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2. | being male | null | null | null | null |
3. | being Caucasian | null | null | null | null |
4. | being over the age of 50 | null | null | null | null |
5. | having H pylori gastritis | null | null | null | null |
6. | smoking | null | null | null | null |
7. | being obese | null | null | null | null |
8. | smoking | null | null | null | null |
9. | alcohol | null | null | null | null |
10. | frequent use of NSAIDS or Aspirin | null | null | null | null |
11. | eating large portions at meals | null | null | null | null |
12. | diets high in saturated fats | null | null | null | null |
13. | spicy foods | null | null | null | null |
14. | going to bed or lying down less than four hours after eating | null | null | null | null |
null | null | null | null | null | null |
Risk | factor of stomach cancer: | null | null | null | null |
1- | Age. Stomach cancer occurs most commonly in people older than 55. Most people diagnosed with stomach cancer are in their 60s and 70s. | null | null | null | null |
2- | Gender. Men are twice as likely to develop stomach cancer as women. | null | null | null | null |
3- | Bacteria. A common bacterium called Helicobacter pylori, also called H. pylori, causes stomach inflammation and ulcers. It is also considered one of the main causes of stomach cancer. Testing for H. pylori is available and an infection can be treated with antibiotics. Testing for H. pylori is recommended if you have had a first- degree relative, such as a parent, sibling, or child, who has been diagnosed with stomach cancer or an H. pylori infection. Other family members could have it as well, and the infection should be treated if found. | null | null | null | null |
4- | Family history/genetics. People who have a parent, child, or sibling who has had stomach cancer have a higher risk of the disease. In addition, certain inherited genetic disorders, such as hereditary diffuse gastric cancer, Lynch syndrome, hereditary breast and ovarian cancer (HBOC), and familial adenomatous polyposis (FAP) may increase the risk of stomach cancer. Learn more about genetics and cancer. | null | null | null | null |
5- | Race/ethnicity. Stomach cancer is more common in Black, Hispanic, and Asian people than in white people. | null | null | null | null |
6- | Diet. Eating a diet high in salt has been linked to an increased risk of stomach cancer. This includes foods preserved by drying, smoking, salting, or pickling and foods high in added salt. Eating fresh fruits and vegetables may help lower the risk. | null | null | null | null |
7- | Previous surgery or health conditions. People who have had stomach surgery, pernicious anemia, or achlorhydria have a higher risk of stomach cancer. Pernicious anemia happens when the stomach cannot take in enough vitamin B12. This causes a severe decrease in red blood cells. Achlorhydria is when there there is no hydrochloric acid in the gastric juices, which help digest food. | null | null | null | null |
8- | Occupational exposure. Exposure to certain dusts and fumes may increase the risk of developing stomach cancer. | null | null | null | null |
9- | Tobacco and alcohol. Tobacco use and drinking a lot of alcohol may increase the risk of developing stomach cancer. | null | null | null | null |
10- | Obesity. Excess body weight increases a man's risk of developing stomach cancer. It is not clear whether obesity increases a woman's risk of stomach cancer. | null | null | null | null |
null | Child-Turcotte-Pugh | score system for | cirrhosis | null | null |
Clinical variable | 1 point | 2 point | 3 point | null | null |
Encephalopathy | None | Stage 1-2 | Stage 3-4 | null | null |
Ascites | Absent | Slight | Moderate | null | null |
Bilirubin(mg/dl) | <2 | 2-3 | >3 | null | null |
Bilirubin in PSC or PBC (mg/dl) | <4 | 4-10 | >10 | null | null |
Albumin (g/dl) | >3.5 | 2.8-3.5 | <2.8 | null | null |
Prothrombin (sec) or INR | <4 sec or INR< 1.7 | 4-6 sec or INR 17-2.3 | > 6 sec or INR > 2.3 | null | null |
null | Disease | Pathogenesis | Characteristics | Dx and Tx | null |
Familial non- hemolytic unconjugated hyperbilirubinemia | Criglar - Najjar type 1 | Glucuronosy transferase deficiency ( autosomal recessive ) | - Rapid rise of unconjugated bilirubin in the first day of life - Persistence of bilirubin >20 mg/dl in absence of hemolysis after first week - Almost all infant have kernicterus | Dx: closed liver biopsy to measure glucuronosy| transferase Tx : intensive phototherapy and exchange therapy | null |
