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Heartback?1. Myocardial infarctiona. Is characterized by necrosis beginning approximately 30 minutes after coronary occlusionb. Most often involves occlusion of the left circumflex coronary arteryc. Are apparent macroscopically at around one hour after coronary occlusiond. Typically results in liquefactive necrosise. Is subendocardial if only two thirds of the ventricular wall is involved2. regarding the changes to myocardium after MIa. pallor at 24 hoursb. wavy fibres are found centrallyc. decreased contractility after 5 minutesd. liquefactive necrosis is typicale. sarcoplasm is resorbed by leukocytes3. In compensated cardiac hypertrophy changes include:a. Diffuse fibrosisb. Hyperplasiac. Decreased sarcomeresd. Increased capillary densitye. Increased capillary/myocyte ratio4. endocarditis in IV drug abusers typicallya. involves the mitral valveb. is caused by candida albicansc. does not cause feverd. has a better prognosis than other types of endocarditise. is caused by staph aureus5. The commonest cause of fungal endocarditis isa. Actinomycosisb. aspergillusc. ?d. candidae. blatomycosis6. With regard to MIa. Gross necrotic changes are present within 3-5 hoursb. Irreversible cell injury occurs in less than 10 minutesc. Fibrotic scarring is completed in less than 2 weeksd. Death occurs in 20% of cases in less than 2 hourse. Is most commonly caused by occlusion of the left circumflex coronary artery7. Regarding pericarditisa. Constrictive pericarditis only rarely follows suppurative pericarditisb. Primary pericarditis is usually bacterial in originc. Serous pericarditis may be due to uraemiad. Fibrinous pericarditis is due to Mycobacterium tuberculosis infection until proven ptherwisee. Haemorrhagic pericarditis is most commonly due to Klebsiella infection8. A young man presents with central chest pain presumed to be associated with vasoconstriction. The most likely cause of the pain is locala. Hypoxiab. Decreased ATPc. Increased CO2d. Catecholamines acting on alpha 1 receptorse. Acetylcholine stimulation9. An adult male with an ejection fraction of 80% could be due toa. Myocardial ischaemiab. Arrythmiac. Thiamine deficiencyd. ?e. ?10. The cause of fluid retention peripherally with congestive cardiac failure isa. Increased reninb. Increased GFRc. Increased angiotensin IId. Increased aldosteronee. ?11. rheumatic carditis is associated witha. Curschmann spiralsb. Ito cellsc. Aschoff bodiesd. Nutmeg cellse. Reed-Sternberg cells12. Regarding myocardial infarction:a. The size of the infarct is independent of collateral circulationb. Is mainly precipitated by vasospasmc. Irreversible tissue damage appears within 30 minutesd. Acute cellular swelling is due to ATP depletione. Occlusion of right coronary artery is responsible for most infarcts in the anterior wall of the left ventricle13. The most common form of congenital heart disease isa. Coarctation of the aortab. Tetralogy of Fallotc. ASDd. PDAe. VSD14. Myocardial infarction:a. Is usually a consequence of coronary vessel occlusion by embolusb. Is characterized morphologically by liquefactive necrosisc. Is most commonly complicated by ventricular ruptured. Can be either transmural or subendocardiale. Is apparent on light microscopy within minutes15. All of the following are cardiac compensatory responses that occur in heart failure except:a. Cardiac muscle fibre stretchingb. Increased adrenergic receptors on cardiac cellsc. Chamber hypertrophyd. Decreased heart ratee. Increased vasopressin levels16. The most common cause of pericarditis isa. SLEb. Drug hypersensitivityc. Traumad. Post myocardial infarctione. Bacterial17. all of the following are features of rheumatic fever EXCEPTa. carditisb. subcutaneous nodulesc. erythema nodosumd. elevated antistreptolysine. Aschoff bodies in the heart18. The histological appearance of contraction bands in association with acute myocardial infarction indicate:a. Previous old myocardial infarctionb. Early aneurismal formationc. Compensatory responses to decreased myocardial contractilityd. A right ventricular infarcte. Recent reperfusion therapy19. After occlusion of a coronary arterya. The ischaemia is most pronounced in the epicardial regionb. Loss of contractility only occurs when ultrastructural changes in the myocyte are presentc. Reperfusion of the ischaemic area can result in new cellular damage, due to the generation of oxygen free radicalsd. Q waves on the ECG are diagnostic of transmural infarctione. None of the above are true20. In compensated heart failurea. Right atrial pressure dropsb. Maximum cardiac