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Cardiovascular Pathology > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

All cusps of the heart valves are attached to what?

A

attached to ring of dense tissue (annulus fibrosus) around the orifice

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2
Q

What attaches to the AV valves to prevent them bulging into the atria?

A

papillary muscles

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3
Q

Coronary arteries come off where?

A

come off the sinus in the out-flow tract of the aortic valves

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4
Q

Valves consist of

A

folds of endocardium covering a core of dense fibrous connective tissue which are continuous with the annuli fibrosis and the chordae tendinae

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5
Q

What are valves lined on both sides by

A

endothelial layers

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6
Q

How are the AV valves histologically different from the semilunar valves?

A

AV valves have smooth muscle on the atria side and are thicker than semilunar valves

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7
Q

Mechanics of how valves open and close

A

valves close passively when backflow pressure is greater than chamber pressure
valves open when chamber pressure is greater than outflow pressure

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8
Q

What is directional flow dependent on

A

competency of the valves

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9
Q

Why is velocity of blood through the semilunar valve greater?

A

due to smaller openings and greater chamber pressure (ventricles have more muscle than atria); therefore the edges of the pulmonic and aortic valves are subject to greater mechanical abrasion

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10
Q

insufficiency

A

failure to close completely, allowing regurgitation and backflow into the chamber

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11
Q

stenosis

A

narrowing or constriction of an orifice; most frequently involving the pulmonic or aortic opening

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12
Q

current formation

A

abnormal valve function may cause “jet streams” which can damage vessels, or current eddies which allow thrombosis and bacterial deposition on either side of the valve

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13
Q

Left-sided flow disruptions

A

mitral stenosis; mitral regurgitation; aortic stenosis; aortic regurgitation

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14
Q

mitral stenosis

A

most often caused by post-inflammation scarring due to rheumatic fever; often coexists with insufficiency; takes decades to develop and is remarkably well tolerated

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15
Q

mitral regurgitation

A

failure of valves to close completely; caused by infection and papillary muscle abnormality

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16
Q

aortic stenosis

A

may be congenital or acquired; most commonly caused by calcific degeneration of bicuspid valves; obstruction of left ventricular outflow leads to pressure overload and left ventricular hypertrophy

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17
Q

Infection with aortic stenosis may lead to?

A

acute cusp destruction and sudden decompensation resulting in rapidly fatal cardiac failure

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18
Q

aortic regurgitation

A

results from intrinsic valvular disease or aortic root disease (syphilis); leads to volume overload and left ventricular hypertrophy

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19
Q

Insufficient cardiac output leads to

A

syncopal episodes (acute); chronic results in left ventricular hypertrophy and attempts by the kidney to increase volume by retaining salt and water; increased peripheral resistance also tries to compensate

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20
Q

Mechanical valve damage

A

“jet stream” damage to aortic and pulmonic outflow tracts

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21
Q

Types of embolic thrombi

A
  1. infectious - vegetations in endocarditis

2. thrombotic - vegetations (both infectious and inflammatory); small clots

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22
Q

Clinical consequence of embolic damage

A

occlusion of vessels; seeding of infections

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23
Q

Congenital valvular lesions

A
  1. Bicuspid aortic valve

2. Mitral valve prolapse

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24
Q

Incidence of bicuspid aortic valve

A

presents in 6th - 7th decade

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25
Q

Pathology of bicuspid aortic valve

A

nodules restricted to base and lower halves of cusps; rarely involve free margins of leaflets

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26
Q

Pathogenesis of bicuspid aortic valve

A

congenital bicuspid aortic valve -> progressive calcification of cusps -> calcific aortic stenosis

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27
Q

gross features of bicuspid aortic valve

A
  1. heaped-up, calcified masses within aortic cusps that protrude in the sinuses of Valsalva
  2. architectural distortion
  3. no comissural fusion
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28
Q

microscopic features of bicuspid aortic valve

A

fibrosed and thickened cusps

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29
Q

Clinical significance of a bicuspid aortic valve

A

little functional significance at birth; but predisposes to secondary calcification in adult life

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30
Q

Clinical progression of a stenosed/bicuspid aortic valve

A

stenosed valve -> increased pressure gradient across valve -> left ventricular hypertrophy -> decompensation -> angina, syncope -> cardiac failure

