Flashcards in MI Pathology Deck (47):
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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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