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CV Quiz 2 > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

What are the semilunar valves?

A

aortic and pulmonary

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2
Q

What are the AV valves?

A

mitral and tricuspid

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3
Q

Describe the AV valve structure…

A

free margins attached to the ventricular wall via chordae tendinae and papillary muscles

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4
Q

What is stenosis?

A

failure of a valve to open completely– Usually a chronic process affecting a valve cusp

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5
Q

What is insufficiency?

A

failure to close completely

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6
Q

Causes of insufficiency?

A

– Functional regurgitation: valvular incompetence due to disruption of supporting structures (Aorta root dilation &Left ventricle dilation)
–Intrinsic disease of valve cusps

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7
Q

Major causes of Vavlular Disease

A

• Congenital causes– Bicuspid aortic valve (most common)
-Acquired causes–
Aortic valve –Stenosis: senile calcific aortic stenosis & Insufficiency: dilation of ascending aorta related to hypertension and aging
Mitral valve –Stenosis: Rheumatic heart disease & Insufficiency: Myxomatous degeneration

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8
Q

Is stenoses or insufficiency more frequent cause?

A

Stenosis

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9
Q

What is dystrophic calcification?

A

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

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10
Q

Risk factors for dystrophic calcification?

A

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

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11
Q

Most common of all valvular abnormalities?

A

Calcific Aortic Stenosis (AS)

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12
Q

When does AS occur in life?

A

– 5th/6th decades - bicuspid, unicuspid valves • Occur in 1-2% of population, association w/ Notch mutation
–8th/9th decades – normal valves (“senile”)

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13
Q

What are the clinical effects of AS?

A

LV: increased pressure causes hypertrophy• Angina, ischemia, & CHF• Syncope (mechanism is not clear)• 50% with CHF will die within two years

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14
Q

Treatment for AS?

A

valve replacement

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15
Q

Describe the morphology of AS.

A

Heaped up calcified masses in cusps, primarily at the bases• Free cuspal edges not involved• No fusion of commissures

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16
Q

What is Mitral Annular Calcification?

A

Degenerative calcific deposits on fibrous ring, at base of valve

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17
Q

Risk factors for mitral annular calcification?

A

Women > 60 years old • Increased in patients with myxomatous valves or elevated LV pressure

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18
Q

Does mitral annular calcification affect function?

A

Usually does not affect valve function BUT, calcifications are sites for thrombi/infection

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19
Q

What happens in Myxomatous Degeneration of Mitral Valve (Prolapse)?

A

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)

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20
Q

How common and who gets Myxomatous Degeneration of Mitral Valve?

A

Very common (3% of adults) & Young women

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21
Q

Pathogenesis of Myxomatous Degeneration of Mitral Valve?

A

Unknown• ? Developmental anomaly of connective tissue
• Feature of Marfan syndrome (fibrillin gene mutation) and other hereditary disordersDeposition of mucoid material in valve

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22
Q

Clinical features of Myxomatous Mitral Valve?

A

• Asymptomatic - Incidental finding: mid systolic click on auscultation• When regurgitation occurs - Late systolic/holosystolic murmur

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23
Q

Complications of Myxomatous Mitral Valve?

A

uncommon• Infective endocarditis• Mitral insufficiency• Thrombi on atrial surfaces lead to stroke or other systemic infarcts due to emboli• Arrhythmias –>sudden death• Most often seen with advanced mitral insufficiency

24
Q

What causes rheumatic fever?

A

Acute, immunologically mediated, multisystem, inflammatory disease with major cardiac manifestations• Occurs following an episode of group A Streptococcal (pyogenes) pharyngitis

25
Q

Most important complication of RF?

A

progression to chronic valvular dysfunction (mitral stenosis)

26
Q

How does RF affect the heart?

A

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 fibrous thickening of endocardium

27
Q

What is the classic lesion seen in RF?

A

Aschoff body – Foci of swollen eosinophilic collagen surrounded by T lymphocytes, plasma cells and plump macrophages –Anitschkow cells, caterpillar cells

28
Q

Chronic rheumatic heart disease inflammation and fibrosis leads to what?

A

Thickened valve leaflets– Fusion of commissures (fishmouth or buttonhole deformities)– Fusion/thickening of chordae tendineae

29
Q

Major effect of of chronic rheumatic heart disease is mitral stenosis which leads to what?

A

– Leads to left atrial dilatation (sometimes thrombus formation)• Reduced cardiac output (mechanical obstruction prevents filling of LV)– Pulmonary congestion, eventual right ventricular hypertrophy, and right-sided heart failure

30
Q

What percentage of time does chronic rheumatic heart disease affect the following:mitral valvemitral and aortic vavlestricuspid valvepulmonary valve

A

• Mitral valve alone in 65 – 70%
Mitral and aortic 25%
Tricuspid less often
Pulmonary rare

31
Q

Ab cross react after group A strep infection to cause rheumatic heart disease, what’s going on?

