basic science Flashcards
Describe the main cell of athero
Foam cells –> macrophages
stages of athero
fatty streaks–> foam cells within aorta—>lipid core free cholesterol esters—>
mature athoro plaqus –> fibrous cap is smooth mucle cells and collegens produced by them
Plaque mineralizes –> circulating osteoprogenitor cells find
hydroxyapotite crystals
athero why at bifurcations
nonlaminar flow lowering shear stress so adehsion can happen (less forces taing away)
glagovs remodeling concept
artery exands and lumen doesnt changes. –> limit in amount the overall artery can expand then plaqye impinges
ACH response
normal - mod vasodil
athero - vascocaonstriction –> the hallmark of endothelial dysfunction
endothelial independent (direct and metab) and endothelium dependent
independent
direct No donors
-NO gas
Na Nitroprrusside
NO donors req metabolism
-NTG
ISDN
amlnitrate
dependent
-ACH
what is the general process of acute plaque rupture
Thin cap fibroatherom (thrombogenic lipid rich core underneath it)–> the cap ruptures and exposes the core to blood which then forms a thrombus.
What is in the fibrous cap
sm cells making ecm (collagens and elastins)
infammatory calls in athero
key cell is macrophage that turn into foam cells
where do plaques tend to rupture
sholder region
3 triggers of plaque rupture
- emotional stress
- Physcial activity
sympathetic tone.
POBA response hyperplasia
stent
medial
stent-> neointimal hyperplasia
loss index
late loss/acute lumen gain
When does neointimal hyperplasia occur\\
- neointimal hyperplasia what is it?
mostly in first 6 months
- sm cells–> 3 maj
3 major predictors of ISR (pre des)
small stent size (esp 2.5)/MLD
DM
Length
