoskeletal system: Muscle and joint aches are common. Complications Stroke Heart failure resulting from cardiomyopathy and pericarditis Intestinal necrosis and perforation Causes PAN has no association with anti-neutrophil cytoplasmic antibodies, but about 30% of people with PAN have chronic hepatitis B and deposits containing HBsAg-HBsAb complexes in affected blood vessels, indicating an immune complex-mediated cause in that subset. Infection with the hepatitis C virus and HIV are occasionally discovered in people affected by PAN. PAN has also been associated with underlying hairy cell leukemia. The cause remains unknown in the remaining cases; there may be causal and clinical distinctions between classic idiopathic PAN, the cutaneous forms of PAN, and PAN associated with chronic hepatitis. In children, cutaneous PAN is frequently associated with streptococcal infections, and positive streptococcal serology is included in the diagnostic criteria. Diagnosis No specific lab tests exist for diagnosing polyarteritis nodosa. Diagnosis is generally based on the physical examination and a few laboratory studies that help confirm the diagnosis: CBC (may demonstrate an elevated white blood count) ESR (elevated) Perinuclear pattern of antineutrophil cytoplasmic antibodies (p-ANCA) - not associated with "classic" polyarteritis nodosa, but is present in a form of the disease affecting smaller blood vessels, known as microscopic polyangiitis or leukocytoclastic angiitis Tissue biopsy (reveals inflammation in small arteries, called arteritis) Elevated C-reactive proteinA patient is said to have polyarteritis nodosa if he or she has three of the 10 signs known as the 1990 American College of Rheumatology (ACR) criteria, when a radiographic or pathological diagnosis of vasculitis is made: Weight loss greater than/equal to 4.5 kg Livedo reticularis (a mottled purplish skin discoloration over the extremities or torso) Testicular pain or tenderness (occasionally, a site biopsied for diagnosis) Muscle pain, weakness, or leg tenderness Nerve disease (either single or multiple) Diastolic blood pressure greater than 90 mmHg (high blood pressure) Elevated kidney blood tests (BUN greater than 40 mg/dL or creatinine greater than 1.5 mg/dL) Hepatitis B (not C) virus tests positive (for surface antigen or antibody) Arteriogram (angiogram) showing the arteries that are dilated (aneurysms) or constricted by the blood vessel inflammation Biopsy of tissue showing the arteritis (typically inflamed arteries): The sural nerve is a frequent location for the biopsy. In polyarteritis nodosa, small aneurysms are strung like the beads of a rosary, therefore making this "rosary sign" an important diagnostic feature of the vasculitis. The 1990 ACR criteria were designed for classification purposes only, but their good discriminatory performances, indicated by the initial ACR analysis, suggested their potential usefulness for diagnostic purposes as well. Subsequent studies did not confirm their diagnostic utility, demonstrating a significant dependence of their discriminative abilities on the prevalence of the various vasculitides in the analyzed populations. Recently, an original study, combining the analysis of more than 100 items used to describe patients characteristics in a large sample of vasculitides with a computer simulation technique designed to test the potential diagnostic utility of the various criteria, proposed a set of eight positively or negatively discriminating items to be used as a screening tool for diagnosis in patients suspected of systemic vasculitis. Differential diagnosis Polyarteritis nodosa rarely affects the blood vessels of the lungs and this feature can help to differentiate it from other vasculitides that may have similar signs and symptoms (e.g., granulomatosis with polyangiitis or microscopic polyangiitis). Treatment Treatment involves medications to suppress the immune system, including prednisone and cyclophosphamide. When present, underlying hepatitis B virus infection should be immediately treated. In some cases, methotrexate or leflunomide may be helpful. Some patients have entered a remission phase when a four-dose infusion of rituximab is used before the leflunomide treatment is begun. Therapy results in remissions or cures in 90% of cases. Untreated, the disease is fatal in most cases. The most serious associated conditions generally involve the kidneys and gastrointestinal tract. A fatal course usually involves gastrointestinal bleeding, infection, myocardial infarction, and/or kidney failure.In case of remission, about 60% experience relapse within five years. In cases caused by hepatitis B virus, however, recurrence rate is only around 6%. Epidemiology The condition affects adults more frequently than children and males more frequently than females. Most cases occur between the ages of 40 and 60. Polyarteritis nodosa is more common in people with hepatitis B infection. History The medical eponyms Kussmaul disease or Kussmaul-Maier disease reflect the seminal description of the disease in the medical literature by Adolph Kussmaul and Rudolf Robert Maier. Culture In the 1956 American film Bigger Than Life, the protagonist character played by James Mason is diagnosed with polyarteritis nodosa after experiencing excruciating chest pain and is treated with cortisone. References == External links ==

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What is the significance of the term 'Ectopic testis' in the medical field?

