Atherosclerosis Flashcards
Define atherosclerosis
Accumulation of lipid in the intima and media of medium and large sized arteries
Name some factors that predispose to atherosclerosis
Age Sex Ethnicity Smoking Hyperlipidaemia Obesity Lack of exercise Alcohol Diabetes Infection
Name 6 cell types involves in atherosclerosis
Endothelial cells Platelets SMCs Macrophages Lymphocytes Fibroblasts - cap Neutrophils
What kind of arteries does atherosclerosis commonly form in (2)?
Elastic - e.g. aortic (particularly abdominal)
Medium-large muscular - e.g. coronaries
What is arteriosclerosis? Where does this often occur?
Hardening of arterioles - particularly around kidney e.g. in hypertension or diabetes
What is Monkebergs disease?
Rate disease where there is calcification of the media of large arteries
What is atheroma?What is it made up of?
Necrotic core of the plaque
Dead cells debris and cholesterol crystals
How can an atherosclerotic plaque be complicated/complex (8)?
Form: Ulceration Spasm Embolisation Thrombus Aneurysm Calcification Haemorrhage Rupture
What is an aneurysm?
Local dilation of an aftery due to weakening of the arterial wall. Large arteries mostly due to atherosclerosis
What is a dilation of a vein called?
Varices
What are some of the less obvious modifiable risk factors that contribute to atherosclerosis?
Chlamydia pneumoniae or CMV
Why is prevention key with atherosclerosis?
As its normally silent until plaque becomes complicated then it may be too late
What are the 5 stages of plaque development?
1) Endothelial insult
2) Foam Cells
3) Fatty Streak
4) Plaque with cap
5) Mature plaque
What occurs in endothelial insult?
E.g. due to hyperlipidaemia, hypetension, other haemodynamic effects that cause damage to the endothelium
What occurs in the making of foam cells?
LDLs lipid droplets can cross endothelium - become oxidised in intima
Oxidised LDLs are phagocytosed by macrophages and they become foam cells
Fatty streak
Crowded foam cells make endothelium bulge
SMCs migrate and begin to proliferate in intima
Plaque with cap
SMCs also take up LDLs and become foamy, and some lay over plaque but under endothelium forming a roof. roof reinforces with collagen, elastin and other matrix proteins = fibrous cap
Stretching of endothelium creates gaps - gaps recruit platelets.
Mature plaque
Centre cells of plaque die and necrosis develops
Dead cells release cholesterol - forms cholesterol crystals inside cell
Angiogenesis from the adventitia
Calcification
What prevention mechanisms is there for atherosclerosis?
Diet - low sat fats to reduce LDLs
Stop smoking
Moderate alcohol
Control weight and do exercise
Antioxidants e.g. vit E may be protective
Control hypertension
Treat diabetes mellitus
What lipid lowering therapeutics are there/other treatments?
Statins
Aspirin prophylaxis
Thrombolysis
Angioplasty
Stents
CABG
What 5 major organs can be affected by complications of atherosclerosis? What can occur at each?
Brain - TIA, multiple infarct dementia Kidney - HTN, renal failure Bowel - infarct/iscahemic colitis Heart - Angina/MI/Death/arrhythmias etc Legs - peripheral arterial disease -gangrene
What 3 major things are in plaques?
- Cells (SMC/macrophages/platelets)
- Intra and Extracellular lipid
- Extracellular matrix - collagen, elastin and proteoglycans
What are three historical theories about atherosclerosis development?
1) Reponse to injury - chronic inflammation involving T cells
2) Encrustation of thrombus over thrombus
3) Benign tumour of monoclonal content e.g. induced by virus
Which cells take up lipid in a plaque (2)
SMCs and macrophages
