University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

233

Pages:

2
Author:

Mariam A.

Atherosclerosis and strokes       Occlusion of a cerebral artery most commonly occurs as a result of underlying atherosclerosis, an inflammatory disease resulting from damage to the endothelium. Normal artery: Loss of function of the endothelium precedes the formation of lesions of atherosclerosis. o Risk factors: hypertension, diabetes, smoking, chronic renal failure, genetic influences, other inflammatory diseases. o Manifests as increased endothelial permeability to lipoproteins and other plasma constituents and migration of leukocytes into the artery wall. Developing plaque result from increased endothelial permeability and the migration of leukocytes and LDLs, a fatty streak develops. o These initially consist of lipid-laden monocytes and macrophages (foam cells) together with T lymphocytes. o Later, they are joined by various numbers of smooth muscle cells. Fatty streaks progress to intermediate and advanced lesions, and tend to form a fibrous cap that walls off the lesion from the lumen. o Cap usually represents bulk of the plaque. o Covers a mixture of leukocytes, lipid and debris, which may form a necrotic core. o Lesions expand at their shoulders by means of continued leukocyte adhesion. Eventually, the plaque ruptures as a result of the turbulent flow of blood. o The composition and vulnerability of plaque, rather than its volume or consequent severity of stenosis produced, have emerged as being the most important determinants for the development of the thrombus-mediated syndromes.  o Lipid-rich and soft plaques are more dangerous than collagenrich and hard plaques because they are more unstable, rupture-prone and highly thrombogenic after disruption. When the vessel wall is disrupted or punctured, there is thrombus formation. o Collagen and tissue factor associated with the vessel wall provide a haemostatic barrier to maintain the high-pressure circulatory system. o After vessel damage, tissue factor (in medial and adventitial layers) and collagen come in contact with flowing blood and activate the clotting cascade and initiate thrombus formation.