Cholesterol emboli syndrome pathophysiology: Difference between revisions
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{{Cholesterol emboli syndrome}} | {{Cholesterol emboli syndrome}} | ||
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==Overview== | |||
==Pathophysiology== | |||
Cholesterol emboli occur when atheromatous plaques rupture and release cholesterol crystals, either spontaneously or as a result of iatrogenesis. | |||
Cholesterol emboli syndrome (CES) is defined as the occlusion of 55-900 um arterioles by cholesterol crystals after their dislodgment from eroded upstream atheromatous plaques. The occlusion site is subsequently surrounded by intimal tissue, fibrin and platelet thrombi, and foreign-body giant cells. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} |
Revision as of 14:13, 27 September 2012
Cholesterol emboli syndrome Microchapters |
Differentiating Cholesterol emboli syndrome from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Cholesterol emboli occur when atheromatous plaques rupture and release cholesterol crystals, either spontaneously or as a result of iatrogenesis. Cholesterol emboli syndrome (CES) is defined as the occlusion of 55-900 um arterioles by cholesterol crystals after their dislodgment from eroded upstream atheromatous plaques. The occlusion site is subsequently surrounded by intimal tissue, fibrin and platelet thrombi, and foreign-body giant cells.