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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

25
Ezetimibe mechanism of action
Inhibits intestinal absorption of cholesterol by interfering with NPC1L1 transport protein - decreased LDL and VLDL
26
Ezetimibe PK
Oral Absorbed into intestinal epithelial cells Active metabolites Enterohepatic recycling slows elimination
27
What does NPC1L1 transport protein do
Takes cholesterol out of intestine and deposits into cardiovascular system
28
Ezetimibe clinical use
Hyperlipidaemia in combination with statins
29
Ezetimibe adverse effects
Diarrhoea, abdominal pain, headache Rash and angioedema
30
Contraindication of Ezetimibe
Breastfeeding - secreted into breast milk
31
2 other cholesterol absorption inhibitors
Colestipol, cholestyramine
32
Colestipol mechanism of action
Binds bile acid in gut, prevents reabsorption Upregulates LDL receptors Bile acids and LDL removed from blood
33
Colestipol PK
Oral - stays in GIT
34
Colestipol clinical use
Primary hypercholesterolaemia when statin is contraindicated Bile acid diarrhoea
35
Colestipol adverse effects
Constipation, bloating Malabsorption of vitamin K, folic acid Disrupts absorption of warfarin, thiazides
36
Nicotinic acid (Niacin) mechanism of action in liver
Reduced VLDL synthesis Reduces VLDL and LDL
37
Nicotinic acid (Niacin) mechanism of action in adipose
Reduced hormone sensitive lipase activity Reduced TG
38
Nicotinic acid effect of HDL
Increases HDL
39
Nicotinic acid effect on lipoprotein lipase
Activates lipase so increases clearance of VLDL
40
Niacin PK
Absorbed in GIT after oral administration Metabolised in liver Excreted via kidneys
41
Nicotinic acid clinical use
Hypercholesterolaemia Hypertriglyceridemia with low levels of HDL
42
Niacin adverse effects
Cutaneous flushing Nausea and abdominal discomfort
43
What is apoA1
HDL
44
Which cholesterol carries the highest risk of cardiovascular disease
LDL
45
What is the prevalence of FH
1/250
46
What percentage of males with FH will have symptomatic heart disease by age 50
50%

Cardiovascular (6 decks)

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