BIOC 3300 Lecture Notes - Lecture 14: Fibrous Cap, Foam Cell, Atheroma
4 Apr 2016
School
Department
Course
Professor
Document Summary
Mainly intracellular lipid accumulation present in first decade clinically silent. Type ii lesion changes to contain small extracellular lipid pools. Growth of lesion in mainly through further lipid accumulation. Type iii lesion progresses to contain a core of extracellular lipid. Defect develops in fibrous cap presence of thrombus and hematoma. Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans: what are the components of a necrotic center, what is the thrombogenic theory? cell debris cholesterol crystals, foam cells, calcium. Atherosclerotic lesions develop as a result of repeated clot formation and organization, eventually occluding the vessels. Atherosclerotic lesions develop from a single cell which changes to a proliferative state at the lesion site viral or chemical mutagen. Atherosclerotic lesions develop as a result of an imbalance on the entry and exit of lipoproteins from the intima. Atherosclerosis associated with increased ldl and decreased hdl. Focal lesions - sites of stress or injury are sites of lipid accumulation.
