Atherosclerosis Flashcards

1
Q

Define atherosclerosis

A

Accumulation of lipid in the intima and media of medium and large sized arteries

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2
Q

Name some factors that predispose to atherosclerosis

A
Age
Sex
Ethnicity
Smoking
Hyperlipidaemia
Obesity
Lack of exercise
Alcohol
Diabetes
Infection
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3
Q

Name 6 cell types involves in atherosclerosis

A
Endothelial cells
Platelets
SMCs
Macrophages
Lymphocytes
Fibroblasts - cap
Neutrophils
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4
Q

What kind of arteries does atherosclerosis commonly form in (2)?

A

Elastic - e.g. aortic (particularly abdominal)

Medium-large muscular - e.g. coronaries

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5
Q

What is arteriosclerosis? Where does this often occur?

A

Hardening of arterioles - particularly around kidney e.g. in hypertension or diabetes

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6
Q

What is Monkebergs disease?

A

Rate disease where there is calcification of the media of large arteries

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7
Q

What is atheroma?What is it made up of?

A

Necrotic core of the plaque

Dead cells debris and cholesterol crystals

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8
Q

How can an atherosclerotic plaque be complicated/complex (8)?

A
Form:
Ulceration
Spasm
Embolisation
Thrombus
Aneurysm
Calcification
Haemorrhage
Rupture
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9
Q

What is an aneurysm?

A

Local dilation of an aftery due to weakening of the arterial wall. Large arteries mostly due to atherosclerosis

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10
Q

What is a dilation of a vein called?

A

Varices

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11
Q

What are some of the less obvious modifiable risk factors that contribute to atherosclerosis?

A

Chlamydia pneumoniae or CMV

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12
Q

Why is prevention key with atherosclerosis?

A

As its normally silent until plaque becomes complicated then it may be too late

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13
Q

What are the 5 stages of plaque development?

A

1) Endothelial insult
2) Foam Cells
3) Fatty Streak
4) Plaque with cap
5) Mature plaque

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14
Q

What occurs in endothelial insult?

A

E.g. due to hyperlipidaemia, hypetension, other haemodynamic effects that cause damage to the endothelium

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15
Q

What occurs in the making of foam cells?

A

LDLs lipid droplets can cross endothelium - become oxidised in intima

Oxidised LDLs are phagocytosed by macrophages and they become foam cells

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16
Q

Fatty streak

A

Crowded foam cells make endothelium bulge

SMCs migrate and begin to proliferate in intima

17
Q

Plaque with cap

A

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.

18
Q

Mature plaque

A

Centre cells of plaque die and necrosis develops

Dead cells release cholesterol - forms cholesterol crystals inside cell

Angiogenesis from the adventitia

Calcification

19
Q

What prevention mechanisms is there for atherosclerosis?

A

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

20
Q

What lipid lowering therapeutics are there/other treatments?

A

Statins
Aspirin prophylaxis

Thrombolysis
Angioplasty
Stents
CABG

21
Q

What 5 major organs can be affected by complications of atherosclerosis? What can occur at each?

A
Brain - TIA, multiple infarct dementia
Kidney - HTN, renal failure
Bowel - infarct/iscahemic colitis 
Heart - Angina/MI/Death/arrhythmias etc
Legs - peripheral arterial disease -gangrene
22
Q

What 3 major things are in plaques?

A
  • Cells (SMC/macrophages/platelets)
  • Intra and Extracellular lipid
  • Extracellular matrix - collagen, elastin and proteoglycans
23
Q

What are three historical theories about atherosclerosis development?

A

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

24
Q

Which cells take up lipid in a plaque (2)

A

SMCs and macrophages

25
Q

What role do prostcyclin and thrombomodulin have in normal endothelium?

A

Thrombosis prevention

Thrombomodulin prevents thrombin
(prostacyclins are platelet inhibitors and vasodilators)