Valvular Heart Disease Flashcards

1
Q

Functional regurgitation

A

Valve incompetence due to pathology in support structures

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2
Q

Mitral stenosis

A

Rheumatic heart disease

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3
Q

Mitral insufficiency

A

Mitral valve prolapse

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4
Q

Aortic stenosis

A

Calcification

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5
Q

Aortic insufficiency

A

Dilation of ascending aorta

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6
Q

Calcification aortic stenosis

A

Most common valvular abnormality

Age related degenerative calcification

If aortic valve is congenitally bicuspid, comes to attention in 50 to 70

If previously normal, comes to attention in 60s to 80s

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7
Q

Calcification aortic stenosis morphology

A

Rheumatic stenosis has commissar always fusion (degenerative usually does not)

Mitral valve involvement in rheumatic heart disease

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8
Q

Calcification aortic stenosis clinical

A

Obstruction causes concentric LV hypertrophy

May cause systolic and diastolic (CHF) dysfunction

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9
Q

Senile aortic stenosis

A

Tricuspid aortic valve undergone calcification

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10
Q

Congenital bicuspid aortic valve

A

Cusps usually unequal

Mitral valve normal

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11
Q

Acquired bicuspid aortic valve

A

Post inflammatory commissural fusion in rheumatic heart disease

Mitral valve is also abnormal

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12
Q

Myxomatous degeneration of the mitral valve

A

Most often young women

Most common valvular disease in industrialized nations

One or both mitral leaflets are enlarged,hooded, redundant, or floppy

Rarely lead to serious complications

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13
Q

Myxomatous degenerative of mitral valve morphology

A

Hooding of mitral leaflets
Leaflets are thick and rubbery
Cords often elongated, thinned, and occasionally ruptured

Commissural fusion is absent unlike in rheumatic heart disease

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14
Q

Myxomatous degen of the mitral valve histology

A

Attenuation of collagenous fibrosa layer

Thickening of spongiosa layer

Deposition of mucous material in the leaflets

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15
Q

Myxomatous degen of the mitral valve PE

A

Midsystolic click

May have late systolic or holosystolic murmur

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16
Q

Rheumatic fever

A

Occurs a few weeks after an episode of group A streptococcal pharyngitis

Often involves heart acutely but may progress to chronic valvular disease

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17
Q

Acute rheumatic fever morphology

A

Aschoff bodies

Anitschkow cells

Pancarditis

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18
Q

Aschoff bodies

A

T lymphocytes

Occasional plasma cells

Plump macrophages

Found in all layers

19
Q

Anitschkow cells

A

Plump macrophages

Abundant cytoplasm

Nuclear chromatin is central, slender, wavy ribbon

Larger ones form giant cells

20
Q

Pericarditis

A

Fibrinous or serofibrinous exudate

21
Q

Myocarditis

A

Aschoff bodies often perivascular

22
Q

Endocarditis

A

See fibrinoid necrosis within the cusps or along the tendinous cords

Verrucae along line of closure of valves

23
Q

MacCallum plaques

A

Rheumatic heart disease

Irregular subendocardial thickening usually in left atrium

24
Q

Acute rheumatic fever pathogenesis

A

Damage to heart caused by:

Immune response to group A strep which cross reacts with host tissue

CD4+ cells specific for strep peptides also react with self proteins

25
Q

Acute rheumatic fever clinical

A

Evidence of preceding group A strep pharyngitis (10 days to 6 weeks) and

Jones criteria:
2 major or 1 major and 2 minor

Most often in children ages 5 to 15

Lab antibodies to streptolysin O and DNAse B

26
Q

Jones criteria

Major manifestations

A

Migratory polyarthritis

Carditis

Subcutaneous nodules

Erythema marginatum of the skin

Sydenham chorea

27
Q

Jones criteria

Minor manifestations

A

Fever

Arthralgias

Elevated acute phase reactant (C reactive protein)

28
Q

Carditis

A

Pericardial friction rubs

Weak heart sounds

Tachycardia

Arrythmias

29
Q

Consequence of rheumatic fever

A

Chronic rheumatic heart disease

30
Q

Chronic rheumatic heart disease

A

Deforming fibrotic heart disease

Particularly mitral stenosis
Leaflet thickening
Commissural fusion
Shortening, thickening, and fusion of the tendinous cords

31
Q

Chronic rheumatic heart disease morphology

A

LA dilation with possible mural thrombus

May cause RV hypertrophy 2* pulmonary congestion leading to vascular and parenchymal changes

32
Q

Infective endocarditis

A

Serious infection of heart valves or mural endocardium

Invasion by a microbe-> formation of vegetation’s with destruction of underlying tissue

Usually do to bacteria

Can be in aorta, aneurysmal sacs, other blood vessels, prosthetic devices

33
Q

Acute endocarditis

A

Highly virulent organisms

Frequently affect normal valves, as well as abnormal

Destructive, tumultuous infection

50% die even with antibiotics and surgery

34
Q

Subacute endocarditis

A

Organisms with low virulence

Previously abnormal valve

Most recover after appropriate therapy

35
Q

Agents causing Infective endocarditis

A

Strep viridans

  • oral flora
  • damaged abnormal valves

Staph aureus

  • found on skin
  • # 1 in drug abusers

Enterococci and HÁČEK

Staph epidermidis
-prosthetic valves

36
Q

Infective endocarditis morphology

A

Friable vegetation’s composed of fibrin, inflammatory cells, bacteria

aortic and mitral valves are usual sites
Right-sided valves may be involved esp IV drug users

May produce abscess in myocardium-ring abscess

37
Q

Infective endocarditis clinical

A

Fever

Fatigue, wt loss, flu like syndrome

Murmur (90%)

Less frequently Janeway lesions, Oiler nodes, Roth spots

Positive blood culture

Echocardiography- mass or abscess

38
Q

Janeway lesions

A

Erythematous lesions on palms or soles in infective endocarditis

39
Q

Older nodes

A

Subcutaneous nodules in pulp of digits in infective endocarditis

40
Q

Roth spots

A

Retinal hemorrhages in infective endocarditis

41
Q

Complications of artificial valves

A

Thromboembolic complications

  • long term anticoagulation
  • may cause hemorrhage complications
42
Q

Structural deterioration of artificial valves

A

Major failure mode of bioprostheses

43
Q

Other complications of artificial valves

A

Intravascular hemolysis from shear forces

Paravalvular leak from inadequate healing

Obstruction from overgrowth by fibrous tissue during healing