Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > 2nd Exam: Myocardial Disease > Flashcards

2nd Exam: Myocardial Disease Flashcards

1
Q

When does the heart undergo hyperplasia?

A

never

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

These grow in hypertrophy:

A

contractile filaments, cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 types of hypertrophy:

A

concentric, eccentric, compensatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Myocardium will hypertropy in response to:

A

an infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Types of compensatory hypertrophy:

A

diffuse, localized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

compensatory hypertrophy is a response to:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Concentric hypertrophy is a response to:

A

pressure overload, hypertension, R ven looks about normal size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

concentric, eccentric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Eccentric:

A

m. lengthening and contracting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

aortic insufficiency is aka:

A

aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is end diastolic volume effected with aortic insufficiency?

A

inc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Functional issue in aortic insufficiency:

A

incompetent valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Heavy heart is characteristic of:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Laplace’s Law:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens as the ven chamber dilates

A

more tension required to reduce the increased radius (volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TF? hypertrophy can be either pathologic or physiologic.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ex of physiologic hypertrophy:

A

marathon runner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

myotrophin:

A

GF, stimulates heart m., hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

aging myocardium:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

Pathology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions