(3.2) Cholesterol and Lipid Metabolism Flashcards
What is the pathology of Famalial Hypeerlipidaemia? Suggest a treatment for it.
- Mutation of LDL receptor -> increased LDL (moving cholesterol from liver to tissue) in circulation
- Statin: increases LDL receptors and inhibits HMG-CoA reductase -> reduces Cholesterol synthesis
What is the normal range of Cholesterol and when fasting?
- Normal:
Suggest some ADRs of Statin use.
- Myopathy & Myositis
- Headache
- GI complaints
- Type 2 Diabetes
Suggest two types of Statin and how should each be prescribed (e.g. time of a day)?
- Simvastatin: given before bed (a short half life, to coincide cholesterol peak production in the morning)
- Rosuvastatin & Atorvastatin: during day (a longer half life, given to those who don’t take before bed)
How do Fibrates work?
PPAR-alpha antagonists -> + FA uptake & oxidation & action of lipoprotein lipase -> —TAG & -LDL
Suggest some possible ADRs of fibrates.
- GI complaints
- Myositis
- Cholelithiasis
Why shouldn’t Statin and Fibrates be prescribed together?
Both cause myopathy -> Rhabdomyolysis
How does Ezetimibe work?
Cholesterol lipase inhibitor -> inhibits INTESTINAL cholesterol absorption -> –LDL
Suggest some possible ADRs of Ezetimibe.
- Headache
- GI complaints
- Headache
- Rhabdomyolysis
Suggest the actions of Nicotinic Acid.
- —TAG
- -LDL
- +++HDL
Suggest some possible ADRs of Nicotinic Acid.
- Headache
- Flushing
- Hepatoxicity
- Reduced insulin sensitivity -> hyperglycaemia
How does Bile Acid Sequesterants work?
- Bind bile acid -> reduce their reabsorption
- Bile acid synthesis requires cholesterol, reduced reabsorption leading to increased synthesis -> increase utilisation of cholesterol -> lowers cholesterol level