lecture 16 kemp
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| valvular stenosis | failure of a valve to open completely due to calcification or prev infection, prevents forward flow of blood, almost always due to chronic process
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| valvular insufficiency (regurgitation) | failure of a valve to completely close, allowing for backward flow of blood. may be either acute or chronic onset
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| 3 forms of aortic stenosis | degenerative calcification of a nl tricuspid aortic valve, stenosis due to chronic rheumatic valvulitis, stenosis due to calcification of a bicuspid aortic valve
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| how one might acquire a bicuspid aortic valve | due to infective endocarditis causing scarring of leaflets during healing
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| major sequelae of aortic stenosis | LVH over time, if perfusion is no longer sufficient for the LV then angina develops, syncope due to hypoperfusion of brain, CHF can be precipitated. bicuspid aortic valves are associated with aortic dissections
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| myxomatous mitral valve | mitral valve prolapse - redundancy or balooning of leaflets with resultant chordae tendinae elongation, can be associated with Marfan and Ehler-Danlos syndromes, occurs in women 7x more than men. PEx: mid-systolic click
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| bicuspid valves acquire calcification earlier than nl tricuspid valves | 40-50 y/o vs 70-80 y/o for nl aortic valves with 3 leaflets
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| causes of aortic regurgitation | damage to cusps: endocarditis, bicuspid valve OR damage to annulus: dissection, syphilis or in Marfan syndrome
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| Jones criteria for acute rheumatic fever (must have 2+ to make dx) | carditis (peri-, endo- or myo-), migratory polyarthritis, erythema marginatum, subcutaneous nodules, Sydenham chorea // leads to mitral valve stenosis
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| chronic rheumatic fever | causes scarring of mitral (and maybe aortic) valve = thick leaflets and thick, fused and shortened chordae tendinae
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| infective endocarditis | infection of cardiac valves with vegetations composed of necrotic debris, thrombus and organisms on the leaflets
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| pathogenesis in acute rheumatic fever | body makes Ab against M proteins on GABHS that cross-react with glycoproteins in the body, especially the heart valves
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| 2 types of infective endocarditis | acute: develops rapidly even on nl valves, usually a very virulent organism, results in high mortality rate (S. aureus) // subacute: develops insidiously, usually on already abnl valves, less virulent organism like viridans Strep
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| complications of infective endocarditis | glomerulonephritis, septicemia, septic emoblizations, local myocarditis, perforations of cusps
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| marantic (nonbacterial thrombotic) endocarditis | due to sterile vegetations of just plts, fibrin and other blood components found on nl valves. may make strands of tissue called Lambl excrescences. usually occurs in hypercoagulable states
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| cardiomyopathy | either congenital or acquired (developed over time as compensation or in response to an insult) defects in the myocardium
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| dilated cardiomyopathy | all 4 chambers dilated, heart is round/globular without a true apex, non-specific fibrosis and hypertrophy, CHF; associated with EtOH, viral infections, peripartum period, doxorubicin, idiopathic causes, strucutral protein mutations (dystrophin)
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| dilated LV can't produce sufficient force for forward blood flow | dilated LV streches annulus, causes mitral valve insufficiency and LAE
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| hypertrophic cardiomyopathy | myocardial hypertrophy without dilation or increase in size, thick inverventricular septum, patch of fibrosis from thick septum striking anterior mitral valve leaflet during systole. microscopic appearance: whorled pinwheel cardiac myocytes
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| clinical features of hypertrophic cardiomyopathy | less compliance of LV during diastole, decreased LV output, backup into lungs causing dyspnea. may cause coronary artery ischemia. complications: arrhythmias, CHF. beta-myosin heavy chain mutation
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| restrictive cardiomyopathy | ventricles are normal size or slightly enlarged but infiltrative process like sarcoidosis or amyloidosis causes reduction in ventricular compliance and poor filling during diastole
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| myocarditis | inflammatory infiltrate (lymphocytes) with resultant necrosis of the myocardium. caused by viruses, fungi, protozoa, immune dz like SLE or other unk dz like sarcoidosis
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| lymphocyte myocarditis | mononuclear inflammatory infiltrate associated with cardiac myocyte necrosis, usually viral origin
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| hypersensitivity vs giant-cell myocarditis | hypersensitivity: high proportion of eosinophilic infiltrate especially around vessels // giant-cell: lots of macrophage and multinucleated giant cells, associated with high mortality rate
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| clinical course of myocarditis & complications | pts may be asymptomatic or have sudden CHF/arrhythmias due to altered depol from necrotic myoctes. sx: fatigue, dyspnea, palpitations, CP and/or fever // complications: dilated cardiomyopathy
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| pericarditis | inflammatory infiltrate of the pericardial sac due to viral, bacterial, fungal infections. can be from SLE, post-MI, uremia, rheumatic fever, mets. fibrinous exudate that can heal as scar and cause constriction
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| clinical findings of pericarditis | friction rub on exam, maybe tamponade // sx: atypical CP
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