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Cardiovascular > 04.25 - CV Misc 2 (Nichols) > Flashcards

04.25 - CV Misc 2 (Nichols) Flashcards

1
Q

What usually causes V Tach in adults

A

IHD

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2
Q

100% of Hypertrophic CM is due to

A

Genetic causes (sarcomeric proteins)

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3
Q

3 Main Causes of Long QT

A

(1) IHD; (2) Low K, Ca, Mg; (3) Channelopathy

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4
Q

3 major forms of Restrictive CM

A

Amyloidosis (TTR or systemic), Endomyocardial Fibrosis, Loeffler Endomyocarditis

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5
Q

40 yo Asian male with syncope or SCD due to ventricular tachycardia, especially during sleep

A

Presentation of Brugada Syndrome

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6
Q

5 general pathways leading to end-stage DCM

A

(1) Genetic causes; (2) Infection; (3) Alcohol, other toxic; (4) Peripartum CM; (5) Iron Overload

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7
Q

8 yo with syncope or SCD due to V Tach during emotional or physical stress

A

Presentation of Catecholaminergic Polymorphic V Tach

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8
Q

Are V Tach’s usually mono or polymorphic?

A

Mono

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9
Q

Asteroid Bodies are most often seen in

A

Sarcoidosis

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10
Q

Asystole =

A

No electrical activity at all

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11
Q

Begins in RV with fatty replacement of myocytes, frequently w lymphocyte infiltration and later fibrous scarring

A

Morphological progression of Arrhythmogenic RV CM

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12
Q

Cardiac involvement is found in what percent of Sarcoidosis

A

76%

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13
Q

Cause of Arrhythmogenic RV CM

A

Mutations in genes encoding desmosomal proteins; Possibly with enteric viral infection of Right Heart

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14
Q

Causes of Chylous Effusion

A

Mediastinal Lymphatic Obstruction

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15
Q

Causes of Restrictive CM

A

Amyloidosis, Radiation-induced fibrosis; Idiopathic

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16
Q

Causes of Seroanguineous Effusion

A

Blunt Chest Trauma, Malignancy, Ruptured MI, Aortic Dissection

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17
Q

Causes of Serous Effusion

A

CHF, Hypoalbuminea

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18
Q

Characteristic histologic features of HCM

A

Marked myocyte hypertrophy; Haphazard Myocyte Disarray, Interstitial Fibrosis

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19
Q

Constrictive Pericarditis

A

Extensive Dense, Fibrotic Scarring

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20
Q

Dilated CM when describing a functional entity usually means

A

Idiopathic Dilated CM

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21
Q

Distinctive “spongy appearance of ventricles, associated with CHF and arrhythmias

A

Left Ventricular Compaction

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22
Q

EKG of Brugada

A

Presistently elevated ST segments descending w/ upward convexity to an inverted T wave (V1-V3)

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23
Q

Endomyocardial Fibrosis is characterized by

A

Dense diffuse fibrosis of the ventricular endocardium and Subendocardium

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24
Q

Endomyocardial Fibrosis is principally a disease of

A

children and young adults in Africa and other tropical areas

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25
Q

Epsilon Wave

A

Notch in terminal QRS, most prominent in V1

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26
Q

Epsilon Wave can be manifestation of

A

RV CM

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27
Q

Extensive replacement of myocytes by adipocytes and fibrous tissue

A

Arrhythmogenic RV CM

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28
Q

Feature of inherited forms of DCM

A

Congenital conduction abnormalities

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29
Q

Functional Manifestation of Dilated CM

A

Impaired contractility and Systolic Fxn

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30
Q

Functional Manifestation of Hypertrophic CM

A

Impaired compliance and diastolic function

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31
Q

Functional Manifestation of Restrictive CM

A

Impaired compliance and diastolic function

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32
Q

Fundamental defect in DCM

A

ineffective contraction

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33
Q

Genetics of Brugada

A

Autosomal Dominant

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34
Q

Gross appearance of Myocarditis

A

Acute: Normal of Dilated; Advanced: Flabby and Mottled

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35
Q

Group of channelopathies causing shortened myocyte AP’s and risk of V Tach, SCD

A

Brugada

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36
Q

HCM is fundamentally a disorder of

A

Sarcomeric Proteins (GOF)

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37
Q

Histology of Cardiac Myxoma

A

Stellate, frequently multinucleated Myxoma cells with other cell types

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38
Q

How does DCM usually present

A

Signs of slowly progressive CHF, including dyspnea, easy fatiguability, and poor exertional capacity

