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Pathology > 2nd Exam: Vavular and Endocardial Heart Disease > Flashcards

2nd Exam: Vavular and Endocardial Heart Disease Flashcards

1
Q

Trauma valves experience:

A

mechanical, shearing, friction

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2
Q

Changes per minute of valves under mech stress:

A

60-80 times per minute

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3
Q

Shearing forces of the valve come from:

A

blood flow

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4
Q

Friction of valves occurs here:

A

points of coaptation (where they come together)

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5
Q

Aging changes to aortic valve:

A

fibrosis, thickening of leaflets, loss of elasticity, lipid deposition, aortic root/ ring/ anulus dilates

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6
Q

Consequences of age changes of heart valves:

A

murmurs, stenosis, insufficiency, endocarditis, calcification

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7
Q

This leads to aortic insufficiency:

A

loss of elasticity of valves

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8
Q

Root/ ring/ anulus:

A

where leaflets attach, dilate

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9
Q

Do these aging changes to the valves happen to valves throughout the body?

A

yes

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10
Q

Calcification of aortic valve is seen in:

A

aortic stenosis

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11
Q

Valve thickening can lead to:

A

benign murmor, or more severe disease

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12
Q

Acute rheumatic fever:

A

kids 5-15yo, no organism, AI, hypersensitivity d., Ab response, indirectly related to Group A strp infection (GAS, B-hemolytic), can lead to heart infection, inflammation of myocardium, valves and pericardium

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13
Q

Cross reactions, antistrep Ab’s and heart muscle:

A

vegetations, Aschoff body (only RF), fibrinous pericarditis

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14
Q

How long after GAS infection does RF present as immune mediated carditis?

A

1-4wks

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15
Q

Site of infection for RF:

A

pharyngitis, usually not skin or other sites

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16
Q

Common M types of acute RF:

A

1, 3, 5, 6,18, 24

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17
Q

What bind, leading to RF?

A

Ag’s in heart bind M protein epitopes on bacteria that are shared with myosin, tropomyosin

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18
Q

Contributing factors to the prevalence of acute RF:

A

poverty, crowding, cold climate

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19
Q

Why we are we at lower RF risk in U.S.:

A

less virulent organisms, earlier dx, tx, and rx

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20
Q

Antibodies w this cross react with heart Ag’s, producing heart disease (?) rf (?):

A

M proteins

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21
Q

disorder of kidneys, occurs after infection w some strains of strep bacteria:

A

poststreptococcal nephritis

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22
Q

Test to determine if pt has strep infection:

A

If they are producing Abs to streptolysin secreted by strep

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23
Q

streptolysin is an:

A

exotoxin

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24
Q

Substances secreted by strep:

A

Streptolysin, streptokinase, strepteornases, pyrogenic exotoxins, DNAase, Hyaluronidase

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25
Q

m protein projects directly out of:

A

the cell mem

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26
Q

Cx dx of acute RF:

A

Jones criteria: evidence of inflammation w a rheumatic (joint) component, polyarthritis, evidence of HD, recent GAS infection, skin lesions, carditis

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27
Q

acute RF affects what parts of the heart?

A

all

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28
Q

arthritis, part of acute or chronic rf?

A

acute

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29
Q

Most severe long term disease in rheumatic fever

A

heart disease

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30
Q

Polyarthritis:

A

transient, migratory joint pain and swelling, many joints affected, nonsuppurative, usually no residual disability

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31
Q

Erythema marginatum:

A

serpiginous(wavy margin), erythematous, non-pruritic (not itchy), on trunk/ extremities, circular, thin line of hyperemia, small % of pts with acuter RF get this

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32
Q

Erythema marginatum is assoc w:

A

acute RF

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33
Q

Cx dx of rheumatic pericarditis:

A

friction rubbing sounds in stethoscope

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34
Q

Parts of heart invovled in Rheumatic pericarditis

A

peri-, myo- , endo-, epicardium

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35
Q

This disorder has a bread and butter appearance w fibrinous exudate:

A

Rheumatic Pericarditis

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36
Q

This disorder has a bread and butter appearance w fibrinous exudate:

A

Rheumatic Pericarditis

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37
Q

Aschoff bodies are usually seen in:

A

acute RF, occasionally in old d.

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38
Q

Aschoff body:

A

acute RF, usually only in h., granuloma-like lesion, multifocal, chronic inflammatory rxn, possible necrosis T cells, macs (antischkow “myocytes”, Aschoff (giant) cells)

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39
Q

Giant cells are aka:

A

Aschoff cells

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40
Q

TF? Aschoff bodies are granulomatous lesions.

A

F. granuloma-like

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41
Q

Multinucleated Aschoff/giant cells:

A

linear, fusiform, fused macs in Aschoff body (looks like a fibroblast)

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42
Q

Antischkow myocyte:

A

linear chromatin, “caterpillar cells”

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43
Q

acute RF valvulitis:

A

most important long term consequence of the d., affects valves preferentially, stenosis and/or regurgitation later on

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44
Q

Valves affected by ARF valvulitis, greatest to least:

A

mitral, aortic, tricuspid, pulmonary

45
Q

most important aspect of ARF in the long run:

A

ARF valvulitis

46
Q

acute ARF valvulitis:

A

verrucae (small wart) at line of closure of valve leaflets, inflammation, edema and fibrinoid necrosis, may dissipate

47
Q

If valve is damaged by ARF valvulitis you will get:

A

chronic valve disease

48
Q

Valves on this side of heart are more commonly affected by ARF valvulitis:

A

L, bc higher pressure = more damage, maybe

49
Q

wart like lesions:

A

veruci

50
Q

Acute RF valvulitis causes:

A

acute rheumatic endocarditis, tiny lesion at line of closure

51
Q

Acute rheumatic endocardiits:

