Hyperlipidemias Flashcards
Atherosclerosis
Cholesterol/lipid plaques in coronary arteries
What increases atherosclerotic risk
An increase in LDL, IDL, and VLDL, with a decrease in HDL
How to prevent atherosclerosis
Decrease the plasma lipoproteins like LDL
How LDL becomes a plaque
It gets engulfed by a macrophage, oxidized, and turned into a plaque
Pathogenesis of atherosclerosis
The smooth muscle in the intima proliferates and LDLs enter the intima and accumulate, where they are engulfed by macrophages to make lesions. These damage the endothelium so platelets adhere, the muscle proliferates and it continues to build
HMG-CoA
Enzyme that mediates early steps of hepatic sterol synthesis
Statins mechanism
Structural anologs of HMG-CoA that inhibit HMG-CoA reductase an increase LDL receptors in the liver
Statin examples
Lovastatin and rosuvastatin
Additional pharmacologic effects of statins
Decrease inflammation, improve vasodilation to nitric oxide, decrease thrombosis, increase stability of atherosclerotic plaques
Toxicities of statins
Teratogenic, liver toxicity, drug interactions
Niacin mechanism
Vitamin b3 when converted to NAD, but when unconverted it inhibits VLDL production and secretion and decreases adipose LPL, also raises HDL
Toxicities of niacin
Cutaneous flushing and itching from PG release, GI distress and ulcers
Cholestryamine and colestipol mechanism
Are large and positively charged so they bind to negatively charged bile acids and inhibit their reabsorption, which increases LDL receptors so LDL gets taken up
Pk of cholestryamine and colestipol
Insoluble in water, not absorbed by GI tract so they’re taken orally and with meals
Toxicities of cholestryamine and colestipol
Constipation and bloating, drug interactions
