Path slide set 4 Flashcards

1
Q

3 causes of left to right shunts

A
  • ASD
  • VSD
  • PDA
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2
Q

Genes for Tetrology of Fallot

A

JAG1 and NOTCH2

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3
Q

Valve doesn’t open completely, occurs chronically and impedes forward flow

A

Stenosis

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4
Q

age for dilated cardiomyopathy

A

usually between 20-50

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5
Q

What congenital defect can cause shunting that causes volume overload on the right side leading to

  • pulmonary hypertension
  • right heart failure
  • Paradoxical embolization
A

Atrial septal defect

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6
Q

with IV drug users, what side of the heart is often involved in infective endocarditis

A

right

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7
Q

Valve doesn’t close completes, may occur acutely or chronically. allows reversed flow

A

insufficiency

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8
Q

Gender and age for mitral annular calcification

A

Females more and >60

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9
Q

What cardiotoxic drugs/substances are associated with dilated cardiomyopathy?

A
  • doxorubicin (chemotherapy)
  • cobalt
  • iron overload (repeated transfusions)
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10
Q

What time frame does Acute RF occur after grp A strep infection

A

10 days to 6 weeks with Anti-Streptolysin O

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11
Q

Apical ballooning of left ventricle with abnormal wall motion and contractile dysfunction

A

Takotsubo cardiomypathy

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12
Q

fish mouth stenosis

A

RHD

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13
Q

most common primary tumor of adult heart?

A

Myxomas

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14
Q

Most common genetic cause of congenial heart disease

A

Trisomy 21

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15
Q

What is the coarctation in relationship to the vessels that supply the upper body?

A

After

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16
Q

Bizarre Enlarged myocytes with a cytoplasm appearance of “spider cells”

A

Rhabdomyoma

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17
Q

Genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to reduced stroke volume and often ventricular outflow obstruction

A

Hypertrophic cardiomyopathy

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18
Q

Excess catecholamines following extreme emotional or psychological stress

A

Takotsubo cardiomyopathy

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19
Q

Most are asymptomatic but a miniority might have pain mimicking angina and dyspnea

A

mitral valve prolapse

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20
Q

SUBACUTE infective endocarditis vegetations may have what component

A

granulation tissue

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21
Q

the vegetations in infective endocarditis are mixtures of what?

A

fibrin, inflammatory cells (neutrophils) and organisms

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22
Q

Nonbacterial thrombotic endocarditis may be a source of what?

associated with what?

A

emboli

malignancies (especially mucinous adenocarcinomas)

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23
Q

Extracellular deposition of proteins which from an insoluble beta-pleated sheet

A

Amyloid

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24
Q

decrease in ventricular compliance leading to diastolic dysfunction

A

Restrictive cardiomyopathy

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25
Q

What valvular problem comes about from mitral annular calcification?

A

mitral valve prolapse

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26
Q

what type of hypertrophy does Calcific aortic stenosis cause?

A

pressure overload hypertrophy

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27
Q

What do affected valves with calcific aortic stenosis contain?

A

osteoblast-like cells, which deposit an osteoid-like substance–>ossifies

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28
Q

This is generally seen with a PDA if found in infancy and without a PDA in adults form

A

Coarctation of the Aorta

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29
Q

Mutations for Myxomas

A
  • GNAS (McCune-Albright syndrome)

- PRKAR1A (null mutation in Carney complex)

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30
Q

immune response to streptococcal M protein cross reacts with cardiac self antigens

A

Pathogeneis of Rheumatic heart disease

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31
Q

Collapse of young athlete and sudden death

A

Hypertrophic cardiomyopathy

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32
Q

What organism causes infective endocarditis in really acute setting or with IV drug user

A

S. aureus

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33
Q

if you have mitral valve stenosis what is most likely the cause?

A

Rheumatic heart disease

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34
Q

Where do calcific deposits occur in Mitral annular calcification?

A

the fibrous annulus

  • NOT leaflets like in aortic
  • doesn’t affect valve function
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35
Q

what organism causes infective endocarditis in someone with a prosthetic valve

A

S. epidermidis

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36
Q

a slower progressing infection of a PREVIOUSLY deformed valve (such as in chronic RHD)

A

SUBACUTE infective endocarditis

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37
Q

What valve abnormality shows accelerated course for calcific aortic stenosis?

A

bicuspid valve

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38
Q

Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

A

dilated cardiomyopathy

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39
Q

Binucleated macrophages and T cells (Aschoff Bodies)

A

Rheumatic Heart Disease

40
Q

What is the most common valve abnormality

A

calcific aortic stenosis

41
Q

What type of morphology is seen with dilated cardiomyopathy

A

interstitial fibrosis

42
Q

Right ventricle hypertrophies and left atrophied

A

Transposition of Great vessels

43
Q

Describe the size of the chambers in restrictive cardiomyopathy

A

Ventricles are usually of normal size, but both atria can be enlarged

44
Q

describe the immune response in rheumatic heart disease

A

both humoral and T cell

45
Q

What’s the most common mutation involved in hypertrophic cardiomyopathy

A

B-myosin heavy chain

-usually involving sarcomeric protein

46
Q

What has a STONG association with dilated cardiomyopathy

A

alcohol abuse

47
Q

Gene for Bicuspid Aortic valve

A

NOTCH1

48
Q

gender preference for mitral valve prolapse

A

7:1 f:m

49
Q

Inflammation of the MYOCARDIUM is most commonly due to what?

