Valvular heart disease Flashcards

1
Q

Cardiac valves

A

Maintain unidirectional flow of blood
Lined by endothelium
Semi lunar valves- Aortic and pulmonary
AV valves- mitral and tricuspid (free margins attached to ventricular wall via chordae tendinae and papillary muscles

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2
Q

Valvular heart disease

A

Stenosis- failure of a valve to open completely (usually a chronic process affecting a valve cusp)

Insufficiency: failure of a valve to close completely (functional regurgitation-valvular incompetence due to disruption of supporting structures, Aorta root dilation and LV dilation, Intrinsic disease of Valve cusps

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3
Q

Cause of valvular disease major cause

A

Congenital causes (bicuspid aortic valve), Acquired causes (aortic valve stenosis (senile calcific), Insufficiency (ilation of ascending aorta related to HTN and age)

Mital valve Stenosis: Rheumatic heart disease, Insufficiency: Myxomatous degeneration

Stenosis»> insufficiences

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4
Q

Calcific Valvular Disease

A

Dystrophic calcification: damage caused by wear and tear complicated by deposits of calcium phosphate

distinct from atherosclerosis, but shares some risk factors (hyperlipidemia, hypertension, inflammation)

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5
Q

Calcific aortic stenosis

A

Most common of all valvular abnormalities
Occurence: 5os 60s - bicuspid, unicspid valve (notch mutation, 890s normal valves senile

Clical effects: LV: increased pressure causes Hypertrophy
Angina, ischemia and CHF, syncope,
Treatment valve replacement

Heaped up calcified masses in cusps, primarily at the bases, free cuspal edges not involved, no fusion of commisures

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6
Q

Mitral annular calcification

A

Degenerative calcific deposists on fibrous ring, at base of valve
Women> 60 Yrs old
increased in patients with myxomatous valves or elevated LV pressure
Usually doesnt affect valve function but site of thrombi/infection

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7
Q

Myxomatous degeneration of mitral valve (prolapse)

A

very common, young women, usually not serious

One or both leaflets enlarged, hooded redundant floppy

Prolapse or balloon back into left atrium during systole
Pathogenesis unknown: developmental anomaly of CT, marfan syndrome

Clinical features/complication: asymptomatic, regurgitation (late systolic/holosystolic murmur)
Complications uncommon (IE, Mitral insuf, thrombi on atrial surfaces, arrhythmias-> sudden death
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8
Q

Rheymatic fever and heart disease

A

Acute, im mune mediated, multisystem, inflammatory disease
Occurs after group A strep (pyogenes) pharyngitis

Most important complciation: progresion to chronic valvular dysfunction (mitral stenosis)a\

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9
Q

Acute rheumatic fever morphology

A

widely disseminated inflammatory lesion found in many sites
Pancarditis (affects all three layers)-pericarditis, myocarditis with aschoff bodies, endocardium and left sided valves with fibrinoid necrosis and verrucae, subendocardial Maccallum plaques: irregular fibrous theckening of endocardium

Classic lesion is Aschoff body (foci of swollen eosinophillic collagen surrounded by Tcell, plasma cells and plump Macrophages- Anitschkow cells, caterpillar cells

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10
Q

Chronic rheumatic heart disease

A

inflammation and fibrosis leads to thickened valve leaflets, fusion of commissures (fishmouth or buttonhole deformaties), fusion/thickening of chordae tendinaee

Major effect is mitral stenosis– left atrial dilatation (thrombus) reduced cardiac output, pulmonary congestion eventual right ventricular hypertrophy and right sided heart failure
Pathogenesis: HS reaction induced by group A Streptococci, antibodies against M protein cross react with gcp Ag in the heart joints and other tissues

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11
Q

JONES

A

Preceding group A strep infection and 2 major manifestaion (or 1 maj and 2 min)

Major: migratory polyartheritis, carditis, Nodules, Erythema marfinatum, Synednham chorea

Minor: Fever, arthralfia, elevated acute phase reactants

Clinical features and course: ASO tites

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12
Q

Inefective endocarditis

A

Acute: highly virulent organism, normal valve, mortality, necrotizing ulcerative invasive infection

Subacute: low virulence, deformed valve, less destructive lesions, respond to antibiotics

Etiology/pathogenesis: CV abnormalities, host factors

Strep viridans 50-60%
S aureus organism in

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