Pathb2: Heart Iii Valves

Front 1

calcific aortic stenosis, most common of all valvular abnormalities, leads to LVH=>angina, ischemia, CHF, syncope, if occurs 5th-6hth decade=bicuspid valve

Back 1

-

Front 2

mitral annular calcification, degenerative calcific deposities on fibrous ring at base of valve, women >60, usually does not affect fxn but site for thrombus/ embolus

Back 2

-

Front 3

MV prolapse, caused by myxomatous degeneration. Usually no serious complications, leads to mid systolic click. Can progress to mitral regurg

Back 3

-

Front 4

"bread and butter" pericarditis typical of the pancarditis associated with acute rheumatic fever. Can lead to a friction rub

Back 4

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Front 5

Aschoff body. Characteristic lesion of the myocarditis assoicated with acute rheumatic fever.

Back 5

-

Front 6

Anitschkow cell, macrophages with long, flattened nuclei. Loacted in Aschoff body, the characteristic lesion of acute rhumatic fever

Back 6

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Front 7

Thickening of the chordae tendineae, characteristic of chronic rheumatic heart disease

Back 7

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Front 8

Vegetations associated with non-infective thrombotic endocarditis. The lesions are sterile and non-inflammatory and are located along the lines of closure

Back 8

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Front 9

Endocarditis associated with Libman-Sacks non-infective endocarditis. The lesions can be located on both sides of the valve and may have intense inflammation. LSE is assoicated with SLE and primary antiphospholipid syndrome

Back 9

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Front 10

Patterns of vegetations with the vaious endocarditises, note the location of the lesion and the degree of destruction

Back 10

-

Front 11

Endocardial plaque like fibrosis assoicated with carcinoid heart diseease. SMC's and colagen are embeded in a MPS matrix. Caused by a carcinoid tumor with hepatic mets or direct secretion into systemic circulation producing various mediators. Results in TV insufficiency or PV stenosis

Back 11

-

Front 12

major causes of aquired aortic valve disease

Back 12

senile calcific stenosis, insufficiency-dilation of thoracic aorta related to HTN, aging

Front 13

major cuases of aquired mitral valve disease

Back 13

rheumatic HD=stenosis, insufficeincy=myxomatous degneration (prolapse)

Front 14

which is more common stenosis or insufficiency

Back 14

stenosis

Front 15

describe calcific aortic stenosis

Back 15

dystrophic calcification of the aortic valve, occurs in 5th/6th decade w. bicuspid valve, 8th/9th if normale, Clinical effects-LVH, angina, ischemia, CHF, syncope, microangiopathic hemolytic anemia

Front 16

Aortic stenosis auscutation finding

Back 16

systolic ejection click with crescendo-decresendo murmur, S4

Front 17

treatment of calcific aortic stenosis

Back 17

valve replacement

Front 18

the most common of all valvular anbormalities

Back 18

calcific aortic stenosis

Front 19

morphology of calcific aoric stenosis

Back 19

calcified masses in cusps primarily ab the base, free cuspal edge is not involved and there is no fusion of the commusiures (distinuish from rheumatic HD)

Front 20

mitral annular calcification

Back 20

degenreative calcific deposite at base of MV ring, women >60, increased in pts with myxomatous valves or elevated Lvpressure, usually does not effect valve fxn but te for thrmobi

Front 21

Pathogenesis of myxomatous mitral valve (prolapse)

Back 21

very common esp young women, developmental anoamly of CT leads to deposition of mucoid material in valve

Front 22

Clinical findings of MVP

Back 22

usually asymptomatic, can have regurg. Complications include:infective endocarditis, mitral insufficiency, thrombi, arrythmia (with advacned insufficiency)

Front 23

auscultaiton of MVP

Back 23

mid systolic click, late systolic/ holosysolic murmur if regurgitation

Front 24

pathogenesis of rheumatic heart disease

Back 24

hypersensitivity rxn induced by group A beta hemolytic strep, antibodies against viral M protein cross react with glycoprotein antigen in heart

Front 25

Most significant complication of Rheumatic HD

Back 25

mitral stenosis

Front 26

Morphology of acute Rheumatic HD

Back 26

pancarditis: 1. bread and butter pericarditis 2. Myocarditis with Achoff bodies 3. Endocartitis affecting left sided valves with fibrinoid necrosis

Front 27

the Achoff body is the classic leasion of

Back 27

rheumatic HD

Front 28

Describe Aschoff bodies

Back 28

classic lesion of rheumatic HD. Found in the myocardium, contain collagen, swollen degenerated inflammation (lymphs, macs, plasma cells), contain Anitschkow cells (macs in aschoff bodies," Caterpillar cells")

Front 29

describe the effect of rheumatic HD on the endocardium

Back 29

fibrinoid necrosis and verrucae (lines of closure of valve cusps_

Front 30

describe the effect of rheumatic HD on the myocardium

Back 30

inflammation characterizied by Aschoff bodies with Anitschkow cells

Front 31

describe the complications of CRHD

Back 31

thickned valve leaflets, fusion of commissures (fishmouth/ button hole), fusion/ thickening of chordae tendineae

