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A13THP @ UoN > Atherosclerosis & Lipid Lowering Drugs > Flashcards

Atherosclerosis & Lipid Lowering Drugs Flashcards

1
Q

What is Hypercholesterolaemia?

A

Elevated plasma cholesterol, often leading to Atherosclerosis

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2
Q

What is Atherosclerosis?

A

Focal lesions (plaques) on the inner surface of an artery

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3
Q

What can Atherosclerosis lead to?

A

Ischaemic heart disease (IHD)
Peripheral vascular disease (PVD)
Cerebrovascular disease

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4
Q

What are the non modifiable risk factors for Atherosclerosis?

A

Genetics

Infection (dental)

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5
Q

What are the modifiable risk factors for Atherosclerosis?

A 
Hypercholesterolaemia (raised LDL/lowered HDL)
Hypertension
Smoking
Obesity
Hyperglycaemia
Reduced physical activity
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6
Q

What is dyslipidaemia?

A

Abnormal levels of lipids in the blood

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7
Q

What drugs are known to induce dyslipidaemia?

A 
Beta-blockers
Thiazides
Corticosteroids
Retinoids
Oral contraceptives
Anti-HIV
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8
Q

What are lipoproteins?

A

A group of soluble proteins that transport lipids in the blood

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9
Q

What is the structure of lipoproteins?

A

Central hydrophobic lipid core

Encased in phospholipid, cholesterol & apolipoproteins

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10
Q

What are the four main types of lipoprotein?

A

HDL - High density lipoprotein
LDL - Low density lipoprotein
VLDL - Very low density lipoprotein
Chylomicrons

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11
Q

What are Chylomicrons?

A

Type of lipoprotein that transport TGs/cholesterol from GI tract to the liver
Free FA released
Cholesterol stores/oxidised

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12
Q

What is the function of VLDL?

A

Transports cholesterol/TGs to tissues –> becomes LDL

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13
Q

What is the function of LDL?

A

Transports cholesterol to liver/tissues, taken up by endocytosis

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14
Q

What is the function of HDL?

A

Transports cholesterol from cell breakdown to VLDL/LDL (in liver)

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15
Q

What is the ideal level of cholesterol?

A

<5.0 mmol/L

High HDL:LDL

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16
Q

What are the diagnostic criteria for Hypercholesterolaemia?

A

TC >6.5 mmol/L

High LDL:HDL

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17
Q

What are some diagnostic signs of Hypercholesterolaemia?

A

Xanthoma (cutaneous fatty deposit)
Xanthomata - nails
Xanthelasma - around eyes

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18
Q

What is Atherogenesis?

A

An inflammatory response to injury leading to the development of atheromatous plaques

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19
Q

What are risk factors for damage to the arterial endothelium?

A

Turbulent flow
Smoking
Hypertension

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20
Q

What causes Atherosclerosis?

A

Damage to the endothelium followed by the inflammatory response

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21
Q

What cells make up the inflammatory response in Atherogenesis?

A

Monocytes/Macrophages

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22
Q

What is the main effect of Monocytes/Macrophages in Atherogenesis?

A

Release of Ox radicals

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23
Q

What effect does the release of Ox radicals have on LDL?

A

Converts it to oxLDL

24
Q

What is oxLDL?

A

Oxidised LDL
Damages receptor
Cholesterol accumulates underneath endothelium

25
Q

How do fatty streaks form?

A

Cholesterol rich foam cells forming underneath endothelium

26
Q

What is an atherosclerotic plaque?

A

Cholesterol rich plaque, calcified w/ connective tissue

27
Q

At what point does narrowing of an artery due to an atherosclerotic plaque lead to symptoms?

A

70% occlusion

28
Q

What are the three main stages of Atherosclerotic formation?

A

Damage to blood vessel - inflammation/infiltration
Formation of fatty streaks - deposition of foam cells
Formation of plaques - calcification of cholesterol deposits

29
Q

What are the causes of symptoms in Atherosclerosis?

A

Stenosis (70%) - angina

Rupture of plaque - clot formation/platelet aggregation

30
Q

What are the main treatments for Atherosclerosis?

A

Lifestyle measures/hyperlipidaemia treatments
Angioplasty & stenting
Antiplatelets/clot-busting drugs

31
Q

How is most cholesterol produced?

A

In the liver (70%)

Key enzyme - HMG-CoA Reductase

32
Q

How do Statins work?

A

HMG-CoA Reductase Inhibitors

33
Q

What are the clinically most common Statins?

A

Simvastatin
Atorvastatin
Pravastatin
Fluvastatin

34
Q

What is the effect of Statins?

A

Reduced plasma cholesterol (therefore)

Upregulation of hepatic LDL receptors - LDL uptake

35
Q

In what condition are Statins less effective?

A

Homozygous familial hypercholesterolaemia (cannot make LDL-receptor)
ATORVASTATIN

36
Q

What is the most important metabolic factor of Statins?

A

Hepatoselective - 95% 1st pass metabolism

37
Q

In what conditions are Statins effective?

A

Types IIa & IIb Hyperlioproteinaemia
(LDL & LDL/VLDL)
Heterozygous Familial Hypercholesterolaemia

38
Q

Are Statins effective at reducing CV risk?

A

Yes, even if normal cholesterol

  • Improve endothelial function
  • Reduce atherosclerosis
  • Reduce progression of carotid disease
39
Q

To what patients should Statins be given?

A

Hypocholesterolaemia
Raised LDL
Atherosclerosis
Patients w/ >10% risk of CVD

40
Q

How should Statins be given?

A

At night - increased cholesterol synthesis at night

EXCEPT ATORVASTATIN

41
Q

What is the dosing structure of Statins in patients with low risk of CVD?

A

Low intensity

ie. 20 mg Atorvastatin

42
Q

What is the dosing structure of Statins in patients with high risk/secondary prevention of CVD?

A

High intensity

ie. 80 mg Atorvastatin

43
Q

When should Statins be avoided?

A

Use in care with liver disease - serious risk of dysfunction

Monitor function

44
Q

What is the main ADR of Statins?

A

Myopathy leading to Rhabdomyolysis
1:1000/10,000
Fibrates increase risk
PRAVASTATIN

45
Q

Which drugs interact with Simvastatin?

A 
Contraindication with Macrolides
Interactions
-Amlodipine
-Verapamil
-Diltiazem
46
Q

What Statin can be given OTC?

A

Simvastatin 10 mg

47
Q

Which patients can receive Simvastation OTC?

A 
All males >55
Males 45-55/Females >55 with
-Family history IHD
-Smokers
-Overweight
-S. Asian ethnicity
48
Q

What are Fibrates?

A

Derivatives of fibric acid used to reduce the levels of TGs

49
Q

How do Fibrates work?

A

Activate PPAR-a - alters lipoprotein metabolism

50
Q

What are the effects of Fibrates?

A

Promote breakdown in VLDL
Reduce TGs
Decrease glucose
Reduce IHD (not mortality)

51
Q

What are the adverse effects of Fibrates?

A

Rhabdomyolysis

52
Q

What is Ezetimibe?

A

Cholesterol Absorption Inhibitor

53
Q

How do fish oils affect lipid levels?

A

Contain EPA
EPA competes w/ Arachidonic acid for COX
Reduce TGs/Increase LDL

54
Q

What effect do supplemental Vitamins have on lipid levels?

A

No benefits seen with supplementation

55
Q

What is Sitostanol?

A

A phytosterol that prevents absorption of cholesterol

Reduces LDL 10-15%

A13THP @ UoN (19 decks)

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