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