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Atherosclerosis CVS lecture 2 Atherosclerosis

Atherosclerosis CVS lecture 2 Atherosclerosis. Vessel wall structure. Atherosclerosis. Atherosclerosis is a specific type of arteriosclerosis ( thickening & hardening of arterial walls) affecting primarily the intima of large and medium-sized muscular arteries .

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Atherosclerosis CVS lecture 2 Atherosclerosis

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  1. AtherosclerosisCVS lecture 2Atherosclerosis

  2. Vessel wall structure

  3. Atherosclerosis • Atherosclerosis is a specific type of arteriosclerosis (thickening & hardening of arterial walls) affecting primarily the intima of large and medium-sized muscular arteries. • Chronic inflammatory response in the walls of arteries. • Slowly progressive. • A build-up of fat (cholesterol) within the artery wall. • Characterized by intimal lesions called: atheromas, atheromatous or fibrofatty plaques

  4. AtherosclerosisCommon sites • Abdominal aorta • Coronaries • Popliteal artery • The internal carotid arteries • The vessels of the circle of Willis

  5. Atherosclerosis Risk factors

  6. LDL Vs. HDL • LDL cholesterol : deliver cholesterol to peripheral tissues. • HDL, "good cholesterol“: mobilizes cholesterol from developing and existing atheromas and transports it to the liver for excretion in the bile

  7. Pathogenesis of Atherosclerosis •Cause? - Current hypothesis: Response to Injury - Initiated by endothelial dysfunction •–The main component of fibro-fatty plaque are: • Lipid containing macrophages • Extracellular matrix • Cells, Proliferating smooth muscle cells

  8. Atherosclerosis Pathogenesis Response-to-injury hypothesis • Endothelial injury • Not completely understood • Nevertheless, the two most important causes of endothelial dysfunction are: • Hemodynamic disturbances (HTN) • Hypercholesterolemia • Inflammation is also an important contributor.

  9. Response to injury hypothesis Injury to the endothelium (dysfunctional endothelium) Chronic inflammatory response Migration of SMC from media to intima Proliferation of Smooth Ms Cells in intima Excess production of Extra cellular Matrix Enhanced lipid accumulation

  10. Evolution of arterial wall changes in the response to injury hypothesis. • Normal. • Endothelial injury with adhesion of monocytes and platelets (the latter to sites where endothelium has been lost). • Migration of monocytes and smooth muscle cells into the intima.

  11. Smooth muscle cell proliferation in the intima with ECM production. • Well-developed plaque

  12. Fatty streak, a collection of foamy macrophages in the intima. A, Aorta with fatty streaks (arrows), associated largely with the ostia of branch vessels. B, Intimal, macrophage-derived foam cells

  13. Plaques vary from 0.3 to 1.5 cm in diameter, but can coalesce to form larger masses

  14. Atherosclerosis Consequences

  15. Atherosclerosis Clinical Complications • Myocardial infarction (heart attack) • Cerebral infarction (stroke) • Aortic aneurysms • Mesentric occlusion • Peripheral vascular disease (gangrene of the legs)

  16. Morphological changes that are seen on macro and microscopic levels in atherosclerosis • Neovascularization (formation of new blood vessels) • Calcification • Hemorrhage • Fissure • Ulcer • Thrombosis • Medial thinning • Cholesterol microemboli • Aneurysmal dilatation

  17. Neovascularisation • Calcification • Inflam. cells Elastin membrane destroyed Fibrous cap Cholesterol clefts

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