A

Hypersensitivity reaction induced by group A Streptococci• Antibodies against M protein cross react with glycoprotein antigens in the heart, joints and other tissues– Specific antigen not yet definitively identified• ? Glycoprotein in heart valves• ? Protein in sarcolemma of myocyte

32
Q

JONES criteria?

A

2 major or 1 major and 2 minor:
major- joints, heart, subQ nodules, erythema marginatum, sydenham chorea
minor- fever, arthralgia and elevated acute phase reactants

33
Q

Prognosis of acute RF?

A

good for primary attack; increased vulnerability to reactivation

34
Q

Course and prognosis of chronic rheumatic carditis?

A

– Years or decades after initial episode– Valvular disease (valvulitis)– Prognosis: surgical repair of valves improves outlook

35
Q

What are the two 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

36
Q

Risk factors for infective endocarditis?

A

More common in patients with cardiovascular abnormalities, neutropenia, immunodeficiency, malignancy, diabetes, alcoholics and IV drug users

37
Q

Causes 50-60% of infective endocarditis for deformed valves?

A

Strep viridans for deformed valves

38
Q

Causes 10-20% of infective endocarditis overall?

A

Staph aureus

39
Q

Describe acute infective endocarditis?

A

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 –> ring abscess

40
Q

Describe subacute infective endocarditis.

A

Less valvular destruction, fibrosis and granulation tissue reaction at the base of vegetation

41
Q

What are the Duke Criteria for bacterial endocarditis?

A

Major Positive blood cultures Echocardiographic findings (valve-related mass/abscess) New valvular regurgitation (new murmur on auscultation)
Minor  Predisposing heart lesion or IVDA Fever Uncommon findings resulting from septic emboli: petechiae, splinter hemorrhages, Janeway lesions (palms, soles hemorrhagic lesions), Osler nodes (digits), Roth spots (retina)

42
Q

Complications of bacterial endocarditis?

A

Valvular insufficiency or stenosis and possible heart failure– Myocardial abscesses and possible perforation– Vegetations break off  embolic complications• Brain, kidneys, spleen, etc.– Glomerulonephritis (immune complexes)

43
Q

Treatment of bacterial endocarditis?

A

– IV antibiotics, valve replacement if necessary– Prophylactic antibiotics after valve damage

44
Q

What can cause nonbacterial thrombotic endocarditis?

A

– Hypercoagulable states– Associated with mucin producing adenocarcinomas (DVTs & Trousseau syndrome)– Endocardial trauma - Swan-Ganz catheter

45
Q

What is nonbacterial thrombotic endocarditis?

A

Depositions of small masses of fibrin, platelets and other blood products on leaflets

46
Q

Endocarditis associated with Systemic lupus erythematosus:– Mitral & tricuspid valves involved– Antiphospholipid antibodies presentWhat is it?

A

Libman-Sacks Endocarditis

47
Q

Carcinoid tumors produce what?

A

serotonin, kallikrein, bradykinin, histamine, prostaglandins, and tachykinins

48
Q

Symptoms of carcinoid syndrome?

A

flushing, cramps, nausea, vomiting, diarrhea

49
Q

Serotonin and bradykinin inactivated by what?

A

MAO in pulmonary vasculature AND also inactivated by passage through functioning liver

50
Q

What is carcinoid heart disease?

A

In 50% of patients with carcinoid syndrome -plaque-like fibrosis of right-heart endocardium and valves

51
Q

Where does carcinoid heart disease usually occur?

A

Usually occurs on right side of heart (not left) because of inactivation of mediators by MAO in lung

52
Q

What is the cause of carcinoid heart disease?

A

Exact cause is unknown; believed to be related to endothelial injury caused by vasoactive agents

53
Q

What happens when pt has GI carcinoids with hepatic mets?

A

Normally, bioactive proteins are inactivated by liver• With mets to liver, secretion occurs directly into the hepatic vein & reaches right-side of heart

54
Q

What happens when pt has carcinoids outside of the portal system of venous drainage?

A

Direct secretion into systemic circulation – Example: carcinoids arising in ovary, testes• Very high blood levels may prevent complete inactivation by the lung MAO– Example: primary lung carcinoid

55
Q

Which valves are usually involved in carcinoid heart disease?

A

– Tricuspid and pulmonic valves equally affected• Usually tricuspid insufficiency or pulmonic stenosis

56
Q

Complications with mechanical valves?

A

Thromboembolic complications &Infective endocarditis

57
Q

Complications with bioprothesis artificial valves?

A

• Structural deterioration - 50% need replacement by 15 years • Infective endocarditis

CV Quiz 2 (16 decks)

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