Term
| In transmural infarction, what is the extent of necrosis? |
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Definition
| There is necrosis that spans the entire thickness of the myocardial wall, but it is laterally limited by the area of distribution of the now-occluded coronary artery. |
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Term
| What are the features of subendocardial infarction? |
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Definition
1. necrosis limited to inner 1/3 of the ventricular wall
2. damage can extend laterally beyond area of distribution
3. subendocardial zone normally the least perfused area, so more prone to necrosis |
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Term
| With subendocardial infarction, is there an increase or decrease in blood pressure? |
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Definition
| decrease; it's been postulated that the prolonged, severe reduction in systemic blood pressure, as in shock superimposed on chronic coronary stenosis can lead to subendocardial infarct |
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Term
| What are the 3 steps of pathogenesis of the myocardial infarction? |
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Definition
1. coronary occlusion
2. myocardial response
3. infarct modification by reperfusion |
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Term
| What things modify the effects of coronary artery occlusion? |
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Definition
1. increased O2 demand
2. decreased blood pressure |
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Term
| In the myocardial response, what two things happen within a minute? |
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Definition
| There is cessation of aerobic glycolysis, and there is |
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Term
| In order for there to be irreversible damage, how long does ischemia have to occur? |
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Definition
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Term
| When does classic acute myocardial infarction begin? |
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Definition
| 2-4 hours after occlusion of the coronary artery |
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Term
| During an MI, what part of the myocardium is preserved (unaffected) and why? |
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Definition
| There is a narrow rim (1cm ) of preserved subendocardium due to direct diffusion of oxygen and nutrients in the lumen |
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Term
| If the patient has died 2-3 hours after an MI, how might it be possible to highlight the area of necrosis? |
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Definition
| We immerse the tissue slices in either triphenyltetrazolium chloride solution or nitroblue tetrazolium. |
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Term
| From 12-24 hours to 10 days, describe the change in the general morphology of the infarct. |
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Definition
| We start with dark, mottling reddish color due to the trapping of blood. Then, there is the development of tannish-yellow core. The area gets softer, and there is surrounding the center reactive hyperemia. |
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Term
| From 10 days to 2 months, describe the change in the general morphology of the infarct. |
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Definition
| We start with red-gray depressed infarct borders, and then we have the formation of a collagen scar starting from the border and heading toward the center of the infarct. Two months later, we have a complete fibrous scar formation. |
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Term
| In an MI, what does the histology look like 4-12 hours out? |
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Definition
| There are "wavy" fibers and myocytolysis- large vacuolar spaces that are within cells and probably contain water |
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Term
| When do we start to see prominent macrophages and then formation of granulation tissue? |
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Definition
| We start to see macrophages 7-10 days out, followed by granulation tissue formation between 10-14 days out |
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Term
| Why is a reperfused infarct usually hemorrhagic? |
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Definition
| When there is ischemia, the vasculature is injured. So, when red cells rush in again, there is leakage. |
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Term
| During microscopic examination, what might be noticed of the myocytes afte rreperfusion? |
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Definition
| The myocytes may be irreversibly damaged, containing contraction bands (eosinophilic stripes of sarcomeres due high exposure of calcium from reperfused red cells) |
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Term
| Cardiogenic shock occurs in what percentage of contractile dysfunction cases, and what is the mortality rate? |
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Definition
| 10-15% of cases/ mortality associated with cardiogenic shock is 70% |
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Term
| What percentage of acute MI's involve arrythmias and mural thromboses, respectively? |
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Definition
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