Flashcards in Atherosclerosis Deck (40):
differences in cardiovascular disease prevalence
race and gender, as well as environmental factors
normal vessel wall composition
intima, media, adventitia
endothelium and ECM
inner/outer elastic lamina, SM, ECM,
vasa vasorum, CT
specialization in blood vessels arose from
aorta/brances. Have media with alternating layers. elastic lamina and smooth muscle
smaller aorta branches. mainly SMC, regional flow controlled by the SMC
in CT of organs. Media, regulate flow resistance
states of endothelial cells (3)
constitutive activities, endothelial activation, dysfunction
normal functions for homeostasis
response to stimuli - adhesion molecules, cytokines, coag factors: DOES NOT REQUIRE DENUDING
large amount of inducer exposure- hyper coag, ROS, thrombosis
not able to function correctly!
smooth muscle cells proliferate under
SMC synthesize what?
ECM collagen, elastin, proteoglycans
effect of endothelial injury on SMC
stimulates growth and synthesis in INTIMA (not supposed to be there!) these cells do not contract, leading to stiff lumen
hardening of arteries, three types; atherosclerosis, monckeberg arteriosclerosis, arteriolosclerosis
lg/med arteries. lipid deposits in tunica intima. Most common
calcification of periferial muscular arteries MEDIA. little lumen encroachment . (pipe stem arteries) common in legs of elderly
small, usually related to HTN/DM
pathogenesis of arteroosclerisis
chronic inflammation response to injury. lesion progression, lipoproteins, mphage, T lymph
stages of arteriosclerosis
intimal cell mass (NO LIPID), fatty streak (foam cells, no flow issues), lipid plaque (atheroma- raised within intimate, fibrous cap- may lead to stenosis
clinical complications (4)
rupture/ulceration, hemorrhage into a plaque atheroembolism, aneurysm
aneurysm vs disection
dilation vs surfas defects. both have risk of rupture/thrombus.
causes of endothelial injury (3)
hemodynamic disturbance, lipids, inflammation
hemodynamic disturbance and endothelial injury
turbulent blood flow at OSTIA, branch points, bifurcation, results in plaque and calcification
lipids and endothelial injury
plaques are filled with cholesterol
inflammation and endothelial injury
macrophages create foam cells, T cells in intima lead to inflammation, measure CRP!
principle plaque components
Cells (SM, macrophage, T cell), ECM, lipid (intra and extra)
crystallization of cholesterol
problem with stable plaques
70% fixed occlusion
two main causes of AA
atherosclerosis and hypertension (also Marfan, ED)
small, diabetes and hypertension, walls thicken, lumen narrows> perfusion of organs (Kidney)
severe hypertension, onion skin of arteriole wall, narrowing of lumen
intimal cell mass
first step in lesion, SM, ECM, no lipid.
stable vessels have
dense cap! but more stenosis!
weakness of ALL THREE LAYERS
direction pushes apart layers of?