Valvular Heart Disease Flashcards

(43 cards)

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
Acute rheumatic fever clinical
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
Jones criteria Major manifestations
Migratory polyarthritis Carditis Subcutaneous nodules Erythema marginatum of the skin Sydenham chorea
27
Jones criteria Minor manifestations
Fever Arthralgias Elevated acute phase reactant (C reactive protein)
28
Carditis
Pericardial friction rubs Weak heart sounds Tachycardia Arrythmias
29
Consequence of rheumatic fever
Chronic rheumatic heart disease
30
Chronic rheumatic heart disease
Deforming fibrotic heart disease Particularly mitral stenosis Leaflet thickening Commissural fusion Shortening, thickening, and fusion of the tendinous cords
31
Chronic rheumatic heart disease morphology
LA dilation with possible mural thrombus May cause RV hypertrophy 2* pulmonary congestion leading to vascular and parenchymal changes
32
Infective endocarditis
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
Acute endocarditis
Highly virulent organisms Frequently affect normal valves, as well as abnormal Destructive, tumultuous infection 50% die even with antibiotics and surgery
34
Subacute endocarditis
Organisms with low virulence Previously abnormal valve Most recover after appropriate therapy
35
Agents causing Infective endocarditis
Strep viridans - oral flora - damaged abnormal valves Staph aureus - found on skin - #1 in drug abusers Enterococci and HÁČEK Staph epidermidis -prosthetic valves
36
Infective endocarditis morphology
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
Infective endocarditis clinical
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
Janeway lesions
Erythematous lesions on palms or soles in infective endocarditis
39
Older nodes
Subcutaneous nodules in pulp of digits in infective endocarditis
40
Roth spots
Retinal hemorrhages in infective endocarditis
41
Complications of artificial valves
Thromboembolic complications - long term anticoagulation - may cause hemorrhage complications
42
Structural deterioration of artificial valves
Major failure mode of bioprostheses
43
Other complications of artificial valves
Intravascular hemolysis from shear forces Paravalvular leak from inadequate healing Obstruction from overgrowth by fibrous tissue during healing