Valvular Heart Disease Flashcards Preview

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Flashcards in Valvular Heart Disease Deck (57):
1

What are the semilunar valves?

aortic and pulmonary

2

What are the AV valves?

mitral and tricuspid

3

Describe the AV valve structure...

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

4

What is stenosis?

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

5

What is insufficiency?

failure to close completely

6

Causes of insufficiency?

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

7

Major causes of Vavlular Disease

• 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

8

Is stenoses or insufficiency more frequent cause?

Stenosis

9

What is dystrophic calcification?

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

10

Risk factors for dystrophic calcification?

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

11

Most common of all valvular abnormalities?

Calcific Aortic Stenosis (AS)

12

When does AS occur in life?

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

13

What are the clinical effects of AS?

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

14

Treatment for AS?

valve replacement

15

Describe the morphology of AS.

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

16

What is Mitral Annular Calcification?

Degenerative calcific deposits on fibrous ring, at base of valve

17

Risk factors for mitral annular calcification?

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

18

Does mitral annular calcification affect function?

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

19

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

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)

20

How common and who gets Myxomatous Degeneration of Mitral Valve?

Very common (3% of adults) & Young women

21

Pathogenesis of Myxomatous Degeneration of Mitral Valve?

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

22

Clinical features of Myxomatous Mitral Valve?

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

23

Complications of Myxomatous Mitral Valve?

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

What causes rheumatic fever?

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

25

Most important complication of RF?

progression to chronic valvular dysfunction (mitral stenosis)

26

How does RF affect the heart?

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

What is the classic lesion seen in RF?

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

28

Chronic rheumatic heart disease inflammation and fibrosis leads to what?

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

29

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

– 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

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

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

31

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

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

JONES criteria?

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

Prognosis of acute RF?

good for primary attack; increased vulnerability to reactivation

34

Course and prognosis of chronic rheumatic carditis?

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

35

What are the two basic forms of infective endocarditis?

– 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

Risk factors for infective endocarditis?

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

37

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

Strep viridans for deformed valves

38

Causes 10-20% of infective endocarditis overall?

Staph aureus

39

Describe acute infective endocarditis?

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

Describe subacute infective endocarditis.

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

41

What are the Duke Criteria for bacterial endocarditis?

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

Complications of bacterial endocarditis?

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

Treatment of bacterial endocarditis?

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

44

What can cause nonbacterial thrombotic endocarditis?

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

45

What is nonbacterial thrombotic endocarditis?

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

46

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

Libman-Sacks Endocarditis

47

Carcinoid tumors produce what?

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

48

Symptoms of carcinoid syndrome?

flushing, cramps, nausea, vomiting, diarrhea

49

Serotonin and bradykinin inactivated by what?

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

50

What is carcinoid heart disease?

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

51

Where does carcinoid heart disease usually occur?

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

52

What is the cause of carcinoid heart disease?

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

53

What happens when pt has GI carcinoids with hepatic mets?

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

54

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

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

Which valves are usually involved in carcinoid heart disease?

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

56

Complications with mechanical valves?

Thromboembolic complications &Infective endocarditis

57

Complications with bioprothesis artificial valves?

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