null | Criglar - Najjar type 2 | Partial enzymatic deficiency ( autosomal dominant ) | - May be similar to type 1 or milder with delayed onset . Kernicterus is not common | Dx and Tx different from type I: will respond to oral phenobarbital | null |
null | Gilbert syndrome | Low glucuronosy transferase with unconjugated hyperbilirubinemia | Benign disorder | No treatment necessary | null |
Inherited conjugated hyperbilirubinemia | Dubin - Johnson syn, Rotor syn | Transfer of bilirubin and other organic anions from liver to bile is defective (autosomal recessive | Chronic, mild conjugated hyperbilirubinemia | Dx : usually detect in adolescence | null |
Area of infarction | ECG changes | Artery involved | null | null | null |
Anterior MI | V2-V4 | Left anterior descending | null | null | null |
Anteroseptal MI | V1-V3 | Left anterior descending | null | null | null |
Inferior MI | ST elevation II,III,aVF | Right coronary, left circumflex | null | null | null |
Lateral MI | ST elevation I, aVL, V5 ,V6 ST depression II, III, aVF | Left circumflex | null | null | null |
Posterior MI | ST depression V1-V3 ST elevation I ,aVL (left circumflex) ST depression I, aVL (right coronary ) | Left circumflex, , right coronary | null | null | null |
Right ventricle MI | ST elevation V4-V6 | Right coronary | null | null | null |
null | null | null | null | null | null |
Substances | Drug | Administration | Monitori ng during therapy | Antidote | null |
Unfractionated heparin | Heparin | Prophylaxis : SC Therapeutic : IV | aPTT | Protamine sulfate | null |
Low molecular weight heparin | Enoxaparin Dalteparin Tinzaparin Nadroparin | SC | anti-factor Xa activity | protamine sulfate (partial reversal 50 %) | null |
Synthetic heparin | fondaparinux | SC | Anti- factor Xa activity | activated prothrombin complex concentrates (aPCC) | null |
Direct thrombin inhibitors | Argatroban Bivalirudin Desirudin Dabigatran | Argatroban, Bivalirudin, Desirudin : IV Dabigatran: oral | aPTT | aPCC and/or antifibrinolytics(tranex amic acid) -Dabigatran : idarucizumab (monoclonal antibody) | null |
Direct factor Xa inhibitors | Apixaban Rivaroxaban Edoxaban | Oral | Not required | andexanet alfa | null |
Vit K antagonist | Warfarin | Oral | PT/INR | IV vit K and fresh frozen plasma | null |
Systolic murmur | Diastolic murmur | null | null | null | null |
Mid systolic : AS,PS,ASD,HOCM | Early diastolic : AR,PR,Austin flint | null | null | null | null |
Holosystolic : MR, TR, VSD | Mid and late diastolic : MS,TS,graham-steel (murmur of PR) | null | null | null | null |
Late systolic : MVP | null | null | null | null | null |
null | Discrete juxtaductal coarctation (adult type) | Tubular hypoplasia (preductal, infantile type) | null | null | null |
null | B | A | null | null | null |
Pathophysiology: | - Ascending aortic blood flows normally through narrowed segment to reach Descending aorta >> left ventricular hypertrophy and hypertension | - Severe narrowing starting at one of the head or neck vessels and extending to the Ductus - Right ventricular blood flows across the PDA to supply the descending aorta so the Perfusion of the lower part of the body is dependent upon right ventricular output | null | null | null |
null | null | null | null | null | null |
Clinical pictures: | 1. - No symptoms if mild 2- Blood pressure : high in upper half of the body low in lower half of the body leg systolic pressure is decreased (>5%) than arm Note: Normally, leg systolic pressure is 10-20 mm Hg higher than in arms If pressure is greater in right arm than left arm, suggests coarctation involving left subclavian artery 3- pulse : weak or absent in lower half of the body bounding (very strong ) in upper half of the body delay in femoral pulse compared to radial Note: femoral normally occurs slightly before radial) 4- Short systolic murmur along left sternal border at third-to-fourth intercostals space >> left scapula and neck 5- Hypertension due not only to mechanical but also to neurohormonal reasons 6- extensive collateral circulation >> systolic or continuous murmurs over left and right sides of chest with thrills 7- rib notching (dilated intercostal arteries) | 1- - differential cyanosis : upper body is pink, lower is cyanotic 2- prominent heart failure as ductus closes 3- lower body hypoperfusion 4- acidosis 5- large heart 6- systolic murmur along left sternal border | null | null | null |