A

tiny lesion at line of closure, tiny white bumps, ai inflammation

52
Q

Valve fluid from necrosis and edema during acute valvulitis can lead to:

A

scarring of valve, stiffer, thicker, now more prone to chronic rheumatic valve disease

53
Q

Chronic rheumatic valve disease:

A

yrs after ARF, turbulence adds to original damage, deformed, thickened, fibrotic, stenotic and/or insufficient

54
Q

Disease pt most likely has if heart valve won’t open:

A

chronic RF

55
Q

This will appear white on a valve leaflet w chronic RH disease:

A

necrosis

56
Q

Signature lesion of RF:

A

mitral stenosis

57
Q

mitral stenosis:

A

classic murmurs (snap open), inc L atrial P, atrial dilation/ hypertrophy, atrial thrombi, arrhythmias (atrial fibrillation), IE is secondary

58
Q

This results in fish mouth valve:

A

mitral stenosis

59
Q

IE is secondary to:

A

acute RF and mitral stenosis

60
Q

Is a damaged valve due to mitral stenosis from ARF more like to bc IE because the damage has created a good host environment for the bacteria?

A

ask

61
Q

sequela of damaged tissue:

A

calcification, calcific valve disease, dystrophic calcification, heart murmurs, valve opening narrowing leading to inc L atrial P

62
Q

Is valve damage slight or severe from RF?

A

severe

63
Q

2 types of IE:

A

bacterial, fungal

64
Q

Which type of IE is further broken down to acute and subacute?

A

bacterial

65
Q

Ppl prone to fungal IE:

A

IV drug users, IC pts, i.e. HIV

66
Q

Types of non-rheumatic endocarditis:

A

infective and non-infective

67
Q

More common, bacterial or fungal infective endocarditis?

A

bacterial

68
Q

Most common organism to cause acute bacterial endocarditis (ABE):

A

staph a., virulent = acute

69
Q

Infective endocarditis is infection of:

A

heart valve, prosthetic valve or catheter

70
Q

ABE:

A

virulent organisms like Staph A., valve not damaged, more destructive than Subacute BE (SBE)

71
Q

SBE:

A

lower virulence like Strep viridans, valve already damaged, may incur more

72
Q

This is like a revolving door:

A

endocarditis, contaminated blood goes to heart, heart valves sheds organism into blood

73
Q

Sx and Dx of endocarditis:

A

fever, chills, pos blood culture

74
Q

Source of infection for endocarditis:

A

IV lines, IV drugs, dental procedures, unknown

75
Q

dental procedures that can lead to endocarditis:

A

AGE: abscess, gum disease, extraction

76
Q

1st step in pathogenesis of endocarditis:

A

altered or damaged endo

77
Q

steps in pathogenesis of edocarditis:

A

altered or damaged endo, exposure of collagen and matrix substances, platelet aggregation, and fibrin deposits (nidus)

78
Q

This is the nidus for endocarditis:

A

fibrin deposits

79
Q

Pws to endo damage:

A

normal/ abnormal valve, previously injured valve, endo MAY already be damage, turbulence and stasis put platelets at the endo

80
Q

What can put platelets at the endothelium?

A

turbulence and stasis

81
Q

This can lead to endo damage:

A

mitral stenosis

82
Q

Each vegetation from IE and CRF contains:

A

inflammatory cells and bacteria

83
Q

Types of non-infective/ non-rheumatic endocarditis:

A

NBTE (“marantic”), atypical verrucous endocarditis (Libman-Sacks)

84
Q

“marantic” is assoc with:

A

NBTE

85
Q

Libman-Sacks is assoc w:

A

Atypical verrucous endocarditis (Libmann-Sacks)

86
Q

This is characterized by large vegetations that can embolize, shower into brain, kidney, etc. producing infarcts:

A

NBTE vegetation

87
Q

shown destroying the valve, seen in endocarditis-cotran:

A

IE

88
Q

NBTE “marantic”:

A

pancreatic cancer, emboli, infarct (check)

89
Q

When does NBTE often occur?

A

hypercoagulabe state (60%)

90
Q

NBTE is often assoc w:

A

mal d. such as adenocarcinomas-pancreas, GI, lung

91
Q

NBTE freq affects normal:

A

valve

92
Q

This disease often does not change the valve:

A

NBTE

93
Q

This often gives rise to emboli:

A

NBTE

94
Q

‘Marantic” endocarditis:

A

bulky, more frialbe lesions tha IE

95
Q

These are vegetations in row, not damaging valve, but can embolize
no inflammation, no bacteria:

A

“marantic” endocardiits

96
Q

Characteristics of NBTE in slides:

A

friable (easily crumbled), fibrin, sterile deposits

97
Q

Tiny vegetations in endocarditis are assoc w:

A

RF

98
Q

Variable size vegetations in endocarditis are assoc w:

A

IE

99
Q

Large vegetations in endocarditis are assoc w:

A

NBTE

100
Q

line of closure is assoc w:

A

RF

101
Q

Destruction is assoc w:

A

IE

102
Q

“Friable” is assoc w:

A

NBTE

103
Q

Friable:

A

easily pulverized or crumbled

104
Q

Vegetations in endocarditis that can lead to emboli:

A

IE, NBTE

105
Q

Specific valve lesions:

A

aortic stenosis, myxomatous (benign ct tumor containing gelatinous or mucous material) degeneration, mitral valve prolapse, mitral valve ring calcification, carcinoid valve disease

106
Q

Aortic stenosis means:

A

less blood can flow through valve

107
Q

Causes of aortic stenosis:

A

RF, age

108
Q

Complications of aortic stenosis:

A

L ven hypertrophy, agina, sudden death

Pathology (23 decks)

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