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CV 3 > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

what is the function of normal cardiac valves? what are the different valves

A

to maintain unidriectional flow of blood

lined by endothelium

semilunar: aortic and pulmonary

AV valves: mitral and tricuspid, free margins attached to ventricular wall via chordae tendinae and papillary muscle

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2
Q

What is stenosis? What is insufficiency? what is more common, stenoses or insufficiencies?

A
  • Stenosis: failure of a valve to open completely, usually a chronic process affeting a valve cusp
  • Insufficiency: aka regurgitation.
    • functional regurgitation: valvular incompetence due to disruption of supporting structures
      • aorta root dilation, left ventricle dilation
      • intrinsic disease of valve cusps
  • stenoses are more frequent thatn insufficiencies
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3
Q

What are the major causes of valvular disease?

A
  • Congenital causes: bicuspid aortic valve (most common)
  • Acquired causes:
    • aortic valve
      • stenosis: senile calcific aortic stenosis
      • insufficiency: dilation of ascening aorta related to hypertension and aging
    • mitral valve
      • stenosis: rheumatic heart disease
      • insufficiency: myxomatous degeneration
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4
Q

What is dystrophic calcification? 2 specific examples?

A

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

distinct from atherosclerosis, but shares some risk factors (hyperlipidemia, hypertension, inflammation)

while some people are affected and others are not is unknown

ex: calcific aortic stenosis, mitral annular calcification

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5
Q

what is the most common valvular abnormality?

A

calcific aortic stenosis

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6
Q

When in life does calcific aortic stenosis usually occur? what are the clinical effects? what is the treatment? morphology? what mutation is it associated with

A
  • 5th/6th decades- bicuspid, or unicuspid valves. occurs in 1-2% of population and is associated with Notch mutation
  • clinical effects:
    • LV: increased pressure causes hypertrophy
      • angina, ischemia, CHF
      • syncope
      • 50% with CHF will die within 2 years
  • treatment: valve replacement
  • morphology: heaped up calcified masses in cusps, primarily at the bases, free cuspal edges not involved, no fusion of commissures
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7
Q

What is mitral annular calcification? who gets it?

A
  • degenerative calcific deposits on fibrous ring, at base of vlalve
  • women>60, increased in pts. with myxomatous valves or elevated LV pressure
  • usually does not affect valve function
  • BUT, calcifications are sites for thrombi/infection
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8
Q

What is myxomatous degeneration of mitral valve? (prolapse) Who gets it?

A

very common (3% of adults), young women

usually no serious complications

one or both leaflets enlarged, hooded, redundant, floppy (myxoid)

prolapse or balloon back into left atrium during systole (mid-systolic click)

pathogenesis is not clear but it is a feature of marfan syndrome

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9
Q

If myxomatous degeneration of the mitral valve is asymptomatic what would be the incidental finding on physical exam? WHen does the regurgitation occur? What are some uncommon complications?

A
  • Asymptomatic
    • incidental finding: mid systolic click on aucultation (between s1 and s2)
  • when regurgitation occurs: late systolic/ holosystolic murmur
  • complications: uncommon
    • infectious endocarditis
    • mitral insufficiency
    • thrombi on atrial surfaces lead to stroke or other systemic infarcts due to emboli
    • arrhythmias lead to sudden death
      • most often seen with advanced mitral insufficiency
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10
Q

What is acute rheumatic fever and heart disease? what is the classic lesion?

A
  • acute, immunologically mediated multisystem, inflammatory disease with major cardiac manifestations
  • occurs following an episode of group A streoptococcal (pyogenes) pharyngitis
  • most important complication progression to chronic valvular dysfunction (mitral stenosis)
  • widely disseminated inflammaotry lesions found in many sites
  • pancarditis (affects all three layers)
    • bread and butter pericarditis
    • myocarditis with Aschoff bodies
    • endocardium and left sided valves with fibrinoid necrosis and verrucae
    • subendocardial (MacCallum) plaques: irregular fibrosus thickening of endocardium
  • classic lesion? Aschoff body
    • foci of swollen eosinophilic collagen surrounded by T lymphocytes, plasma cells and plump macrophages- anitschkow cells, caterpillar cells
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11
Q

What is this image showing?

A

Pericarditis

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12
Q

what is this image showing?

