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Flashcards in 2nd Exam: Myocardial Disease Deck (101)
1

When does the heart undergo hyperplasia?

never

2

Causes of hypertrophy:

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

3

These grow in hypertrophy:

contractile filaments, cytoplasm

4

3 types of hypertrophy:

concentric, eccentric, compensatory

5

Myocardium will hypertropy in response to:

an infarct

6

Types of compensatory hypertrophy:

diffuse, localized

7

compensatory hypertrophy is a response to:

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

8

Concentric hypertrophy is a response to:

pressure overload, hypertension, R ven looks about normal size

9

Indicative of concentric hypertrophy:

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

10

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

concentric, eccentric

11

Indicative of eccentric hypertrophy:

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

12

Eccentric:

m. lengthening and contracting

13

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

T

14

aortic insufficiency is aka:

aortic regurgitation

15

How is end diastolic volume effected with aortic insufficiency?

inc

16

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

because it is dilated

17

Functional issue in aortic insufficiency:

incompetent valve

18

Heavy heart is characteristic of:

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

19

Laplace's Law:

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

20

What happens as the ven chamber dilates

more tension required to reduce the increased radius (volume)

21

TF? hypertrophy can be either pathologic or physiologic.

T

22

Ex of physiologic hypertrophy:

marathon runner

23

myotrophin:

GF, stimulates heart m., hypertrophy

24

aging myocardium:

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

25

Effect of reactive interstitial fibrosis:

reduced elasticity, dilation, filling, and CO

26

What happens after myocardial injury?

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

27

Myofiber hypertrophy:

Hyperchromatic, large, blunt nuclei, large diameter fibers

28

Atrophic heart fibers are often seen:

in elderly

29

Cause of atrophy:

unclear

30

CM's:

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

31

Ven usually affected be dilated CM's:

L ven

32

dilated CM is aka:

congestive CM

33

Causes of congestive CM's:

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

34

% of congestive CM's that are genetic:

30-40%

35

TF? Inflammation of the heart can cause CM.

T

36

__ deficiency leads to BeriBeri:

B1

37

Dilated/ congestive CM:

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

38

Why are dilated CM's slowly progressive?

bc the diseases that cause them are

39

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

dilated CM

40

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

restrictive CM

41

3 types of CM's:

dilated/ congestive, hypertrophic, restrictive

42

How is the L atrium affect for each CM?

Similar inc in size for all 3

43

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

dilated, restrictive, hypertrophic

44

Leads to mural thrombus formation in dilated CMs:

blood stasis

45

Dilated CM pathology:

nonspecific, variation in fiber size, interstitial fibrosis

46

There is increased ___ in dilated CM:

fibrosis, collagen

47

Metabolic CM's:

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

48

hemochromatosis

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

49

Iron is removed from here in hemochromatosis:

hemosiderin

50

Causes of hemochromatosis (HC):

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

51

Why can transfusions lead to HC?

iron overload, body can't handle

52

Effects of iron deposition/ HC on heart:

decreased force, brown coloration

53

Disease of children:

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

AMD sf:

Acid maltase deficiency

55

PAS stains for:

glycogen/ polysacs

56

These get filled w glycogen in AMD:

vacuoles, huge, dilated h. chamber

57

Genetics and Dilated CM:

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

These CM's are often protein myopathies:

dilated CMs ( L ven )

59

Wo dystrophin, the h. is:

weaker

60

Genetic CM's:

DMD, MyD

61

Fxn of dystrophin:

connects membane to contratile apparatus

62

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

acute MI

63

Type of MI assoc w chest pain:

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

64

Artery involved in MI:

coronary a., undergoes thrombosis

65

Leads to elevated CK levels in blood:

MI, myocardial necrosis

66

CK is found in __ cells:

myocardial

67

Causes of myocarditis (inflammation of heart muscle):

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

68

causes of viral myocarditis:

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

69

Ex's of bacterial causes of myocarditis:

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

70

Immune related causes of myocarditis:

Giant cell type, transplatation

71

Most common viral cause of myocarditis:

Coxsackie

72

TF? Myocarditis is a disease.

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

73

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

myocarditis

74

Cx ft of myocarditis:

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

75

Acute/ fulminant viral myocarditis (MC):

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

76

Chronic active or persistent viral MC:

less distinct onset, ven dysfunction, dilated CM

77

Mechs of viral MCs:

cytotoxic effect, secondary immune response, cytokine mediated

78

cytotoxic effect leading to viral MC:

due to causative agents (viruses) killing myocyte,

79

Secondary IR, viral MC:

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

80

Cytokine mediated damage, viral MC's:

Ex: IL-1, TNF, and ions

81

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

F. often false neg

82

Self-limited viral MC:

A9

83

Severe MC:

B3, high mortality

84

Cellular appearance during viral MC:

lymphocyte infiltration, myocardial cell necrosis

85

Characteristic to MC:

Myocardial death and inflammation

86

Etiology of hypertrophic CMs:

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

87

Cx px of hypertrophic CMs:

CHF, arrhythmias, sudden, unexplained death in youth

88

dilated/ congestive CMs are usually related to:

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

89

Hypertrophic CM:

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

Haphazard myoctyte arrangement is indicative of:

hypertrophic CM

91

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

restricvtive

92

Effect of restrictive CMs on heart:

impaired ven filling, normal contraction

93

Causes of restrictive CM:

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

94

Arrhythmogenic R ven CM:

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

Cx px of Arrhythmogenic R ven CM:

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

96

Mutations here can lead to arrhythmia:

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

97

Genes usually involved in Arrhythmogenic R ven CM:

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

98

Pathogenesis of Arrythmogenic R ven CM involves:

myocyte loss

99

Most common mutation of Arryhthmogenic R ven CM:

desmoglein 2 mutation

100

Appearance of R ven with Arrhythmogenic R ven CM:

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

101

Drinking this can lead to cardiomyopathy:

alcohol