Nov22 M2-Pathology - Atherosclerosis Flashcards
ats composition
soft granulous necrotic core + thick fibrous cap
ats step 1
endoth injury: lets lymphocytes, macrophages, monocytes through
ats step 2 (after macrophages in)
are activated, secrete ECM and induce other cells to do so. LDL gets in intima, oxidized and taken up by activated macrophages
ats step 3
macrophages activated form foam cells
ats step 4
SM cells, normally contractile, become synthetic: mitosis + make ECM + move from media to intima
ats step 5
SM cells activate macrophages, take lipids and form foam cells
foam cells origin
from macrophages and SM that take cholesterol (LDL)
why calcification in ats sometimes
SM (now synthetic) can become chondrocytes, deposit Ca, calcification
effect of ats on platelets
aggregate and adhere bc endoth dysfunctional now
fatty streaks cause
when both SM and macrophages take cholesterol
what causes stenosis
thickening of intima
fibrotic cap name + origin
atheroma. origin is ECM from SM
what’s found in center of atheroma
CH esters, lipid debris
fibrous cap components
SM cells, inflam cells, collagen, elastin, proteoglycans, new vessels
necrotic center composition
cell debris, cholesterol crystals, foam cells, calcium
vulnerable plaque def
big lipid core, thin fibrous cap. likely to rupture
stable plaque def
thick fibrous cap, less lipid core: less likely to rupture
inflam in vuln vs stable plaque
stable less inflammed
why vuln plaque can rupture
lot of inflam, macrophages’ metalloproteinases, thin fibrous cap
consequence of cap rupture
thrombus formation (core is very thrombogenic)
complicated plaques
fissures, erosion, ulceration, calcification, thrombus, rupture
pathophgy of aneurysm and rupture
thick cap and core, SM atrophy
thrombotic stroke def
ulceration, rupture and thrombus or hemorrhage in plaque cause narrowing of lumen
ats risk factor not usually covered
homocysteine mild elevation (can cause endoth damage and promote thrombosis)
