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Pathology > HEART 3 > Flashcards

HEART 3 Flashcards

1
Q

is the failure of a valve to open completely, obstructing forward flow

A

stenosis

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2
Q

calcification or valve scarring may lead to

A

chronic stenosis

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3
Q

failure of valves to close completely

A

insuffiency

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4
Q

result from intrinsic disease of the valve leaflet or disruption of supporting structures

A

insifficiency

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5
Q

supporting structures

A 
aorta
mitral annulus
tendinous cords
papillary muscles
ventricular free wall
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6
Q

consequence of leaflet scarring and retraction

A

insidiously

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7
Q

chest rising during the contraction of the heart

A

thrills

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8
Q

exacerbate valve disease and lead to unfavorable maternal or fetal outcomes

A

pregnancy

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9
Q

calcification and
sclerosis of aortic valves, when you say
calcification, it also includes aging, your
wear and tear

A

aortic stenosis

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10
Q 
dilation  of  the
ascending  aorta,  the aortic  valve  cannot
compensate to the increased diameter of
the  aorta,  secondary  to  hypertension
and/ or aging
A

aortic insufficiency

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11
Q

rheumatic heart disease

A

mitral stenosis

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12
Q

myxomatous
degeneration (MVP) or your mitral valve
prolapse, or left ventricular dilation due to
heart failure

A

mitral insufficiency

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13
Q

Most common of all valvular abnormalities

A

calcific aortic stenosis

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14
Q

clinically significant

one to two decades earlier.

A

stenotic bicuspid valve

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15
Q

consequence of
recurrent chronic injury due to hyperlipidemia,
hypertension, inflammation, and atherosclerosis

A

aortic valve calcification

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16
Q

T or F
Bicuspid valves incur greater mechanical stress
than normal tricuspid valves, which may explain
their accelerated stenosis

A

T

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17
Q 
clinical feature (aortic stenosis) 
Left ventricular pressures rise to
A

200mmHg or more

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18
Q

die within __ years of developing angina

A

5

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19
Q

die within _ years of developing syncope

A

3

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20
Q

die within _ yrs of CHF onset

A

2

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21
Q

Some with familial clustering, often with
associated aortic or left ventricular
outflow tract malformations

A

calcific stenosis of congenitally bicuspid aortic valve

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22
Q

in BAV, there is loss-of-function mutations in

A

NOTCH1 (9q34.3)

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23
Q

major site of calcific deposits

A

raphe

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24
Q

in BAV:

larger cusp having a ________

A

midline raphe resulting from incomplete commissural separation during development

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25
Q

In mitral annular calcification, degenerative calcific deposits in the mitral valve develop in the ___________

A

fibrous annulus

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26
Q

appear as irregular stony hard ulcerated nodules at the base of the leaflets (2-5 mm)

A

mitral annular calcification

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27
Q

Mitral annular calcification can lead to the following

A

regurgitation
Stenosis
Arryhthmias

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28
Q

one or both mitral valve leaflets are floppy

A

mitral valve prolapse (protrusion of mitral valve into the left atrium)

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29
Q

MVP is associated with disorders of connective tissue including marfan syndrome caused by

A

fibrillin 1 mutations

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30
Q

mutated FBN1 develop a form of MVP that is prevented by

A

TGF B inhibitors

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31
Q

the characteristic anatomic change in MVP

A

ballooning of the mitral leaflets

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32
Q

key histologic change in the tissue (mvp)

A

myxomatous degeneration of the spongiosa layer

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33
Q

secondary changes (mvp)

A 
fibrous thickening of the valve leaflets
Linear fibrous thickening of the left ventricular endocardial surface
Thickening of the mural endocardium
Thrombi
Focal calcifications
34
Q

mocat pentachrome stain

A

collagen yellow
elastin black
proteoglycan blue

35
Q

auscultation of mid-systolic clicks, caused by abrupt tension in the redundant valve leaflets and chordae tendinae as the valve attempts to close

A

MVP

36
Q

MVP can be confirmed by

A

echocardiography

37
Q

can be done for for symptomatic patients or those with increased risk for significant complications

A

valve repair or replacement surgery

38
Q

is an acute, immunologically

mediated, multisystem inflammatory disease classically occurring a few weeks after group A streptococcal pharyngitis.

A

Rheumatic fever

39
Q

is a common
manifestation of active RF and may progress to
chronic Rheumatic heart disease.

A

acute rheumatic carditis

40
Q

Rheumatic heart disease characterized by
deforming fibrotic valvular disease,
particularly involving

A

mitral valve

only cause of mitral stenosis

41
Q

are the predictable

consequence of healing and scarring associated with the resolution of the acute inflammation.