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31
Q

Incidence of mitral valve prolapse

A

7% of US population; females:males = 6:4; 20-40 years of age; often associated with Marfan’s syndrome and connective tissue disorders

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32
Q

pathogenesis of mitral valve prolapse

A

floppy enlarged mitral leaflets balloon into left atrium during systole; snapping or tensing of everted cusps or chordae tendineae; incompetent valve

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33
Q

Murmur heard in mitral valve prolapse

A

midsystolic click; late systolic click; or holosystolic murmur

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34
Q

gross features of mitral valve prolapse

A

billowing of mitral valve leaflets (prolapse); pathologic hooding if >4mm above base of cusp; stretched, elongated, or ruptured chordae tendineae; may also have tricupid and pulmonary valve involvement

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35
Q

microscopic features of mitral valve prolapse

A

degeneration/attenuation of zona fibrosa; thickening of spongiosa layer; loose connective tissue on collage of chordae tendineae; fibrosis of valve/and ventricular surface, also calcification

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36
Q

Clinical correlations with mitral valve prolapse

A

most are asymptomatic; symptomatic MVP: some chest pain like angina, dyspnea, fatigue, depression, personality disorders, anxiety reactions

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37
Q

Major concerns with mitral valve prolapse

A

infective endocarditis; mitral valve insufficiency; arrhythmia; sudden death

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38
Q

Inflammatory causes of valvular lesions

A
  1. Rheumatic heart disease

2. SLE

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39
Q

Rheumatic heart disease

A

an acute, recurrent inflammatory disease, principally of children, that follows pharyngeal infection with group A-hemolytic streptococci (S. pyogenes)

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40
Q

Incidence of rheumatic heart disease

A

steadily declining; important pre-disposing factor for degenerative heart disease in later decades; leading cause of death from heart disease between the ages 5 and 25

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41
Q

pathogenesis of rheumatic heart disease

A

heightened immunologic activity to streptococcal antigens; antibodies cross react with other tissues; hyaluronate capsules of strep are identical to hyaluronate; antibodies cross react with glycoproteins in heart valves

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42
Q

What kind of antibodies correlate with development of rheumatic heart disease

A

antibodies to streptolysin O

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43
Q

gross features of rheumatic heart disease

A

most often involves mitral and aortic valves; mitral valvulitis results in stenosis; acute rheumatic pericarditis (fibrinous)

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44
Q

characteristic vegetations of rheumatic heart disease

A

verrucae

45
Q

Major criteria of acute rheumatic fever

A

i. migratory polyarthritis
ii. pancarditis
iii. subcutaneous nodules
iv. erythemia marginatum
v. sydenham chorea

46
Q

Pathognomonic for rheumatic myocarditis

A

Aschoff bodies

47
Q

Describe an Aschoff body

A

foci of fibrinous necrosis surrounded by lymphocytes and macrophages, Anitschkow cells (reactive histiocytes with slender, wavy nuclei) giant cells, and fibrinoid material

48
Q

Anitschkow cells

A

reactive histiocytes with slender, wavy nuclei; seen in rheumatic myocarditis

49
Q

valvular lesions of rheumatic heart disease

A

verrucae vegetations with beading of vegetations along the liens of closure; focal collagen degeneration surrounded by inflammation; ulceration of valve surface with deposition of fibrin;

50
Q

Where are valvular lesions of rheumatic heart disease also found

A

also found in pericardium (pericarditis), myocardium, endocardiu, and subendocardium (MacCallum plaques)

51
Q

friction rub and chest pain are symptoms of

A

pericarditis

52
Q

Minor criteria of rheumatic heart disease

A

history of rheumatic fever, arthralgias, fever, lab tests indicative of inflammation (increased sed. rate, leukocytosis, C-reactive protein), EKG changes

53
Q

major cause of death with rheumatic heart disease

A

congestive heart failure from myocarditis (although valve dysfunction may play a role)

54
Q

clinical correlations with rheumatic fever

A

increased vulnerability to reactivation of disease with subsequen pharyngeal ifnections

55
Q

Rheumatic heart disease most often affects which valves

A

mitral and aortic valves

56
Q

Describe chronic rheumatic heart disease

A

may involve recurrent attacks with different forms of streptococci; sometimes subacute form of single attack; permanent deformity of the valves; conspicuous, irregular thickening/fusion of leaflets; MacCallum’s patches