A

aschoff body which is collagen, swollen, degenerated inflammation (lymphs, macrophages aka caterpillar cells, plasma cells)-giant cells and fibrinoid necrosis

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13
Q

what are these images showing?

A

Anitschkow cells: macrophages in Aschoff bodies (caterpillar cells)

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14
Q

what is being shown in these images?

A

fibrinoid necrosis and verrucae: lines of closure of valve caps (endocardial involvement)

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15
Q
  • Chronic Rheumatic heart disease: organization of inflammation and fibrosis leads to _________
  • the major effect is __________
A
  • In chronic rheumatic heart disease, organization of inflammation and fibrosis leads to:
    • thickened valve leaflets
    • fusion of commissures (fishmouth or buttonhole deformities)
    • fusion/thickening of chordae tendinae
  • major effect is mitral valve stenosis
    • leads to left atrial dilation (sometimes thrombus formation)
      • reduced cardiac output (mechanical obstruction prevents filling of LV)
    • pulmonary congestion, eventual right ventricular hypertrophy, right-sided heart failure
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16
Q

what valve is most commonly involved in chronic rheumatic heart disease?

what other valves are involved?

A
  • chronic rheumatic heart disease:
    • mitral valve alone (65-70%)
    • mitral and aortic
    • tricuspid less often
    • pulmonary rare
17
Q

WHat is this image ilustrating?

A
  • mitral stenosis in chronic rhematic heart disease
    • “fishmouth” or buttonhole deformities
18
Q

What is this picture showing?

A

chronic rheumatic heart disease-mitral stenosis, fusion/thickening of chordae tendinae and thickened valve leaflets

19
Q

describe the pathogenesis of rheumatic heart disease. what is the genetic susceptibility?

A
  • hypersensitivity reaction induced by group A streptococci
  • antibodies against M protein cross react with glycoprotein antigens in the heart, joints and other tissues
  • genetic susceptibility varies between individuals (not all with group A strep infections develop rheumatic fever)
20
Q

WHat are the diagnositc criteria for rheumatic fever?

A

preceding group A strep infection and

2 major manifestations

or 1 major and 2 minor

21
Q

What are the major manifestations of rheumatic fever? what are theminor manifestations?

A
  • Major:
    • migratory polyarthritis (large joints)
    • carditis-pericardial friction rub, weak heart sounds, tachycardia, arrhythmia
    • subcutaneous nodules-rare (extensor surfaces of joints)
    • erythema marginatum of skin- rare (trunk)
    • syndenham chorea (involuntary purposeless, rapid movements)
  • minor:
    • non-specific signs and symptoms
    • fever
    • arthralgia
    • elevated acute-phase reactants
22
Q

describe the clinical features and curse of acute rheumatic fever.

how long after a strep infection does it develop

who gets it

what is the prognosis

A

acute rheumatic fever

  • 1-4 weeks after group A (B hemolytic)streptococcal pharyngitis (only in 3%)
  • children between 5 and 15 years
  • ASO titers and antibodies to DNAase B
    • ASO=antistreptolysin O
      • streptolysin O and DNAase are protein produced by group A strep
  • prognosis: good for primary attack; increased vulnerability to reactivation
23
Q

how long after the initial episode do you get chronic rheumati fever? what is the prognosis?

A

years or decades after initil episode

valvular disease (valvulitis)

prognosis: surgical repair of valves improves outlook

24
Q

WHat are the 2 basic forms of infective endocarditis

A
  • Acute
    • highly virulent organism,normal valve, 50% mortality
    • necrotizing ulcerative invasive infection, requiring surgery
  • subacute
    • low virulence, deformed valve
    • less destructive lesions, respond to antibiotics
25
Q

who typically gets IE?

A
  • it is more common in patients with cardiovascular abnormalities
    • RHD, myomatous mitral valve, calcific valvular stenosis, artificial valves
  • host factors: neutropenia, immunodeficiency, malignancy, diabetes, alcoholics, and IV drugs users
26
Q

what are the main causative organisms for IE?

A

strep viridans: causes 50-60%

staph aureus causes 10-20% most common in IVDA

other organisms: commensal organisms f mouth, staph epidermidis in prothetic valves

27
Q

what is acute and subacute endocarditis like?

