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PATH: Valvular

valvular disease

Stenosis is almost always? cusp related
what is problematic about an abnormal valve increased work of teh heart and increased susceptibility to infection
when do you get rheumatic fever 1-4 weeks after GAS infection
what are the mortality rates of rheumatic fever 1% or so
what are the general characteristics of rheumatic fever fever, migratory polyarthritis, subcutaneous nodules erythema marginatum, syderham's chorea
in addition to general features or rheumatic fever what else can be effected carditis (75% of children and 35% of adults) and pancarditis
what do you find when the myocardium is affected by RF aschoff bodies (necrotic foci) surrounded by mononuclear inflammatory cells
what does the pericardium look like when it is affected by Acute Rheumatic fever? aschoff bodies (necrotic foci) and bread and butter pericarditis
what does the endocardium look like when itis affected by acute rheumatic Fever aschoff bodies and maccalum's patches (LA foci of endocardial fibrosis)
what are aschoff bodies necrotic foci seen with heart layers affected by rheumatic fever
what are Maccalum's patches LA foci of endocardial FIBROSIS)
what do valves affected by Acute Rheumatic fever look like necrotic and verrucae along the closure (chrodae fusion)
what happens to the valve lesions after an acute attack of rheumatic fever they undergo organization and fibrosis
what happens when there are repeat attacks of rheumatic fever on the valves there is scaring and blunting
what valves are most affected by chronic rheumatic fever 70% mitral, 25% mitral and aortic and 2-3% aortic only
when the mitral valve is stenotic what part of the heart is affected the LA is dilated resulting in pulmonary congestion and RV hypertrophy
what are the secondary affects of chronic RF on the heart CHF, Dilation, mural thrombi, increased endocarditis
etiology of myocarditis with chronic RF anti strep abs react with myocardial and valvular Ags
what are the two theories used to explain the myocarditis of chronic RF cross reaction and autoimmune (less likely)
how does a mitral valve prolapse work during systole the MV enters the LA
what characteristics could be noted with a mitral valve prolapse leaflets enlarged with parchute like outpouchings with fusion
how do the chordae respond to the prolapse they are elongated and prone to rupture
what does a mitral valve prolapse look like microscopically myxoid degeneration (mucus like) with myxoid acumulation and destruction of the zona fibrosa substructures
what percent of the population has mitral valve prolapse 3-6%
what do you hear in someone with a mitral valve prolapse a loud mid systolic click that is the chordae snapping
what happens in severe cases of mitral valve prolapse you have regurge which can enlarge the left side of the heart, may also have endocarditis and arrythmia
why would you have a mitral valve prolapse growth imbalance b/t leaflets and the heart
when do you get ischemic mitral regurge when you have papillary infarct
when do you see commissural fusion in the mitral valve prolapse
what does long standing aortic stenosis cause LV hypertrophy and CHF
etiology of aortic stenosis cong. (valve is too small) or acquired(most wear and tear 10%=RF)
do more virulent stains cause acute or subaccute endocartitis acute ( highly destructive)
acute endocarditis affects individuals with what kind of heart normal and abnormal
what is the mortality associated with acute endocarditis 50%
how do the vegetations differ between acute and subacute endocarditis acute=huge vegetations with valve perforation and myocardial extension with ring absess vs smaller vegetations with subacute endocarditis
outcome with subacute endocarditis most recover
who causes subacute endocarditis having an abnormal heart
who are the bugs 50% strep viridans 20% aureus 10 or so unknown
what does NBTE stand for non-bacterial thrombotic emboli
what is NBTE small sterile vegetations on both sides of the valve usually at the closure (fibrin and blood elements)
Libman Sacks Endocarditis associated with SLE (50% of lupus patients) may embolize or be colonized
Carcinoid Heart disease plaque like pearly whit fibrous thickening of the RV endocardium they can secreate bioactive amines and will mimic sympathetic nervous system activation
aortic stenosis calc, cong, RF
aortic regurge cong. RF, Endocarditis, SLE (2nd)
Mitral stenosis RF, Calc, SLE
Mitral Regurge Degenerative ischemia, RF, Annular calcification, endocarditis, SLE 2ndary
Tricuspid stenosis RF carcinoid
Tricuspid regurge RF, Endocarditis, 2ndary
Pulmonary stenosis cong. carcinoid
Pulmonary regurge secondary
Created by: jmuame03