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39
Q

How is Brugada recognized

A

Persistently elevated ST segs, with upward convexity to inverted T wave (V1-V3)

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40
Q

In what age range does DCM most commonly present

A

20-50 years

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41
Q

Life-saving preventive tx of Arrhythmogenic RV CM

A

defibrillator device

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42
Q

Life-saving preventive tx of Brugada

A

defibrillator device

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43
Q

Life-saving preventive tx of CPVT

A

BB’s or defib implant

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44
Q

Life-saving preventive tx of TDP is

A

defibrillator device

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45
Q

Lyme Myocarditis manifests primarily as

A

Self-limited conduction system disease

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46
Q

Major clinical manifestations of Myxomas

A

Ball-valve obstruction, Embolization, IL-6

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47
Q

Mechanism of Arrhythmias in CPVT

A

Triggered activity resulting from delayed after-depolarizations due to high intracellular calcium

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48
Q

Mechanism of HF in Restrictive CM

A

Impairment of compliance (diastolic dysfunction)

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49
Q

Microscopic findings in Loeffler Endomyocarditis

A

Eosinophilic infiltrates, Myocardial Necrosis

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50
Q

Microscopic findings in Restrictrive CM

A

Interstitial fibrosis common

51
Q

Morphological progression of Arrhythmogenic RV CM

A

Begins in RV with fatty replacement of myocytes, frequently w lymphocyte infiltration and later fibrous scarring

52
Q

Morphology of ARVC

A

RV wall is severely thinned owing to myocyte replacement by massive fatty infiltration and less amounts of fibrosis

53
Q

Mortality after DCM presentation

A

50% in 2 years

54
Q

Most characterstic cells in Rhabdomyomas

A

Spider Cells

55
Q

Most common appearance of Myxomas

A

Soft, translucent, villous lesions with gelatinous appearance

56
Q

Most common cause of Myocarditis in US

A

Viral Infections (Coxsackieviruses)

57
Q

Most common cause of rhythm disorders

A

Ischemia

58
Q

Most common form of Restrictive CM worldwide

A

Endomyocardial Fibrosis

59
Q

Most common major cardiomyopathy pattern

A

Dilated CM

60
Q

Most common malignancy of heart

A

Mets

61
Q

Most common primary malignant tumor of heart

A

Angiosarcoma

62
Q

Most common primary tumor of adult heart

A

Myxoma, Usually Left Atrial

63
Q

Most common primary tumor of heart in infants and children

A

Rhabdomyosarcomas

64
Q

Most common systemic disorder associated with pericarditis

A

Uremia

65
Q

Most frequently affected protein in HCM

A

Beta-myosin heavy chain

66
Q

Most myocytes in DCM exhibit

A

Hypertrophy with enlarged nuclei

67
Q

Murmur in HCM?

A

Harsh Systolic Ejection murmur if dynamic obstruction present (25 % of cases)

68
Q

Mutations in ARVC involve

A

Desmosomal junctions

69
Q

Mutations in Cardiac Ryanodine Receptor

A

Familial Catecholaminergic Poly V Tach

70
Q

Mutations in Desmosomal Proteins

A

Arrhythmogenic RV CM

71
Q

Mutations in Desmosomal proteins causes

A

Re-entrant V Tach, originating in RV

72
Q

Mutations in genes encoding desmosomal proteins; Possibly with enteric viral infection of Right Heart

A

Cause of Arrhythmogenic RV CM

73
Q

Noncaseating granulomas in lungs, lymph nodes, liver, etc

A

Sarcoidosis

74
Q

One unifying feature of HCM mutations

A

All affect Sarcomeric proteins and increase microfilament activation

75
Q

Pericardial exudate in Acute Viral Pericarditis/Uremia vs Acute Bacterial Pericarditis

A

Fibrinous vs Fibrinopurulent (Suupurative)

76
Q

Pericarditis classically manifests with

A

Atypical Chest pain (not related to exertion, worse in recumbency), and a prominent friction rub

77
Q

Presentation of ARVC

A

Right-sided HF and rhythm disturbances that can cause sudden cardiac death

78
Q

Presentation of Brugada Syndrome

A

40 yo Asian male with syncope or SCD due to ventricular tachycardia, especially during sleep

79
Q

Presentation of Catecholaminergic Polymorphic V Tach

A

8 yo with syncope or SCD due to V Tach during emotional or physical stress

80
Q

Presistently elevated ST segments descending w/ upward convexity to an inverted T wave (V1-V3)

A

EKG of Brugada

81
Q

Primary Pericarditis is most often due to

A

Viral infection (typically with concurrent Myocarditis)