A
  • acute
    • friable, large, bulky destructive vegetations
    • fibrin, inflammatory cells and bacteria (less often fungi)
    • mitral valve and aortic valve most common sites
    • tricuspid valve in IV drug users
    • may erode myocardium leading to ring abscess
  • subacute
    • less valvular destruction, fibrosis and granulation tissue reaction at the base of vegetation
28
Q

What is seen on histology for infective endocarditis?

A

abundant acute inflammation, clusters of bacteria

29
Q

what are the major and minor duke criteria for bacterial endocarditis?

A
  • major:
    • positive blood cultures
    • echocardiographic findings (valve-related mass/ abscess)
    • new valvular regurgitation (new murmur on asucultation)
  • minor
    • predisposing heart lesion or IVDA
    • fever
    • uncommon findings resulting from septc emboli: petechiae, splinter hemorrhages, janeway lesions (palms, soles hemorrhagic lesions), osler nodes (digits), roth spots (retina)
30
Q

what are the complications of bacterial endocarditis? treatment?

A
  • valvular insufficiency or stenosis and possible heart failure
  • myocardial abscesses and possible perforation
  • vegetations break off lead to embolic omcplications
    • brain kidneys, spleen etc,
  • glomerulonephritis (immune complexes)
  • treatment: IV antibiotics, valve replacement if necessary
  • prophylactic antibiotics after valve damage
31
Q

what are the 2 kinds of non-infective vegetations?

A

nonbacterial thrombotic endocarditis

libman-sacks endocarditis

32
Q

what is a nonbacterial thrombotic endocarditis?

A
  • deposition of small masses of fibrin, platelets and other blood products on leaflets
    • often in debilitated patients (cancer, sepsis)
  • pathogensis and etiology:
    • hypercoagulable states
    • associated with mucin producing adenocarcinomas (DVTs and Trosseau syndrome)
    • ENdocardiak trauma-Swan-Ganz catheter
33
Q

what is the morphology of a non-infective thrombotic endocarditis like?

A

sterile, nondestructive, noninflammatory, small (1-5mm), along lines of closure

34
Q

What is Libman-Sacks endocarditis associated with?

A
  • systemic lupus erythematosus
    • mitral and tricuspid valves involved
    • antiphospholipid antibodies present
  • primary antiphospholipid syndrome
  • morphology
    • either or both sides of leaflets; may also be on endocardium
    • 1-4mm verrucae with firbous material
    • may have intense inflammation
35
Q

what is carcinoid syndrome?

A
  • carcinoid tumors produce serotonin, kallkrein, bradykinin, histamine, prostaglandins, and tachkinins
    • carcinoid syndrome: flushing cramps, nausea, vomiting, diarrhea
    • serotonin and bradykinin inactivated by MAO in pulmonary vasculature AND also inactivated by passage through functioning liver
36
Q

What is carcinoid heart disease?

A
  • cardiac manifestations of the systemic syndrome caused by carcinoid tumors
  • in 50% of patients with carcinoid syndrome-plaque-like fibrosis of right heart endocardium and valves
    • usually occurs on right side of heart (not left)
    • because of inactivation of mediators by MAO in lung
    • exact cause is unkown; believed to be realted to endothelial injury caused by vasoactive agents
37
Q

what type of patient does carcinoid syndrome/heart diseases occur in?

A
  • GI carcinoids with hepatic mets
    • normally, bioactive proteins are inactivated by liver
    • with mets to liver, secretion occurs directly into the hepatic veins and reached right side of heart
  • Carcinoids outside portal system of venous drainage
    • direct secretion into systemic circulation
      • example: carcinoids arisingin ovary, testes
    • very high blood levels may prevent complete inactivation by the lung MAO
      • ex: primary lung carcinoid
38
Q

when are endocardial plaque like thickenings found?

A

carcinoid heart disease

  • endocardial plaque like thickenings
    • smooth muscle cells and collagen embedded in mucopolysaccharide matrix
    • tricuspid and pulmonic valves equally afected
      • usually tricuspid insufficiency or pulmonic stenosis
39
Q

what are complications of a mechanical prosthetic valve? how about a bioprosthesis?

A
  • mechnical
    • thromboembolic complications
    • infective endocarditis
  • bioprosthesis
    • structural deterioration
      • 50% need replacement by 15 years
    • infetive endocarditis

CV 3 (7 decks)

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