Dyslipidaemia

Question 1

Primary prevention vs secondary prevention

Answer 1

Primary prevention - pt has no history of CV events (decision is based on lipid levels and CV risks)

Secondary prevention - pt with history of CV events (on statins regardless of lipid levels due to other benefits)

Question 2

What 3 drug classes are used in dyslipidaemia

Answer 2

Statins, fibrates and ezetimibes

Question 3

Statins - e.g., MOA, AE, precautions, monitoring

Answer 3

e.g. - simvastatin, rouvastatin, atorvastatin

MOA - inhibit enzyme involved in synthesis of cholesterol –> reduced cholesterol production

AE - muscle related side effects e.g. pain, spasms

Precautions - atorvastatin and rouvastatin most potent (should be give during the day when pt are eating)

Monitoring - monitor creatine kinase if muscle related side effects occur + liver function

STRONGEST EVIDENCE - MOST COMMONLY USED

Question 4

Fibrates - e.g., MOA, AE, precautions, monitoring

Answer 4

e.g. fenofibrate, gemfibrozil

MOA. - lowers TG, increases HDL, lowers LDL by promoting lipolysis
- better than statins at lowering LDLs

AE - GI side effects, photosensitivity, myopathy

Precautions - renally cleared

Question 5

Ezetimibe

Answer 5

Inhibits cholesterol absorption
- used in issues with statin therapy (no effect, muscle effects, sensitivity etc.)

Question 6

A pt presents with high LDLs

Answer 6

initial - statins
second line - statins + ezetimibe OR ezetimibe OR fibrate

Question 7

Causes of dyslipidaemia

Answer 7

dyslipidaemia - abnormal lipids (high LDL and TC)

causes:
- dietary fat intake
- alterations in lipoprotein metabolism (genetics)
- medication side effects
- level of physical activity
- medical conditions e.g. hypothyroidism

Question 8

Pharamcology for high LDLs vs high TG

Answer 8

statins and fibrates both reduce LDL and TG
- fibrates more preferred for reducing TG (statins better at reducing LDLs)