Drugs Used in the Treatment of Hyperlipidemias Flashcards
MOA of statins
Inhibit HMG CoA reductase, which inhibits the synthesis of cholesterol. This, in turn, causes the liver to compensate by increasing the number of LDL receptors, which clear LDL and VLDL from the blood.
Adverse side effects of statins
Hepatotoxicity (must monitor liver enzymes)
Myopathy
Teratogenic
MOA of resins
Prevent the recycling of bile acids. This diverts hepatic cholesterol to synthesis of new bile, thereby reducing the cholesterol pool. A compensatory increase in the synthesis of LDL receptors occurs.
*NB: interferes with absorption of some drugs and vitamins (e.g., vitamin K)
Which class of hyperlipidemic drugs are contraindicated in patients with familial combined hyperlipidemia because they increase triglycerides and VLDL?
Resins (cholestyramine, colestipol, colesevelam)
Member of a family of nuclear transcription regulators that participate in the regulation of metabolic processes; target of the vibrates and omega-3 fatty acids
PPAR-alpha
What are the primary effects of fibrates on lipid profiles?
**reduce triglycerides
slight increases in HDL
No effects on LDL
Adverse side effects of fibrates
myopathy, hepatic dysfunction, cholestasis (increased risk of gallstones)
Effects of niacin on lipid profiles
Decreases VLDL synthesis and LDL cholesterol concentrations
**Increases HDL!!
Adverse effects of niacins
GI irritation, hyperuricemia (do not use if pt has gout), flushing, hepatic toxicity, may reduce glucose tolerance
Consumption of alcohol is associated with increases in which serum lipid concentrations?
Triglycerides