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Sem4-AcuteMI
Sem 4 - Path - Acute MI
| Question | Answer |
|---|---|
| What are the three types of angina pectoris? | Stable, variant and unstable. |
| What type of angina pectoris is caused by >70% lumen narrowing by uncomplicated AS plaque? | Stable angina |
| Chest pain induced by physical exertion, emotional stress, exposure to cold, or overeating. | Stable angina |
| What kind of angina: Chest pain not associated with precipitating factors and usually occurs at rest due to uncomplicated AS plaque w/ coronary artery spasm ? | Variant angina |
| What kind of angina: ST depression or elevation during angina | Variant angina |
| What is the cause of variant angina? | Uncomplicated AS plaque with coronary a. spasm |
| What type of angina: Transient ST elevation during angina, ST depression, and/or T-wave changes | Unstable angina |
| Chest pain due to destabilized AS plaque, that is increasing in severity, frequency, and duration. | Unstable angina |
| What type of angina is caused by AS plaque destabilization leading to rupture, hemorrhage or thrombosis | Unstable angina |
| Angina upon exposure to cold? | Stable angina |
| What is the leading cause of MI? | Coronary AS. (other causes include coronary a. thromboembolism, coronary arteritis (ie PAN or kowasaki), dissectiving aortic aneurysm, and severe systemic htn |
| Describe the pathogenesis of AS-associated MI | Plaque destabilization -> platelet aggregation --> thrombus formation --> ischemia --> necrosis. |
| What type of MI results from a complete obstruction of a single coronary artery? | Transmural MI. |
| What is the cause of a circular subendocardial MI? | severe systemic hypotension (ie collapse or shock) |
| What is the cause of a localized subendocardial MI? | coronary a. obstruction with subsequent thrombolysis. |
| MI effecting only inner 1/3 ventricular wall? | Subendocadial MI |
| What area if ventricular wall is most vulnerable to ischemia | inner 1/3 |
| Dark brown cardiac tissue following an MI indicates what? | Reperfusion of the tissue |
| An obstruction of the LAD will affect what areas the heart? | LV anterior wall near apex, Ant 2/3 of IV septum, and apex circumferentially |
| An obstruction of the RCA will affect what areas of the heart? | Post wall of LV, Post 1/3 if IV septum, Post inferior free wall of RV |
| An obstruction of the LCX will affect what areas of the heart? | LV lateral wall, except apex. |
| What is the duration of an MI with no associated findings on LM, and MC swelling and glycogen loss on EM. | 0-1/2 hr (all reversible injuries) |
| What is the duration of an MI with findings of wavy myocardial fibers and staining defect with TTC on LM, along with Sacolemmal ruptures and MC amorphus densities on EM | 1/2 - 4 hours |
| What is the duration of an MI with associated LM findings of coagulative necrosis(pyknosis, karyorrhexis), deeply eosinophilic cytoplasm, and PMN infiltrate. Necrotic debris found on EM study. | 4-12 hours. |
| Pallor and matting on gross examination are indicative of an MI of what duration? Other expected LM and EM findings? | 12-24hrs. LM findings of coag necrosis and EM findings of necrotic debris are expected. |
| At what duration MI does gross morphological changes begin to occur? | 12-24 hrs |
| Staining defect with TTC dye occurs at what duration MI? | 1/2-4hrs |
| Nuclear changes (pyknosis, karyorrhexis, etc) do not occur until what duration MI? | 4-12 hours |
| At what time following onset of an MI does karyolysis occur? | 24-48 hours (day 2-3) |
| Gross cardiac appearance of mottling with yellow tan center… time after MI? | 2-3 days |
| Gross cardiac appearance of central yellow-tan softening with hyperemic borders… time after MI? | 4-7 days |
| At what point after onset of an MI is macrophage infiltration found? | 4-7 days (myocyte and PMN disintegration also occurs at this point) |
| At what point after onset of an MI does marginal phagocytosis and granulation tissue formation occur? | 4-7 days! |
| How long after an MI would a gray white scar growing from border toward center be found? | 2 – 8 weeks. |
| Histological finding of absence of nuclei in cardiac bx… how long ago did MI occur? | appx 24 hours ago. (absence of nuclei is due to karyolysis) |
| Morphological findings of a cardiac reperfusion injury. | Brown in color (hemorrhagic infarction), presence of accentuated contraction bands (***hypercontraction of sarcomeres with z line thickening due to massive Ca2+ influx***) |
| What is the most effective serum marker in dx of MI ? | troponin I (elevates ***2-4 hours following MI****, peaks at 12h, and normalizes in 7-10 days) |
| What is the most common fatal complication of MI? | v-fib. |
| How long after an MI is a cardiac tamponade most likely to occur? What is the cause? | 4-7 days… caused by a free wall rupture due to action of PMN disintegration causing the release of lytic enzymes ‡ softens tissue. Connective tissue has not yet been synth’d, so tissue is weak. |
| In what situation is a mural thrombus actually beneficial? | in the case of an acute MI, because it strengthens the ventricular wall. |
| Death within 1 hour of cardiac symptoms (may also occur without symptoms) in a person with no previously diagnosed fatal conditions. | Sudden cardiac death. |
| What is the leading cause of death in 20-30 y/o men. | sudden cardiac death. |
| What is the most common post-mortem finding of sudden cardiac death? | Ischemic heart diasease: Healed MI (40-70%), destabilized plaque with acute coronary syndrome (20%) |
| What are 3 major causes of Chronic Ischemic Heart Disease (CIHD) ? | IMPAIRED CONTRACTILITY DUE TO: 1) Healed MI (scars), 2)Ischemic cardiomyopathy: degeneration of cardiomyocytes without obvious MI (hibernating myocardium) and/or 3) Diffuse myocardial fibrosis. |
| What artery supplies the LV lateral wall, except the apex? | LCX |
| What artery supplies the apex, circumferentially? | LAD |
| Most common vessel implicated in an MI? | LAD> RCA > LCX |
| What changes in cardiac enzymes are associated with angina pectoris? | NO CHANGES! Cardiac enzymes are not elevated in angina pectoris. |
| Destabilized AS plaque causes what type of angina? | Unstable angina. (angina increasing in frequency and severity) |
| Reduced stroke volume in a pt with severe coronary arteriosclerosis w/o EKG and troponin I level changes. Dx? | CIHD |
| Reduced stroke volume in a pt with multiple minute myocardial scars... DX? | CIHD |
| 4 classifications of ischemic heart disease? | Angina pectoris, acute MI, sudden cardiac death, and chronic ischedmic heart disease |
Created by:
rkirchoff
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