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40 Cards in this Set
- Front
- Back
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Intimal plaque is a core of ______ with a _______ cover. |
lipid, fibrous cap |
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What are the most common areas for atheromas to develop? |
coronary arteries, abdominal aorta, popliteal arteries |
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What are intimal lesions composed of? |
cells: endothelial, smooth muscle, macrophages, inflammatory extracellular matrix: collagen, elastin, proteoglycan lipid: many cholesterol esters |
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Necrotic center of atheroma is composed mainly of what? |
macrophages with phagocytosed lipis= foam cells |
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______ hypothesis is the theory that best fits the current understanding of atherosclerosis. |
"response to injury" |
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What is the "response to injury" hypothesis characterized by? (3) |
-endothelial dysfunction -lipid insudation -monocyte/macrophage infiltration -smooth muscle cell migration |
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A Fatty Streak is characterized by an accumulation of? |
foam cells in the intima.
present universally for those >10 years old.
does not obstruct blood flow
probable precursor to artheroma, but not all become plaques |
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List chronic causes of endothelial injury. |
-hyperlipidemia -hypertension -smoking -hemodynamic factors -toxins -viruses -immune reactions |
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How does HTN contribute to endothelial injury? |
-Mechanical stress -Angiotensin II
both cause downstream increase in reactive oxygen species |
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Endothelial dysfunction directly causes? (2) |
-lipoprotein entry and modification (oxidation) -increase in inflammatory cytokines.
cytokines cause increased luminal expression of ICAM and VCAM, which in turn cause increased leukocyte adhesion and migration. |
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Oxidation of lipoproteins entering the intima creates ______. These are taken up by ______ which then develop into _____. |
remnants. macrophages, foam cells.
macrophages upregulate scavenger receptors that pick up remnants.
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Foam cells are a major source of? |
superoxide anion and matrix metalloproteinases |
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What is responsible for macrophage recruitment into subintimal space? |
MCP-1; macrophage chemotactic protein |
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Il-1 and TNF-1 are responsible for? |
leukocyte recruitment |
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What is the major factor leading to development of foam cells from macrophages? |
mLDL (oxidized LDL) ingestion by scavenger receptors evades nigative feedback (unlike typical LDL receptor) and results in engorgement of macrophages with cholesterol and cholesterol ester. |
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______ dominates early plaque progression. |
smooth muscle cell migration. |
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Most acute coronary symtpoms occur when _____ ruptures. |
the fibrous cap of an atherosclerotic plaque.
exposes prothrombotic molecules and leads to sudden occlusion |
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Erosion and rupture is more likely to occur in plaques that? |
have a large core (>40% atheroma volume) with many macrophages
have a thin cap with little fibrous material or muscle |
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_____ is more likely with rupture in large vessels, while _____ is more likely in small vessels. |
embolus, occlusion |
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What are the characteristics of complicated atheromas? |
-calcification: increases rigidity and reduces vessel compliance -evidence of rupture or erosion: can cause thrombosis and occlude -Internal hemorrhage into the plaque forming intramural hematoma, further narrows lumen -Associated thrombosis: embolus formation -Medial atrophy/ replacement: weaking vessel wall can cause aneurysm -Microvessel growth within plaques |
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Arterial stenosis generally occurs at what point over the length of the vessel? |
usually within the first 2cm; more likely to occur in areas that have high shear stress or branching |
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Define "significant" lesion. |
>50% reduction in diameter 75% cross sectional area nutritional demand is still met at rest symptoms with exertion
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define "critical" lesion. |
>75% reduction in diameter 90% cross sectional area chronic ischemic heart disease |
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What should be given when a coronary plaque is found early? |
Tissue plasminogen activator |
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3 clinical consequences of plaques? |
occlusion by stenosis occlusion by thrombus aneurysm |
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Two types of aneurysm? |
saccular- localized bulging wall fusiform- bulging wall all around artery |
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What is a false aneurysm? |
an extravasation of blood into the extravascular connective tissue |
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What are the IHD syndromes? |
-Angina pectoris -Myocardial infarction -Sudden cardiac death -chronic ischemic heart disease |
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Stages of gross appearance of infarct? |
0-4 hours: invisible 4-24 hours: dark mottling (blood extravasation into muscle 1-14 days: progressively more pale 14 days onward: gray scarred area |
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Explain the histopathological changes of infarct to 4 days |
Wavy fiber change: hours 1-3 Coagulation necrosis: hours 4-12 Nuclear pyknosis: 12 hours Karyolysis: 24-48 hours Neutrophilic infiltration: 6-8 early, peaks at 48 hours Vessel proliferation: 3 days Macrophage infiltration: 4 days
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Histopathological changes after 4 days |
Fibroblast proliferation: 4 days Collagen deposition: 9 days Granulation tissue peak: 2-4 weeks Mature scar > 6 weeks |
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______ span the entire thickness of the myocardium and result from a total, prolonged, occlusion of an epicardial coronary artery. |
transmural infarct |
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______ involve the innermost layers of the myocardium. |
subendocardial infarcts |
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Why is the subendocardium particularly susceptible to ischemia? |
it is supplied by vessels that pass through the contracting layers of myocardium, is subjected to the highest pressure from the ventricle, and has few collateral connections. |
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What are the determinants of the amount of tissue that succumbs to infarction? |
-mass of myocardium perfused by occluded vessel -magnitude and duration of impaired coronary flow -oxygen demand of affected region -adequacy of collateral vessels that provide blood flow -degree of tissue response that modifies the ischemic process |
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Sequelae of transmural infarcts? |
-Pericarditis: acute fibrinous pericarditis w/ transmural infarct (2-3 days) -Myocardial rupture with cardiac tamponade (3-6 days) -Mural thrombi: can develop anytime -Papillary muscle infarct/rupture -Ventricular aneurysm -Chronic IHD |
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_____ accumulates in damaged myocytes, and is though to contribute to the final common pathway of cell destruction through the activation of ____ and _____. |
calcium, lipases, proteases |
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When does contraction band necrosis occur? |
numerous in infarcts after reperfusion; can occur in as little as 2 minutes following reperfusion.
occurs in margins between dead and viable zones.
Also occur through hypercontraction: increased Ca causes overlapping of sarcomeres where z lines overlap causing hypereosinophilic areas on microscopy |
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How is chronic IHD defined? |
Ischemic cardiomyopathy: progressive microinfarcts over time causing scarring and dilatation Gross pathology: cardiac hypertrophy, dilation of all 4 chambers Histopath: myocardial atrophy w/ myocyte hypertrophy, subendocardial myocytolysis, replacement fibrosis
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Other features of CHF? |
pulmonary edema (characterized by iron containing "heart failure cells"= macrophages), hepatic congestion "nutmeg liver" |
