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Pathology of Valvular Heart Disease
Terms in this set (43)
What are the 3 layers of each valve leaflet?
fibrosa - provides fibrous support
spongiosa - centrally located loose connective tissue
venticularis - rich in elastic fibers for elasticity of valve
What is an important cause of mitral stenosis?
Chronic rheumatic valvulitis (PIS)
Define rheumatic fever
immunologically mediated, multisystem inflammatry disease which follows a few weeks after episode group A streptococcol pharyngitis (3%)
Which layers are involved in the inflammatory changes in acute rheumatic carditis?
all three layers --> pancarditis
What is the pathological hallmark of myocarditis?
Aschoff bodies within connective tissue of heart
What is the pathological hallmark of endocarditis
edematous and thickened valves with foci of fibrinoid necrosis (verrucous vegetatations) on line of closure
What is the pathological hallmark of pericarditis
What are 3 cell types/features seen in acute rheumatic carditis?
1. aschoff bodies
- inflammatory lesion present: comprises T cells, plasma cells, and macrophages
2. Anitschkow cells
- activated macrophages
- "caterpillar" cells pathognomonic
3. Aschoff cells - binucleate macrophage
What are 4 consequences of chronic rheumatic mitral valvulitis?
1. chronic scarring
- functional stenosis, regurgitation, or both
2. pure mitral stenosis
- left atrial dilation (pressure overload), atrial fibrillation, atrial thrombus)
3. added MR - LVH (volume overload)
4. scarred valves with predisposition to infection
What are 3 potential causes of aortic stenosis?
1. chronic rheumatic valvulitis
2. senile calcific (dystrophic) stenosis
3. calcification of congenital deformed valve (bicuspid)
How does senile calcific aortic stenosis differ pathologically from RHD?
NO FUSION of valve commissures
What is the pathophysiological result of senile calcific aortic stenosis?
resultant AS - concentric LVH
What are 3 clinical consequences of senile calcific aortic stenosis?
congestive heart failure
When does congenital bicuspid aortic valve calcification generally become sympomatic? How does this compare to senile calcific aortic stenosis?
5th to 6th decades versus 8th-9th
What is the most common cause of mitral stenosis, aortic stenosis, mitral regurgitation, and aortic regurtitation
mitral sten - chronic RHD
aortic sten - degenerative calcification of valve
mitral regurg - myxomatous degeneration
aortic regurg - dilation of aortic root
- old age, atherosclerosis and HTN
What are two causes of aortic regurgitiation?
2. degenerative aortic root dilation
What are 3 causes of degenerative aortic root dilation?
1. Marfan syndrome
3. syphilic aortitis
Describe the histological features of mitral valve prolapse
excessive amounts of loose, edematous, faintly basophilic, myxomatous material in valve
Describe the morphology and pathophysiology of mitral valve prolapse
soft and enlarged mitral valve cusps
- ballooning of the valve leaflets into the let atrium during systole, causing MIDSYSTOLIC CLICK
chordae teninae often elongated and fragile, may rupture in severe cases
mitral annulus may be dilated
What are the clinical features and complications of MVP
mitral regurgitation and congestive heart failure
thrombus formation and emboliation
Marfan's may similar valvular change
**most are asymptomatic
What are two clinical classifications of infectious endocarditis?
1. acute endocarditis
2. sub acute endocarditis
What is the cause of acute endocarditis
destructive necrotizing lesion infection of normal heart valve with a highly virulent organism
What is the mortality associated with acute endocarditis?
>50% of patients despite antibiotics and surgery
What is the cause of subacute endocarditis
infection in a previously abnormal deformed valve with a low virulence organism
What are 5 predisposing factors for infectious endocarditis?
1. prexisitng valvular abornmality
- chronic rheumatic valvulitis
- degenerative calcific aortic stenosis/BAV
2. prosthetic heart valves (10-20%)
3. repaired/unrepaired congenital defects
4. IV drug abuse (tricuspid)
5. transient bacteremia
Describe the 2 mechanisms for the predisposion of abnormal heart valves to endocarditis
1. hemodynamic factors
- abnormal blood flow across damaged valve --> endothelial injury --> focal deposition of platelets and fibrin
2. adherent properties of microorganisms
- adhesion factors - polysaccharides
What is the most common virulent and non virulent organism that causes endocarditis?
virulent - staph aureus
non virulent - streptococcus viridans
Which valves are most commonly affected by acute bacterial endocarditis
mitral and aortic valve
Which valve is most commonly affected by IV drug abuse?
What are 3 gross features of acute bacterial endocarditis
1. bulky, friable vegetations, obstruct the valve orifice
2. rapid destruction of the valves
- rupture of the leaflets, chordae tendinea, and papillary muscles
3. ring abscess
- abscesses erode into perivalvular myocardium
What are the microscopic features of acute bacterial endocarditis?
- large number of organisms mixed with fibrin and blood cells
- minimal inflammatory response
What are the gross features of suabcute endocarditis in comparison to acute bacterial endocarditis
1. vegetations are less friable
2. associated with less valve destruction
3. ring abscesses uncommon
What are the microscopic features of subacute endocarditis?
- presence of granulation tissue
- fibrosis, calcification
- chronic inflammatory infiltrate
What are 3 complications/sequelae of vegetations?
1. valvular regurgitation
- perforation of valve
- rupture of chordae tendinae
2. immune complex disease
- small vessel vasculitis
3. vegetations prone to embolization
- embolic fragmens with virulent organisms
- lodge at distant sites with abscess formation
- septic infarcts
- mycotic aneurysms
What is non-bacterial thrombotic endocariditis?
NBTE is characterized by deposition of sterile thrombi (vegetations) on valve leaflets
What are 3 potential contributors to the pathogenesis of NBTE?
1. endothelial abormalities
2. hypercoagulable states
Which valve is most commonly affected by NBTE
What are the gross and microscopic features of NBTE?
gross - multiple small nodules along the line of closure
microscopic - nodules are composed of bland fibrin thobi
- NO INFLAMMATION OR FIBROSIS
What is the effect of MV disease on LAP?
What are the pulmonary vascular changes secondary to MV disease with acute increase in LAP? What are the associated clinical features?
venous congestion with increased pulmonary venous pressure, leading to increased pressure in alveolar capillaries and interstitial and alveolar edema and hemorrhage
- SOB, othopnea, PND
What are the pulmonary vascular changes secondary to MV disease with chronic increase in LAP? What are the associated clinical features?
fibrous thickening of pulmonary veins
- severe increase in pressure transmitted to pulmonary arterioles --> structural changes --> increased arterial resistance, --> PULMONARY HYPERTENSION
- pressure overload of RV --> RHF if RV unable to compensate
- brown lung induration in the lung (interstitial fibrosis and hemosiderin)
What is a microscopic change seen in small pulmonary arteries due to chronic mitral stenosis?
concentric intimal thickening --> pulmonary hypertension
Which type of remodeling and in which chambers occurs in response to stenosis and regurgitation, respectively?
stenosis - concentric hypertrophy in upstream chamber
regurgitiation - eccentric hypertrophy in upstream and downstream chambers
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