Ischaemic Heart Disease/ Atherosclerosis Flashcards
Modifiable risk factors of atherosclerosis
smoking lipid intake BP diabetes obesity sedentary lifestyle
Non-modifiable risk factors of atherosclerosis
age
sex
genetic background
By how much does smoking, hypertension and high cholesterol increase risk
16 times
Changes in epidemiology over the last decade for hyperlidaemia, hypertension, obesity
hyperlidaemia - reduced due to statins
hypertension - reduced to due antihypertensives
obesity - increased
Where does atherosclerosis often occur
- bifurcation of carotid arteries
- origins of subclavian and carotid arteries
- where aorta branches into iliac arteries
- particularly at the inside of bends/ at bifurcations
where is the fat mainly deposited in atherosclerosis
LDL deposit in the sub-intimal space + binds to matrix proteoglycans
Type II lesion
macrophage foam cells in sub-intimal space
Type III lesion
Foam cells accumulate until small pools of extracellular lipid
Type IV lesion
Core of extracellular lipid
Type V lesion
Fibrous thickening - lipid pool with scar tissue over it
Type VI lesion
Fissure and haematoma - when material in plaque hits blood, stimulates a clot
Role of monocyte macrophages in atherosclerosis
foam cell formation
cytokine + GF release (for scar formation)
Source of free radicals (damage DNA + RNA)
Metalloproteinases - cut up collagen
Role of vascular endothelial cells in atherosclerosis
barrier function - eg. to lipoproteins
leukocyte recruitment
Role of platelets in atherosclerosis
thrombus generation
cytokine + GF release
Role of vascular smooth muscle cells in atherosclerosis
Migration + proliferation
collagen synthesis
remodelling + fibrous cap formation
Role of T cells in atherosclerosis
Macrophage activation
why are high risk of atherosclerosis patients injected with antibodies to IL-1
cholesterol crystal formation triggers inflammation - injected patients have lower risk of CVD event
what is atherosclerosis
inflammatory disease of the arteries that cause most heart attacks/ strokes
What is low density lipoprotein
‘bad’ cholesterol - synthesised in liver - carries cholesterol from. liver to body (need some - usually it is in excess so seen as bad)
what is high density cholesterol
‘good’ cholesterol - carries form peripheral tissues back to liver - reverse cholesterol transport
Oxidised/ modified LDL
free radicals + LDL = family of highly inflammatory + toxic form of LDL found in vessel walls
Why are oxidised/ modified LDL bad
Oxidised/ modified LDL gets phagocytosed by macrophages = become foam cells + stimulates chronic inflammation
What is familial hyperlipidaemia
autosomal dominant - massively elevated cholesterol due to a failure to clear LDL (liver has lost receptors to take it back in)
what is a macrophage scavenger receptor
expressed on macrophages and they bind and internalise modified forms of LDL in blood vessel
