Atherosclerosis Flashcards
How does hypertension increase changes of atherosclerosis?
leads to a higher chance of endothelial injury due to greater pressure within the aorta e.g. aneurysm
How does impaired glucose tolerance lead to higher chance of atherosclerosis
more circulating glucose –> lipoproteins leading to greater risk of atheroma
How does age lead to increased risk of atherosclerosis?
thickening & hardening of artery walls
How does gender affect chances of developing atherosclerosis?
women > male esp. post menopause
How does hyperlipidaemia lead to increased chances of atherosclerosis
high LDL, carry cholesterol to body cells from liver
How does alcohol lead to increased chances of atherosclerosis?
increased risk of ischaemic heart disease (IHD) - fatty liver
How does apolipoprotein E genotype lead to increased chances of atherosclerosis?
linked to LDL levels
How does familial hyperlipidaemia lead to atherosclerosis?
genetic, early development of atheroma
How does haemodynamic stress lead to atherosclerosis?
Means that certain areas of body are more likely to develop atheroma
How does infection increase the chances of atherosclerosis?
e.g. chlamydia: secretes cytokines & cause inflammatory response to endothelial cell injury
can also be caused by helicobacter pylori & cytomegalovirus
What are the epidemiology of atherosclerosis?
smoking, hypertension, impaired glucose tolerance, age, gender, hyperlipidaemia, alcohol, apolipoprotein E genotype, familial hyperlipidaemia, haemodynamic stress, infection
What are the preventions of atherosclerosis?
stop smoking, decrease fat intake, treat hypertension, aspirin, sensible alcohol intake, regular exercise & control of weight, treat D.Mellitus, Lipid lowering drugs where needed
How does stoping smoking prevent atherosclerosis?
prevents endothelial damage from the toxins in cigarettes
How does decreasing fat intake prevent artherosclerosis?
reduce LDL & cholesterol circulating
How does treating hypertension prevent atherosclerosis?
prevents aneurysm
How does taking aspirin help prevent atherosclerosis?
prevent aneurysm
How does sensible alcohol intake prevent atherosclerosis?
prevents liver damage (fatty liver) prevent atheroma through LDL circulating or blocking function of liver
How does regular exercise & control of weight prevent atherosclerosis from forming?
reduce cholesterol
How does treating D.M. prevent atherosclerosis?
lower levels of circulating glucose & lipids
How does lipid lowering drugs where needed prevent atherosclerosis?
prevent accumulation - preventing formation of atheroma
How does smoking increase the chances of atherosclerosis?
toxins from cigarette smoke can lead to endothelial injury
What are the cells involved in atherogenesis?
endothelial cells: line arteries, altering permeability to lipoproteins
platelets: aggregate, migration of SM cells (PDGF)
SM cells: take up LDL –> foam cells (collagen synthesis)
Macrophage: become foam cells
Neutrophils: secrete proteases (break down proteins) –> continued local damage + inflammation
What is the monoclonal hypothesis?
1 smooth muscle cell gives rise to all smooth muscle cells
What is the lipid oxidation hypothesis?
antioxidants help prevent atherosclerosis
atherosclerosis is from oxidative damage from oxidised LDL - inhibited by antioxidants
What is insudation hypothesis?
LDL is taken up endothelial cells (receptor mediated) and transcytosed into CT underneath and taken up by macrophage (foam cell)
so when there is endothelial damage, inflammation leads to increased permeability of lipid from plasma
What is the encrustation hypothesis?
SM cells react to thrombi + lipids that aren’t associated with vessel walls
(mural thrombi (not in contact with vessel walls) is organised to lead to formation of plaques)
What causes and what happens when there is endothelial damage?
hypercholestrolaemia leads to endothelial damage
plaques form in response
injury increases permeability - allowing platelet adhesion
monocytes penetrate endothelium to become macrophage
SM cells prolife + migrate
Response to injury hypothesis
SMC proliferation induced by growth factors e.g. PDGF
repetitive injury to endothelial cells lead to release of GF
GF stimulates inflammatory cells + macrophage + SM cells to release more GF
leading to increased SM cell proliferation –> atherosclerosis
What is the unifying hypothesis to atherosclerosis?
endothelial injury –> platelet adhesion, releasing platelet derived growth factor, SMC prolife + migrate, becomes foam cells (taken up oxidised LDL), foam cells secrete cytokines, leading to further SMC stimulation (prolife + migrate) and recruitment of other inflammatory cells
monocytes migrate to intima, SMC produce matrix
