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MHD 1 > L43 Valvular Heart Disease and Cardiac Neoplasms > Flashcards

L43 Valvular Heart Disease and Cardiac Neoplasms Flashcards

1
Q

What are the two types of semilunar valves in the heart and how many cusps do they have?

A

Aortic and pulmonary; three

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2
Q

Upon what does the function of semilunar valves depend?

A

Integrity and coordinated movement of cusps and attachments

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3
Q

What are the two types of atrioventricular valves in the heart?

A

Tricuspid and mitral

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4
Q

Upon what does the function of AV valves depend?

A

Integrity of valve apparati (including leaflets, annulus, chordae tendinae, papillary muscles, ventricular wall)

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5
Q

Describe the basic histology of a valve.

A

Lined by endocardium with a connective tissue core of variable density

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6
Q

What is the difference between regurgitant and stenotic valvular heart disease?

A

Regurgitant: insufficient, allows backflow of blood

Stenotic: tight valve

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7
Q

What is the most common congenital valvular heart disease?

A

Biscupid aortic valve

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8
Q

Describe the etiology of a bicuspid aortic valve.

A

Normally, the aortic valve has three cusps. Here, there is incomplete embryonic separation, leading to 2 cusps

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9
Q

What does bicuspid aortic valve cause?

A

Aortic stenosis and increased pressure load on L ventricle

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10
Q

Any kind of abnormal valve can be predisposed to developing what infection?

A

Endocarditis

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11
Q

What is the most common cause of aortic stenosis?

A

Calcific aortic degeneration

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12
Q

What happens in calcific aortic degeneration?

A

Dystrophic calcification - deposition of calcium at sites of cell injury and necrosis

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13
Q

Discuss the development of calcific aortic stenosis.

A

Over time, calcified masses develop within aortic cusps. This prevents the cusp from opening, which obstructs outflow, increases pressure gradient across the valve, and leads to concentric LVH development.

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14
Q

What are the symptoms of calcific aortic stenosis?

A

Congestive heart failure, angina due to myocardial ischemia, and syncope

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15
Q

What happens in mitral valve prolapse?

A

Mitral valve leaflets are enlarged, redundant, and floppy; they balloon into the atrium during systole. This can injure the atrium.

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16
Q

What can be seen histologically in mitral valve prolapse?

A

Expansion of the spongiosa via deposition of myxomatous (mucoid) material; this makes the valve more floppy.

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17
Q

What is the pathogenesis of mitral valve prolapse?

A

Unknown; some patients have a developmental defect of connective tissue (Marfan Syndrome), but not all patients

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18
Q

Describe the epidemiology of mitral valve prolapse.

A

Occurs in 3% of the population, particularly in young women

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19
Q

What are the symptoms of mitral valve prolapse?

A

Majority are asymptomatic, midsystolic click (snapping of chorda tendinae); minority of patients have non-specific symptoms such as chest pain, dyspnea, fatigue, depression, and anxiety

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20
Q

What are the rare, serious complications of mitral valve prolapse seen in 3% of patients?

A
  1. Infective endocarditis
  2. Mitral insufficiency (regurgitation)
  3. Stroke/systemic infarction (due to embolism of thrombi formed in atria due to ballooning)
  4. Arrhythmia
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21
Q

What is infective endocarditis?

A

Destructive inflammation of cardiac valves and endocardium caused by infection (most commonly bacterial)

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22
Q

What is a hallmark of infective endocarditis?

A

Vegetation

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23
Q

What is vegetation?

A

Warty excrescences on the valves of the heart composed of various tissue elements including fibrin and collagen

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24
Q

Describe the vegetations of infective endocarditis.

A
  1. Composed of thrombotic debris, fibrin, inflammatory cells, microorganisms
  2. Large and bulky
  3. Destructive and erosive
  4. Friable, apt to embolize
25
Q

What are the two types of infective endocarditis?

A
  1. Acute

2. Subacute

26
Q

Describe acute infective endocarditis.

A

Involves highly virulent microorganisms (classically S. aureus), usually involves a previously normal valve with rapid, severe destruction; patients present as very sick (50% mortality)

27
Q

Describe subacute infective endocarditis.

A

Involves low virulence organisms (classically S. viridans), usually involves a previously deformed valve, recovery with appropriate treatment

28
Q

Who is at risk for infective endocarditis?

A

Patients with valvular disease and prosthetic valves, immune deficient patients, patients with diabetes, people who use IV drugs, people with alcohol use disorder

29
Q

What are portals of entry for infective endocarditis?

A
  1. Injection of contaminated material into bloodstream
  2. Infections elsewhere (bacteremia, goes to heart)
  3. Dental or surgical procedures with bacteremia
  4. Occult source (gut, oral cavity, trivial injury)
30
Q

How do we diagnose infective endocarditis?

