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Pathology > 2nd Exam: Myocardial Disease > Flashcards

2nd Exam: Myocardial Disease Flashcards

1
Q

When does the heart undergo hyperplasia?

A

never

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2
Q

Causes of hypertrophy:

A

work (adaptive change), GF’s, i.e., myotrophin causing myocyte hypertrophy (activation of sig pw), inc expression of filament genes

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3
Q

These grow in hypertrophy:

A

contractile filaments, cytoplasm

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4
Q

3 types of hypertrophy:

A

concentric, eccentric, compensatory

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5
Q

Myocardium will hypertropy in response to:

A

an infarct

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6
Q

Types of compensatory hypertrophy:

A

diffuse, localized

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7
Q

compensatory hypertrophy is a response to:

A

loss of myocardium, i.e., MI, aging

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8
Q

Concentric hypertrophy is a response to:

A

pressure overload, hypertension, R ven looks about normal size

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9
Q

Indicative of concentric hypertrophy:

A

P overload, hypertension, stronger initially, heavy heart, thick ven wall, smaller ven chamber, inc diameter of myoctes, large nuclei, sarcomeres side by side

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10
Q

Sarcomeres are added sided by side in ____ and end to end in ___.

A

concentric, eccentric

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11
Q

Indicative of eccentric hypertrophy:

A

V overload, aortic insufficiency/ regurgitation, heavy heart, dil, thin walled ven, inc length of myocytes, sarcomeres end to end, reduced # of cross bridges, chamber/wall thickness more proportional, both ven have larger chambers

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12
Q

Eccentric:

A

m. lengthening and contracting

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13
Q

TF? In addition to sarcomere being added end to end with eccentric hypertrophy, there is also side to side addition.

A

T

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14
Q

aortic insufficiency is aka:

A

aortic regurgitation

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15
Q

How is end diastolic volume effected with aortic insufficiency?

A

inc

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16
Q

Why does a heart w eccentric hyp look thin even though the chamber is dilating at the same time as hypertrophy?

A

because it is dilated

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17
Q

Functional issue in aortic insufficiency:

A

incompetent valve

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18
Q

Heavy heart is characteristic of:

A

(4) eccentric, concentric, hypertrophic and dilated/ congestive CM:

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19
Q

Laplace’s Law:

A

tension in wall = (Pressure)(radius) / 2h

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20
Q

What happens as the ven chamber dilates

A

more tension required to reduce the increased radius (volume)

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21
Q

TF? hypertrophy can be either pathologic or physiologic.

A

T

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22
Q

Ex of physiologic hypertrophy:

A

marathon runner

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23
Q

myotrophin:

A

GF, stimulates heart m., hypertrophy

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24
Q

aging myocardium:

A

fewer, smaller, weaker myocytes, interstitial fibrosis/ stiffening of heart, compensatory hypertrophy, may be accom by ischemia, hypert., etc.

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25
Q

Effect of reactive interstitial fibrosis:

A

reduced elasticity, dilation, filling, and CO

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26
Q

What happens after myocardial injury?

A

compensatory hypertrophy: Larger fibers try to compensate for smaller, weaker

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27
Q

Myofiber hypertrophy:

A

Hyperchromatic, large, blunt nuclei, large diameter fibers

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28
Q

Atrophic heart fibers are often seen:

A

in elderly

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29
Q

Cause of atrophy:

A

unclear

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30
Q

CM’s:

A

(HARDAR) hypertrophic, aging, restrictive, dilated, arrhythmogenic R ven CM

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31
Q

Ven usually affected be dilated CM’s:

A

L ven

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32
Q

dilated CM is aka:

A

congestive CM

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33
Q

Causes of congestive CM’s:

A

heterogenous group w many causes: BIG MAMA: beriberi, idiopathic, genetic, metabolic, alcohol, myocarditis, age

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34
Q

% of congestive CM’s that are genetic:

A

30-40%

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35
Q

TF? Inflammation of the heart can cause CM.

