Valvular Heart Disease Pathology Flashcards
commissures
the points of lateral attachment between adjacent cusps
layers of the valve leaflets
fibrosa, spongiosa, and ventricularis
fibrosa
constitutes the major structural component of the cusp
consists of dense fibrous tissue
spongiosa
beneath the fibrosa and occupies a central position
consists of proteolgycan, loosely arranged collagen fibrils, and scattered fibroblasts
ventricularis
subadjacent to the spongiosa
in direct contact with the endothelium of the inflow surface of the cusp
contains a large amount of elastic fibrils
major causes of acquired valvular stenosis
postinflammatory (rheumatic) mitral or aortic stenosis
calcific aortic stenosis
causes of valvular incompetence/regurgiation
leaflet abnormality
papillary muscle damage
valve ring abnormalities
types of noninfective endocarditis
nonbacterial thrombotic endocarditis
rheumatic endocarditis
Libman-Sacks endocarditis
nonbacterial thrombotic endocarditis
the deposition of small masses of fibrin, platelets,and other blood components on leaflets of cardiac valves
lesions do not contain microorganisms
valvular damage is not a prerequisite
valves are usually previously noromal
aka NBTE or marantic endocarditis
pathogenesis of NBTE
subtle endothelial abnormalities
hypercoagulable states from malignancies (especially adenocarcinomas) in 50% of cases
morphologic features of NBTE
small nodules on lines of valve closure
nodules may be bulky and friable
valve leaflets otherwise normal
aortic valve most common, mitral valve next most frequently involved
infective endocarditis
infection of the cardiac valves or mural surface of the endocardium, with formation of adherent mass of thrombotic debris and organisms, termed a “vegetation”
any microorganism may be present, but most cases are bacterial
broken down into acute bacterial endocarditis (ABE) and subacute bacterial endocarditis (SBE)
ABE
acute and rapidly progressive valvular dysfunction
can be fatal in up to 50% of patients
due to highly vurilent organisms such as staphylococcus aureus
organisms affect normal valves
SBE
usually presents as a more insiduous process that can progress slowly over time (weeks)
prognosis is markedly better than ABE
usually due to low virulence organisms such as alpha-hemolytic streptococci
affects previously abnomral valves
infection due to abnormal hydrodynamics and surface irregularieis of the abnormal valve, leading to microscopic surface thrombosis
acute infective endocarditis morphology
small to large vegetations
rapid destruction of valve leaflets - rupture of leaflets, chordae tendinae, or papillary muscles
organisms, fibrin, blood cells
virtually no inflammatory response
systemic embolization infarcts of brain, kidneys, myocardium, etc.
abscesses at site of infarcts
subacute infective endocarditis morphology
firmer than in acute
cause less valve damage
granulation tissue at base of lesions
eventual fibrosis and calcification may occur
systemic emboli - infarcts (less likely to supprate)
complications of infective endocarditis
septicemia
emboli and septic emboli - infarcts to heart, brain, kidney, and spleen
immun complex mediated injury - focal glomerulonephritis (flea bitten), vasculitis in skin
valve perforation - congestive heart failure
clinical mainfestations of infective endocarditis
infection - prolonged fever
vegetations - changing heart murmur
emboli - symptoms of cardiac, renal, plenic, or cerebral infarction
immune complex disease:
- > kidney - hematuria, renal failure
- > subcutaneous - splinter hemorrhages, Osler’s nodes
- > retina - Roth’s spots
valve rupture - congestive heart failure
symptoms of rheumatic fever
Syndehams chorea
polyarticular arthritis
skin changes
carditis (pancarditis)
Aschoff nodule
a collection of lymphocytes and histiocytes most easily found in the fibrous interstital septa of the myocardium
lesions indicative of rheumatic carditis
fibrinous pericarditis
results from rheumatic heart disease
gives rise to a friction ribe
“bread-and-butter” pericarditis
supporting evidence of Streptococcal infection
increased titer of anti-strep antibodies
positive throat culture (group A strep)
recent scarlet fever
major Jones criteria
carditis
polyarthritis
chorea
erythema marginatum
subcutaneous nodules
minor Jones criteria
previous RF or RHD
arthalgia
fever
actue phase reactants
prolonged P-R interval
Antichow cell
round or oval nucleus with chromatin condensed at the nuclear periphery and along the center
results in an appearance like an owl eye or caterpillar
seen around the area of fibrinoid necrosis
verrucous endocarditis
mall excrescences along lines of valve closure
lesions may resolve or undergo fibrosis
causes of mitral valve regurgitation
abnormalities of leaflets and commissures
abnormalities of tensor apparatus
abnormalities of the mitral valve annulus or left ventricle
abnormalities of leaflets and commissures leading to MR
postinflammatory scarring
infective endocarditis
floppy mitral valve
abnormalities of tensor apparatus leading to MR
rupture of papillary muscle
papillary muscle dysfunction (fibrosis)
rupture of chordae tendinae
abnormalities of the mitral valve annulus or left ventricle leading to MR
LV enlargement (myocarditis, dilated cardiomyopathy)
calcification of mitral annulsus
morphology of mitral valve prolapse
mitral valve cusps are soft, enlarged, and ballooned into the left atrium during systole
cordae may rupture
loose, edematous, basophilic ground substance in valve leaflets and chordae
causes of aortic stenosis
postinflammatory scarring
senile calcific aortic stenosis (>60 yrs)
calcification of congenitally deformed valve (30-50 yrs)
causes of aortic regurgitation
intrinsic valvular disease:
postinflammatory scarring
infective endocarditis
aortic disease:
syphilitic aortitis
anylosing spondylitis
rheumatoid arthritis
Marfan’s disease
ankylosing spondylitis
systemic disease affecting joints, lungs, heart, and eyes
inflammation can involve the aorta and heart
can cause aortic regurgitation due to dilatation of the aorta and scarring of the valve cusps
etiology of aortic root disease
