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Flashcards in MI Pathology Deck (47):
1

Ischemia

Injury resulting from hypoxia induced by reduced blood flow

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Effects of impaired inflow of blood

Reduced oxygen, reduced nutrients

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Effects of impaired outflow of blood

Insufficient removal of metabolites

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Ischemic heart disease

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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Principal presentations of ischemic heart disease

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

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MI

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

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Circumflex artery supplies

Lateral edge of left ventricle

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LAD supplies

Front and bottom of left ventricle. Anterior edge of IVSeptum

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RCA supplies

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

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Progression of MI

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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Transmural infarct

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

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What causes transmural infarcts

Acute plaque change and superimposed thrombus with sustained obstruction.

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Common complications of transmural infarcts

Pericarditis or ventricular rupture

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Subendocardial infarct

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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Regional subendocardial infarct

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

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Circumferential subendocardial infarct

Due to prolonged severe hypotension.

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Multifocal microinfarction

Due to pathology only involving smaller intramural vessels.
Can be from microemboli, vasculitis, vascular spasm (cocaine/adrenaline)

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Outcome of multifocal microinfarcts

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

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What do the cellular consequences of myocardial ischemia depend on?

Severity and duration of the blood flow deprivation

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Characteristics of early ischemia

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

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Characteristics of late ischemia

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

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Effect of ischemia on mitochondria

Creation of amorphous densities

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Curve of ATP concentration vs minutes

Decreasing exponentially

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Curve of lactate concentration vs minutes

Increasing sigmoidally

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When is myocardial injury reversible

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

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When is myocardial loss of viability after MI complete?

6-12 hours after onset of severe ischemia

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

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

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Is MI apparent on gross exam?

Yes, but only after 12 hours or so

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Gross features 12-24 hours post MI

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

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Gross features3-7 days

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

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Gross features >2 months

Complete scarring (grey-white)

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Microscopic features 12-24 hours post MI

Coagulative necrosis with wavy fibers

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Microscopic features 3-7 d

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

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Microscopic features >2 months

Fibrous tissue and collagenous scar stained blue with trichrome.

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Can you see histologic changes very early after infarction?

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

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Features of coagulative necrosis

Loss of nuclei

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When are neutrophils most common?

1-3 days post MI

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When are macrophages most common?

3-7 days post MI

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Granulation tissue

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

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Does >2 months look like 10 years after MI?

Yes.

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Old MI Scar

Dense collagen fibrous tissue, no inflammatory infiltrates.

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Myocardial rupture

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

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True aneurysms

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

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MI induced pericarditis

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

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Dressler Syndrome

Autoimmune mediated pericarditis months after MI

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Proposed mechanisms of reperfusion injury

1. Oxidative stress from reoxygenation (ROS cause injuries)

2. Intracellular calcium overload (causes bands)

3. Inflammation (brings neutrophils)

4. Complement activation

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Common pathologic findings in reperfusion injury

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)