Atherosclerosis Flashcards
(19 cards)
Define atherosclerosis
accumulation of intracellular and extracellular lipids in the intima of large and medium sized arteries
(arteriosclerosis = smaller sized arteries)
What happens to the arterial walls during atherosclerosis?
Thicken and elasticity is lost
What is Monkeberg’s disease?
Calcification of the media of large arteries
What is atheroma and what does it consist of?
The necrotic core of atherosclerotic plaque.
It consists of dead cells, debris and cholesterol crystals
What are MACROscopic features of atherosclerosis?
- Fatty streaks = lipid deposits in the intima (yellow)
- Simple plaques = development from fatty streaks (yellow to white)
- Complicated plaques = calcified
What are MICROscopic features of atherosclerosis?
- Fibrosis
- Necrosis
- Cholesterol clefts
- Disruption of internal elastic lamina
- Ingrowth of small vessels in adventitia
What are some plaque formation complications?
- Ulceration
- Thrombosis on plaque
- Spasms at the site
- Embolisation
- Calcification
- Aneurysm formation
What are some clinical effects of atherosclerosis?
- Ischaemic heart disease (e.g. sudden death, MI)
- Cerebral ischaemia (e.g. cerebral infarction)
- Mesenteric ischaemia (e.g. intestinal infarction)
- Peripheral vascular disease (e.g. gangrene, Leriche syndrome)
What are aneurysms?
Local dilations of an artery from weakened arterial wall (elastic tissue destroyed)
What are the 4 proposed theories for Atherogenesis?
1) Thrombogenic theory
2) Insudation theory
3) Reaction to injury theory
4) Monoclonal hypothesis
What happens in thrombogenic theory (encrustation hypothesis)?
Plaques formed by repeated thrombi
-lipid core derived from thrombi
What happens in insudation theory?
1) Endothelial injury
2) Inflammation
3) Increased permeability to lipids from plasma
What happens in reaction to injury theory?
Plaques form in response to endothelial injury
- injury increases permeability and allows platelet adhesion
- monocytes penetrate endothelium
- smooth muscle cells proliferate and migrate
What happens in monoclonal hypothesis?
Plaques are monoclonal
- raises question wether they are from benign neoplastic growths
- could they have a viral aetiology?
What are non-modifiable risk factors for atheroscleorsis?
- Age
- Gender (women protected relatively before menopause)
- Genetic predisposition (familial hyperlipidaemia and genetic variations in apoE)
What are modifiable risk factors of atherosclerosis?
- Cigarette smoking
- Hypertension
- Hyperlipidaemia
- Infections (e.g. chlamydia pneumoniae)
- Obesity
- Alcohol consumption
Describe a unified hypothesis of atherogenesis
1) Chronic endothelial insult (e.g. from hypertension)
2) Lipid droplets and monocytes cross endothelium to intima
3) Lipids get oxidised and they get ingested by macrophages = turn into foam cells
4) Fatty streaks start to form as foam cells and smooth muscle cells proliferate and migrate
5) Further growth of fatty streaks lead to development of a plaque
6) Cells in the centre of the plaque die and necrosis develops
How can atherosclerosis be prevented?
- no smoking
- reduce fat intake
- treat hypertension
- decrease alcohol intake
- regular exercise
What are some intervention strategies for atherosclerosis?
- Modify diet
- Lipid lowering drugs e.g. statins
- Treat diabetes
- Thrombolysis
