atherosclerosis Flashcards
what is arteriosclerosis
hardening of arterioles. effects arterioles in body especially kidney. occurs In diabetes and hypertension
what is atherosclerosis
plaques form in arterial wall, filled with atheroma. then often calcify
what is atheroma
necrotic glue like material
how does an atherosclerotic plaque form
- chronic endothelial adult from hyperlipidaemia, hypertension, smoking or haemodynamic factors= endothelial dysfunction. leads to platelets, growth factors and cytokines
- oxidised lipids accumulate in the intima and are engulfed by macrophage = foam cells.
- causes bulge and smooth muscle cells begin to migrate from the media and proliferate = FATTY STREAK
- plaque grows as muscle cells increase. roof formed over plaque by muscle cells, collagen and elastin.endothelium stretches over plaque and holes appear= more platelets attracted.
- cells at centre die = necrosis. dead cells release cholesterol seen as cholesterol clefts under microscope
morphological appearance of atherosclerosis over time (macroscopic)
- fatty streak (flat, no disturbance to blood flow)
- simple plaque (white/yellow and impinges lumen)
- complicated fatty streak
complications of atherosclerosis
ulceration - fibrous cap eroded= plaque core exposed. v thrombogenic
thrombosis- if ulcerated often occludes vessel
spasm at site of plaque- by vasocontrciters of thrombi
embolism
calcification - makes even stiffer
haemorrhage - of new vessel in plaque (weak) may cause occlusion
aneurysm - because elastic tissue around plaque destroyed
rupture of atherosclerotic artery -= bleeding. occurs when weekend media
microscopic appearance of atherosclerotic plaque over time
inflammatory cells foam cells proliferation of smooth muscle cells extracellular lipid deposition fibrosis necrosis cholesterol clefts disruption of elastic extension into media ingrowth of blood vessels plaque fissuring (splits open)
effects of atherosclerosis
heart - MI, arrhythmia, cardiac failure, abdominal aortic aneurysm
brain- TIA, cerebral infarction and ischameia
kidneys - hypertension and renal failure
legs - peripheral vascular disease, gangrene
bowel - mesenteric ischaemia, bowel infarction, ischameic colitis
common sites for atherosclerosis
aorta (especially abdominal) coronary arteries carotid arteira cerebral arteries leg arteries
what is the response to injury hypothesis
atherosclerosis= chronic inflammatory response of arterial wall because injured endothelium =. progresses due to interaction between modified lipoproteins, macrophages, T lymphocytes and cells of arterial wall
encrustation hypothesis
thrombi over thrombi. lipid core derived from thrombi
monoclonal hypothesis
found that some plaques are monoclonal and some olgocolocnal. are plaques benign neoplastic growths? BUT normal arteries are colonel = unpopular opinion
what is the lipid oxidation hypothesis
oxidation of LDL responsible for atherosclerosis. this is actual reason for it
risk factors contributing to atherosclerosis
smoking - damages blood vessels = increased chance of thrombosis and lipid oxidation
hypertension - damages blood vessel walls
impaired glucose tolerance
age
gender - more common in men but prevalence increases after women hit menopause
hyperlipidaemia- increases cholesterol
alcohol
apolipoprotein E genotype - high LDL levels
familial hyperlipidaemia - defect in LDL receptor= more LDL. often have MI before 20
geography - to do with diet
infection - chlamidia pneumonie - increases risk of atherosclerosis
diabtes
obesity - causes hypertension, diabetes, hypertriglycaridiaemia, reduced HDL
prevention of atherosclerosis
should begin in childhood low fat, high fibre diet to increase HDL and decrease LDL no smoking control hypertension control weigh and regular exercise sensible alcohol treat diabetes aantioxidants e.g vitamin E may be protective