A

chronic fibrotic lesions

42
Q

in RHD, damage to heart tissue may thus be caused by a combination of

A

antibody and T cell-mediated rxns

43
Q

composed of foci of
Tlymphocytes, plasma cells, and plump activated
macrophages called Anitschkow cells

A

aschoff bodies

44
Q

During acute RF, diffuse inflammation and
Aschoff bodies may be found in three layers of
the heart, resulting in

A

pericarditis, myocarditis, or endocarditis

45
Q

small vegetations, very typical and a feature where you can differentiate the other types if disease causing vegetation

A

verrucae

46
Q

Subendocardial lesions, exacerbated by
regurgitant jets, can induce irregular thickenings
called

A

MacCallum plaques (left atrium)

47
Q

Changes of the mitral valve in chronic RHD are
leaflet thickening, commissural fusion and
shortening, and thickening of the tendinous
cords. This will add to severity of the patients
symptoms. This is now you call

A

fish-mouth stenosis

48
Q

Rheumatic fever is characterized by a constellation of major manifestations:

A 
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erytheme marginatum
Sydenham chorea (involuntary rapid movements)
49
Q

Diagnosis (RF)

A

presence of 2 major

or 1 major and 2 minor manifestations (fever arthralgia, elevated blood levels of acute phase reactants)

50
Q

antibodies to streptococcal enzymes

A

streptolysin O and DNAse B

51
Q

pericardial friction rubs

tachycardia, and arrhythmias

A

acute carditis

52
Q

cause cardiac dilation that
culminates in functional mitral valve insufficiency
or heart failure.

A

myocarditis

53
Q

T or F
Surgical repair or replacement of diseased valves
has greatly improved the outlook for persons with
RHD

A

T

54
Q

Is a microbial infection of the heart valves or the
mural endocardium that leads to the formation of vegetation composed of thrombotic debris and organisms, associated with destruction of the underlying cardiac tissues.

A

Infective endocarditis

55
Q

is typically caused by infection of a
previously normal heart valve by a highly
virulent organism (e.g. Staphylococcus aureus)
that rapidly produces destructive lesions

A

Acute IE

56
Q

Is characterized by organisms with lower

virulence (viridans streptococci) that cause insidious infections of deformed valves with less destruction

A

subacute IE

57
Q

major antecedent disorder (IE)

A

RHD with valvular scarring

58
Q

Endocarditis of native but previously damaged or
otherwise abnormal valves is caused most
commonly by

A

Streptococcus viridans

59
Q

minor causes of IE

A 
Enterococci
Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
60
Q

prosthetic valves (1-2 mts)

A

s. aureus, s. epidermidis

61
Q

prosthetic valve (1 yr)

A

Streptococcis, s. aureus

62
Q

classic hallmark of IE

A

Vegetations on heart valves

63
Q

most common sites of infection in IE

A

aortic and mitral valves

64
Q

typically exhibit granulation tissue at their bases indicative of healing
o With time, fibrosis, calcification, and
chronic inflammatory infiltrate can develop

A

vegetations of subacute IE

65
Q

present in the majority of patientswith left-sided IE

A

murmurs

66
Q

cure rate for low-virulence organisms

A

98%

67
Q

enterococci and s aureus cure rates

A

60-90%

68
Q

erythematous or hemorrhagic nontender lesions on the palms or soles

A

Janeway lesions

69
Q

subcutaneous nodules in the pulp of the digits

A

osler nodules

70
Q

retinal hemorrhages in the eyes

A

roth spots

71
Q

When you say non-infective endocarditis, we think of two:

A 
o  Noninfected  (sterile)  vegetations  occur in  nonbacterial  thrombotic  endocarditis (NBTE)
o  Endocarditis  of  systemic  lupus erythematosus  (SLE)/  Libman-sacks endocarditis
72
Q

Characterized by the deposition of small (1 to 5 mm)

sterile thrombi on the leaflets of the cardiac valve

A

NBTE

73
Q

endocarditis due to sepsis

A

marantic endocarditis

74
Q

likely related to the procoagulant effects of tumor-derived mucin of tissue factor that can also cause migratory thrombophlebitis

A

mucinous adenocarcinoma

75
Q

consequence of immune complex deposition, with activation of complement and recruitment of Fc-receptor bearing cells

A

NBTE (SLE)

76
Q

intense valvulitis and fibrinoid necrosis of valve substance

A

NBTE SLE

77
Q

systemic disorder marked by flushing, diarrhea, dermatitis and bronchoconstriction that is caused by bioactive compounds such as serotonin released by carcinoid tumors

A

Carcinoid syndrome

78
Q

primarily affected carcinoid syndrome

A

endocardium and valves of the right heart

79
Q

Valvular plaques in carcinoid syndrome are also

similar to lesions that occurred in patients taking

A

fenfluramine (an appetite suppressant) or ergot

alkaloids (for migraine headaches)

80
Q

Distinctive, glistening white intimal plaque like

thickenings of the endocardial surfaces of the cardiac chambers and valve leaflets

A

carcinoid heart disease

Pathology (31 decks)

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