output is unchangedc. Resting cardiac output is unchangedd. Renin level eventually drops below premorbid levele. Fluid retention plays no role21. Infective endocarditisa. In the acute form, is most commonly caused by streptococcib. Involves abnormal valves in most acute casesc. Is confirmed by positive blood cultures in less than 50% of casesd. May cause splenic infarctione. May cause MacCallum’s plaques to form on affected valves22. cor pulmonale may be caused bya. congenital heart diseaseb. mitral stenosisc. left ventricular failured. primary pulmonary hypertensione. aortic regurgitation23. Post myocardial infarctiona. ATP is down to 50% at 10 minutesb. Irreversible cell injury occurs within 5 minutesc. ATP depletion begins at 2 minutesd. Microvascular injury occurs within 30 minutese. Wavy fibres are seen within 20 minutes24. congestive heart failure can be caused by:a. vitamin A deficiencyb. niacin deficiencyc. vitamin D deficiencyd. thiamine deficiencye. vitamin B2 deficiency25. Regarding acute endocarditisa. It has a mortality of <20%b. It is caused by virulent organismsc. 30% is caused by bacteriad. ?e. ?26. A 50 year old man with an acute myocardial infarction has a BP 130/80. He can maintain his BP because of:a. An absolute increase in cardiac outputb. Increased systolic filling pressurec. Increased right atrial pressured. Increased water absorptione. Decreased sympathetic outflow27. What is the most common histological change seen in myocardial infarction less than 24 hours duration?a. Pallor and oedemab. Haemorrhagec. Hyperaemic borderd. Liquefactive necrosise. ?28. With regard to acute coronary occlusiona. Collaterals do not flow for 4-6 hoursb. Striking loss of contractility within 60 secondsc. 50% recanalise spontaneouslyd. ischaemia occurs after 60 minutese. ?29. In hypertensive cardiac disease there is:a. Flattening of trabeculaeb. Insterstitial fibrosisc. Dilation of the left ventricled. ?e. ?30. Acute severe MI causes:a. Pulmonary oedemab. Thoracic pressurec. Increased right atrial pressured. Decreased aterial pressuree. ?31. Coronary thrombusa. If asymptomatic, carries a low riskb. Increased tissue plasminogen activator inhibitor causes extension of thrombusc. Vessels mostly occluded to decrease blood velocityd. Is at increased risk of because of mechanical stressorse. 50-75% occlusion is likely to cause infarction32. The most common complication of acute myocardial infarctionisa. Sudden cardiac deathb. Congestive cardiac failurec. Valvular dysfunction due to papillary muscle ruptured. Ventricular aneurysme. Arrythmia33. in the developed world, the most common cause of myocarditis isa. SLEb. HIVc. Enterovirusesd. Chlamydiaee. Drug hypersensitivity34. Plaque associated thrombosis is associated with all EXCEPT:a. Transmural MIb. Subendocardial MIc. Unstable anginad. Stable anginae. Sudden cardiac death35. in left heart failurea. failure is typically secondary to right heart failureb. ascites is a predominant featurec. right heart failure is rarely, if ever, associated with left heart failured. renal congestion and acute tubular necrosis are less commone. pulmonary congestion and oedema are rare36. Regarding myocardial infarctiona. Subendocardial infarcts are most commonb. Approximately 30% of transmural infarcts are due to vasospasmc. Irreversible cell injury occurs within 20-40 minutesd. Reperfusion does not salvage reversibly damaged cellse. Irreversible injury does not first occur in the subendocardial zone37. congestive cardiac failure is characterized by all of the following EXCEPT:a. perivascular and interstitial transudateb. Kerley A lines on chest Xrayc. Activation of renin-angiotentin-aldosterone systemd. Haemosiderin-containing macrophages in the alveolie. Progressive oedematous widening of alveolar septa38. Pertaining to ischaemic heart disease:a. Coronary atherosclerosis begins to form in middle ageb. 50% of people with this condition have underlying atherosclerotic plaquesc. acute myocardial infarction occurs mostly by embolus occluding the arteryd. Prinzmetal angina occurs due to coronary artery spasme. Subendocardial infarcts always occur from reduced systemic blood pressure39. Regarding macroscopic changes in myocardial infarcts:a. Changes may be accentuated as early as 1-2 hours by histochemical stainsb. By 18-24 hours infarcted tissue becomes dark and swollenc. In the first week, the lesion becomes sharply defined, yellow and softd. At four days, a rim of hyperaemic granulation tissue appearse. A fibrous scar is well established at two weeks ................
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