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CV Module > Myocardial Ischemia and infarction > Flashcards

Myocardial Ischemia and infarction Flashcards

1
Q

What is myocardial ischemia

A

A condition of reversible inadequate blood supply to the heart due to fixed coronary stenosis, increased myocardial demand, coronary vasospasm, intraplaque hemorrhage, super imposed thrombosis or any combination of these factors

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2
Q

What defines acute ischemia?

A

Ischemia that has lsted only minutes to hours at the most a few days

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3
Q

What are some of the occurences that happen after only 1 minute of ischemia?

A

Loss of glycogen, mitochondrial swelling, cellular swelling and loss of contractility occur after only one minute of ischemia, and a fata arrhythmia may preceede irreversible injury to myocytes

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4
Q

Can the manifestation of acute myocardial ischemia be visualized by Light microscopy?

A

No

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5
Q

How would acutely ischemic myocytes appear under light microscope?

A

Normal, they are not dead yet but they do not work

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6
Q

What can gradually cause these non-fuctional myocytes of acute ischemia to gradually regain their contractile function?

A

Restoration of adequate blood supply

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7
Q

What are the features of the “stunned myocytes?”

A
  1. Accumulated excess Calcium
  2. Oxygen derived free radicals
  3. Damage to its cytoplasmic proteins and organelles which takes time to reverse
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8
Q

What is Chronic Ischemia?

A

Ischemia last weeks months or years

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9
Q

What are the features of Chronic Ischemia

A

These myocytes catabiloze their contractile proteins and revert to primitive state limited to survival functions

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10
Q

How would myocytes of the chronic ischemia (hibernating myocytes) appear under light microscopy?

A

They would show clear vacuolization of their cytoplasm due to the catabolism of contractile proteins

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11
Q

What is Myocytolysis?

A

The light microscopy appearance of hibernating myocytes

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12
Q

Can function of chronically ischemic myocytes return?

A

Yes with adequate blood flow restored there will be gradual regeneration of all the normal cytoplasmic proteins

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13
Q

What develops in response to chronic mycardial ischemia?

A

Collateral coronary arteries

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14
Q

What is ischemic pre-conditioning?

A

Resistance to mild-moderate ischemia due to induction of protective proteins by brief episodes of ischemia

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15
Q

What is myocardial infarction

A

The irreversible necrosis of heart muscle due to prolonged ischemia (greater than 20 minutes)

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16
Q

How the the myocardial infarction/necrosis occur?

A

Thought to occur in a wavefront starting in the subendocardial region and not complete until 6 hours after it is started

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17
Q

What is the time fram where thrombolytic therapy or angioplasty is thought to be beneficial?

A

20minutes -6hours after the onset of ischemia

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18
Q

What is Chronic ischemia?

A

Repeated episodes of ischemia too brief to cause infarction or inadequate perfusion that is low injure myocytes but not low enough to kill them

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19
Q

What is the most common cause of Myocardial infarctions?

A

Coronary atherosclerosis

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20
Q

What are some of the other causes of MI?

A
  1. Coronary vascilitis
  2. Coronary emboli
  3. Endocarditis
  4. Vasospasm (Cocaine)
  5. Antiphospholipid antibody syndrome
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21
Q

What is meant by transmural infaction?

A

Infaction affecting the full thickening of the heart wall

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22
Q

What is associated with Transmural infarcts 90% of the time?

A

Occlusive thrombosis superimposed on an Atherosclerotic plaque than undergoes an acute change typically disruption of an unstable vulnerable plaque by ulceration or rupture

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23
Q

What are subendocardial infarctions?

A

Infarctions involving the inner portion of the heart wall, and are more likely to be patchy and to have episodes of extension with additional infarction at the periphery

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24
Q

What is the gross pathology of an unreperfused myocardial infarction after 01-12 hours?

A

None

25
Q

What is the gross pathology of an unreperfused myocardial infarction after 12-24 hours?

A

Progressive pallor

26
Q

What is the gross pathology of an unreperfused myocardial infarction after 2-3 days?

A

Yellow and softened

27
Q

What is the gross pathology of an unreperfused myocardial infarction after 4-7 days?

A

Red (granulation tissue) border

28
Q

What is the gross pathology of an unreperfused myocardial infarction after 1-6 weeks?

A

Gradual replacement of infarct by red granulation tissue

29
Q

What is the gross pathology of an unreperfused myocardial infarction after 6-12 weeks?

A

Gradual white scarring

30
Q

What is the earliest microscopic finding that is not always present 1-3 hours post infarct?

