Valvular Heart Disease, Murmurs Flashcards

1
Q

What is the etiology for mitral stenosis?

A

a. rheumatic valve disease (99%)
b. calcification
c. congenital abnormalities
d. medications (ergotamines, pergolide)

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2
Q

What is the pathophysiology of mitral stenosis?

A

a. A-Fib in 50%
b. high risk of thromboembolism
c. high LA pressure leads to pulmonary congestion
d. Aschoff Bodies

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3
Q

What sounds does mitral stenosis make?

A

Opening snap and diastolic ruble

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4
Q

What is the presentation of MS?

A

a. fish mouth
b. hocky stick valves
c. dyspnea/pulmonary edema/thromboembolism
d. hemoptysis in extreme cases

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5
Q

What is the prognosis and treatment of MS?

A

a. progressive loss of valve area
b. pulmonary congestion, can lead to R heart dysfunction
c. hypertrophy
d. LEFT ATRIAL APPENDAGE CLOT

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6
Q

What is the primary etiology of MR?

A

a. mitral valve prolapse
b. myxomatous degen. (gel-like valve)
c. infectious endocarditis (staph aureus from IVs or strep viridans if congenital)
d. rheumatic heart disease
e. trauma
f. anoretic drug: fen-phen
g. cleft mitral valve

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7
Q

What is the acute pathophysiology of MR?

A

Acute:

a. decrease in LV afterload
b. increase in LV preload
c. increased SV
d. press. and vol. overload of LA

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8
Q

What is the secondary etiology of MR?

A

a. enlarged LV and mitral valve annulus bc of ischemic heart disease
b. papillary muscle of chordae tendinae rupture/malfunction
c. clacification of mitral annulus (women > 60)

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9
Q

What is the chronic pathophysiology of MR?

A

a. decrease in LV afterload
b. increase in LV preload
c. eccentric LV hypertrophy
d. LA enlargement

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10
Q

What is the sound of MR? What makes it better or worse?

A

Click during systole (prolapse only!) and the holosystolic murmur.

Squatting makes it quieter.

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11
Q

What is the presentation of MR?

A

a. pulmonary edema

b. V wave shows increased pressure in LA during systole

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12
Q

What is the prognosis and treatment of MR?

A

Acute: poorly tolerated
Chronic: prolonged asymptomatic, but CHF, A Fib, and pulmonary hypertension. 5 year survival = 22%

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13
Q

What is the etiology of MVP?

A

billowing of a leaflet past plane of valve annulus.

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14
Q

What is the pathophysiology of MVP?

A

thickened, redundant leaflets, stretched chordae and dilated annulus.

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15
Q

What is the sound of MVP?

A

a click! in systole and a subsequent systolic murmur.

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16
Q

What is the presentation of MVP?

A

can be same as MR (dilated LA, pulmonary congestion, reduced SV, etc. ), and it occurs in 4-5% of adults

17
Q

What is the etiology of aortic stenosis?

A

a. degenerative: calcification, leaflet thickening, inflammatory pathway
b. congenital bicuspid valve (pts. less than 70): 3:1 males to females, in 1% of population
c. rheumatic: most common in world (but not US), causes commissures to fuse and thickens subvalvular apparati

18
Q

What is the pathophysiology of AS?

A

a. increased LV afterload
b. LV concentric hypertrophy
c. diastolic LV dysfunction is common
d. valve area of 2cm^2 or smaller

19
Q

What murmur does AS make?

A

a systolic crescendo/decrescendo (whoosh!)

20
Q

How does AS present?

A

a. late peaking systolic ejection murmur

b. weakened and delayed upstroke of carotid artery pulsations

21
Q

What is the treatment and prognosis of AS?

A

angina, syncope, CHF (5, 3, and 2 year survival rate, respectively)

aortic valve replacment

22
Q

What is the etiology of AR?

A

a. dilated aortic root
b. Marfan’s
c. endocarditis
d. dissection
e. bicuspid valve issues
f. trauma
g. rheumatic fever

23
Q

What is the pathophysiology of AR?

A

a. increased preload
b. increased afterload
c. LV pressure/volume overload
d. LV dilates
e. LV eccentric hypertrophy

24
Q

What is the murmur associated with AR?

A

diastolic murmur with absence of S2.

25
Q

What is the presentation of AR?

A

Acute: LV normal size but non-compliant
Chronic: increased LV SV, widened pulse pressure, decreased coronary artery perfusion

26
Q

What is the treatment and prognosis for AR?

A

a. can have a prolonged asymptomatic period
b. Ab prophylaxis
c. long-standing volume overload can lead to LV dysfunction

27
Q

What is the etiology of TS?

A

almost always due to rheumatic heart disease.

28
Q

What is the pathophysiology of TS?

A

RA enlargement.

29
Q

What is the presentation of TS?

A

results in elevated RA/SVC/IVC pressures; leg edema, hepatomegaly

30
Q

What is the treatment and prognosis of TS?

A

It is very RARE!

31
Q

What is the etiology of TR?

A

a. function TR 90% of the time
b. endocarditis
c. trauma
d. rheumatic HD
e. carcinoid syndrome (tumor with serotonin)
f. myxomatous degeneration
g. ebstein’s anomaly
h. anoretic drugs

32
Q

What is the pathophysiology of TR?

A

RV volume overload

33
Q

What is the presentation of TR?

A

elevated RA/SVC/IVC pressures, ascites, leg edema, hepatomegaly

34
Q

What is the treatment and prognosis of TR?

A

often tolerated and asymptomatic.

35
Q

What is the etiology of pulmonic stenosis?

A

a. common congenital abnormality (Tetralogy of Fallot)
b. congenital rubella syndrome
c. noonan syndrome

36
Q

What is the pathophysiology of PS?

A

RV hypertrophy

37
Q

What is the etiology of PR?

A

usually secondary to pulmonary hypertension and/or dilated pulmonary artery

38
Q

What is the presentation of PR?

A

rarely clinically significant.