MEDI213 Lecture Notes - Lecture 11: Cholesteryl Ester, Familial Hypercholesterolemia, Team Ldlc.Com
7 Aug 2018
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Document Summary
Pathology: response to injury hypothesis, progression of atherosclerosis, role of macrophages & oxidised ldl, regression of atherosclerosis. Response to injury hypotheses 2 intima from media taken up oxidised ldl and store lipids. Foam cell = macrophage to brought site and move into. It is now thought that the endothelial cells are structurally intact in the early stages of lesion formation, but are functionally abnormal. Progression of atherosclerosis: fatty streaks are earliest visible lesion of atherosclerosis, found as early as 3 years of age, covers 20-30% surface of abdominal aorta by age 30. Second one less likely to: not size of lesion that is important mechanical stability is important. Role of macrophages: background: we know plaque contains macrophages which are full of cholesterol esters (foam cells) If monocytes are incubated with ldl do not form foam cells because monocytes have receptors for ldl which can be downregulated: monocytes also have other receptors scavenger receptors which are not downregulated by intracellular cholesterol.
