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Cardio > Myocardial Ischemia and Infarction > Flashcards

Myocardial Ischemia and Infarction Flashcards

1
Q

reversible inadequate blood supply

A

ischemia

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2
Q

What is myocardial ischemia due to?

A 
fixed coronary stenosis
increased myocardial demand
coronary vasospasm 
intraplaque hemorrhage
superimposed thrombosis
**any combo of these factors
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3
Q

myocytes that look normal by microscopy but do not work

A

stunned myocytes

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4
Q

fatal arrhythmia may precede ______

A

irreversible injury to myocytes/infarct

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5
Q

T or F: fatal arrythmias can occur prior to in infarct

A

T

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6
Q

Stunned myocytes are (reversible or irreversible)

A

reversible

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7
Q

What causes stunned myocytes

A

ischemia

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8
Q

T or F: stunned myocytes can initiate an arrhythmia

A

T

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9
Q

myocyte with cytoplasm cleared of contractile proteins

A

hibernating myoctes (breaks doen the contractile protein for fuel to stay alive)

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10
Q

chronically ishemic myocyte

A

hibernating myocytes

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11
Q

acutely ischeic myocte

A

stunned myocytes

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12
Q

growth into or enlargement of arteries in areas of chronic ischemia

A

collateral coronary arteries

  • *not unique to the heart
  • **neovascualrization and enlargement of existing ones
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13
Q

myocytolysis

A

cleared cytoplasm of hibernating myocyte

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14
Q

Hibernating myocyte is a reversible or irreversible cellular change

A

reversible; just need to make new contractile proteins

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15
Q

T or F: rapid ischemia will result in collateral coronary arteries

A

F: ischemia must occur slowly

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16
Q

irreversible necrosis of heart muscle from prolonged ischemia

A

myocardial infarction

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17
Q

a myocyte can go without blood/O2 for ___ mins

A

20 mins

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18
Q

In an MI, the infarction is thought to occur in a wavefront starting ____ (where) and not complete until ___ (time) after it started

A

subendocardial region

6 hrs

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19
Q

MI involving full thickness of heart wall

A

transmural MI

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20
Q

90% of transmural MIs are assc with

A

occlusive thrombosis superimposed on atherosclerotic plaque with an acute change (disruption of an unstable vulnerable plaque by ulceration or rupture)

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21
Q

Surgery causes _____ state. How does this relate to artherlosclerosis?

A

hypercoagulable

  • *imp for people that have artherlosclerotic disease = inc risk of MI, stroke, and death with surgery
  • **superimposed thrombosis on artherlosclerosis
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22
Q

What arteries does artherlosclerosis favor?

A

cerebral and coronary arteries

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23
Q

MI involving the inner portion of the heart wall

A

subendocardial MI

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24
Q

more likely to be patchy infarcts with episodic extension

A

subendocardial MI

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25
Q

Can subendocardial MIs be detected with ECG?

A

not all the time

need greater than 1/3 of the wall thickness affected??

26
Q 
gross pathology in unreperfused MI after...
0-12 hrs
12-24 hrs
2-3 days
4-7 days
1-6 weeks
6-12 weeks
A

0-12 hrs: none
12-24 hrs: progressive pallor
2-3 days: yellow
4-7 days: red boarder (granulation tissue)
1-6 weeks: yellow –> red (granulation tissue) *thinning of wall @ infarct and thickening at other parts of wall
6-12 weeks: gradual white scarring –> thinned wall

27
Q

microscopic pathology at acute phase of MI: 1-3 hrs

4-12 hrs

A 
thin wavy myocytes 
coagualtion necrosis (hypereosinophillia + loss of striations + nuclear pyknosis --> karyorrhexis, karyolysis, loss)
28
Q

thin wavy myocytes

A

1-3 hrs after acute MI (irreversible)

29
Q

hypereosinophillia + loss of striations + nuclear pyknosis –> karyorrhexis, karyolysis, loss

