Atherosclerosis Flashcards

1
Q

Define atherosclerosis

A

accumulation of intracellular and extracellular lipids in the intima of large and medium sized arteries
(arteriosclerosis = smaller sized arteries)

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2
Q

What happens to the arterial walls during atherosclerosis?

A

Thicken and elasticity is lost

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3
Q

What is Monkeberg’s disease?

A

Calcification of the media of large arteries

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4
Q

What is atheroma and what does it consist of?

A

The necrotic core of atherosclerotic plaque.

It consists of dead cells, debris and cholesterol crystals

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5
Q

What are MACROscopic features of atherosclerosis?

A
  • Fatty streaks = lipid deposits in the intima (yellow)
  • Simple plaques = development from fatty streaks (yellow to white)
  • Complicated plaques = calcified
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6
Q

What are MICROscopic features of atherosclerosis?

A
  • Fibrosis
  • Necrosis
  • Cholesterol clefts
  • Disruption of internal elastic lamina
  • Ingrowth of small vessels in adventitia
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7
Q

What are some plaque formation complications?

A
  • Ulceration
  • Thrombosis on plaque
  • Spasms at the site
  • Embolisation
  • Calcification
  • Aneurysm formation
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8
Q

What are some clinical effects of atherosclerosis?

A
  • 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)
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9
Q

What are aneurysms?

A

Local dilations of an artery from weakened arterial wall (elastic tissue destroyed)

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10
Q

What are the 4 proposed theories for Atherogenesis?

A

1) Thrombogenic theory
2) Insudation theory
3) Reaction to injury theory
4) Monoclonal hypothesis

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11
Q

What happens in thrombogenic theory (encrustation hypothesis)?

A

Plaques formed by repeated thrombi

-lipid core derived from thrombi

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12
Q

What happens in insudation theory?

A

1) Endothelial injury
2) Inflammation
3) Increased permeability to lipids from plasma

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13
Q

What happens in reaction to injury theory?

A

Plaques form in response to endothelial injury

  • injury increases permeability and allows platelet adhesion
  • monocytes penetrate endothelium
  • smooth muscle cells proliferate and migrate
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14
Q

What happens in monoclonal hypothesis?

A

Plaques are monoclonal

  • raises question wether they are from benign neoplastic growths
  • could they have a viral aetiology?
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15
Q

What are non-modifiable risk factors for atheroscleorsis?

A
  • Age
  • Gender (women protected relatively before menopause)
  • Genetic predisposition (familial hyperlipidaemia and genetic variations in apoE)
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16
Q

What are modifiable risk factors of atherosclerosis?

A
  • Cigarette smoking
  • Hypertension
  • Hyperlipidaemia
  • Infections (e.g. chlamydia pneumoniae)
  • Obesity
  • Alcohol consumption
17
Q

Describe a unified hypothesis of atherogenesis

A

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

18
Q

How can atherosclerosis be prevented?

A
  • no smoking
  • reduce fat intake
  • treat hypertension
  • decrease alcohol intake
  • regular exercise
19
Q

What are some intervention strategies for atherosclerosis?

A
  • Modify diet
  • Lipid lowering drugs e.g. statins
  • Treat diabetes
  • Thrombolysis