Diagnosis: | 1 - chest X- ray : increased heart size and pulmonary congestion 2- ECG : left ventricular hypertrophy 3- Echocardiogram (gold standard) | I - Chest x-ray : occur after first decade: A. Increased size of subclavian artery-prominent shadow in left superior mediastinum B. Notching of inferior border of ribs from passive erosion of increased collaterals in late childhood C. Poststenotic dilatation of ascending aorta | null | null | null |
null | null | 2- ECG :biventricular hypertrophy 3- Echocardiogram (gold standard) | null | null | null |
Treatment: | - treat heart failure and hypertension, and then follow with surgery | I - PGE1 infusion to maintain patent, ductus, which establishes adequate lower extremity blood flow; surgery after stabilization 2- Surgery soon after diagnosis of any significant coarctation | null | null | null |
Answer: B | null | null | null | null | null |
Clinical pictures of left sided heart failure | Clinical pictures of right sided heart failure | null | null | null | null |
1. Dyspnea | 1. Peripheral edema | null | null | null | null |
2. orthopnea | 2. ascites | null | null | null | null |
3. paroxysmal nocturnal dyspnea | 3. Jugular venous distention | null | null | null | null |
4. Fatigue - weakness | 4. Hepatomegaly | null | null | null | null |
null | 5. Paroxysmal nocturnal dyspnea | null | null | null | null |
Central cyanosis | Peripheral cyanosis | null | null | null | null |
bluish or purple discoloration of tongue and linings of the mouth. | blue tint in fingers or extremities, due to an inadequate or obstructed circulation | null | null | null | null |
1. Decreased arterial oxygen saturation 2. Decreased atmospheric pressure high altitude 3. Impaired pulmonary function 4. Alveolar hypoventilation 5. Uneven relationships between pulmonary ventilation and perfusion (perfusion of hypoventilated alveoli) 6. Impaired oxygen diffusion 7. Anatomic shunts 8. Certain types of congenital heart disease 9. Pulmonary arteriovenous fistulas 10. Multiple small intrapulmonary shunts 11. Hemoglobin with low affinity for oxygen 12. Hemoglobin abnormalities 13. Methemoglobinemia: hereditary, acquired 14. Sulfhemoglobinema: acquired 15. Carboxyhemoglobinemia (not true cyanosis) | 1. central cyanosis and its causes are all associated with peripheral cyanosis 2. Decreased pumping of blood by the heart or reduced cardiac output. This is seen in heart failure or circulatory shock. 3. Diseases of circulation like thrombosis or embolism. 4. Constriction of blood vessels of the limbs, fingers and toes. This could be due to: cold exposure, Raynaud's phenomenon, spasm of the smaller skin capillaries or arteries called acrocyanosis, erythrocyanosis occurring in young women and as side effects of beta blocker drugs taken for high blood pressure. | null | null | null | null |
Contraindications of | thrombolytic therapy | null | null | null | null |
Absolute | Relative | null | null | null | null |
1. Any prior intracranial hemorrhage | 3- > 75 years age | null | null | null | null |
2- Known intracranial malformation and | 4- Current anticoagulant | null | null | null | null |
neoplasm | 5- Pregnancy | null | null | null | null |
3- Ischemic stroke <3 month | 6- Cardiopulmonary resuscitation > 10 min | null | null | null | null |
4 Suspected dissection | 7- Recent internal bleeding (2-4 week) | null | null | null | null |
5- Recent surgery | 8- Uncontrolled hypertension (180/ 110) | null | null | null | null |
6- Recent head trauma | 9- Remote ischemic stroke | null | null | null | null |
7- Bleeding diathesis | 10- Major surgery within 3 weeks | null | null | null | null |
null | ECG changes in MI | null | null | null | null |
ECG abnormalities | Onset | Disappearance | null | null | null |
Hyperacute T wave | Immediately | 6-24 hours | null | null | null |
ST segment elevation | Immediately | 1-6 weeks | null | null | null |
Q waves longer than 0.04 sec | One to several days | Years to never | null | null | null |
T wave inversion | 6-24 hours | Months to years | null | null | null |
Jones criteria for Rheumatic | fever | null | null | null | null |
Major criteria | Minor criteria | null | null | null | null |
Carditis | Fever | null | null | null | null |
Polyarthritis ( migratory ) | Arthralgia | null | null | null | null |
Erythema marginatum | Elevated ESR, CRP | null | null | null | null |
Chorea | Prolonged PR interval on ECG | null | null | null | null |
Subcutaneous nodules | Plus evidence of preceding streptococci infection | null | null | null | null |
Causes of | BNP elevation | null | null | null | null |
Cardiac | Non-cardiac | null | null | null | null |