histo cardio Flashcards
atherosclerosis definition
an srteriosclerosis characterised by atheromatous deposits and fibrosis in the inner lining of arteries tunica intima but protrude into vessel lumen
stages of atherosclerosis
- damage to endothelium 2. platelet deposition on damaged tissue 3. endothelial proliferation 4. fibrous cap 5. cholesterol deposits in core 6. plaque enlarges blocking artery
macroscopic description of a atherosclerotic plaque
raised lesion lipid core white fibrous cap
major RF for atherosclerosis
age gender genetics HTN hyperlipidaemia DM smoking
how does multiplicitive effect in atheroclerosis work
2RF- 4x risk 3RF-7x risk
murmer in mitral prolapse
late systolic murmer and mid systolic click
most significant independent RF in atherosclerosis
genetics
how does DM increase atherosclerosis risk
induces hypercholesterolaemia
injury hypothesis of atherosclerosis
Endothelial injury Lipoprotien accumulation (LDL) Monocyte adhesion to endothelium Monocyte migration into intima -> macrophages & foam cells Platelet adhesion Factor release Smooth muscle cell recruitment Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells chronic inflammation and atherosclerosis e.g. metabolic stress
two complications of atheromatous plaque
rupture obstruction
at what point does stenosis cause symptoms
70% occlusion causes stable angina
changes seen in acute plaque change
erosion haemmorhage rupture
effect of a haemmorage into atheroscerotic plaque
increase in plaque size
effect of atherosclerotic plaque rupture
exposure of prothrombotic plaque contents
effect of atherosclerotic plaque erosiion
exposure of prothrombotic sub-endothelial basement membrane
characteristics of a avulnerable atherosclerotic plaque
thin cap many foam cells few smooth muscle cells many inflammatory cell clusters
how does vasoconstriction increase risk of plaque rupture
smaller lumen so greater local mechanical forces
factors increasing risk of plaque rupture by vasoconstriction
adrenergic agonists reduced endothelial relaxins platelet contents
what causes prinzmetal angina
coronary artery vasospasm
what is seen in the first 6 hours after an MI
no histological change
what is seen between 6 and 24 hours after MI
loss of nuclei homogeneous cytoplasm necrosis
what is seen 1-4 days after MI
invasion of polymorphs then macropahges
what is seen 5-10 days post MI
clearing up debris
what is seen 1-2 weeks post MI
granulation tissue restructuring new blood vessels, collagen synthesis