2nd Exam: Vavular and Endocardial Heart Disease Flashcards Preview

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Flashcards in 2nd Exam: Vavular and Endocardial Heart Disease Deck (108)
1

Trauma valves experience:

mechanical, shearing, friction

2

Changes per minute of valves under mech stress:

60-80 times per minute

3

Shearing forces of the valve come from:

blood flow

4

Friction of valves occurs here:

points of coaptation (where they come together)

5

Aging changes to aortic valve:

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

6

Consequences of age changes of heart valves:

murmurs, stenosis, insufficiency, endocarditis, calcification

7

This leads to aortic insufficiency:

loss of elasticity of valves

8

Root/ ring/ anulus:

where leaflets attach, dilate

9

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

yes

10

Calcification of aortic valve is seen in:

aortic stenosis

11

Valve thickening can lead to:

benign murmor, or more severe disease

12

Acute rheumatic fever:

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

13

Cross reactions, antistrep Ab's and heart muscle:

vegetations, Aschoff body (only RF), fibrinous pericarditis

14

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

1-4wks

15

Site of infection for RF:

pharyngitis, usually not skin or other sites

16

Common M types of acute RF:

1, 3, 5, 6,18, 24

17

What bind, leading to RF?

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

18

Contributing factors to the prevalence of acute RF:

poverty, crowding, cold climate

19

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

less virulent organisms, earlier dx, tx, and rx

20

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

M proteins

21

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

poststreptococcal nephritis

22

Test to determine if pt has strep infection:

If they are producing Abs to streptolysin secreted by strep

23

streptolysin is an:

exotoxin

24

Substances secreted by strep:

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

25

m protein projects directly out of:

the cell mem

26

Cx dx of acute RF:

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

27

acute RF affects what parts of the heart?

all

28

arthritis, part of acute or chronic rf?

acute

29

Most severe long term disease in rheumatic fever

heart disease

30

Polyarthritis:

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

31

Erythema marginatum:

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

32

Erythema marginatum is assoc w:

acute RF

33

Cx dx of rheumatic pericarditis:

friction rubbing sounds in stethoscope

34

Parts of heart invovled in Rheumatic pericarditis

peri-, myo- , endo-, epicardium

35

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

Rheumatic Pericarditis

36

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

Rheumatic Pericarditis

37

Aschoff bodies are usually seen in:

acute RF, occasionally in old d.

38

Aschoff body:

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

39

Giant cells are aka:

Aschoff cells

40

TF? Aschoff bodies are granulomatous lesions.

F. granuloma-like

41

Multinucleated Aschoff/giant cells:

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

42

Antischkow myocyte:

linear chromatin, "caterpillar cells"

43

acute RF valvulitis:

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

44

Valves affected by ARF valvulitis, greatest to least:

mitral, aortic, tricuspid, pulmonary

45

most important aspect of ARF in the long run:

ARF valvulitis

46

acute ARF valvulitis:

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

47

If valve is damaged by ARF valvulitis you will get:

chronic valve disease

48

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

L, bc higher pressure = more damage, maybe

49

wart like lesions:

veruci

50

Acute RF valvulitis causes:

acute rheumatic endocarditis, tiny lesion at line of closure

51

Acute rheumatic endocardiits:

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

52

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

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

53

Chronic rheumatic valve disease:

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

54

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

chronic RF

55

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

necrosis

56

Signature lesion of RF:

mitral stenosis

57

mitral stenosis:

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

58

This results in fish mouth valve:

mitral stenosis

59

IE is secondary to:

acute RF and mitral stenosis

60

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?

ask

61

sequela of damaged tissue:

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

62

Is valve damage slight or severe from RF?

severe

63

2 types of IE:

bacterial, fungal

64

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

bacterial

65

Ppl prone to fungal IE:

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

66

Types of non-rheumatic endocarditis:

infective and non-infective

67

More common, bacterial or fungal infective endocarditis?

bacterial

68

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

staph a., virulent = acute

69

Infective endocarditis is infection of:

heart valve, prosthetic valve or catheter

70

ABE:

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

71

SBE:

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

72

This is like a revolving door:

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

73

Sx and Dx of endocarditis:

fever, chills, pos blood culture

74

Source of infection for endocarditis:

IV lines, IV drugs, dental procedures, unknown

75

dental procedures that can lead to endocarditis:

AGE: abscess, gum disease, extraction

76

1st step in pathogenesis of endocarditis:

altered or damaged endo

77

steps in pathogenesis of edocarditis:

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

78

This is the nidus for endocarditis:

fibrin deposits

79

Pws to endo damage:

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

80

What can put platelets at the endothelium?

turbulence and stasis

81

This can lead to endo damage:

mitral stenosis

82

Each vegetation from IE and CRF contains:

inflammatory cells and bacteria

83

Types of non-infective/ non-rheumatic endocarditis:

NBTE ("marantic"), atypical verrucous endocarditis (Libman-Sacks)

84

"marantic" is assoc with:

NBTE

85

Libman-Sacks is assoc w:

Atypical verrucous endocarditis (Libmann-Sacks)

86

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

NBTE vegetation

87

shown destroying the valve, seen in endocarditis-cotran:

IE

88

NBTE "marantic":

pancreatic cancer, emboli, infarct (check)

89

When does NBTE often occur?

hypercoagulabe state (60%)

90

NBTE is often assoc w:

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

91

NBTE freq affects normal:

valve

92

This disease often does not change the valve:

NBTE

93

This often gives rise to emboli:

NBTE

94

'Marantic" endocarditis:

bulky, more frialbe lesions tha IE

95

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

"marantic" endocardiits

96

Characteristics of NBTE in slides:

friable (easily crumbled), fibrin, sterile deposits

97

Tiny vegetations in endocarditis are assoc w:

RF

98

Variable size vegetations in endocarditis are assoc w:

IE

99

Large vegetations in endocarditis are assoc w:

NBTE

100

line of closure is assoc w:

RF

101

Destruction is assoc w:

IE

102

"Friable" is assoc w:

NBTE

103

Friable:

easily pulverized or crumbled

104

Vegetations in endocarditis that can lead to emboli:

IE, NBTE

105

Specific valve lesions:

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

106

Aortic stenosis means:

less blood can flow through valve

107

Causes of aortic stenosis:

RF, age

108

Complications of aortic stenosis:

L ven hypertrophy, agina, sudden death