Valvular Heart Disease Pathology Flashcards

1
Q

commissures

A

the points of lateral attachment between adjacent cusps

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2
Q

layers of the valve leaflets

A

fibrosa, spongiosa, and ventricularis

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3
Q

fibrosa

A

constitutes the major structural component of the cusp

consists of dense fibrous tissue

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4
Q

spongiosa

A

beneath the fibrosa and occupies a central position

consists of proteolgycan, loosely arranged collagen fibrils, and scattered fibroblasts

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5
Q

ventricularis

A

subadjacent to the spongiosa

in direct contact with the endothelium of the inflow surface of the cusp

contains a large amount of elastic fibrils

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6
Q

major causes of acquired valvular stenosis

A

postinflammatory (rheumatic) mitral or aortic stenosis

calcific aortic stenosis

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7
Q

causes of valvular incompetence/regurgiation

A

leaflet abnormality

papillary muscle damage

valve ring abnormalities

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8
Q

types of noninfective endocarditis

A

nonbacterial thrombotic endocarditis

rheumatic endocarditis

Libman-Sacks endocarditis

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9
Q

nonbacterial thrombotic endocarditis

A

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

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10
Q

pathogenesis of NBTE

A

subtle endothelial abnormalities

hypercoagulable states from malignancies (especially adenocarcinomas) in 50% of cases

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11
Q

morphologic features of NBTE

A

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

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12
Q

infective endocarditis

A

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)

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13
Q

ABE

A

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

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14
Q

SBE

A

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

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15
Q

acute infective endocarditis morphology

A

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

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16
Q

subacute infective endocarditis morphology

A

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)

17
Q

complications of infective endocarditis

A

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

18
Q

clinical mainfestations of infective endocarditis

A

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

19
Q

symptoms of rheumatic fever

A

Syndehams chorea

polyarticular arthritis

skin changes

carditis (pancarditis)

20
Q

Aschoff nodule

A

a collection of lymphocytes and histiocytes most easily found in the fibrous interstital septa of the myocardium

lesions indicative of rheumatic carditis

21
Q

fibrinous pericarditis

A

results from rheumatic heart disease

gives rise to a friction ribe

“bread-and-butter” pericarditis

22
Q

supporting evidence of Streptococcal infection

A

increased titer of anti-strep antibodies

positive throat culture (group A strep)

recent scarlet fever

23
Q

major Jones criteria

A

carditis

polyarthritis

chorea

erythema marginatum

subcutaneous nodules

24
Q

minor Jones criteria

A

previous RF or RHD

arthalgia

fever

actue phase reactants

prolonged P-R interval

25
Q

Antichow cell

A

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

26
Q

verrucous endocarditis

A

mall excrescences along lines of valve closure

lesions may resolve or undergo fibrosis

27
Q

causes of mitral valve regurgitation

A

abnormalities of leaflets and commissures

abnormalities of tensor apparatus

abnormalities of the mitral valve annulus or left ventricle

28
Q

abnormalities of leaflets and commissures leading to MR

A

postinflammatory scarring

infective endocarditis

floppy mitral valve

29
Q

abnormalities of tensor apparatus leading to MR

A

rupture of papillary muscle

papillary muscle dysfunction (fibrosis)

rupture of chordae tendinae

30
Q

abnormalities of the mitral valve annulus or left ventricle leading to MR

A

LV enlargement (myocarditis, dilated cardiomyopathy)

calcification of mitral annulsus

31
Q

morphology of mitral valve prolapse

A

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

32
Q

causes of aortic stenosis

A

postinflammatory scarring

senile calcific aortic stenosis (>60 yrs)

calcification of congenitally deformed valve (30-50 yrs)

33
Q

causes of aortic regurgitation

A

intrinsic valvular disease:

postinflammatory scarring

infective endocarditis

aortic disease:

syphilitic aortitis

anylosing spondylitis

rheumatoid arthritis

Marfan’s disease

34
Q

ankylosing spondylitis

A

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

35
Q

etiology of aortic root disease

A