Antihyperlipidemics

Question 1

What is involved in the non-drug approach?

Answer 1

Diet, weight loss, exercise, no smoking or excess alcohol (to much > increased VLDL/TGs); lots of omega-3s

Question 2

What are the bile acid-binding resins?

Answer 2

Cholestyramine, Colestipol, Colesevelam

Question 3

What is the MOA of Cholestyramine?

Answer 3

Prevents GI bile acid reabsorption into liver > increased bile production and LDL receptor expression

Question 4

When would you use Cholestyramine?

Answer 4

To decrease LDL 10-25%, increase HDL 3-5%; second line drugs used in combo with others

Question 5

What are the side effects of Cholestyramine?

Answer 5

Nausea, bloating, impairs absorption of vitamins ADEK; may increase VLDL < 5% in patients with high TGs

Question 6

What is the MOA of Colestipol?

Answer 6

Prevents GI bile acid reabsorption into liver > increased bile production and LDL receptor expression

Question 7

When would you use Colestipol?

Answer 7

To decrease LDL 10-25%, increase HDL 3-5%; second line drug used with others

Question 8

What are the side effects of Colestipol?

Answer 8

Nausea, bloating, impairs absorption of vitamins ADEK; may increase VLDL < 5% in patients with high TGs

Question 9

What is the MOA of Colesevelam?

Answer 9

Prevents GI bile acid reabsorption into liver > increased bile production and LDL receptor expression

Question 10

When would you use Colesevelam?

Answer 10

To decrease LDL 10-25%, increase HDL 3-5%; second line drug used with others

Question 11

What are the side effects of Colesevelam?

Answer 11

Nausea, bloating; may increase VLDL < 5% in patients with high TGs

Question 12

What are the statins?

Answer 12

Rosuvastatin, Atorvastatin, Simvastatin, Lovastatin, Pravastatin, Fluvastatin

Question 13

What is the MOA of Rosuvastatin?

Answer 13

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 14

When would you use Rosuvastatin?

Answer 14

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; has the highest potency at 20hr HL

Question 15

What are the side effects of Rosuvastatin?

Answer 15

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 16

What is the MOA of Atorvastatin?

Answer 16

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 17

When would you use Atorvastatin?

Answer 17

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; 14 hr HL, decreases TG

Question 18

What are the side effects of Atorvastatin?

Answer 18

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 19

What is the MOA of Simvastatin?

Answer 19

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 20

When would you use Simvastatin?

Answer 20

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; prodrug

Question 21

What are the side effects of Simvastatin?

Answer 21

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 22

What is the MOA of Lovastatin?

Answer 22

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 23

When would you use Lovastatin?

Answer 23

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; prodrug

Question 24

What are the side effects of Lovastatin?

Answer 24

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 25

What is the MOA of Pravastatin?

Answer 25

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 26

When would you use Pravastatin?

Answer 26

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; no increased absorption with food

Question 27

What are the side effects of Pravastatin?

Answer 27

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 28

What is the MOA of Fluvastatin?

Answer 28

Competitive inhibition of HMG-CoA Reductase > reduced liver cholesterol synthesis. Liver pulls from plasma cholesterol to maintain its levels

Question 29

When would you use Fluvastatin?

Answer 29

To decrease LDL 20-60%, increase HDL 5-15%, decrease TGs 10-30%; lowest potency

Question 30

What are the side effects of Fluvastatin?

Answer 30

Increased ALT/AST and CPK > myopathy; skin rxns; possible carcinogenicity and teratogenicity > NO pregnancy

Question 31

What is the MOA of Ezetimibe?

Answer 31

Inhibits jejunal uptake of cholesterol

Question 32

When would you use Ezetimibe?

Answer 32

To decrease LDL additional 12-18%; no effect on TGs or HDL; given with simvastati; 2hr before/4hr after bile resins

Question 33

What are the side effects of Ezetimibe?

Answer 33

GI, headache, muscle/joint pain

Question 34

What are the Vitamin B3 derivatives?

Answer 34

Nicotinic acid and Niacin

Question 35

What is the MOA of Nicotinic Acid?

Answer 35

Inhibits adipose lipolysis by blocking lipase > decreased FA supply to liver > decreased VLDL > decreased LDL > increased HDL

Question 36

When would you use Nicotinic Acid?

Answer 36

To decrease VLDL/TG <50%; decrease LDL 15-30%; increase HDL 15-30%

Question 37

What are the side effects of Nicotinic Acid?

Answer 37

Peptic ulceration; severe vasomotor flushing, increase insulin resistance, hyperuricemia, gout; increases endothelial/tPA function, decreases fibrinogen

Question 38

What is the MOA of Niacin?

Answer 38

Inhibits adipose lipolysis by blocking lipase > decreased FA supply to liver > decreased VLDL > decreased LDL > increased HDL

Question 39

When would you use Niacin?

Answer 39

To decrease VLDL/TG <50%; decrease LDL 15-30%; increase HDL 15-30%; also lowers Lp(a); contraindicated with diabetes, peptic ulcers, liver disease, pregnancy, gout

Question 40

What are the side effects of Niacin?

Answer 40

Peptic ulceration; severe vasomotor flushing, increase insulin resistance, hyperuricemia, gout

Question 41

What are the fibric acid derivatives?

Answer 41

Gemfibrozil, fenofibrate

Question 42

What is the MOA of Gemfibrozil?

Answer 42

Increase liver FA oxidation via LPL > decreased VLDL and TGs; decreased LDLs and increased HDL due to increased apoAI/II

Question 43

When would you use Gemfibrozil?

Answer 43

To decrease VLDL/TG <30%, decrease LDL 5-20%, increase HDL 10-20%

Question 44

What are the side effects of Gemfibrozil?

Answer 44

GI, gallstones, increased liver enzymes when used with statins (except rosuvastatin)

Question 45

What is the MOA of Fenofibrate?

Answer 45

Increase liver FA oxidation via LPL > decreased VLDL and TGs; decreased LDLs and increased HDL due to increased apoAI/II

Question 46

What are the side effects of Fenofibrate?

Answer 46

Same as gemfibrozil with less GI effects

Question 47

When would you use Fenofibrate?

Answer 47

To decrease LDL (better than Gemfibrozil)