A

T

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36
Q

__ deficiency leads to BeriBeri:

A

B1

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37
Q

Dilated/ congestive CM:

A

25-50yo onset, impaired contractility/ dec inotropy, heavy heart, low EF, CHF, dilated ventricles, endocardial fibrosis, mural thrombi (systemic emboli), arrythmias, slow progression, poor prognosis, late stage, more acute disease

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38
Q

Why are dilated CM’s slowly progressive?

A

bc the diseases that cause them are

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39
Q

This CM often simmers for a long time before it is noticed:

A

dilated CM

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40
Q

Myopathy in which the heart m is infiltrated by some process like a tumor, heart can’t completely fill:

A

restrictive CM

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41
Q

3 types of CM’s:

A

dilated/ congestive, hypertrophic, restrictive

42
Q

How is the L atrium affect for each CM?

A

Similar inc in size for all 3

43
Q

L vent: inc in chamber size, small decrease, if at all, in chamber size, decrease in chamber size:

A

dilated, restrictive, hypertrophic

44
Q

Leads to mural thrombus formation in dilated CMs:

A

blood stasis

45
Q

Dilated CM pathology:

A

nonspecific, variation in fiber size, interstitial fibrosis

46
Q

There is increased ___ in dilated CM:

A

fibrosis, collagen

47
Q

Metabolic CM’s:

A

hemochromatosis, mito d., glycogen/lipid/ mucopolysaccharide/ mineral storage d.’s (i.e., iron, copper)

48
Q

hemochromatosis

A

hereditary, iron storage d., iron salt deposition, produces free radicals, leads to DM, CM, liver damage, bronze coloration of skin

49
Q

Iron is removed from here in hemochromatosis:

A

hemosiderin

50
Q

Causes of hemochromatosis (HC):

A

Hereditary?, hemolysis (anemia), multiple transfusion, iron deposits in liver cells and bile ducts

51
Q

Why can transfusions lead to HC?

A

iron overload, body can’t handle

52
Q

Effects of iron deposition/ HC on heart:

A

decreased force, brown coloration

53
Q

Disease of children:

A

acid maltase deficiency, storage of glycogen in tongue m., macroglossia, heart m. enlarged due to dilation, globular, thick walls, dec contractility, fibers filled w glycogen, mem bound vacuoles, sarc vacuoles, PAS+

54
Q

AMD sf:

A

Acid maltase deficiency

55
Q

PAS stains for:

A

glycogen/ polysacs

56
Q

These get filled w glycogen in AMD:

A

vacuoles, huge, dilated h. chamber

57
Q

Genetics and Dilated CM:

A

dominant, recessive, or X-linked (includes dystrophin, some wo Duchenne or Becker type phenotype (muscular dystrophy)), often involves proteins in cytoskeleton, desmin aggregate disease (mutation of cytoskeleton protiens), mutation of a-actin gene

58
Q

These CM’s are often protein myopathies:

A

dilated CMs ( L ven )

59
Q

Wo dystrophin, the h. is:

A

weaker

60
Q

Genetic CM’s:

A

DMD, MyD

61
Q

Fxn of dystrophin:

A

connects membane to contratile apparatus

62
Q

Case: man, substernal, crushing/. burning, elevated serum CK, EKG w ST changes:

A

acute MI

63
Q

Type of MI assoc w chest pain:

A

acute (didn’t we learn that chronic coronary artery obstruction leads to angina? Yes, but this is not a MI)

64
Q

Artery involved in MI:

A

coronary a., undergoes thrombosis

65
Q

Leads to elevated CK levels in blood:

A

MI, myocardial necrosis

66
Q

CK is found in __ cells:

A

myocardial

67
Q

Causes of myocarditis (inflammation of heart muscle):

A

viral, bacterial (Rickettsia), fungi (candida), Chagas disease, toxoplasmosis, trichinosis, sarcoidosis, immune related

68
Q

causes of viral myocarditis:

A

Coxsackie A and B, echovirus, parvovirus B19, adenovirus, CMV, HIV

69
Q

Ex’s of bacterial causes of myocarditis:

A

DR LYENEI: diptheria, rheumatic fever, Rickettsia, Lye, Neisseria

70
Q

Immune related causes of myocarditis:

A

Giant cell type, transplatation

71
Q

Most common viral cause of myocarditis:

A

Coxsackie

72
Q

TF? Myocarditis is a disease.