A

Thin Wavy myocytes

Thin wavy myocytes are dead and they persist at the periphery of an infarct

31
Q

What is the characteristic (necrosis) pathology of an unreperfused myocardial infarct?

A

Coagulation necrosis

32
Q

What are the three components of coagulation necrosis?

A
  1. Hypereosinophilia
  2. Loss of striations
  3. Nuclear changes (pyknosis then karyorrhexis, karyolysis and disappearance
33
Q

When does coagulation necrosis first become visible?

A

4-12 hours

34
Q

When is neutrophilic infiltration (acute inflammation) first visible

A

6-12 hours it follows myocyte necrosis and is usually associated with edema and sometimes hemorrhage as well

35
Q

When does Neutrophilic infiltration peak?

A

In the third day

36
Q

What usually happens during the subacute phase (days4-10)

A

Characterized by infiltration of lymphocytes, macrophages and fibroblasts

37
Q

When do the first lymphocytes (small round cells with dense nuclei and scant cytoplasm) sometime arrive?

A

Day 2

38
Q

When do the first few Macrophages arrive?

A

Day 3

39
Q

When do the fibroblasts first arrive?

A

day 4

40
Q

What happens during the Late subacute phase (day 11-week12)

A

Ingrowth of capillaries (angiogenesis) and proliferation of fibroblasts converts the issue cleared of dead myocytes into granulation tissue

41
Q

How do fibroblasts replace the granulation tissue

A

By acellular fibrous collagen scar

42
Q

What is the form of irreversible myocyte injury associated with reperfusion?

A

Contraction band necrosis

43
Q

What are the ways in which one can reperfuse an MI?

A
  1. Angioplasty
  2. Thrombolytic therapy
  3. Coronary bypass
44
Q

What is the best way to minimize an MI?

A

Restoring the blood flow (reperfusion)

45
Q

What are the benefits of reperfusion?

A

MI is

  • smaller than it would have been
  • patchier than it would have been
  • with hemorrhage into it
  • more contraction band necrosis
  • accelerated inflammation and repair
  • diffusion of inflammation and repair
  • fewer neutrophils
  • more macrophages
  • more interstitial fibrosis
46
Q

The gross pathology of an average reperfused myocardial infarction after 1-3 days

A

Dark mottling and hemorrhage immediately following reperfusion

47
Q

The gross pathology of an average reperfused myocardial infarction after 4-5 days

A

Dark mottled red and brown (no change)

48
Q

The gross pathology of an average reperfused myocardial infarction after 6-10 days

A

Shrunken red and brown and bits of grey-white

49
Q

The gross pathology of an average reperfused myocardial infarction after 11-14

A

Brown and intermingled with grey-white

50
Q

The gross pathology of an average reperfused myocardial infarction after 2-7 weeks

A

Progressive white, intermingled normal

51
Q

What is the microscpic pathology of an average reperfused MI after 1-3 days

A
  1. Contraction band necrosis
  2. Hemorrhage immediately following reperfusion
  3. Coagulation necrosis occurs too especially in the center of the big infarct
  4. Followed by neutrophilic infiltration
52
Q

When is coagulative necrosis first visible following reperfusion?

A

First visible 2 hours following reperfusion

53
Q

What is no reflow phenomenon?

A

Failure of relieving obstruction at the arterial level to restore

54
Q

What are the causes of no-reflow phenomenon?

A
  1. Capillary endothelial swelling
  2. Capillary plugging by neutrophils
  3. Microthrombosis
  4. Microembolism
  5. The hemorrhage cause by reperfusion also contributes to microvascular injury
55
Q

How does reperfusion affect macrophage infiltration of an infarct?

A

Macrophage infiltration is sooner and heavier than in an unreperfused infarct

56
Q

How does the cell infiltration date change with reperfusion?

A
  1. Macrophages arrive in 2 days

2. Fibroblasts arrive in 3 days

57
Q

What occurs in the early subacute phase (days 4-10) in a repurfused infarct

A

Infiltration by lymphocytes, eosinophils and sometimes plasma cells followed by formation of granulation tissue, and the collagen

58
Q

What effect does reperfusion have on infarcts in general?

A

It accelerates healing from about 12 weeks to about 7 weeks on average an acceleration of 40%

59
Q

What is reperfusion injury?

A

Hemorrhage and other injurious phenomena associated with bringing oxygen and calcium to injured tissue, attributed to reactive Oxygen species and metabolic effects of calcium

CV Module (24 decks)

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