Valvular Disease Flashcards
functional regurgitation
incompetence due to disruption of supporting structures
(as in aorta root dilation, left ventricle dilation)
damage caused by wear and tear complicatedby deposits of calcium phosphate
dystrophic calcification
clinical effects of calcific aortic stenosis
LV increased pressure casues hypertrophy
angia, ischemia, CHF
syncope
morphology of calcified aortic stenosis
calicified masses in cusps, primarily at base
no fusion of commissures
mitral annular calcification
degenrative calicific dposits on fibrous ring at base of valve,
usually doesn’t impact function
thrombis possible
mxyomatous degeration of mitral valve (prolapse)
enlarged leaflets, prolaps into left atrium during systole
(mid-systolic click)
complciations of mxomatous mitral valve
late systolic murmor,
rare: endocarditis, mitral insufficiency, thrombi, arrhythmias
most serious complication of RA
progression to chronic vavlular dysfxn (mitral stenosis)
classic lesion of RA
aschoff body - swollen eosinophillic collogen surroudned by t lymphocytes, plasma, and plump macrophages.
caterpillar cells
pancarditis of RA
bread and butter pericardiits
myocarditis w/ aschoff bofdies
subendochondrail maccullum plaques (fibrous thickening of endocardium)
chonic RA >chronic inflammatior and fibrosis leads to -
thickened leaflets
fusion of commisures
thickening/fusion of chordae tendinae
clinical impact of chronic RA
mitral stenosis > atrial dilatation > reduced output
pathogenesis RA
hypersensitivity induced by Group A Strep >
> Abs against Mm proteins cross react to glycoproteins inheart, joints >
>protein in sarcolemma of myocyte
Jones criteria of RA
Joints
Heart (carditis, weakened heart sounds, tachy, arrhythmia)
Nodules
Erythema marginatum of skin (trunk)
Sydenham chorea
protein produced by group A stresp
Steptolysis O and DNAase
2 forms of ineffective endocarditis
acute - virulent organism, normal valve, (or necrotizing infection needing surgery)
subacute - low virulance with deformed valve, responds to AB
common organisms of Ineffective Endocardits
Strep viridans (50-60%)
Staph A (10-20%) (most common in all IVDA)
acute inefective endocarditis morphology
friable destructive vegetations
inflammatory cells and bacteria, fibrin
triscuspid valve in IV users
ring abcesses in erosion of myocardium
differing factors in subacute ineffective endocarditis
less valvular destruction, fibroiss and granulation tissue reaction at base of vegetaion
clinical features of Bacterial endocardiits
Dukes criteria
blood culture, valve related mass, abcesses
new vale regurgiation, new murmur on auscultation
Minor: fever, predisposing heart lesion of IVDA
complciations bacterial endocarditis
valve insuf
myocaridal abcesses > perforation
vegetations embolize (kidneys, spleen)
glomulonephritis (immune complexes)
pathogenesis of non-iffective vegetations- non bacterial thrombotis endocarditis
hypercoag. state
mucin producing adenocarcinomas
endocardial trauma (swan-ganz catherter)
morphology liban sacks endocarditis
1-4 mm verrucae with fibrinous material on leaflets and pos endocardium
posible intense inflammation
carcinoid syndrome- - tumors produce
carcinoid tumors produce serotonin, kallifkrein, brady kinin, histamine, prostagalndins, tachykinins
presentation carcinoid syndrome
flushing, cramps, nausea, vomiting, diarrhea
plaqaue like fibrosis of heart endocardium, usually right heart
(becsaue of inactivation of mediators by MAO in lung)
