atherosclerosis Flashcards
what is atherosclerosis?
appearance of soft material and its deposition—> resulting in stiffening vessels
LESION formation in INTIMA of larger arteries
layers of a vessel?
tunica externa= OUTERMOST layer, collagen and elastic
tunica media= middle layer, SM and elastic (vasoconstricts and dilates)
tunica intima= INNERMOST, simple squamous, reduce friction
where does atherosclerosis occur?
in arteries in INTIMA or vessel—>
lesion STRETCHES vessel wall and slowly CLOSES off LUMEN
process of atherosclerosis?
50% patency of lumen, compromised perfusion—> ISCHEMIA—> infarction (necrosis from ischemi)
ischemic pain!
what is the lesion known as?
atheroma (deposited in vessel wall not lumen!)
-made of fat and fibrous tissue “fibro-fatty lesion”
the tissue _____ to the occlusion suffers damage?
distal to the occlusion—> PVD, MI, Stroke
what are the 3 stages of lesion?
1) fatty streak
2) calcification
3) complicated lesion
what is the fatty streak stage?
discolouration of wall in vessel (yellow streak)
- macrophages, lipids, foam cells
- pt asymptomatic
what is the calcification stage?
-accumulation of calcium crystals from necrotic cells
-scar tissue forms on vessels
“clinical lesion” presents with manifestations
what is the complicated lesion?
hemorrhaging into plaque (bleeding into lesion), develops into a thrombus (blood clot)
pathogenesis of atherosclerosis (4 things)
- endothelial cell injury
- migration of inflammatory cells
- lipid accumulation and smooth muscle cell proliferation
- plaque structure
endothelial cell injury..
-late 20s, early 30s subtle changes begin in endothelial lining in vessels (vasc epithelial w single layer of cells that protect)
risk factors: smoking, increased levels of LDL, immune mechanisms and mechanical stress associated with HTN
CRP levels increase, serum marker of inflammation but increased CRP with no inflammation may also indicate atherosclerosis
migration of inflammatory cells?
monocytes and other inflammatory cells adhere to epithelium and migrate from endothelial cells to intima
—> transform into macrophages
lipid accumulation and smooth muscle cell proliferation?
activated macrophages release toxic oxygen species that oxidize lipids (mostly LDL) forming free radicals that damage the wall of vessels, attracts platelets
- —> clot inside lumen forms
- –> macrophages engulf oxidized lipids to become foam cells; this is protective because it removes excess lipids from circulation BUT leads to lipid progression
- —> FOAM cells release growth factors that contribute to SM cell proliferation and migrate from smooth muscle layer to INTIMA
plaque structure?
an atheroma forms = atherosclerotic plaque
- aggregation of smooth muscle cells, macrophage, other WBC, collagen, elastic fibers
