Hyperlipidemia Treatment Flashcards
What will ‘statins’ do?
Inhibit HMB-CoA competitively. Reduces total serum cholesterol, and triggers response which increases LDL receptors, which then greatly reduce LDL and VLDL in blood.
What are the main adverse effects of statins?
incerase in creatine kinase from skeletal muscle. Can cause severe muscle pain and rhabdomyolysis. CP450 metabolized so must avoid cyp inhibitors. Teratogenic.
How do cholesterol resins work?
They bind to bile acids in the GI tract and prevent their recycling. This reduces cholesterol and triggers compensatory increase in LDL receptors, which remove LDL from blood. Can increase VLDL and TGs, but no effects on HDL.
What are the main adverse effects from bile acid resins?
bloating, constipation and malabsorption of vitamins and other drugs.
What is ezetimibe? What is its mechanism? What is unique about it?
Prodrug converted in liver to active form that inhibits transporters of GI cholesterol uptake. Compensatory increases in LDL receptors removes LDL from blood. Hepatic toxicity and can have interactions with fibrates and cholestramine.
What is niacin? What is its mechanism? What is unique about it?
Reduces LDL, TG and VLDL by various mechanisms. Increases HDL. Reduces liver VLDL synthesis. Reduces adipose tissue lipase activity to reduce TG levels. Reduces catabolism of HDL. Causes cutaneous flushing due to PGE release, and severe hepatotoxicity. Also hyperuricemia.
What is gemfibrozil? What is its mechanism? What is unique about it?
Fibric acid derivative that stimulates PPAR-alpha to upregulate LPL production. Also incresaes TG clearance. In liver stimulates fatty acid oxidation to limit TGs and ecrease VLDL synthesis. Decreases expression of ApoC-III, which would normally hinder VLDL clearance. Increases expression of apoA-I and II, which increase HDL levels. LITTLE or NO effect on LDL levels. Can increase LDL in patients with familial combined hyperlipoproteinemia. Can cause nausea or rash and Gallstones (cholelithiasis).
What is fenofibrate? What is its mechanism? What is unique about it?
Renally excreted Fibric acid derivative that stimulates PPAR-alpha to upregulate LPL production. Also incresaes TG clearance. In liver stimulates fatty acid oxidation to limit TGs and ecrease VLDL synthesis. Decreases expression of ApoC-III, which would normally hinder VLDL clearance. Increases expression of apoA-I and II, which increase HDL levels. LITTLE or NO effect on LDL levels. Can increase LDL in patients with familial combined hyperlipoproteinemia. Can cause nausea or rash and Gallstones (cholelithiasis).
What are the main adverse effects of fibric acid derivatives?
they can cause nausea, rashes, and cholelithiasis. (gallstones)
What is cholestyramine? What is its mechanism? What is unique about it?
Bile acid resin. bind to bile acids in the GI tract and prevent their recycling. This reduces cholesterol and triggers compensatory increase in LDL receptors, which remove LDL from blood. Can increase VLDL and TGs, but no effects on HDL.
What is colestipol? What is its mechanism? What is unique about it?
Bile acid resin. bind to bile acids in the GI tract and prevent their recycling. This reduces cholesterol and triggers compensatory increase in LDL receptors, which remove LDL from blood. Can increase VLDL and TGs, but no effects on HDL.
What is nicotinic acid? What is its mechanism? What is unique about it?
AKA niacin or Vitamin B3. Reduces LDL, TG and VLDL by various mechanisms. Increases HDL. Reduces liver VLDL synthesis. Reduces adipose tissue lipase activity to reduce TG levels. Reduces catabolism of HDL. Causes cutaneous flushing due to PGE release, and severe hepatotoxicity. Also hyperuricemia (can cause GOUT)
What is the extended release form of vitamin B3 called?
niaspan. Useful because it will maintain PGE desensitization to prevent flushing.
Why shouldn’t you give a patient with gout niacin?
it causes hyperuricemia and will exacerbate it.
What are N-3 Fatty acids? What is its mechanism? What is unique about it?
reduce TGs by 35% by reducing liver synthesis by reducing SREBP. increases PPAR alpha activation. Little or no effect on HDL and LDL.