A

F. not per se, it is inflammation of the h.

73
Q

Pt: not MI, normal angiogram, no occluded artery, think:

A

myocarditis

74
Q

Cx ft of myocarditis:

A

variable symp, asymptomatic, chest pain, tachycardia, dyspnea, fatigue, EKG change, CHF in severe cases, 7% of autopsies

75
Q

Acute/ fulminant viral myocarditis (MC):

A

often viral prodmrom-flulie, fever, arthralgia, possible sudden death

76
Q

Chronic active or persistent viral MC:

A

less distinct onset, ven dysfunction, dilated CM

77
Q

Mechs of viral MCs:

A

cytotoxic effect, secondary immune response, cytokine mediated

78
Q

cytotoxic effect leading to viral MC:

A

due to causative agents (viruses) killing myocyte,

79
Q

Secondary IR, viral MC:

A

E.g., coxsackie: IS attacks virus infected myocytes, mostly T cells

80
Q

Cytokine mediated damage, viral MC’s:

A

Ex: IL-1, TNF, and ions

81
Q

TF? Viral cultures of viral MC’s often return a true positive result.

A

F. often false neg

82
Q

Self-limited viral MC:

A

A9

83
Q

Severe MC:

A

B3, high mortality

84
Q

Cellular appearance during viral MC:

A

lymphocyte infiltration, myocardial cell necrosis

85
Q

Characteristic to MC:

A

Myocardial death and inflammation

86
Q

Etiology of hypertrophic CMs:

A

familial, often dominant, mutations in sarcomere protein genes, myosin heavy chain most common

87
Q

Cx px of hypertrophic CMs:

A

CHF, arrhythmias, sudden, unexplained death in youth

88
Q

dilated/ congestive CMs are usually related to:

A

mutations in actin DAHM: dilated: actin, hypertrophic: myosin

89
Q

Hypertrophic CM:

A

thick wall, esp. upper septum, heavy, big heart, aortic stenosis, contraction impaired, L ven outflow impaired bc of thick septum, leads to diastolic filling, myocyte hypertrophy, enlarged nuclei, haphazard arrangement of myocardial fibers

90
Q

Haphazard myoctyte arrangement is indicative of:

A

hypertrophic CM

91
Q

heart can’t fill/ dilate properly in this type of CM:

A

restricvtive

92
Q

Effect of restrictive CMs on heart:

A

impaired ven filling, normal contraction

93
Q

Causes of restrictive CM:

A

idiopathic, amyloidosis, sarcoidosis, tumor infiltration of h., storage disease (i.e., glycogen (infiltrated, stiffer heart can’t’ pump enough blood)

94
Q

Arrhythmogenic R ven CM:

A

sometimes involves L ven, diverse group of d.’s, children, peak onset: 35yo, several possible causes, most likely genetic, dominant inheritance, several genes implicated, thin walled, not hypertrophic, R ven dilated, myocardium replaced by fat and scar tissue.

95
Q

Cx px of Arrhythmogenic R ven CM:

A

bundle branch block, arrhythmias, R heart failure, sudden death

96
Q

Mutations here can lead to arrhythmia:

A

of adhesion molecules b the myocardial fibers, can lead to sudden death

97
Q

Genes usually involved in Arrhythmogenic R ven CM:

A

those encoding components of cardiac desmosomes (cell adhesion molecules, desmoglein 2: 1 of most imp causes

98
Q

Pathogenesis of Arrythmogenic R ven CM involves:

A

myocyte loss

99
Q

Most common mutation of Arryhthmogenic R ven CM:

A

desmoglein 2 mutation

100
Q

Appearance of R ven with Arrhythmogenic R ven CM:

A

transmural fat replaces myocardium along entire lateral border of R ven, wall remains thin

101
Q

Drinking this can lead to cardiomyopathy:

A

alcohol

Pathology (23 decks)

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