atherosclerosis + MI Flashcards
define atherosclerosis
changes of vessel layers over decades.
normal healthy artery
in to out:
- intima - thin endothelial cell layer (non stick)
- media
- adventitia - connective tissue sheath
atherosclerotic plaque
smooth muscle cells migrate from media to intima to produce ECM and form fibrous cap.
macrophages have engulfed lipids and produces a pool of lipoproteins = necortic core.
thinned media, thick intima
intimal injury (active endothelial cells)- results
platelet adhesion.
monocyte (WBC) recruitment - become macrophages in tissue which become foam cells once their cytoplasm is filled w lipid material
smooth muscle migration + production ECM = fibrous cap
monocytes
type of WBC that become macrophages once migrated into tissue.
have a high affinity for LDL, become foam cells
produce proteases that destabilise ECM = fibrous cap destruction
stimulate proliferation and migration of SMC to intima
lymphocytes
mostly T cells
secrete cytokines which influence lipoprotein accumulation in plaque
stimulate proliferation + migration of SMC (like monocytes)
stable plaque
thick fibrous cap with dense collagen fibre
relatively small lipid core
minimal inflammatory cells
unstable/vulnerable plaque
thin fibrous cap
lots of inflammatory cells
large lipid core
clinical phase of atherosclerosis
aneurysm and rupture
occlusion by thrombus
critical stenosis
risk factors atherosclerosis
age - older
men have them more, women die of them more
hypertension - rupturing
hypercholesterolemia
DM - increased calcification of plaques
smoking
obesity
family hx
lifestyle
social deprivation
prior CVD
LV blood supply
all 3 arteries:
left - LACx
front - LAD
back and right - right CA
coronary artery lesions - clinical presentation
angina pectoris (severe referred chest pain from heart)
MI - severe sustained BF occlusion = ischemia of cardiomyocytes
cardiac arrhythmia - abnormal/irregular rhythm of heart beat
early MI
after 2 hours there is necrosis in the inner part of the endocardium.
necrosis starts further from occluded BV since its harder for blood to get there
right chronic heart failure
pumps to pulmonary circuit = perfusion pressure changes
congestion of peripheral tissues
backflow effect on R ventricle from not being able to push blood to the lungs
left chronic heart failure
pumps to systemic circuit = decreased cardiac output
backflow into LV, in pulmonary veins coming in to LV (fluid leaks from pulmonary capillaries and accumulates in the blood brain barrier = pulmonary edema)
