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6 Cards in this Set

  • Front
  • Back

Arteriosclerosis

= thickening & loss of elasticity of arterial walls




- Mönkeberg medical calcific sclerosis - muscular arteries, do not encroach vessel lumen


- Arteriolosclerosis - small aa.'s, narrowing of lumen, downstream ischemia (HT, DM)


- Atherosclerosis - large aa.'s, localized thickening of the wall, lumen narrowing

Atherosclerosis

= wear & tear of large arteries; chronic inflammatory disease, large aa.'s, progresses w/ age until symptomatic; endothelium injury -> progression


- fatty streak = foam cells in intima as a result of a lesion


-> atheroma(tous core): intimal thickening, lipid accumulation


-> fibroatheroma (cap): collagen production, fibrofatty plaque


-> complications: calcification, ulceration, thrombosis, hemorrhage, rupture (-> symptomatic in aa.'s of heart, brain, kidneys, legs)


=> blood flow obstruction, atheroemboli, thrombosis, aneurisms

Atheroma

= atherosclerotic plaque

Plaque

= atherosclerotic fatty accumulation in large aa.'s




- stable - dense fibrous cap, minimal lipid accumulation, little inflammation


-> chronic ischemia


- unstable - thin cap, large lipid core, dense inflammatory infiltrates


-> sudden & potentially fatal ischemia

Response to Injury hypothesis


progression sequence in atherosclerosis

- Endothelial cell injury -> (hemodynamic disturbances, hypercholesterolemia ->) dysfx - vascular permeability, thrombosis


- Accumulation of lipoproteins in vessel wall


- Monocyte adhesion to endothelium -> intima -> macrophage, foam cell


- Platelet adhesion -> factor release -> SM cell recruitment


- SM cell proliferation, extracellular matrix production, T cell recruitment


- Lipid accumulation

Risk factors for


Atherosclerosis

Family history


Genetic abnormalities


Increasing age


Male gender (estrogen?)


Hyperlipidemia - ↑ cholesterol, LDL, ↓ HDL


HT, Diabetes


Cigarette smoking


Inflammation, C-reactive protein - produced by liver, predicts CV risk