Monckeberg arteriosclerosis A form of characterized by of the and There is no blood flow obstruction. Mainly affects medium-sized Causes: and/or progressive disease : pipestem appearance Arteriolosclerosis: the thickening and loss of elasticity of the small and Hyaline arteriolosclerosis Deposition of below the due to leakage H&E: pink amorphous deposits () within the arteriolar walls Causes: chronic , , and normal Hyperplastic arteriolosclerosis of subendothelial in response to very H&E: "onion-" appearance of the Cause: The terms “” and “” are often used synonymously. Chronic stress on the (e.g., due to and turbulence) cell dysfunction, which leads to: Invasion of inflammatory cells (mainly and ) through the disrupted barrier Adhesion of to the damaged vessel wall → release of inflammatory mediators (e.g., ) and () stimulates the migration and of (SMCs) in the and mediates the differentiation of into Inflammation of the vessel wall and SMCs ingest from oxidized ; and transform into foam cells ( filled with lipid droplets). accumulate to form fatty streaks (early atherosclerotic lesions). Lipid-laden and SMCs produce (e.g., ) deposition → development of a fibrous plaque () Inflammatory cells in the (e.g., ) secrete → weakening of the fibrous cap of the plaque due to the breakdown of → minor stress ruptures the fibrous cap Calcification of the (the amount and pattern of calcification affect the risk of complications) Plaque rupture → exposure of thrombogenic material ; (e.g., )→ formation with vascular occlusion or spreading of thrombogenic material Carotid |