A

Viruses (coxsackie A and B)

50
Q

Familial, usually autosomal dominant

Usually gene involved with desmosome and cardiomyocyte connections - intercalated disc

A

Arrhythmogenic right ventricular cardiomyopathy

51
Q

rapidly progressing, destructive infection of a previously normal valve

A

ACUTE infective endocarditis (Staph Aureus)

52
Q

The clinical severity of Tetrology of Fallot depends on what?

A

Degree of subpulmonary stenosis

53
Q

“broken heart syndrome”

A

Takotsubo cardiomyopathy

54
Q

Chronic stenosis may cause what type of hypertrophy?

Chronic insufficiency?

A

pressure overload

volume overload

55
Q

What organisms causes infective endocarditis if there is a preexisting valve abnormality

A

S. viridans

56
Q

what therapy is needed for acute endocarditis

A

SURGERY and antibiotics

57
Q

What happened to the left atrium in Rheumatic heart disease?

A

LA enlargement –>Afib/thrombosis, pulmonary congestion/RHF

58
Q

Harsh, machinery-like murmur

A

PDA

59
Q

multisystem inflammatory disorder following pharyngeal infection with group A streptococcus

A

Rheumatic fever

60
Q

Friable, bulky, destructive valvular vegetations

A

Infective endocarditis

61
Q

therapy needed for subacute endocarditis

A

antibiotics alone

62
Q

inflammation and fibrinoid necrosis of endocardium and left-sided valves with verucae (vegetations)

A

Acute RF

63
Q

Coarctation with PDA manifests at birth as what?

A

Cyanosis in lower half of body

64
Q

What increases prevalence of calcific aortic stenosis

A
  • Age (usually at 60-80)

- also same risk factors of wear and tear as atherosclerosis (HTN, hyperlipidemia, inflammation)

65
Q

Septal hypertrophy and myocytes disarray

A

Hypertrophic cardiomyopathy

66
Q

What may be secondary to deposition of material within the wall (amyloid) or increased fibrosis from radiation?

A

Restrictive cardiomyopathy

67
Q

Describe the calcifications in calcific aortic stenosis?

A

mounded calcification in cusps that prevent complete opening of valve

68
Q
  • Progressive CHF –> dyspnea, exertional fatigue, lower EF
  • Arrhythmias
  • embolism
A

Dilated cardiomyopathy

69
Q

Morphology for myocarditis

A

LYMPHOCYTIC infiltrate

70
Q

Only an enlarged Atrium. Ventricle is stiff and can’t expand. backup of blood into atrium may lead to Afib and mural thrombosis

A

Restrictive cardiomyopathy

71
Q
  • Right ventricular failure and arrhythmias
  • Myocardium of the right ventricular wall replaced by adipose and fibrosis
  • causes ventricular tachycardia and fibrillation, sudden death
A

Arrhythmogenic right ventricular cardiomyopathy

72
Q

The friability of infective endocarditis leads to what?

A

septic emboli

73
Q

4 cardinal features of Tetrology of Fallot

A
  • VSD
  • Obstruction of RV outflow tract
  • Aorta overrides the VSD
  • RV hypertrophy
74
Q

hypervascularity of valves

A

RHD

75
Q

what side valves are more commonly affected with infective endocarditis

A

left

76
Q

Pathogenesis of Dilated cardiomyopathy

A
  • 30-50% thought to be familial (TTN gene: Titin protein

- autosomal dominan

77
Q

Small, sterile thrombi on cardiac valve leaflets, along line of closure

A

Nonbacterial thrombotic endocarditis

78
Q

what do patients usually present with when they have infective endocarditis?

A
  • Nonspecific symptoms (fever, weight loss, fatigue)

- Murmurs usually present with left-sided lesions

79
Q

Enlarged and “boot shaped” heart due to right ventricular hypertrophy

A

Tetralogy of Fallot

80
Q

symptoms and signs similar to acute myocardial infarction. ECG changes and troponin elevated but not as much as would be in MI

A

Takotsubo

81
Q

When a left to right shunt produces pulmonary pressure that eventually becomes a right to left shunt and introduces deoxygenated blood into systemic circulation

A

Eisenmenger syndrome

82
Q

splinter hemorrhages on fingernails and painful nodules on digits

A

infective endocarditis

83
Q

Which coarctation causes concentric hypertrophy?

A

Without PDA

84
Q

What gives you a systemic Amyloid?

A

Myeloma

85
Q

What give you amyloid restricted to the heart

A

Transthyretin

86
Q

Most common primary tumor of pediatric heart

A

Rhabdomyoma

87
Q

describe the leaflets in mitral valve prolapse

A

thickened and rubbery due to proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption

88
Q

What is the most common form of congenital heart disease

A

VSD

89
Q

Nodules in mitral annular calcification may become sites for what?

A

thrombus formation and infective endocarditis

90
Q

epidemiology for takotsubo cardiomyopathy

A

> 90% women. ages 58-75

91
Q

Pancarditis featuring Aschoff bodies

A

Acute RF

92
Q

What stains green with a conga red stain

A

Amyloid

93
Q

Coarctation without PDA is usually asymptomatic but when it does show symptoms what are they

A
  • HTN in upper extremities
  • hypotension in lower extremities
  • Claudication and cold lower extremities with exercise
94
Q

mid systolic click

A

mitral valve prolapse

95
Q

Predisposing conditions for infective endocarditis

A

Valvular abnormalities

Bacteremia (another site of infection, DENTAL work/surgery, CONTAMINATED NEEDLE, compromised epithelium)

96
Q

mitral leaflet thickeing, fusion and shortening of commisures, fusion and thicking of tendinous cords resulting in mitral stenosis

A

CHRONIC RHD

97
Q
  • Globular heart (dilation of all chambers)
  • Mural thombi are common
  • functional regurgitation of valves
A

Dilated cardiomyopathy