Question | Answer |
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 |