57
Q

Incidence of Libman-Sacks disease

A

vegetations on the mitral and tricuspid valves occur in approximately half the cases of SLE; unlike rheumatic heart disease, often involves valves on the RIGHT side of the heart

58
Q

Libman-Sacks disease often involves which valves

A

valves on the RIGHT side of the heart

59
Q

Libman-Sacks vegetations are composed of

A

composed of necrotic debris, fibrinoid material, disintegrating fibroblasts and inflammatory cells

60
Q

Describe Libman-Sacks vegetations

A

small; usually occur on flow side of leaflets, but can occur behind them; usually occur/multiply in random fashion; rarely spread to mural endocardium or chordae tendineae

61
Q

Pathology of Libman-Sacks disease

A

“fibrinoid necrosis” with neutrophils and mononuclear infiltrate; myocardial arterioles and small arteries may undergo necrosis

62
Q

Compare the affected valves in IE, rheumatic endocarditis, and Libman-Sacks

A

IE: any
rheumatic endocarditis: mitral (sometimes aortic)
Libman-Sacks: mitral > tricuspid > pulmonic

63
Q

Compare the size of vegetations in IE, rheumatic endocarditis and Libman-Sacks

A

IE: large
RE: small
LS: small

64
Q

Distribution of vegetations in infective endocarditis

A

not widely dispersed; singly or 2-3 in foci; rarely found behind cusps

65
Q

Distribution of vegetations in rheumatic endocarditis

A

confined to lines of closure of cusps; “beading” verrucae; almost never behind cusps

66
Q

Distribution of vegetations in Libman-Sacks endocarditis

A

multiple, random; usually on flow side, but can occur behind

67
Q

Endocarditis

A

colonization or invasion of valves or mural endocardium by a microbial agent leading to the formation of friable vegetations

68
Q

Endocarditis is most often associated with

A

pre-existing anomaly, valvular disease, or congenital heart disease

69
Q

Prophylaxis with endocarditis patients

A

prophylactic use of antibiotics in any person with cardiac anomalies or artificial valve undergoing dental procedures

70
Q

Organisms that cause endocarditis

A

95% bacteria: Strep viridans; Staph; enterococci; Pneumococci; Gram negative rods
5% viruses: rickettsia, chlamydia, fungi

71
Q

Predisposing conditions to endocarditis

A

any anomaly leading to abnormal flow, shunting (particularly right to left), exposure of collagen, or damage to valves

72
Q

Predisposing diseases to endocarditis

A

Rheumatic heart disease, congenital heart disease, bicuspid aortic valve, mitral valve prolapse, aortic stenosis, cardio-vascular surgery (sutures), IV drug abuse, immunosuppression, bacterial seeding with any of the above agents

73
Q

IV drug use predisposes to

A

right sided endocarditis infections (S. aureus, Candida, Aspergillus)

74
Q

Pathogenesis of endocarditis

A

for damaged valves or deranged blood flow: deposition of fibrin and agglutinated organisms;
for right to left shunt: bypass filtering of blood by lungs

75
Q

gross features of endocarditis

A

friable, bulky, usually bacteria-laden vegetations on heart valves; old lesions become fibrotic, calcified masses

76
Q

Valves most often affected by endocarditis

A

mitral and aortic valves

77
Q

Microscopic features of endocarditis

A

vegetations: irregular masses of fibrin strands, platelets, blood cell debris, organisms and inflammatory cells
valve leaflets: vascularizations and nonspecific inflammation

78
Q

What eventually happens to the valves in endocarditis

A

erosion, destruction of valve leaflets (particularly with acute endocarditis); “fenestration”
deformation of valves leaflets: valvular stenosis, insufficiency

79
Q

Acute congestive heart failure in endocarditis

A

cardiogenic shock from acute decompensation of valve

80
Q

Subacute congestive heart failure in endocarditis

A

chronic development of CHF

81
Q

Describe the pericarditis that can occur as a complication of endocarditis

A

suppurative pericarditis (penetration of heart wall or lymphatic extension); myocardial metastatic abscesses

82
Q

Extrinsic clinical consequences of endocarditis

A
  1. seeding of aortia, kidney, spleen, brian with infective emboli
  2. arterial thrombotic emboli
83
Q

Acute bacterial endocarditis

A

bacterial cause endocarditis; acute caused by highly virulent organism which can lead to death in days to a week; may occur in a normal heart