Front 32

The major effect of CRHD is ___ which can lead to…

Back 32

mitral stenosis= LA dilation=reduced CO, Pulmonary congestion, RVH, right sided heart failure

Front 33

valves affected by CRHD

Back 33

mitral alone>mitral _aortic> tricuspid> pulmonary

Front 34

fishmouth or button hole deformitie of the mital valve are characteristic of

Back 34

chornic rheumatic HD

Front 35

fusion/ thickening of the chordae tendinae anthickend valve leaflest are characteristic of

Back 35

CRHD

Front 36

Diagnosis of rheumatic heart diase

Back 36

1. Precedding group A strep infection 2. 2 major or 1 major and 2 minor manifestation

Front 37

Major manifestations of RHD

Back 37

JONES: Joints-migratory polyarthritis, O-Carditis, N-subcutaneous nodules, E-erethema marginatum S-Syndeham chorea

Front 38

minor manifestations of RHD

Back 38

fever, arthralgia, elevated acute phase reactants (ESR)

Front 39

clinical course of RHD

Back 39

acute: 1-4 wks after group A strep infection, kids 5-15, Chronic: years or decades after intial episode, valvular disease,

Front 40

two forms of infectious endocarditis, cause, result

Back 40

1. Acute-highly virulent organism infects normal vavle, necrotizing ulcerative invasive lesion requires surgery 2. Subacute-low virulent organism infects deformed valve, less destructive lesion, responds to antibiotics

Front 41

predispositions for infective endocarditis

Back 41

CV abnormality (RHD, myxomatous mitral valve, calcific valvular stenosis, artifical vavle), host factors (neutropneia, immunodeficiency, malignancy, diabetes, alcoholic, IV drug user

Front 42

causes an endocarditis of deformed valves 50-60%, low virulence

Back 42

Strep viridans (low VIRulence)

Front 43

Causes an infective endocarditis in 10-20% of cases, most common cause in IVDA's

Back 43

staph aureus (drugs give you an aura of hapiness)

Front 44

Causes infective endocarditis in prosthetic valves

Back 44

staph epidermidis (prothetics are Epi the body)

Front 45

frequency of valves infected with endocarditis

Back 45

most common=mitral, aortic, most common in IVDA's=tricuspid

Front 46

criteria used to Dx bacterial endocarditis

Back 46

Duke criteria. Major (positive blood culture, Echo, New valvular regur) Minor: predisposing heart lesion or IVDA, fever, uncommon findings from septic emboli (splinter hemorrhage, Janeway lesion, Osler node, Roth spots)

Front 47

splinter hemorrahges in the finger nails are a sign of

Back 47

septic emboli from bacterial endocarditis

Front 48

Complications of bacterial endocarditis

Back 48

valvular insufficiency, myocardial abcess, vegetations=>emboli, glomerulonephritis (immune complexes)

Front 49

Tx of bacterial endocarditis

Back 49

IV antibiotics (low virulence), valve replacement (high virulence), note use of prophylactic antiobiotics after valve damage

Front 50

pathogenesis and eitology of nonbacterial thrombotic endocarditis

Back 50

depositis of small masses of fibrin/platelets/ blood products on leaflest, often in debilitated pts, hypercoagulable state, mucin producing adenocarcinoma, endocardial trauma

Front 51

Debiliated pts or those in a hypercoagulable state, with a mucin producing adenocarcinoma or endocardial trauma are at risk for what type of endocarditis

Back 51

nonbacterial thrombotic

Front 52

describe the morphology of non-infective thrombotic endocarditis

Back 52

sterile, non-destructive, non inflmmatory vegetations along the lines of valve closure

Front 53

Describe libman-Sacks endocarditis

Back 53

vegetations th virbnous material and intense inflammation on either or both sides of the associated with SLE, primary antiphospholipid syndrome

Front 54

Pts with SLE or primary antiphospholipid syndrome are at risk for what type of endocarditis

Back 54

Libman-Sacks, nondestructive/ inflammatory, either or both sides

Front 55

Describe the pattern of vegetations expected with RHD, IE, NBTE, and LSE

Back 55

RHD-left sided valves, along the lines of closure; IE-friable, large, bulky, destructive, NBTE-small patches on leaflets, LSE-on both sides of valve

Front 56

what is carcinoid syndrome

Back 56

tumor that produces serotonin, kallikrein, bradykinin, histamine, prostaglandins, tachkinins, leads to flushing, cramps nausea, vomiting, diarhhea, leads to plauqe like fibrosis of right heart endocardium and valves (inactivation by lung MAO protects left heart)

Front 57

which pts are are at risk for carcinoid syndrome

Back 57

GI carcinoids with hepatic mets, carconids outside of the portal system of venous drainage leading to direct secretion into the systemic circulation

Front 58

cardiac manifestations of carcinoid syndrome

Back 58

plaque like fibrosis of right heart endocardium and valves (MAO in lungs protects left heart)

Front 59

mitral stenosis ausculation

Back 59

opening snap, diastolic rumble

Front 60

aortic regurg auscultation

Back 60

early blowing systolic murmur