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| Atherosclerosis | ||
| Etiology •Unknown. Although the role of risk factors contributing to the pathogenesis is clear, the problem is that there are a few privileged individuals and experimental animals that are resistant when challenged by risk factors. Knowledge of the resistant factor(s) and their mechanism(s) of action would lead to a solution of the etiology. | ||
| Pathogenesis •Hypotheses: Endothelial damage (dysfunction) with increased permeability, monocyte adhesion, and endothelial proliferation; hyperlipidemia with invasion of intima by foamy macrophages; macrphage derived cytokines (IL-1, TNF) and growth factors (PDGF, FGF) cause inflammatory response and proliferation of smooth muscle with sclerosis; plaque thickened by organization of superimposed thrombi., | ||
| Epidemiology •Causes 50% of all deaths in the U.S. due to coronary, cerebral, peripheral, and mesenteric vascular disease, and aortic aneurysms. •A disease of Western civilization. Absent in certain third world ethnic groups. •Major risk factors are high animal fat diets, hyperlipdemias, hypertension, cigarette smoking, and diabetes. • Other important risk factors are obesity, male gender, family history, and physical inactivity. | ||
| General Gross Description •Lesions in childhood appear as "fatty streaks". •Adult plaques are discrete, yellow white random elevations, more prominent around ostia of large branches, abdominal aorta, and coronary popliteal, internal carotid, and cerebral arteries. •Plaques may have sclerotic firm surfaces, or ulcerate with soft exposed grumous material. •Plaques may become confluent with thrombosis. •Severity increases with age, into very old age. •Examples: | ||
| General Microscopic Description •An intimal lesion, made up of a deposition of neutral fats, cholesterol esters, necrotic debris and foam cells, with a variable chronic fibrotic inflammatory response forming a superficial fibrous cap containing smooth muscle and foam cells and lymphocytes. •Complications are ulcers with thrombi, bleeding into plaque, embolization of thrombi and/or atheromas, calcifications, and atrophy of media with formation of aneurysms. •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 473-484. This link will directly take you to the relevant new literature Atherosclerosis
| Synopsis by: J. Hasson M.D. (T41000M52110)[163]
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