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Pharmacology and Therapeutics 2 Y2 > Atherosclerosis and Lipo-Protein Metabolism > Flashcards

Atherosclerosis and Lipo-Protein Metabolism Flashcards

1
Q

Good cholesterol?

A

HDL

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2
Q

Bad cholesterol?

A

LDL

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3
Q

Exogenous lipid metabolism pathway, mention lipase and their products

A

 Exogenous = Absorb fats from the diet

  • Amount of cholesterol taken from diet is negligible
  • Dietary triglycerides and to a smaller extent cholesterol are converted into chylomicrons
  • Lipases break these down leaving FFAs and chylomicron remnants
  • Chylomicron remnants can contribute to atheromas
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4
Q

Endogenous pathway of lipid metabolism? Where does most circulating cholesterol come from?

A

Endogenous = generation of lipids from bodily tissues (mostly the liver)- contributes about 80% of circulating cholesterol

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5
Q

What enzyme converts HDL to LDL

A

Cholesterol ester transfer protein

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6
Q

What does cholesterol ester transfer protein do

A

Converts HDL to LDL

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7
Q

What is REVERSE CHOLESTEROL TRANSPORT

A

A process where cholesterol is taken out of blood vessels and foam cells (smooth muscle cells/macrophages which are full of lipids/cholesterol)

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8
Q

3 stages of atherosclerosis?

A
  1. ENDOTHELIAL DYSFUNCTION
  2. FATTY STREAK FORMATION
  3. FORMATION OF THE COMPLICATED ATHEROSCLEROTIC PLAQUE
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9
Q

What happens during endothelial dysfunction? (4)

A
  • Increased permeability
  • Upregulation of endothelial adhesion molecules
  • Leukocyte adhesion
  • Migration of leukocytes into artery wall
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10
Q

What happens during fatty streak formation? (5)

A
  • Adherence and entry of leukocytes
  • Migration of smooth muscle cells
  • Activation of T cells
  • Adherence and aggregation of platelets
  • Formation of foam cells
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11
Q

What happens during formation of the complicated atherosclerotic plaque? (3)

A
  • Formation of fibrous cap
  • Accumulation of macrophages
  • Formation of necrotic core
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12
Q

What is used to diagnose type of atherosclerotic plaque?

A

Calcium through CT scans

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13
Q

How does calcium relate to CVS risk

A

More calcium = more risk

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14
Q

What are remnant lipids

A

Remnant lipids come from breakdown of the chylomicron- they are glycoprotein containing elements which are atherogenic- increase risk of CHD

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15
Q

What is inflammation in atherosclerosis associated with

A

inflammation is associated largely with remnant cholesterol levels

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16
Q

Is LDL associated with inflammation?

A

No

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17
Q

What is a ‘vulnerable’ atherosclerotic plaque

A

‘Vulnerable’ plaques show a smaller gap between the lumen and the lipid core- this can break under high pressure and cause many problems – travel and cause thrombosis

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18
Q

10% increase in LDL levels results in X% increase in CHD risk

A

20%

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19
Q

How is HDL protective

A

promotes reverse transport and is also antioxidant to an extent

20
Q

What lowers HDL?

A

smoking, obesity and physical inactivity

21
Q

If triglycerides are high, what is the usual implication of HDL levels

A

Low

22
Q

What do statins do to the cholesterol synthesis pathway

A

Statins block HMG-CoA Reductase in the cholesterol synthesis pathway

23
Q

What enzyme do statins block

A

Statins block HMG-CoA Reductase

24
Q

What cells synthesise cholesterol

A

Most

25
Q

What drug targets HMG-CoA Reductase

A

Statins

26
Q

What do statins do to LDL levels in serum

A
  • Reduce amount of cholesterol synthesised in hepatocyte
  • It responds by expressing more LDL receptors on its surface
  • This causes cell uptake of LDL, which removes it from the circulation
27
Q

Most potent statin?

A

Rosuvastatin

28
Q

What is the rule of 6

A

Double the dose of statin to reduce LDL by 6%

29
Q

Pleiotropic effects of statins? (8)

A
  • Platelet activation
  • Thrombotic effects
  • Plaque stability
  • Vascular inflammation
  • SMC hypertrophy
  • Endothelial dysfunction
  • SMC proliferation
  • Vasoconstriction
30
Q

What do fibrates do

A

activation of PPAR alpha receptors

  • They lower free fatty acids and triglycerides
  • They have some similar effects to statins e.g. reduce inflammation
  • PPAR gamma activators are the thiazolidinediones (glitazones) used in diabetes
31
Q

Which group of people benefit the most from fibrates

A

People with high TG, e.g. diabetics

32
Q

What receptors do fibrates activate

A

PPAR - Peroxisome Proliferator Activated Receptors

33
Q

What activates PPAR Peroxisome Proliferator Activated Receptors?

A

Fibrates

34
Q

Effects of nicotinic acid? (4)

A

Lowers LDL, increase fibrinolytic activity, increases HDL, lowers triglyceride etc.

35
Q

Why is nicotinic acid ineffective?

A

Low compliance

36
Q

What does ezetimibe do?

A

Inhibits cholesterol absorption

37
Q

What is the active form of ezetimibe

A

Glucoronide

38
Q

Effectiveness of Ezetimibe?

A

Reduces LDL by 15-20%- not great

39
Q

How to increase Effectiveness of Ezetimibe?

A

Administer alongside statins, makes it not follow the rule of 6

40
Q

CHOLESTERYL ESTER TRANSFER PROTEIN (CETP) INHIBITORs effectiveness?

A

These seemed ideal, but then they were shown by clinical trials to actually increase mortality- not too sure why (this relates specifically to a drug called torcetrapib)

41
Q

What does PROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9 do?

A

Inhibits LDLR which absorbs LDL

42
Q

What effect does statins have on LDLR and PCSK9

A

Increase

43
Q

What so PCSK9 INHIBITORS do? What do they need to be coadministered with?

A

As a result, PCSK9 inhibition enhances the lipid-lowering effects of statins

44
Q

What are the best PCSK9 inhibitors?

A

Monoclonal antibodies

45
Q

What group of people are most in need of PCSK9 inhibitors

A

Familial hypercholesterolaemic patients

46
Q

Problem with PCSK9 inhibitors?

A

Super expensive

Pharmacology and Therapeutics 2 Y2 (24 decks)

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