82
Q

Proteins most often affected in congenital DCM

A

Cytoskeletal

83
Q

Prototype Restrictive CM

A

Cardiac Amyloidosis

84
Q

Re-entrant V Tach originating from RV, possibly related to abnormalities in Myocyte Adhesion via desmosomal proteins

A

What causes arrhythmia in Arrhythmogenic RV CM

85
Q

Restrictive CM is characterized by

A

Primary decrease in ventricular compliance

86
Q

Secondary cardiomyopathy means

A

Presenting as the cardiac manifestation of a systemic disorder

87
Q

Secondary Myocardial Dysfunction mimicking Hypertrophic CM

A

HTN HD, Aortic Stenosis

88
Q

Secondary Myocardial Dysfunction mimicking Restrictive CM

A

Pericardial Constriction

89
Q

Some fraction of Idiopathic Dilated CM is due to

A

Previous Viral Myocarditis and Alcohol

90
Q

Spider Cells =

A

Rhabdomyomas

91
Q

T/F: 80-90% of patients who suffer SCD but are successfully resuscitated do not show any enzymatic or ECG evidence of myocardial necrosis - even if original cause was IHD

A

TRUE

92
Q

T/F: Clinical progression from myocarditis to DCM is frequent

A

False, rare

93
Q

T/F: Hypertrophic cardiomyopathy (structural) is a genetic disease

A

TRUE

94
Q

The characteristic histologic abnormalities in DCM are

A

nonspecific, and do not typically point to a specific etiologic entity

95
Q

The clinical features of Myocarditis can mimic those of

A

Acute MI

96
Q

Top 3 most common cancers to met to heart

A

Lung, Lymphoma, Breast

97
Q

Toxic agents to heart implicated in CM

A

Alcohol, Doxorubicin, Cobalt

98
Q

Type of V Tach typical of Congenital Long QT is

A

Torsades de Pointes

99
Q

What causes appearance of Torsades de Pointes

A

Early After-Depolarizations from multiple sites causes multifocal ventricular tachycardia with polymorphology, varying over time

100
Q

What causes arrhythmia in Arrhythmogenic RV CM

A

Re-entrant V Tach originating from RV, possibly related to abnormalities in Myocyte Adhesion via desmosomal proteins

101
Q

What causes Catecholaminergic Poly V Tach

A

Mutations in Cardiac Ryanodine Receptor (SR Ca release channel)

102
Q

What causes most of the 300,000 SCD/year in US

A

V Tach

103
Q

What causes V Tach in Brugada

A

Variably blunted Na currents can cause shortened or failed AP’s and localized conduction block in RV, predisposing to phase 2 re-entrant V Tach

104
Q

What channel is affected in Brugada Syndrome

A

Sodium

105
Q

What channel is affected in LQTS1

A

Iks

106
Q

What channel is affected in LQTS2

A

Ikr

107
Q

What channel is affected in LQTS3

A

Ina

108
Q

What is present in childhood with syncope or SCD due to polymorphic ventricular tachycardia?

A

Congenital Long QT Syndrome

109
Q

What is the normal QTc?

A

<440 milliseconds

110
Q

What is the risk of early after-depolarizations

A

V Tach

111
Q

What is the risk of V Tach

A

SCD

112
Q

What is the site and mechanims of Catecholaminergic Polymorphic VT Channelopathy?

A

Delayed After-Depolarization in Left Ventricle

113
Q

What is the site and mechanism of Brugada Channelopathy?

A

Re-entry in Right Ventricle

114
Q

What is the site and mechanism of Long QT Channelopathy

A

Early After-Depolarization in Left Ventricle

115
Q

What leads show Brugada sign

A

V1-V3

116
Q

What percent of DCM are caused by mutations affecting cytoskeletal proteins

A

20-50%

117
Q

What percent of MI’s are unrecognized?

A

up to 30%

118
Q

What percent of patients with HCM have dynamic obstruction of LV outflow

A

25%

119
Q

What’s special about hypersensitivity myocarditis

A

Numerous eosinophils infiltrating tissue

120
Q

When does HCM typically manifest

A

Post-pubertal growth spurt

121
Q

Which chambers are affected in DCM

A

all

122
Q

Which channelopathy benefits from BB’s

A

Familial Catecholaminergic Poly V Tach

123
Q

With extensive _____, healing can result in fibrosis (chronic pericarditis)

A

suppuration or caseation (TB)

124
Q

X-linked DCM is most frequently associated with

A

Dystrophin

Cardiovascular (18 decks)

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