84
Q

Most common overall cause of endocarditis

A 
Streptococcus viridans (low-virulence)
small vegetations
85
Q

Most common cause of endocarditis in IV drug users

A 
Staphylococcus aureus (high-virulence)
large vegetations
86
Q

Clinical features of bacterial endocarditis

A

fever, murmur, Janeway lesions (nontender on palms and soles), Osler nodes (tender on fingers and toes), splinter hemorrhages, Roth spots (embolism), anemia of chronic disease

87
Q

Clinical circumstances of acute bacterial endocarditis

A

destructive, tumultuous infection; organisms tend to produce necrotizing, ulcerative, invasive valvular infections; may be predisposed by heart defects, but often occurs in a normal heart; may be associated with IV catheter or prosthetic valves

88
Q

Leading cause of acute bacterial endocarditis

A

Staph aureus

89
Q

Pathogenesis of S. aureus acute bacterial endocarditis

A

seeding of blood; may develop in any individual when organism is sufficiently virulent, bacterial invasion is sufficiently large, and resistance of host is depressed

90
Q

Morphology of acute bacterial endocarditis

A

friable, bulky, bacteria-laden vegetations

91
Q

Acute bacterial endocarditis may lead to

A

perforation or erosion of leaflet, invasion of underlying tissue, or may undergo progressive sterilization, fibrosis, organization, calcification

92
Q

clinical course of acute bacterial endocarditis

A

prompt diagnosis and treatment greatly improve prognosis; fever most common sign; rapidly developing fever, chills

93
Q

Subacute bacterial endocarditis usually occurs in the presence of which previous heart diseases/conditions

A

congenital heart disease (MVP most common); rheumatic heart disease; previous surgery; previous endocarditis; IV drug use

94
Q

Most common cause of subacute bacterial endocarditis

A

Strep viridans

95
Q

Other organisms that can cause subacute bacterial endocarditis

A

Group D strep, enterococci

96
Q

How do patients present with subacute bacterial endocarditis

A

with risk factors; flu-like illness that has been going on for months; heart murmur, signs of systmeic infections

97
Q

How do you treat subacute bacterial endocarditis

A

need antibiotics to cure infection; difficult to treat because bacterial hide on valves

98
Q

Complications from subacute bacterial endocarditis

A

heart failure; MI from embolism; mycotic aneurysm; glomerulonephritis

99
Q

How do you get non-bacterial thrombotic endocarditis (NBTE)

A

endothelial damage -> platelet and fibrin deposition on valve leaflets -> formation of nodular vegetations

100
Q

What is non-bacterial thrombotic endocarditis associated with

A

SLE; cachexia, mucin-producing tumors, or damage to endothelium

101
Q

Occurrence of carcinoid heart disease

A

1% of all patients who have argentaffinoma and 10% of those with GI carcinoids with hepatic metastases

102
Q

Clinical features of carcinoid heart disease

A

distinctive episodic flushing of the skin, and cramps, nausea, vomiting, and diarrhea; cardiac lesions in about 50%

103
Q

Pathology of carcinoid heart disease

A

deposits of pearly gray, uniform fibrous tissue on tricuspid and pulmonic valves leading to insufficiency and stenosis

104
Q

Which side of the heart does carcinoid heart disease affect and why?

A

Carcinoids affect the right heart because the tumor products are metabolized in the lungs and do not reach the left heart

105
Q

Fibrous tissue reaction in carcinoid heart disease is due to

A

elaboration of bioactive products by argentaffinomas, including serotonin, kallikrein, bradykinin, histamine, prostaglandins, and newly described tachykinins P and K

106
Q

Gross features of carcinoid heart disease

A

plaque like thickenings composed of an unusual type of fibrous tissue are superimposed on the endocardium of the cardiac chambers and valvular cusps; mainly on the outflow tract of the right ventricle

107
Q

Microscopic features of carcinoid heart disease

A

fibrous thickening resembling cellular atheromas

108
Q

Pathogenesis of ischemic valvular dysfunction

A

lack of oxygen perfusion mainly affects annulus rings behind valves, not the actual leaflets; leads to calcium deposition with no inflammatory change
ischemia can affect papillary muscles

109
Q

Indications for artificial heart valve

A

congenital disorders; valvular stenosis; valvular regurgitation; destruction of cusp by infection

Cardiovascular Pathology (8 decks)

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