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Cardio > MI Pathology > Flashcards

MI Pathology Flashcards

1
Q

Ischemia

A

Injury resulting from hypoxia induced by reduced blood flow

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2
Q

Effects of impaired inflow of blood

A

Reduced oxygen, reduced nutrients

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3
Q

Effects of impaired outflow of blood

A

Insufficient removal of metabolites

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4
Q

Ischemic heart disease

A

A group of syndromes that result from inadequate blood supply to meet the oxygen demands of the heart resulting from ischemia.

90% caused by coronary artery disease

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5
Q

Principal presentations of ischemic heart disease

A

Angina
MI
Chronic IHD w/HF
Sudden Cardiac Death - regional ischemia causes fatal ventricular arrhythmia

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6
Q

MI

A

Irreversible myocardial muscle damage caused by prolonged cardiac ischemia.
Discrete focus of ischemic muscle necrosis.

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7
Q

Circumflex artery supplies

A

Lateral edge of left ventricle

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8
Q

LAD supplies

A

Front and bottom of left ventricle. Anterior edge of IVSeptum

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9
Q

RCA supplies

A

Blood to the right atrium, ventricle, and bottom of left ventricle, and posterior edge of septum. Also, PAPILLARY MUSCLE

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10
Q

Progression of MI

A

Starts in the subendocardium and in the central portion of the area at risk. Progresses as a wavefront of necrosis moves from subendo to subepicardium

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11
Q

Transmural infarct

A

Ischemic necrosis involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery.

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12
Q

What causes transmural infarcts

A

Acute plaque change and superimposed thrombus with sustained obstruction.

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13
Q

Common complications of transmural infarcts

A

Pericarditis or ventricular rupture

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14
Q

Subendocardial infarct

A

ischemic necrosis limited to the inner 1/3 or 1/2 of the ventricular wall. Subendocardial zone is the least perfused and most vulnerable to any reduction in flow.

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15
Q

Regional subendocardial infarct

A

transient obstruction of a coronary artery which is relieved before the necrosis extends across the full thickness of the myocardium.

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16
Q

Circumferential subendocardial infarct

A

Due to prolonged severe hypotension.

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17
Q

Multifocal microinfarction

A

Due to pathology only involving smaller intramural vessels.

Can be from microemboli, vasculitis, vascular spasm (cocaine/adrenaline)

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18
Q

Outcome of multifocal microinfarcts

A

Sudden cardiac death due to fatal arrhythmia, ischemic dilated cardiomyopathy.

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19
Q

What do the cellular consequences of myocardial ischemia depend on?

A

Severity and duration of the blood flow deprivation

20
Q

Characteristics of early ischemia

A

Switch from aerobic to anaerobic metabolism, decreased ATP and accumulation of lactate. Glycogen depletion. ATP deficiency leads to failure of NA K pump, so water rushes in. Mild cellular and mitochondrial swelling.

This is potentially reversible

21
Q

Characteristics of late ischemia

A

This occurs after 20-30 minutes of ischemia. Disruptions in the sarcolemma occur and intracellular molecules leak out (biomarkers).

Amorphous densities in the mitochondria.

This is non-reversible

22
Q

Effect of ischemia on mitochondria

A

Creation of amorphous densities

23
Q

Curve of ATP concentration vs minutes

A

Decreasing exponentially

24
Q

Curve of lactate concentration vs minutes

A

Increasing sigmoidally

25
Q

When is myocardial injury reversible

A

20-30 minutes after onset of severe ischemia. After that, dead myocardium starts to accumulate.

26
Q

When is myocardial loss of viability after MI complete?

A

6-12 hours after onset of severe ischemia

27
Q 
Cellular consequences of myocardial ischemia over the course of:
Seconds
Minutes
20-30 Minutes
1 hour
A

Seconds: Onset of ATP depletion (cessation of aerobic metabolism
Minutes: Decrease in contractility due to depletion of atp
20-30 Minutes: irreversible cell injury
1 Hour is microvascular injury

28
Q

Is MI apparent on gross exam?

A

Yes, but only after 12 hours or so

29
Q

Gross features 12-24 hours post MI

A

Dark Mottling due to coagulative necrosis. Reddish blue discoloration. Looks like red jello.

30
Q

Gross features3-7 days

A

Hyperemic border due to granulation tissue, central yellow-tan softening due to inflammatory infiltrates.

31
Q

Gross features >2 months

A

Complete scarring (grey-white)

32
Q

Microscopic features 12-24 hours post MI

A

Coagulative necrosis with wavy fibers

33
Q

Microscopic features 3-7 d

A

Neutrophils, macrophages and removal of necrotic tissue. Some granulation tissue (very congested vessels)

34
Q

Microscopic features >2 months

A

Fibrous tissue and collagenous scar stained blue with trichrome.

35
Q

Can you see histologic changes very early after infarction?

A

Not on H and E, but if you stain for complement you can!

36
Q

Features of coagulative necrosis

A

Loss of nuclei

37
Q

When are neutrophils most common?

A

1-3 days post MI

38
Q

When are macrophages most common?

A

3-7 days post MI

39
Q

Granulation tissue

A

Very congested vasculature, las lymphoid cells, fibroblasts, lots of capillaries even wtihout blood cells

40
Q

Does >2 months look like 10 years after MI?

A

Yes.

41
Q

Old MI Scar

A

Dense collagen fibrous tissue, no inflammatory infiltrates.

42
Q

Myocardial rupture

A

Due to softening and weakening of necrotic and inflamed myocardium.

Rupture of free wall (most common) causes hemopericardium and cardiac tamponade. Happens in the first 2 weeks post MI

Rupture of the Ventricular septum (L->R shunt can cause death)

Papillary muscle rupture

43
Q

True aneurysms

A

Occur weeks->months post MI. Can cause incompetent mitral valve or mural thrombi.

44
Q

MI induced pericarditis

A

Happens with transmural thrombi only. Can cause fibrinous or fibrinohemorrhagic pericarditis.

45
Q

Dressler Syndrome

A

Autoimmune mediated pericarditis months after MI

46
Q

Proposed mechanisms of reperfusion injury

A
  1. Oxidative stress from reoxygenation (ROS cause injuries)
  2. Intracellular calcium overload (causes bands)
  3. Inflammation (brings neutrophils)
  4. Complement activation
47
Q

Common pathologic findings in reperfusion injury

A

Hemorrhage (due to leakage from weakened ischemic vessels)

Contraction bands in lethally injured cells (exaggerated contraction of sarcomeres due to flooding of new plasma calcium)

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