front 1 What is an example of an HMG-CoA reductase inhibitor? | back 1 Atorvastatin ("statins") |
front 2 What does atorvastatin do? | back 2 inhibits HMG-CoA reductase (enzyme) primarily responsible or hepatic synthesis of cholesterol |
front 3 How would you describe atorvastatin? | back 3 It is the best class for lowering LDL cholesterol and TG while increasing HDL. |
front 4 What is atorvastatin used for? | back 4 Used in patients that have hypercholesterolemia, and to reduce risk of CV events |
front 5 When does atorvastatin peak after administration? | back 5 1-2 hours |
front 6 What are adverse effects of atorvastatin? | back 6 * MYOPATHY*(muscle pain associated w statin use, if severe = RHABDOMYOLYSIS (life threatening bc muscle breakdown releases enzymes (creatinine kinase) that damage kidneys), watch out for dark coca colored urine), hepatic dysfunction, hyperglycemia |
front 7 What is/are contraindications for statins? | back 7 pregnancy category X, take at night |
front 8 What increases risks of statin side effects/toxicity? | back 8
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front 9 What are examples of bile acid sequestrants? | back 9 cholesyramine |
front 10 Where does cholesytamine work in the body? | back 10 in the intestines |
front 11 What does cholestyramine do? | back 11 It binds to bile acids/salts, causing them to be excreted unchanged in the feces (= liver uses excess cholesterol to make new bile acids/salts instead of forming plaques in arteries) |
front 12 How would you describe cholestyramine? | back 12 a bile acid/salt magnet |
front 13 What is cholestyramine used for? | back 13 to decrease LDL (doesn't work too well for HDL/TG) |
front 14 What are some adverse effects of cholestyramine? | back 14 it decreases efficacy of many orally taken drugs (esp statins), GI related (ex. N/V/D) |
front 15 What would you do to allow absorption of orally taken drugs alongside cholestyramine? | back 15 give pt fat soluble vitamin supplements (A,D,E,K) |
front 16 What is an example of a fibric acid derivative (fibrates)? | back 16 Fenofibrate |
front 17 What does fenofibrate do? | back 17 decreases hepatic production of TG and VLDL cholesterol while increasing HDL. |
front 18 How would you describe fenofibrate? | back 18 The best at lowering TG. |
front 19 What kind of patients would use fenofibrate? | back 19 patients that have exceptionally high TG ( >500 md/dL) (they wld also have a very high risk of pancreatitis) associated with diabetes, gout, gastritis, or ulcer disease. Unnecessary otherwise (j use statins) |
front 20 When does fenofibrate peak after administration? | back 20 at around 6-8 hours. |
front 21 What are some adverse effects of fenofibrate? | back 21 increased risk of gallstones and bleeding from anticoagulants |
front 22 What are some contraindications for fenofibrate? | back 22 patients with severe renal impairment or liver disease (fibrates can cause/worsen both) |
front 23 Cholesterol Absorption Inhibitor | back 23 Ezetimibe (Zetia) MOA: blocks biliary and dietary cholesterol absorption Uses: dyslipidemia (monotherapy or in combo w statin) NC: contraindicated in pregnant/lactating, not recommended in pts w severe hepatic impairment |
front 24 PCSK9 Inhibitors | back 24 Alirocumab (Praluent) MOA: increases activity of the receptors that clear cholesterol Uses: Adults w ASCVD, family hc of hypercholesterolemia NC: given subQ, well tolerated but VERY expensive |
front 25 Niacin (Niacor, Niaspan) | back 25 U: no longer recommended NC: only given to pts w high TG (>500). Data did not suggest pt outcomes improved. AE: increases blood glucose and risk of hepatotoxicity. |
front 26 BAD lab value for cholesterol? | back 26 >240 |
front 27 BAD lab value for LDL? | back 27 >160 |
front 28 BAD lab value for triglycerides? | back 28 >200 |
front 29 BAD lab value for HDL? | back 29 <40 |