A
  1. Clinical suspicion
  2. Blood cultures (infection)
  3. Echocardiogram (can see vegetation)
31
Q

What are the cardiac complications of infective endocarditis?

A

Valve insufficiency, abscess, and injury to prosthetic valves

32
Q

What are the other complications of infective endocarditis?

A

Emboli (brain, kidney, spleen, lungs)

Glomerulonephritis (immune complex depositions)

33
Q

How is infective endocarditis treated?

A

IV antibiotics (prolonged course), surgery sometimes; can give antibiotics prophylactically to those at high risk

34
Q

What diseases involve non-infected vegetations?

A
  1. Acute rheumatic fever
  2. Endocarditis of systemic lupus erythematosus (Liebman-Sacks endocarditis)
  3. Nonbacterial thrombic endocarditis (marantic endocarditis)
35
Q

What is Rheumatic fever?

A

A disease that occurs a few weeks after Group A streptococcal pharyngitis; it has acute systemic manifestations and can develop into chronic rheumatic heart valve disease

36
Q

What is the pathogenesis of acute rheumatic fever?

A

Patients have an immune response to GAS which cross-react with host tissues; Ab directed against M proteins of strep cross-react with self-antigens in the heart. CD4+ T cells specific for strep peptides react with cardiac self proteins. This produces cytokines to activate macrophages.

37
Q

What are the major manifestations of acute rheumatic fever?

A
  1. Migratory polyarthritis (large joints)
  2. Carditis
  3. Subcutaneous nodules
  4. Erythema marginatum of skin
  5. Sydenham chorea (involuntary purposeless, rapid movements - St. Vitus’ danse)
38
Q

What are the minor manifestations of acute rheumatic fever?

A

Fever, arthralgia, elevated acute-phase reactants

39
Q

What are the Jones Criteria for acute rheumatic fever?

A

Preceding GAS infection + 2 major manifestations or 1 major + 2 minor manifestations

40
Q

What is pancarditis?

A

Inflammation of all three parts of the heart (pericarditis, myocarditis, endocarditis)

41
Q

Describe the vegetations of rheumatic fever endocarditis grossly and histologically.

A

Gross: tiny little vegetations on the heart valves (typically mitral, L side)

Histology: Aschoff bodies (T cells, plasma cells, macrophages, multinucleated giant cells)

42
Q

What is the special name for macrophages in Aschoff bodies?

A

Antischkow cells/caterpillar cells

43
Q

After the formation of Aschoff bodies, what happens next?

A

Inflammatory injury to the valve, fibrosis during healing, deformation of the normal leaflet structure; this induces turbulence, which leads to further injury and additional fibrosis

44
Q

What can happen years after rheumatic fever?

A

Chronic rheumatic valvular disease

45
Q

What are the hallmarks of chronic rheumatic valvular disease?

A

Fibrosis of valve leaflets, fusion of leaflets (fish mouth stenosis), thickening of chordae tendinae

46
Q

Which valve is most commonly involved in chronic rheumatic valvular heart disease?

A

Mitral valve (65-70%)

Aortic and mitral valves - 25%

Triscuspid/pulmonary - rare

47
Q

Describe the vegetations seen in Libman-Sacks endocarditis (SLE).

A

Small, sterile, found on mitral and tricuspid valves and chords; caused by immune complex deposition, leads to valvulitis, fibrosis, deformity

48
Q

Describe the vegetations seen in non-bacterial thrombotic endocarditis (marantic endocarditis)

A

Small, non-destructive, loosely attached, sterile thrombi

49
Q

What type of patients get marantic endocarditis?

A

Patients who are very sick and wasting away; they are in a hypercoagulable state due to sepsis, cancer, burns, indwelling catheters

50
Q

What happens in marantic endocarditis?

A

The vegetations have little effect on the valve itself, but can embolize and cause infarctions. They can also serve as a nidus for bacterial colonization, leading to infective endocarditis.

51
Q

___ occurs in people who are ill and hypercoagulable.

A

Nonbacterial thrombotic endocarditis

52
Q

___ incidence increases with age.

A

Calcific aortic stenosis

53
Q

___ is a result of post-inflammatory scarring.

A

Chronic rheumatic valve disease

54
Q

___ develops earlier with bicuspid aortic valve.

A

Calcific aortic stenosis

55
Q

Embolization is the most important complication of ___.

A

Nonbacterial thrombotic endocarditis

56
Q

What is a myxoma?

A

Most common primary benign tumor of the heart in adults

57
Q

The myxoma involves which part of the heart in 90% of cases?

A

Atria (L&raquo_space; R)

58
Q

Describe a myxoma grossly and histologically.

A

Gross: mucoid, gelatinous

Histology: mucopolysaccharide, various other types of cells

59
Q

How does myxoma present?

A

Ball-valve obstruction can block the flow of blood, particularly in a position-dependent fashion; fever and malaise (IL-6), embolization

MHD 1 (58 decks)

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