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CR2 > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

Define arteriosclerosis and atherosclerosis.  Describe the risk factors for the development of atheroma and how these may be reduced.  Describe the stages of development of an atheromatous plaque.  Explain the difference between stable and unstable plaques and their different sequelae.

1
Q

What is an arteriosclerosis?

A

General name for atherosclerosis where the arterial wall thickens and loses its elasticity, atherosclerosis is just the most common form

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2
Q

What conditions would lead to arteriosclerosis?

A

coronary artery disease
cerebrovascular disease
peripheral artery disease

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3
Q

What are the 3 stages of development?

A

The 3 I’s - insult, injury, inflammation
insult - endothelial damage where the permeability of it changes to macromolecules
injury - uptake of LDL particles, adhesion and infiltration macrophages
inflammation - SM migration from media to intima, collagen synthesis and plaque hardens forming a fibrous cap and foam cells die

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4
Q

What are the 4 functions of the endothelium?

A

Vasomotor tone - vasodilators/vasoconstrictors
Thrombosis - anti/pro coagulants, platelet inhibitors/activators
Inflammatory factors - leukocytes
Cell adhesion molecules - receptors

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5
Q

how can endothelial damage occur?

A

shear stress
toxic damage
high lipid levels
viral/bacterial infection

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6
Q

What are the different types of lipoproteins?

A 
Chylomicrons
VLDL
IDL
LDL
HDL
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7
Q

What do chylomicrons contain and what apoproteins do they carry?

A

TG

B48 (A,C,E)

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8
Q

What do VLDL’s contain and what apoproteins do they carry?

A

TG

B100 (A,C,E)

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9
Q

What do IDL’s contain and what apoproteins do they carry?

A

TG & cholesterol

B100, E

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10
Q

What do LDL contain and what apoproteins do they carry?

A

cholesterol

B100, E

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11
Q

What do HDL contain and what apoproteins do they carry?

A

Protein

AI, AII

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12
Q

How do macrophages infiltrate?

A

Monocytes bind to the endothelium and cross it to then transform into macrophages. They then accumulate large liquid droplets to become foam cells.

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13
Q

How do LDL’s get uptakes?

A

LDL-receptor mediated endocytosis

via scavenger receptors as modified LDL is not recognised by LDL receptor

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14
Q

How does smooth muscle proliferate?

A

endothelial cells and macrophages release growth factor PDGF
internal elastic lamina breaks down
PDGF is a chemoattractant for SM

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15
Q

What are the types of smooth muscle?

A

Resting contractile

Proliferating which secretes ECM

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16
Q

Where is the most common site for atheroma formation?

A

Carotid artery

17
Q

How can angina be formed from atheroscleroma?

A

An increase plaque volume means stenosis can occur in the lumen leading to angina

18
Q

What is angina?

A

Chest pain due to reduced blood flow to the muscles

19
Q

What can an unstable plaque result in?

A

Plaque can rupture leading to haemorrhages, release of tissue factor, platelet aggregation as collagen becomes exposed

reduces lumen diameter
thrombus formation
MI as may occlude lumen completely

20
Q

What are some unmodifiable RF for an atheromatous plaque?

A

age
sex
family history

21
Q

What are some modifiable RF for an atheromatous plaque?

A 
smoking
hypertension
diabetes mellitus
physical activity
dyslipidaemia
22
Q

What is dyslipidaemia?

A

unhealthy levels of one or more kinds of lipid (fat) in your blood

23
Q

What should total cholesterol levels be for adults?

A

Under 200mg/dl

24
Q

What should LDL, HDL and TG levels be for adutlts?

A

LDL - under 130ml/dl
HDL - over 40 mg/dl
TG - 10-190 mg/dl

25
Q

How can cholesterol be reduced?

A

exercise, diet and drugs

26
Q

What are the treatments for high cholesterol?

A

Modify the risk factors

Statins to reduce plasma lipid levels

27
Q

How do statins work?

A

Inhibit HMG coA reductase to reduce intracellular cholesterol synthesis
increase in lDL receptors
reduce plasma cholesterol

28
Q

What are some complications of atherosclerosis?

A

Coronary artery disease leading to MI and angina

peripheral vascular disease specifically peripheral arterial occlusive disease leading to ulcers, peripheral neuropathy and gangrene

stroke
aneurysm
renal artery stenosis

29
Q

What is PTCA?

A

Percutaneous transluminal coronary angioplasty

minimally invasive procedure to open up blocked arteries allowing blood circulation

30
Q

How is PTCA done?

A

Balloon catheter is threaded into an obstructed area in the artery
Balloon is inflated to stretch arterial wall and squash atherosclerotic plaque
Lumen widened, balloon is deflated and catheter is withdrawn

31
Q

What is the purpose of a stent in an artery?q

A

Maintains the patency of a vessel

32
Q

What is the relationship between density of lipoproteins and their lipid: protein content?

A

Lower density of a lipoprotein means more lipid to protein.

33
Q

How can LDL’s be modified?

A

Entrapped into subendothelial space
Oxidised
Glycation

34
Q

How are LDL’s oxidised?

A

By free radicals

Deoxidised by antioxidants

35
Q

How are LDL’s glycated?

A

By high glucose levels, seen in diabetes mellitus

Glycated LDL’s are more likely to be oxidised

36
Q

How is LDL uptake controlled?

A

Negative feedback
LDL receptors recognise apolipoproteins B100 and so uptake means they accumulate on the inside. This leads to a reduction in LDL surface receptors and therefore uptake.

CR2 (35 decks)

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