A

coagulation necrosis

*visible 4-12 hrs after acute MI event

30
Q

loss of striations

A

coagulation necrosis (4-12 hrs post acute MI)

31
Q

follows myocyte necrosis and is first visible 6-12 hrs most MI, usually assc with edema and sometime hemorrhage; peaks at 3 days

A

neutrophillic infiltration

32
Q

neutrophils move in _____(time) after MI and peak ____ (time)

A

6-12 hrs

3 days

33
Q

neutrophillic infiltration is assc with

A

edema and sometimes hemorrhage

34
Q

dense hypereosinophillic transverse bands of hyper-contracted sacromeres across dead myocytes

A

contraction brand necrosis

35
Q

hypercontracted sarcomeres

A

contraction brand necrosis

36
Q

When does contraction brand necrosis appear pos unreperfused MI

A

1-3 days

37
Q

infiltration by lymphocytes at day ___
macrophages appear at day ___
fibroblasts appear at day ___
***they first appear at the periphery!!

A

2
3
4

38
Q

What is the order of cellular infiltration post MI?

A 
neutrophils
lymphocytes
macrophages
fibroblasts 
(+/- eosinophils and plasma cells)
39
Q

ingrowth of capillaries (angiogeneis) and proliferation of fibroblasts

A

granulation tissue

40
Q

for an unreperfused MI, granulation tissue at day ___ at what part of the heart tissue?

A

11

periphery

41
Q

What pigments are found in macrophages post MI (also color)

A

lipofusion and hemosiderin

brown

42
Q

will pigment laiden macrophages be around at day 12?

A

yes

43
Q

Reperfusion effects after MI (1-9)

A
  1. smaller then it would have been
  2. more patchy
  3. hemorrage into it
  4. more contraction band necrosis
  5. accelerated inflammation and repair
  6. diffusion of infalmmation and repair
  7. fewer neutrophils
  8. more macrophages
  9. more interstitial fibrosis (between myocytes)
44
Q

characteristic feature of reperfusion

A

hemorrhages

45
Q

Why is there more contraction in reperfusion?

A

reperfusion brings in more Ca but there is No ATP to release the contraction (due to lack of blood flow/O2)

46
Q

dark mottling and hemorrhage

A

acute phase (days 1-3) immediately following reperfusion

47
Q

dark mottling + brown (hemosiderin from broken down blood)

A

earliest subacut phase (days 4-5)

48
Q

Shrunken red + brown + bits of gray-white

A

days 6-10
early subacute
reperfused

49
Q

Brown + intermingled gray-white

A

days 11-14
mid subacute
reperfused

50
Q

Progressive white, intermingled normal

A

weeks 2-7
late subacute
reperfused

51
Q

Acute phase of reperfused MI

A

contraction band necrosis with hemorrhage
immediately following reperfusion

Coagulation necrosis (center of big infarct)

Neutrophilic infiltration (acute inflammation) following myocyte necrosis, first visible 2 hours following reperfusion, decreased with reperfusion

52
Q

when flow is restored in major CA that had been occuleded but there is not re-flow

A

no-reflow phenomenon

53
Q

What causes no reflow phenomenon?

A

edema or microthrombi in capilaries

= disease in microvasculatore

54
Q

disease in microvasculature

A

no reflow phenomenon

55
Q

subacute phase of reperfused MI

A

acceleration of repair and scar formation

Lymphocytes (+/- eosinophils, +/- plasma cells)–>
Then granulation tissue–> collagen
Accelerated inflammation and repair:

56
Q

reperfusion can lead to healing of a large infact by ___ and small infarts by ___

A

12-7 weeks

2 weeks

57
Q

patches of preserved myocardium commonly interspereed scar may cause

A

re-entrant ventricular arrhythmias

58
Q

downside of reperfusion?

A

re-entrant ventricular arrhythmias

59
Q

What is the earliest finding of an unreperfused MI?

A

thin wavy myocytes

60
Q

In unreperfused MI, the granulation tissue is gradually replaced by ____

A

acellular fibrous collagen scar

Cardio (26 decks)

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