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CR 2 > Atheroscleorosis > Flashcards

Atheroscleorosis Flashcards

1
Q

What are the three stages of development of atherosclerosis?

A

1) Endothelial damage
2) Uptake of modified LDL particles and adhesion and infilitration of macrophages
3) Smooth muscle proliferation

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2
Q

Name 3 functions of the endothelium

A

1) Maintaining vasomotor tone
2) Regulation of thrombosis- provides receptors for procoagulatants and anticoagulants. Usually the latter
3) Inflammatory factors

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3
Q

What is main vasodilator/ vasoconstrictor in endothlium?

A 
Vasodilator= NO/ PG12
Vasconstriction=  Angiotensin and endothelin
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4
Q

Name 4 ways that the endothelium can be damaged

A

1) Shear stress
2) Infection
3) Toxic damage
4) Hyperlipedemia

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5
Q

What is meant by shear stress?

A

Turbulent flow causing damage

Usually in medium/ large branching arteries

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6
Q

Describe make up of chylomicron

A

50% protein and 50% fat

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7
Q

Role of VLDL

Where is it synthesised?

A

Carries fat from the liver to cells

Synthesised in the liver

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8
Q

Role of IDL

A

Breaks down product of VLDL

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9
Q

Role of LDL

A

Transports fat from cells to blood vessels

BAD

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10
Q

Role of HDL

A

Transports fat from blood vessel to liver

GOOD

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11
Q

The lower the density of lipoprotein….

A

MOre lipid it contains relative to protein

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12
Q

How does damage to the endothelium change the way lipoproteins are uptaken?

A

LDLs can become trapped in subendothelial space when there is substantial damage

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13
Q

What happens when one lipoprotein is trapped

A

Attracts more and undergoes oxidation

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14
Q

What facilitates oxidation of trapped lipoproteins

A

Free radicals

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15
Q

When is glycation of trapped lipoproteins more likely

A

Patients with diabetes

HIgher circulating glucose means glycated LDL

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16
Q

Is glycated LDL more or less likely to be oxidised

A

More

17
Q

How does oxidation of lipoproteins lead to monocyte adhesion

A

Oxidised LDL stimulates expression of inflammatory mediators

Adhesion molecules of monocytes

18
Q

What happens to monocytes when they move into subendothelial space

A

Transformed into macrophages

19
Q

How do macrophages behave in subendothelial space

A

Try to absorb LDLs and accumulate forming foam cells/ fatty streaks

20
Q

Describe normal regulation of LDL uptake

A

LDL-receptor mediated endocytosis
Receptor recognises apolipoprotein B100
B100 is allowed into the cell
Negative feedback occurs as internal accumulation of LDL reduces the number of LDL surface receptors

21
Q

How is regulation of LDL uptake different when LDL are modified

A

Not recognised by LDL receptors
Uptaken by scavenger receptor
No negative feedback- uncontrolled

22
Q

What happens to fatty streak?

A

Matures into a plaque

23
Q

How do endothelial cells respond to a plaque?

A

Endothelial cells and macrophages release growth factors that cause proliferation of smooth muscle in intima
This leads to collagen production and atrophy of internal elastic lamina

24
Q

How does the body try to contain the plaque

A

With a collagen fibrous plaque

25
Q

What is meant by a stable plaque

A

Slow growing plaque embedded in collagen.
Can block vessel
Eg- stable angina

26
Q

What is meant by unstable plaque

A

Fragile cap ruptures
Haemorrhages and release tissue factor
Collagen is exposed leading to platelets leading to a clot

27
Q

Name 3 unmodifiable risk factors for atheroscelorsis

A

Age
Family History
Sex

28
Q

Name 5 modifiable risk factors for atherosclerosis

A 
Dyslipidaemia
Smoking
Hypertension
Diabetes
Physical activity
29
Q

What is meant by homocysteinaemia

A

Too much of the amino acid cysteine increases oxidative stress
Emerging risk factor for atherosclerosis

30
Q

Why is lipoprotein a thought to be an emerging risk factor?

A

It is more easily retained in the vessel wall

31
Q

How do statins work?

A

inhibits hmg cOA
reduces intracellular cholesterol
Increase in LDL receptors
Reduces plasma cholesterol

32
Q

What is contained in polypill?

A

Statin, thiazide, BB, ACE inhibitor

CR 2 (33 decks)

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