100314 valvular disease

Question 1

which are more frequent: stenoses or insufficiencies

Answer 1

stenoses

Question 2

dystrophic calcification

Answer 2

damage caused by wear and tear complicated by deposits of calcium phosphate

risk factors: hyperlipidemia, HTN, inflammation

Question 3

ex of dystrophic calcification

Answer 3

calcific aortic stenosis

mitral annular calcification

Question 4

what is the most common of all valvular abnormalities

Answer 4

calcific aortic stenosis

Question 5

calcific aortic stenosis in 5th or 6th decade of life suggests

Answer 5

bicuspid or unicuspid valves

Question 6

morphology of calcific aortic stenosis

Answer 6

heaped up calcified masses in cusps, primarily at bases

free cuspal edges NOT involved

no fusion of commisures

Question 7

mitral annular calcification

Answer 7

degenerative calcific deposits on fibrous ring at base of valve

usually doesn’t affect valve fxn
but are sites for thrombi or infec

Question 8

myxomatous degeneration of mitral valve (prolapse)

Answer 8

very common (3% of adults)
young women
one or both leaflets are enlarged, hooded, floppy

mid systolic click

Question 9

rheumatic fever causative agent

Answer 9

group A Strep pyogenes-pharyngitis

Question 10

most important complication of rheumatic fever

Answer 10

progression to chronic valvular dysfxn (mitral stenosis)

Question 11

acute rheumatic fever affects what

Answer 11

pancarditis

bread and butter pericarditis (fibrinous)
myocarditis with Aschoff bodies
endocardium and left sided valves with fibrinoid necrosis and verrucae
subendocardial MacCallum plaques

Question 12

what is the classic lesion of acute rheumatic fever

Answer 12

Aschoff body (foci of swollen eosinophilic collagen surrounded by T lymphocytes, plasma cells and plump macrophages)

plump macrophages are called Anitschkow cells or caterpillar cells

Question 13

chronic rhuamtic heart disease

Answer 13

inflam and fibrosis leads to…
thickened valve leaflets
fusion of commissures (fishmouth)
fusion and thickening of chordae tendineae

Question 14

what is the major effect of chronic rheumatic heart disease

Answer 14

mitral stenosis

Question 15

diagonsis of rheumatic fever

Answer 15

jones criteria

preceding group A strep infec and 2 major manifes or (1 major and 2 minor)

Question 16

major manifestations for rheumatic fever

Answer 16

migratory polyarthritis
carditis (percardial friction rub, weak heart sounds, tachycardia, arrhythmia)
subcutaneous nodules - rare
erythema marginatum of skin -rare
sydenham chorea

Question 17

two forms of infective endocarditis

Answer 17

acute-highly virulent organism, normal valve, 50% mortality, requires surgery

subacute-low virulence, deformed valve, less destructive lesions, respond to antibiotics

Question 18

causes of infective endocarditis

Answer 18

more common in pts with cardiovascular abnormalities

host factors-neutropenia, immunodeficiency, malignancy, diabetes, alcholics, IV drugs users

Question 19

organism in 50-60% of cases of infected deformed valves

Answer 19

strep viridans

Question 20

most common causative agent for infective endocarditis in IV drug users

Answer 20

staph aureus

Question 21

morphology of acute and subacute infective endocarditis

Answer 21

friable, large bulky destructive vegetations
fibrin, inflam cells and bacteria (less often fungi)
may erode myocardium–leading to ring abscess

Question 22

Duke criteria for bacterial endocarditis

Answer 22

major:
positive blood cultures
echo findings (valve related mass or abscess)
new valvular regurg (new murmur on auscultation)

minor:
predisposing heart lesion or IV drug abuser
fever
umcommon findings resulting from septic emboli, which are bits of vegetations that fly off (petechiae, splinter hemorrhages, Janeway lesions in palsm and soles, Osler nodes in digits, Roth spots in retina

Question 23

complications of bacterial endocarditis

Answer 23

valvular insufficency or stenosis and possible heart failure

myocardial abscesses and possible performation

vegetations breaking off leading to embolic complications

glomeruloneprhitis (immune complexes)

Question 24

nonbacterial thrombotic endocarditis

Answer 24

depositions of fibrin, platelets and other blood products (RBC) on leaflets

often in debilitated pts
may result in emboli

Question 25

pathogenesis/etiology of nonbacterial thrombotic endocarditis

Answer 25

hypercoagulable states
associated with mucin producing adenocarcinomas
endocardial trauma

Question 26

morphology of noninfec thrombotic endocarditis

Answer 26

nondestructive, noninflammatory, small (1-5 mm)

along lines of closure

Question 27

Libman Sacks endocarditis

Answer 27

non infec vegetation

from SLE
mitral and triscupid valves involved
antiphospholipid antibodies present

Question 28

morphology of Libman Sacks endocarditis

Answer 28

either or both sides of leaflets
may also be on endocardium
may have intense inflam

Question 29

ex of vegetative endocarditis

Answer 29

rheumatic heart disease
infective endocarditis
nonbacterial thrmbotic endocarditis
Libman Sacks endocarditis

Question 30

carcinoid syndrome

Answer 30

flushing, cramps, nausea, vomiting diarrhea

Question 31

carcinoid heart disease

Answer 31

cardiac manifestation of the systemic syndrome caused by carcinoid tumors

in 50% of pts with carcinoid syndrome- plaque like fibrosis of R heart endocardium and valves

Question 32

complications of artifical valves

Answer 32

mechanical prosthesis: thromboemboli, infective endocarditis

bioprothesis: structural deterioration, infective endocarditis