Pathophys of Athero

Question 1

Which areas of the vasculature are more likely to develop plaque?

Answer 1

Bends and branch points with low shear force and turbulence

Ex: lesser curvature of the aortic arch, ostia, bifurcations

Question 2

3 hemodynamic predispositions to athero

Answer 2

Low endothelial shear forces
Activation of pro-atherogenic gene expression by endothelial cells
Loss of endothelial cell alignment and increased permeability

Question 3

Foam cells

Answer 3

Monocytes that engorge on lipids become macrophage foam cells
Elaborate inflammatory cytokines and chemokines
Express unregulated scavenger receptors that mediate modified LDL to the point of self destruction

Question 4

How do smooth muscle cells change in atherogenesis with endothelial dysfunction?

Answer 4

Increased contractile mediators (endothelin, AII)
Decreased vasodilatory mediators (prostacyclin, NO)
Inflammatory mediators are produced (IL-6, TNFa)

Question 5

How is thrombus formation promoted?

Answer 5

Endothelial dysfunction causes cells to become less resistant to PLT aggregation/thrombin formation
Plaque disruption exposes factors to blood to promote thrombus

Question 6

Characteristics of a vulnerable plaque

Answer 6

Large lipid/necrotic core
Few SMC (thin fibrous cap and little ECM)
Many foam cells
Substantial amount of plaque