A ectopic testis is a testicle that, although not an undescended testicle, has taken a non-standard path through the body and ended up in an unusual location.The positions of the ectopic testis may be: in the lower part of the abdomen, front of thigh, femoral canal, skin of penis or behind the scrotum. The testis is usually developed, and accompanied by an indirect inguinal hernia. It may be divorced from the epididymis which may lie in the scrotum. See also Cryptorchidism Orchiopexy References == External links ==

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I'm trying to understand 'Intrahepatic cholestasis of pregnancy' within a medical context. Could you shed some light on it?

Intrahepatic cholestasis of pregnancy (ICP), also known as obstetric cholestasis, cholestasis of pregnancy, jaundice of pregnancy, and prurigo gravidarum, is a medical condition in which cholestasis occurs during pregnancy. It typically presents with itching and can lead to complications for both mother and baby. Pruritus (itching) is a common symptom of pregnancy, affecting around 23% of women. The majority of times, itching is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching may be a symptom of ICP. Although typically noticed on the palms of the hands and the soles of the feet, the itching can occur anywhere on the body. ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy. Signs and symptoms Most women with this condition present in the third trimester (although it can present as early as seven weeks) with itching without a rash. Typically, the itching is localized to the palms of the hands and soles of the feet, but can be anywhere on the body. Hallmarks of ICP include the following symptoms:Most common: Itching, in particular but not limited to that of the palms of the hands and soles of the feet, without presence of a rash Itching that is more noticeable in the evening Darker urineLess common: Lighter stools Increased clotting time (due to possibly associated vitamin K deficiency) Fatigue Increased nausea Decrease in appetite Jaundice (less than 10% of women) Upper right quadrant painNot all ICP sufferers have all of the above symptoms. Mechanism The causes of intrahepatic cholestasis of pregnancy are still not fully understood, but are thought to be caused through a combination of genetics, hormones and environment. Hormones, environmental and genetic factors are all thought to contribute to the condition. ICP commonly occurs in the third trimester at the time when hormone levels are at their highest. Twin and triplet pregnancies, which are associated with higher hormone levels, show a higher incidence of ICP. ICP resolves quickly after delivery, when placental hormone production ceases. Older high-dose estrogen oral contraceptive pills could cause features of ICP. Estrogens Estrogens, and particularly glucuronides such as estradiol-17β-D-glucuronide, have been shown to cause cholestasis in animal studies, by reducing bile acid uptake by hepatocytes. Progesterone Treatment with progesterone in the third trimester of pregnancy has been shown to be associated with the development of ICP, and levels of metabolites of progesterone, particularly sulfated progesterone, are higher in patients with ICP than unaffected women, suggesting that progesterone may have a bigger role than estrogen in ICP. Genetic factors Clustering of cases of ICP in families, geographic variation in rates of ICP, and recurrence of ICP in 45-70% of subsequent pregnancies all suggest a genetic component to the disease. Genetic mutations in the hepatocellular transport protein ABCB4 (MDR3), which controls secretion of phosphatidylcholine into bile, have been found in cases of ICP.Genetic mutations affecting hepatic bile salt transport molecules have also been found in patients with progressive familial intrahepatic cholestasis. It has been found that mothers of patients with this disease have a higher incidence of ICP, suggesting that heterozygote carriers of these mutations are also predisposed to ICP.In addition to genetic changes to bile salt transport molecules, high levels of estrogen glucuronides have been shown to inhibit the bile salt export pump (BSEP) ABCB11, and high levels of progesterone to inhibit the ABCB4 (MDR3) phospholipid transporter.Consequently, both genetic mutations in hepatocyte proteins involved in bile secretion together with inhibition of those proteins by high levels of hormone metabolites in pregnancy may have roles in the pathogenesis of ICP. Environmental factors A number of features of ICP suggest that environmental factors also have a role in the disease: It has been reported that the incidence of ICP is higher in winter than summer. The incidence of ICP in Chile has dropped from 14% of pregnancies before 1975 to 4% in 2016. ICP recurs in between 60% and 90% of subsequent pregnancies. Low serum selenium levels have been linked to ICP, although the role of selenium in bile secretion is not known. Diagnosis ICP is diagnosed by blood tests including a serum bile acid test and liver function test. While most pregnant women experience some itch from time to time, itching without a visible rash, or persistent or extensive itch symptoms should be reported to the midwife or obstetrician. It is important to note that as the level of itch does not correlate with bile acid levels (shown to be the most likely cause of stillbirth in ICP), the itch in ICP can range from being mild to severe.To obtain a diagnosis of ICP, a liver function test and a serum bile acid test should be requested. Although the ALT level may be raised, 20% of women with ICP will always have a normal LFT test result. This, plus pruritus of palms and soles, could be considered as potentially diagnostic of ICP but only with elevated bile acid levels (however LFTs are not always elevated in ICP patients). The serum bile acid blood test for ICP is a quantitative measurement of bile acids. Other problems with the liver that occur in pregnancy should be considered by the treating clinician. These include preeclampsia, the HELLP syndrome, and acute fatty liver of pregnancy. Furthermore, other causes of hepatitis, like hepatitis viruses, cancer and certain medications, should also be considered. Treatment Many providers will prescribe ursodeoxycholic acid. The most recent trial, PITCHES, did not show an overall beneficial effect, but some researchers believe that it may still be useful to offer ursodeoxycholic acid to women whose bile acids are > 40 μmol/litre. While there is no cure for ICP, and no way to guarantee a successful outcome, studies have shown a slightly better fetal and maternal outcome from administration of ursodeoxycholic acid, whereas cholestyramine appears to only relieve itching.There is no evidence that giving oral water-soluble Vitamin K may help to avoid the risk of hemorrhage at delivery. However, experts in ICP will prescribe this if the woman reports pale stools, has very severe ICP (bile acids > 100 μmol/litre) or has a known clotting problem. Delivery from 34 weeks may be important to reduce the risk of stillbirth, as a recent study identified the level of bile acids at which stillbirth risk rises. This research, published in The Lancet, also suggests that around 90% of women with ICP could wait until 39 weeks of pregnancy to be induced. However, this relies on regular bile acid testing with rapid return of results. Risks if untreated Maternal consequences include the following: Itching, which can become intense and debilitating Spontaneous premature labour when bile acids rise above 40 μmol/litreFetal consequences include: Fetal distress Meconium ingestion StillbirthIn most cases induction is typically recommended anywhere from 34–39 weeks.In the United States, some researchers have suggested that the risk of stillbirth is lower if induction occurs at 36 weeks. Whilst Ovadias research suggests differently, it is important to note that in the United States bile acid tests can take up to seven days to be processed, and this means that it may be more prudent to base delivery on the US research. See also Cholestasis Cholestatic pruritus List of cutaneous conditions Pruritic urticarial papules and plaques of pregnancy (PUPPP) an itchy condition of pregnancy that is associated with a rash. References External links E A Fagan "Intrahepatic cholestasis of pregnancy"

