Antihyperlipidemics Flashcards

1
Q

What is involved in the non-drug approach?

A

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

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2
Q

What are the bile acid-binding resins?

A

Cholestyramine, Colestipol, Colesevelam

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3
Q

What is the MOA of Cholestyramine?

A

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

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4
Q

When would you use Cholestyramine?

A

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

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5
Q

What are the side effects of Cholestyramine?

A

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

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6
Q

What is the MOA of Colestipol?

A

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

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7
Q

When would you use Colestipol?

A

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

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8
Q

What are the side effects of Colestipol?

A

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

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9
Q

What is the MOA of Colesevelam?

A

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

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10
Q

When would you use Colesevelam?

A

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

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11
Q

What are the side effects of Colesevelam?

A

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

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12
Q

What are the statins?

A

Rosuvastatin, Atorvastatin, Simvastatin, Lovastatin, Pravastatin, Fluvastatin

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13
Q

What is the MOA of Rosuvastatin?

A

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

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14
Q

When would you use Rosuvastatin?

A

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

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15
Q

What are the side effects of Rosuvastatin?

A

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

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16
Q

What is the MOA of Atorvastatin?

A

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

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17
Q

When would you use Atorvastatin?

A

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

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18
Q

What are the side effects of Atorvastatin?

A

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

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19
Q

What is the MOA of Simvastatin?

A

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

20
Q

When would you use Simvastatin?

A

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

21
Q

What are the side effects of Simvastatin?

A

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

22
Q

What is the MOA of Lovastatin?

A

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

23
Q

When would you use Lovastatin?

A

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

24
Q

What are the side effects of Lovastatin?

A

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

25
Q

What is the MOA of Pravastatin?

A

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

26
Q

When would you use Pravastatin?

A

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

27
Q

What are the side effects of Pravastatin?

A

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

28
Q

What is the MOA of Fluvastatin?

A

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

29
Q

When would you use Fluvastatin?

A

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

30
Q

What are the side effects of Fluvastatin?

A

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

31
Q

What is the MOA of Ezetimibe?

A

Inhibits jejunal uptake of cholesterol

32
Q

When would you use Ezetimibe?

A

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

33
Q

What are the side effects of Ezetimibe?

A

GI, headache, muscle/joint pain

34
Q

What are the Vitamin B3 derivatives?

A

Nicotinic acid and Niacin

35
Q

What is the MOA of Nicotinic Acid?

A

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

36
Q

When would you use Nicotinic Acid?

A

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

37
Q

What are the side effects of Nicotinic Acid?

A

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

38
Q

What is the MOA of Niacin?

A

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

39
Q

When would you use Niacin?

A

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

40
Q

What are the side effects of Niacin?

A

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

41
Q

What are the fibric acid derivatives?

A

Gemfibrozil, fenofibrate

42
Q

What is the MOA of Gemfibrozil?

A

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

43
Q

When would you use Gemfibrozil?

A

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

44
Q

What are the side effects of Gemfibrozil?

A

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

45
Q

What is the MOA of Fenofibrate?

A

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

46
Q

What are the side effects of Fenofibrate?

A

Same as gemfibrozil with less GI effects

47
Q

When would you use Fenofibrate?

A

To decrease LDL (better than Gemfibrozil)