Pathophys of Valvular Heart Disease, Pathology of Acquired Valvular Disease Flashcards

1
Q

Other than changes of stenotic valve, obstruction leading to aortic stenosis can occur via

A

above (supravalvular)

below (HOCM)

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2
Q

aortic stenosis etiology 50-60 y/o

A

bicuspid

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3
Q

aortic stenosis etiology 60-70 y/o

A

rheumatic

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4
Q

aortic stenosis etiology >70

A

senile degenerative

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5
Q

wall stress=

A

Pressureradius/2wall thickness

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6
Q

physical findings of AS

A
  • small/delayed carotid upstroke
  • late peaking systolic aortic murmur
  • absence of S2
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7
Q

AS tx

A

mechanical problem –> surgery

Esp if…

  • severe stenosis and symptomatic (including isolated systolic dysfunc/dec EF)
  • AS and undergoing CABG

baloon valvuloplasty is suboptimal

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8
Q

aortic regurg primary valve etiology

A

congenital, rheumatic, endocarditis, trauma

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9
Q

aortic regurg primary aortic root dilatation etiology

A

rheumatoid syndromes, CMN, Marfan’s, atherosclerotic

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10
Q

aortic regurgitation pathophys

A

huge RDV allows for ejection of large SV to maintain forward SV –> asymptomatic for years

but eventually wall stress inc, EF falls–> fatigue/DOE –> CHF –> death

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11
Q

aortic regurgitation physical exam

A
  • long loud diastolic murmur, Austin-Flint murmur
  • bounding pulses
  • wide pulse pressure
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12
Q

AR tx

A

-afterload reduction (nifedipine, ACE inhib) may slow LV deterioration

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13
Q

aortic valve replacement in AR, when to do

A
  • for symptomatic pts with severe AR

- asymptomatic pts with chronic severe AR and LV systolic dysfunction

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14
Q

mitral stenosis etiology in adults

A

always rheumatic –> inflammation –> deformity and fibrosis of leaflets –> fusion of commissures and chordae –> Ca and stiffening

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15
Q

mitral stenosis eventual outcome

A

inc LAP, LA dilation

inc RV and RA dilation and failure from pulm HTN

–> nutmeg liver

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16
Q

mitral stenosis sx

A
  • none for years
  • DOE, fatigue
  • sx inc w/ onset of afib
  • later, w/ RHF –> edema, venous congestion
  • emboli
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17
Q

mitral stenosis PE

A
  • loud S1, opening snap
  • low diastolic rumble
  • RV enlargement
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18
Q

mitral stenosis therapy

A

early: diuretics, beta blockers
later: MVR, balloon MVP

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19
Q

mitral regurgitation

A
  • ejection of portion of SV into LA (low pressure)

- chronic volume-overload of the LV

20
Q

chronic MR

A
  • rheumatic

- non-rheumatic (MVP, papillary m. dysfunction, endocarditis, LV dilatation, Marfan’s)

21
Q

MR physical exam

A
  • loud, holosystolic murmur. Apex to axilla
  • dec S1
  • S3 rumble
22
Q

chronic MR tx

A
  • afterload reduction and diuretics

- surgical soon after sx develop (prevents irreversible changes in LV, LA, pulm vasculature)

23
Q

tricuspid/pulmonic stenosis

A

usu congenital, early sx

P overload on chamber prod to valve

tx: balloon valvuloplasty

24
Q

tricuspid/pulmonic stenosis in adults

A

carcinoid syndrome

25
Q

tricuspid regurgitation etiology

A

usually secondary to RV/annular dilation

endocarditis in IVDA

RV and RA dilatation

large V waves on PE

systemic venous congestion

26
Q

large V waves on PE

A

tricuspid regurgitation

27
Q

most comm cause mitral stenosis

A

rheumatic heart disease

28
Q

most comm cause aortic stenosis

A

calcification

29
Q

most comm valve abnormalities

A

calcific AS

MVP

30
Q

calcific AS

A

one of the most comm valvular abnormalities

31
Q

myxoid degeneration

A

MVP

32
Q

rheumatic fever

A

heart/joints/skin/brain effets

group A beta hemolytic strep pharyngitis
cross rxn w/ glycoproteins

33
Q

major criteria of rheumatic fever

A
  • migratory polyarthritis of lg joints
  • carditis (PANcarditis)
  • subcutaneous nodules
  • sydenham’s chorea

Jones’ criteria

34
Q

minor criteria of rheumatic fever

A
  • fever
  • arthralgia
  • acute phase reactants
  • antistreptolysin O
  • ESR
35
Q

to dx rheumatic fever, need

A

2 major or 1 major + 2 minor

36
Q

histo findings of rheumatic fever

A

Aschoff nodule (fibrinoid necrosis, inflammatory cells, HISTIOCYTES (aschoff giant cells) Anitschkow cells (caterpillar))

37
Q

Aschoff

A

giant cells (histiocytes

38
Q

Anitschkow cell

A

specialized macrophage

looks like caterpillar

inside Aschoff nodule

39
Q

fish mouth

A

mitral stenosis

40
Q

most common organism in infective endocarditis

A
  • alpha hemolytic strep (VIRIDANS)

^less virulent

41
Q

most common organism in infective endocarditis w/ IV drug use

A

staph aureus

42
Q

HACEK organisms

A
  • hemophilus
  • actinobacillus
  • cardiobacterium
  • eikenella
  • kingells
43
Q

complications of infective endocarditis

A
  • valve destruction
  • ring abscesses
  • suppurative pericarditis (neutrophils)
  • septic emboli forming abscesses (brain, heart, spleen, kidneys, lungs)
44
Q

non-infected endocarditis vegetations

A
  1. nonbacterial thrombotic endocarditis (NBTE)

2. Libman-Sacks endocarditis (SLE)

45
Q

nonbacterial thrombotic endocarditis (NBTE)

A
  • hypercoaguable states
  • other malignant
  • debilitation, burns, sepsis, in-swelling venous catheter
46
Q

Libman-Sacks endocarditis (SLE)

A
  • 1-4mm single or multiple sterile verrucous vegetations (typically UNDERSURFACES aka inflow tract of mitral valve)
  • fibrinoid material within and HEMATOXYPHIL bodies (macrophages or neutrophils which have phagocytksed nucleus of injured cell)