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

The term 'Olecranon bursitis' keeps coming up in medical discussions. What does it stand for?

Olecranon bursitis is a condition characterized by swelling, redness, and pain at the tip of the elbow. If the underlying cause is due to an infection, fever may be present. The condition is relatively common and is one of the most frequent types of bursitis.It usually occurs as a result of trauma or pressure to the elbow, infection, or certain medical conditions such as rheumatoid arthritis or gout. Olecranon bursitis is associated with certain types of work including plumbing, mining, gardening, and mechanics. The underlying mechanism is inflammation of the fluid filled sac between the olecranon and skin. Diagnosis is usually based on symptoms.Treatment involves avoiding further trauma, a compression bandage, and NSAIDs. If there is concern of infection the fluid should be drained and tested and antibiotics are typically recommended. The use of steroid injections is controversial. Surgery may be done if other measures are not effective. Signs and symptoms Symptoms include swelling in the elbow, which can sometimes be large enough to restrict motion. There is pain originating in the elbow joint from mild to severe which can spread to the rest of the arm. If the bursa is infected, there also will be prominent redness and the skin will feel very warm. Another symptom would include the infected bursa possibly opening spontaneously and draining pus. Causes Bursitis normally develops as a result either of a single injury to the elbow (for example, a hard blow to the tip of the elbow), or perhaps more commonly due to repeated minor injuries, such as repeated leaning on the point of the elbow on a hard surface. The chance of developing bursitis is higher if ones job or hobby involves a repetitive movement (for example, tennis, golf, or even repetitive computer work involving leaning on ones elbow). The likelihood of developing the condition is increased as one gets older.As a reaction to injury, the lining of the bursa becomes inflamed. It then secretes a much greater than normal amount of fluid into the closed cavity of the bursa, from where it has nowhere to go. The bursa therefore inflates, producing a swelling over the proximal end of the ulna which is usually inflamed and tender.Another possible cause of inflammation of the bursa is infection, which can usually (but not always) be traced to a crack or other lesion in the skin which allowed for bacteria of the normal skin flora to invade deeper layers of tissue.This bursa is located just over the extensor aspect of the extreme proximal end of the ulna. In common with other bursae, it is impalpable and contains only a very small amount of fluid in its normal state, and fulfills the function of facilitating the joints movement by enabling anatomical structures to glide more easily over each other. Diagnosis Diagnosis is usually based on symptoms. If there is concern of infection the fluid should be drained and tested. Treatments Non-surgical Conservative management of minor cases involves icing, a compression bandage, and avoidance of the aggravating activity. This can also be augmented with NSAIDs taken by mouth or applied as a cream. Elbow padding can also be used for symptomatic relief. The use of steroid injections is controversial.In case of infection, the bursitis should be drained and treated with an antibiotic. Surgery If the fluid continues to return after multiple drainings or the bursa is constantly causing pain, surgery to remove the bursa is an option. The minor operation removes the bursa from the elbow and is left to regrow but at a normal size over a period of ten to fourteen days. It is usually done under general anesthetic and has minimal risks. The surgery does not disturb any muscle, ligament, or joint structures. To recover from surgical removal, a splint will be applied to the arm to protect the skin. Exercises will be prescribed to improve range of motion. References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'd like to learn more about the medical term 'Tarka.' Can you provide some details?

Tarka may refer to: Tarka, also Chhaunk, in Indian cuisine is a method of seasoning food with spices heated in oil or ghee Tarka, Nigeria, a Local Government Area in Benue State, Nigeria Tarka, Niger Tarka the Otter, a 1927 novel by Henry Williamson Tarka Line, a railway line in Devon, England Tarka Trail, a series of footpaths assembled from former railway lines Tarka (medication), a brand name for an antihypertensive medication Tarka (flute), also tharqa, a traditional flute of the Andes David Tarka (born 1983), Australian football player Taharqa, Nubian pharaoh of the twenty-fifth Dynasty of Egypt Tarka (film), a 1988 Kannada language movie Taarka, an Oregonian quartet Tarka Cordell (1968–2008), British musician, writer and record producer Wiesław Tarka (born 1964), Polish diplomat The Tarka, an alien race in the video game Sword of the Stars See also Tarka sastra, an Indian science of dialectics, logic and reasoning

You act as a mediator between medical professionals and the public. Provide comprehensive explanations of medical terms, ensuring they are both precise and easily understood.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Icatibant'?

Icatibant, sold under the brand name Firazyr, is a medication for the symptomatic treatment of acute attacks of hereditary angioedema (HAE) in adults with C1-esterase-inhibitor deficiency. It is not effective in angioedema caused by medication from the ACE inhibitor class.It is a peptidomimetic consisting of ten amino acids, which is a selective and specific antagonist of bradykinin B2 receptors. Mechanism of action Bradykinin is a peptide-based hormone that is formed locally in tissues, very often in response to a trauma. It increases vessel permeability, dilates blood vessels and causes smooth muscle cells to contract. Bradykinin plays an important role as the mediator of pain. Surplus bradykinin is responsible for the typical symptoms of inflammation, such as swelling, redness, overheating and pain. These symptoms are mediated by activation of bradykinin B2 receptors. Icatibant acts as a bradykinin inhibitor by blocking the binding of native bradykinin to the bradykinin B2 receptor. Little is known about the effects of icatibant on the bradykinin B1 receptor. Society and culture Legal status Icatibant received orphan drug status in Australia, the EU, Switzerland, and the US for the treatment of hereditary angioedema (HAE).In the EU, the approval by the European Commission (July 2008) allows Jerini to market Firazyr in the European Unions 27 member states, as well as Switzerland, Liechtenstein and Iceland, making it the first product to be approved in all EU countries for the treatment of HAE. In the US, the drug was granted FDA approval on August 25, 2011. References External links "Icatibant". Drug Information Portal. U.S. National Library of Medicine. "Icatibant acetate". Drug Information Portal. U.S. National Library of Medicine.