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36 Cards in this Set
- Front
- Back
What are 3 forms of aortic stenosis?
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1. degenerative calcification of normal tricuspid aortic valve
2. degenerative calcification of a bicuspid aortic valve 3. aortic stenosis due to chronic rheumatic aortic valvulitis |
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How does dystrophic calcification of the aortic valve lead to stenosis?
How does the effect compare between tricuspid and bicuspid aortic valves? |
Wear and tear on valves --> calcified nodules on outflow surface of valves, fused commissure--> more difficult for valves to open --> stenosis, concentric LV hypertrophy
Bicuspid accumulate damage and calcium sooner |
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Clinical features of aortic stenosis?
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angina, syncope, CHF
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What is myxomatous mitral valve?
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Ballooning of mitral leaflets, chordae tendinae elongated, fibrosa thin
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Clinical features of myxomatous mitral valve?
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Mid-systolic click
Can have chest pain, palpitations, dyspnea, regurgitation can develop regurgitation, infective endocarditis, sudden death due to ventricular arrhythmia |
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What happens in acute rheumatic fever?
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antibodies against M proteins of Group A strep cross-react with glycoproteins in the body
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What are the clinical manifestations of acute rheumatic fever?
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migratory polyarthritis
carditis |
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What are the Jones criteria for diagnosing acute rheumatic fever?
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1. carditis
2. migratory polyarthritis 3. subcutaneous nodules 4. erythema marginatum 5. Sydenham chorea (involuntary movements) must have at least 2 |
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What are Aschoff bodies?
Anitschow cells? |
Aschoff bides = central zone of degenerating, hypereosinophilic material infiltrated by T lymphocytes and large macrophages (Anitschkow cells)
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What happens in chronic rheumatic fever?
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Scarring of valves (mitral, aortic)
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What is the morphology of chronic rheumatic valvulities?
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thick leaflets, chordae tendinae are short and thick
Left atrial dilation from stenosis of mitral valve Fusion of all commissures in aortic valve |
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What is infective endocarditis?
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infection of the cardiac valves, usually bacterial
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What are 2 traditional forms of infective endocarditis?
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acute - rapid, highly virulent
subacute - insidious, infects previous abnormal valve, low virulence |
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How does infective endocarditis come about?
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Abnormal valve produces jet streams --> platelet-fibrin deposits form on valves --> become infected by bacteria
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What are the clinical features of infective endocarditis?
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acute: fever, chills weakness
Subacute: fever may be absent, non-specific Both can have murmur, petechiae hemorrhages |
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What are 3 complications of infective endocarditis?
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Glomerulonephritis, septicemia, emboization
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What are 3 agents of infective endocarditis?
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1. Viridans Strep - infects previously damaged valves
2. S. aureus - infects normal valves 3. HACEK group |
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What is marantic endocarditis (non-bacterial)?
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Sterile vegetations (fibrin, platelets) on valves organize into strands called Lambl excrescences
Occurs in hypercoagulable states |
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What is the difference between a primary and a secondary cardiomyopathy?
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Primary - disease confined to heart
Secondary - multi-organ disorder |
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What is the morphology of dilated cardiomyopathy?
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Dilation of all four chambers from eccentric hypertrophy of the myocardium
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What are the causes of dilated cardiomyopathy?
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viral (Coxasackie B or enterovirus)
alcohol genetic (lamins A and C, B-myosin heavy chain, dystrophin, a-cardiac actin mutations) peripartum state (pregnancy-induced hypertension, volume overload, cardiac defect) |
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What are the clinical features of dilated cardiomyopathy?
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CHF (dilation of LV), mitral insufficiency, abnormal cardiac rhythms, emboli
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What is the morphology of hypertrophic cardiomyopathy?
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Myocardial hypertrophy without dilation; thick interventricular septum;
Myofiber disarray, fibrosis, sclerosis of blood vessels |
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What is the pathogenesis of hypertrophic cardiomyopathy?
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mutations in sarcomeric proteins (dominant) --> B-myosin heavy cahin, myosin-binding protein C, troponin T
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What are the clinical features of hypertrophic cardiomyopathy?
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Impaired diastolic filling --> reduced CO, increase in pulm pressure --> dyspnea
Systolic ejection murmur if outflow obstruction Ischemia |
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What are the complications of hypertrophic cardiomyopathy?
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arrhythmias, CHF, sudden death
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What is the morphology of restrictive cardiomyopathy?
Pathogenesis? |
Ventricles mostly normal (may be enlarged), chambers not dilated
Infiltrative process of myocardium --> reduced ventricular compliance --> impaired diastolic filling |
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What are the causes of restrictive cardiomyopathy?
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idiopathic, amyloidosis, hemochromatosis, sarcoidosis, radiation fibrosis, inborn error of metabolism
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What are 2 variants of restrictive cardiomyopathy?
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1. Endomyocardial fibrosis - fibrosis of endocardium and subendocardium --> reduced compliance
2. Loeffler endomyocarditis - dense endocardial fibrosis + peripheral eosinophilia |
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What is arrhythmogenic right ventricular carddiomyopathy?
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dilation of RV associated with thinning of the wall and fibrosis --> right heart failure or sudden cardiac death
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What is myocarditis?
3 variants? |
Inflammation of heart causing damage to myocardium
Lymphocyte, hypersensitivity (eosinophils), Giant cell (macrophages and giant cells) |
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What are the clinical features of myocarditis?
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asymptomatic
fatigue, dyspnea, palpitations, pain, fever sudden CHF, arrhythmias |
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What is preicarditis?
3 types? |
Inflammatory infiltrate is in the pericardial sac
fibrinous (fibrin) fibrinopurulent (bacteria) fibrinohemorrhagic (malignancy) |
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acute pericarditis?
chronic? constrictive? |
acute = fibrinous and fibrinopurulent, can resolve completely
chronic = pericarditis with scarring constrictive = fibrosis in pericarditis so extensive as to impair diastole |
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clinical findings of pericarditis?
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atypical chest pain (not exertion related)
tamponade (fill sac with fluid --> compress LV, inhibit diasolic filling) |
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What are 3 types of pericardial effusions and their cuases?
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Serous: CHF, hypoalbuminemia
Serosanguinous: trauma, malignancy, ruptured MI Chylous: lymphatic obstruction |