Valvular Disease

Question 1

functional regurgitation

Answer 1

incompetence due to disruption of supporting structures

(as in aorta root dilation, left ventricle dilation)

Question 2

damage caused by wear and tear complicatedby deposits of calcium phosphate

Answer 2

dystrophic calcification

Question 3

clinical effects of calcific aortic stenosis

Answer 3

LV increased pressure casues hypertrophy

angia, ischemia, CHF

syncope

Question 4

morphology of calcified aortic stenosis

Answer 4

calicified masses in cusps, primarily at base

no fusion of commissures

Question 5

mitral annular calcification

Answer 5

degenrative calicific dposits on fibrous ring at base of valve,

usually doesn’t impact function

thrombis possible

Question 6

mxyomatous degeration of mitral valve (prolapse)

Answer 6

enlarged leaflets, prolaps into left atrium during systole

(mid-systolic click)

Question 7

complciations of mxomatous mitral valve

Answer 7

late systolic murmor,

rare: endocarditis, mitral insufficiency, thrombi, arrhythmias

Question 8

most serious complication of RA

Answer 8

progression to chronic vavlular dysfxn (mitral stenosis)

Question 9

classic lesion of RA

Answer 9

aschoff body - swollen eosinophillic collogen surroudned by t lymphocytes, plasma, and plump macrophages.

caterpillar cells

Question 10

pancarditis of RA

Answer 10

bread and butter pericardiits

myocarditis w/ aschoff bofdies

subendochondrail maccullum plaques (fibrous thickening of endocardium)

Question 11

chonic RA >chronic inflammatior and fibrosis leads to -

Answer 11

thickened leaflets

fusion of commisures

thickening/fusion of chordae tendinae

Question 12

clinical impact of chronic RA

Answer 12

mitral stenosis > atrial dilatation > reduced output

Question 13

pathogenesis RA

Answer 13

hypersensitivity induced by Group A Strep >

> Abs against Mm proteins cross react to glycoproteins inheart, joints >

>protein in sarcolemma of myocyte

Question 14

Jones criteria of RA

Answer 14

Joints

Heart (carditis, weakened heart sounds, tachy, arrhythmia)

Nodules

Erythema marginatum of skin (trunk)

Sydenham chorea

Question 15

protein produced by group A stresp

Answer 15

Steptolysis O and DNAase

Question 16

2 forms of ineffective endocarditis

Answer 16

acute - virulent organism, normal valve, (or necrotizing infection needing surgery)

subacute - low virulance with deformed valve, responds to AB

Question 17

common organisms of Ineffective Endocardits

Answer 17

Strep viridans (50-60%)

Staph A (10-20%) (most common in all IVDA)

Question 18

acute inefective endocarditis morphology

Answer 18

friable destructive vegetations

inflammatory cells and bacteria, fibrin

triscuspid valve in IV users

ring abcesses in erosion of myocardium

Question 19

differing factors in subacute ineffective endocarditis

Answer 19

less valvular destruction, fibroiss and granulation tissue reaction at base of vegetaion

Question 20

clinical features of Bacterial endocardiits

Answer 20

Dukes criteria

blood culture, valve related mass, abcesses

new vale regurgiation, new murmur on auscultation

Minor: fever, predisposing heart lesion of IVDA

Question 21

complciations bacterial endocarditis

Answer 21

valve insuf

myocaridal abcesses > perforation

vegetations embolize (kidneys, spleen)

glomulonephritis (immune complexes)

Question 22

pathogenesis of non-iffective vegetations- non bacterial thrombotis endocarditis

Answer 22

hypercoag. state

mucin producing adenocarcinomas

endocardial trauma (swan-ganz catherter)

Question 23

morphology liban sacks endocarditis

Answer 23

1-4 mm verrucae with fibrinous material on leaflets and pos endocardium

posible intense inflammation

Question 24

carcinoid syndrome- - tumors produce

Answer 24

carcinoid tumors produce serotonin, kallifkrein, brady kinin, histamine, prostagalndins, tachykinins

Question 25

presentation carcinoid syndrome

Answer 25

flushing, cramps, nausea, vomiting, diarrhea

plaqaue like fibrosis of heart endocardium, usually right heart

(becsaue of inactivation of mediators by MAO in lung)