Pathology of ischemia and infarction Flashcards Preview

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Flashcards in Pathology of ischemia and infarction Deck (36):

What can cause ischemia?

Reduced blood flow
-CA obstruction
-Tachycardia (dec diastole)
-Dec CO

Increase in myocardial demand
-Inc workload


In what direction does coronary blood flow and when?

Epicardium to endo and during diastole


What kind of necrosis occurs with severe/irrev ischemia?

Coagulative or contraction band necrosis (if reperfused)


What happens in the first 20-40 minutes of ischemia?

Predominantly functional changes
-Anaerobic glycolysis begins
-Cessation of contraction
-Altered electrical activity
-Relaxation of myofibrils-->stretch (contraction of adj cells)

-->myocytes begin to die 20 min after loss of perfusion


Are early changes of ischemia reversible?

Reversible by reperfusion for up to 20-40 min


What happens after 20-40 min of ischemia

Becomes severe/irrev ischemia leading to necrosis


What happens 1-3 days after severe ischemia?

Necrosis followed by phagocytosis
-polys then macrophages


What happens weeks to months after severe ischemia?

healing by replacement with granulation tissue progress to scar


What is prinzmetal's/variant angina?

Cardiac pain occurring at rest/during sleep. Due to vasospasm,


What are acute coronary syndromes?

unstable angina, acute MI, sudden death


What causes acute coronary syndromes?

Acute plaque changes like a rupture wiht superimposed thrombus


What are the properties of a plaque susceptible to rupture?

Thin fibrous cap, lots of lipid, less muscle and/or more inflammation. Disruption of the plaque leads to a superimposed thrombus that can be occlusive or non occlusive


Consequences of incomplete obstruction by a thrombus

Unstable Angina

Subendo MI

Sudden Death


Consequences of complete obstruction by a thrombus

Lethal injury in 15-30 minutes in subendocardium, then injury progresses through endocardium in waves that may take 4-6 hours

Transmural MI

Sudden Death


Consequences of vasospasm

Can contribute to narrowing


What are the 2 possible fates of non-lethal thrombi?

-Can become organized and incorporated into the plaque, contributing to narrowing

-Can be lysed spontaneously or medically


What happens microscopically in acute MI in minutes?

Thin, wavy/stretched myocytes
-still have nuclei and cross striations
-lack of contractile fxn


What happens microscopically in acute MI in 6-24 hours?

Coagulative necrosis:
-loss of nuclei
-cross striations


What happens microscopically in acute MI in 6hr-3 days?

Infiltration by polys


What happens microscopically in acute MI in 7-10 days?

Infiltration by macrophages for clearance


What happens microscopically in acute MI in max 2-4wks?

Ingrowth of granulation tissue


What happens microscopically in acute MI in 8-10 wks

Development of collagenized scar (advanced scar in months to years)


In which direction does ultimate scar formation occur?

From the periphery of the affected area towards the center. It is dependent on the migration of inflammatory cells and neovascularization of neighboring collateral vessels

(ie can have a scar on the outside and necrosis in the center because the outer layer has progressed faster than the inner)


After how long can gross changes be identified in an acute MI?

No gross changes in the first 12 hours


How do we determine where the infarct is within the hours of no gross changes?

Stain for LDH which is present in alive tissue only


Gross image at 12-24 hours

Dark mottling (trapped deoxy blood)


Gross image at 1-3 days

Progressive tan-yellow pallor (necrosis)


Gross image at 3-10 days

Hyperemic border (reactive hyperemia-->brings all of the inflamm agents, polys) with softened yellow, progressively depressed, pale necrotic center


Gross image at 10-14 days

Grey-red depressed periphery (Advancing granulation tissue)


Gross image at 2-8 wks

Grey-white scar progressing from periphery to center


Consequences of reperfusion after ischemic injury

1. rescue of nonlethally injured myocytes
2. alter pattern of necrosis via contraction band necrosis
3. cause additional reperfusion injury


What is contraction band necrosis?

Cells have already undergone ischemia but are reperfused before coagulative necrosis. When myocardium is reperfused, it is overly leaky. It gets flooded with Ca leading to hypercontraction of myofibrils

-this is a marker for reperfusion


What is reperfusion injury?

Myocardium that was not lethally injured gets reperfused and dies because of ROS leading to permeability changes in the mitochondria. Messes with the microvessels and can be associated with myocardial interstitial hemorrhage (white to red infarct)


Danger in evaluating impaired contractility

Amt of irrev injured myocardium may be overestimated due to stunning and hibernation


Complications of MI

-Contractile dysfunction leading to pul edema or cardiogenic shock
-Mural thrombus with or w/o embolization
-Mitral valve regurge
-Pericarditis (autoimmune, usually transmural, associated with inflammation-->friction rub due to fibrinous exudate on epicardial surface)
-Ventricular rupture of free wall, IV septum, pap m-->tamponade
-Remodeling (infarct expansion, distortion by scar, hypertroph of remaining myoc, chamber dilation, interference w mitral valve)
-TGF beta and ACEi and ARBs have a possible role


Why do aneurysms form with MI?

Late complication of transmural MI due to progressive outward bulging and thinning of the area of forming a non contractile scar