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Cardiovascular > Lipid Lowering > Flashcards

Lipid Lowering Flashcards

1
Q

Primary prevention of hyperlipidaemia

A

Statins

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2
Q

What is primary dyslipidaemia

A

Dietary and genetic factors
- familial hyper cholesterolaemia (FD)

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3
Q

What is secondary dyslipidaemia

A

Consequence of other conditions
-diabetes, alcoholism, renal disease

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4
Q

Non-pharmacological treatment for dyslipidaemia

A

Cardioprotective diet
Weight loss
Physical activity
Reduce alcohol
Smoking cessation

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5
Q

Lipid lowering drugs (5)

A

HMG-CoA reductase inhibitors
Fibrates
Cholesterol absorption inhibitors
Omega fatty acids
Nicotinic acid

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6
Q

What are statins

A

HMG CoA reductase inhibitors

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7
Q

3 examples of statins

A

Simvastatin
Pravastatin
Lovastatin

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8
Q

What is CoA reductase essential for

A

Cholesterol synthesis

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9
Q

When are statins taken

A

Tablets taken at night because most cholesterol synthesis occurs at night

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10
Q

Statins Pk

A

Short-acting
Oral
Well absorbed

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11
Q

Metabolism of statins

A

CYP3A4 - except rosuvastatin
Glucuronidation
Simvastain and lovastatin given in inactive form

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12
Q

What conversion to statins inhibit

A

HMG CoA —> mevalonic acid

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13
Q

What to statins unregulate

A

LDL receptors - increases LDL clearance from plasma so are taken up by the liver much quicker

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14
Q

Clinical use of statins

A

Primary hypercholesterolaemia (FH)
- Reduce LDL by 30%
- Reduce HDL by 20%
Secondary hypercholesterolaemia
Secondary prevention of MI & stroke

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15
Q

Adverse effects of statins

A

Muscle pain
GI disturbance
Insomnia
Rash
Rarely - angio-oedema

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16
Q

What is a long lasting statin

A

Atrovastatin

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17
Q

Outcomes of statin treatment

A

Improved endothelial function
Improved vascularisation of ischaemic tissue
Atherosclerotic plaque stabilisation
Reduced vascular inflammatory response
Reduced platelet activation
Enhanced fibrinolysis

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18
Q

3 fibrate examples

A

Gemfibrozil
Fenofibrate
Bezafibrate

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19
Q

Fibrate mechanism of action

A

Agonist of PPAR-alpha nuclear receptor that regulates lipid metabolism

20
Q

Fibrate treatment outcomes

A

Increased lipoprotein lipase synthesis
Stimulated fatty acid oxidation
Increased expression of apoA-1 and apoA5 which are involved in HDL synthesis
Increased hepatic LDL uptake

21
Q

Clinical use of fibrates

A

Hypertriglyceridaemia
Mixed hyperlipidaemia (raised TG plus cholesterol)
- TG reduced by 20-30%
- cholesterol reduced by 10-15%
- rise in HDL

22
Q

Fibrate PK

A

Well absorbed from GI
High degree of albumin binding
Metabolised by CYP3A4
Excreted via kidneys

23
Q

Fibrates adverse effects

A

Rash, GI disturbance
Rhabdomyolysis causing renal failure (skeletal muscle breakdown clogs filtration mechanism)
Gall stones (cholesterol sticks together in fall bladder causing blockage)

24
Q

Cholesterol absorption inhibitor example

A

Ezetimibe

25
Q

Ezetimibe mechanism of action

A

Inhibits intestinal absorption of cholesterol by interfering with NPC1L1 transport protein
- decreased LDL and VLDL

26
Q

Ezetimibe PK

A

Oral
Absorbed into intestinal epithelial cells
Active metabolites
Enterohepatic recycling slows elimination

27
Q

What does NPC1L1 transport protein do

A

Takes cholesterol out of intestine and deposits into cardiovascular system

28
Q

Ezetimibe clinical use

A

Hyperlipidaemia in combination with statins

29
Q

Ezetimibe adverse effects

A

Diarrhoea, abdominal pain, headache
Rash and angioedema

30
Q

Contraindication of Ezetimibe

A

Breastfeeding - secreted into breast milk

31
Q

2 other cholesterol absorption inhibitors

A

Colestipol, cholestyramine

32
Q

Colestipol mechanism of action

A

Binds bile acid in gut, prevents reabsorption
Upregulates LDL receptors
Bile acids and LDL removed from blood

33
Q

Colestipol PK

A

Oral - stays in GIT

34
Q

Colestipol clinical use

A

Primary hypercholesterolaemia when statin is contraindicated
Bile acid diarrhoea

35
Q

Colestipol adverse effects

A

Constipation, bloating
Malabsorption of vitamin K, folic acid
Disrupts absorption of warfarin, thiazides

36
Q

Nicotinic acid (Niacin) mechanism of action in liver

A

Reduced VLDL synthesis
Reduces VLDL and LDL

37
Q

Nicotinic acid (Niacin) mechanism of action in adipose

A

Reduced hormone sensitive lipase activity
Reduced TG

38
Q

Nicotinic acid effect of HDL

A

Increases HDL

39
Q

Nicotinic acid effect on lipoprotein lipase

A

Activates lipase so increases clearance of VLDL

40
Q

Niacin PK

A

Absorbed in GIT after oral administration
Metabolised in liver
Excreted via kidneys

41
Q

Nicotinic acid clinical use

A

Hypercholesterolaemia
Hypertriglyceridemia with low levels of HDL

42
Q

Niacin adverse effects

A

Cutaneous flushing
Nausea and abdominal discomfort

43
Q

What is apoA1

A

HDL

44
Q

Which cholesterol carries the highest risk of cardiovascular disease

A

LDL

45
Q

What is the prevalence of FH

A

1/250

46
Q

What percentage of males with FH will have symptomatic heart disease by age 50

A

50%

Cardiovascular (6 decks)

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