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Pharmacology > Unit 4-Hypolipidemics > Flashcards

Unit 4-Hypolipidemics Flashcards

1
Q

Niacin

Drug class

A

Nicotinic acid

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2
Q

Niacin

Mechanism

A

Reduction of liver triglyceride synthesis, leading to less hepatic VLDL (thus, LDL) production; decreases lipolysis in adipose tissue, leading to lowered FFA transport to liver (thus, less triglycerides); reduced hepatic clearance of ApoAI (raising HDL)

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3
Q

Niacin

Uses

A

Best agent to increase HDL (30-40%); as good as fibrates and statins at lowering triglycerides (35-45%); lowers LDL (20-30%); hypertriglyceridemia and low HDL

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4
Q

Niacin

Side effects

A

Flushing, pruritis of face and upper trunk, rashes, acanthosis nigricans (hyperpigmentation)

Hepatotoxicity, hyperuricemia, hyperglycemia; dyspepsia/reactivation of peptic ulcer disease; rarely, toxic ambylopia, tachyarrhythmias, a-fib (in elderly) and myopathy

Water soluble B vitamin complex at [low]; hypolipidemic at [high]; side effects limit compliance (<50% eligible patients follow on it); contraindicated in DM and gout patients; prevent flushing and pruritus with ASA

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5
Q

Clofibrate

Drug class

A

Fibric Acid Derivatives (Fibrates)

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6
Q

Clofibrate

Mechanism

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)

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7
Q

Clofibrate

Uses

A

Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia

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8
Q

Clofibrates

Side effects

A

Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity; myositis flu-like syndrome in 5%, other effects in 10% (not serious)

Combination w/statin inadvisable due to higher myositis risk

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9
Q

Gemfibrozil

Drug class

A

Fibric Acid Derivatives (Fibrates)

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10
Q

Gemfibrozil

Mechanism

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)

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11
Q

Gemfibrozil

Uses

A

Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia

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12
Q

Gemfibrozil

Side effects

A

Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious)

Combination w/statin inadvisable due to higher myositis risk

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13
Q

Fenofibrate

Drug class

A

Fibric Acid Derivatives (Fibrates)

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14
Q

Fenofibrate

Mechanism

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)

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15
Q

Fenofibrate

Uses

A

Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia

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16
Q

Fenofibrate

Side effects

A

Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious)

Combination w/statin inadvisable due to higher myositis risk

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17
Q

Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

Drug class

A

Bile acid sequestrants

18
Q

Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

Mechanism

A

Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood

19
Q

Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

Uses

A

Decrease LDL (25%), but slight increase (5%) in TG and HDL

20
Q

Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

Side effects

A

Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins)

Bloating, dyspepsia, constipation, gritty/unpleasant taste

Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia

21
Q

Lovastatin

Drug class

A

HMG-CoA reductase Inhibitors (statins)

22
Q

Lovastatin

Mechanism

A

Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG

23
Q

Lovastatin

Uses

A

Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)

24
Q

Lovastatin

Side effects

A

Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)

Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Advicor = niacin + lovastatin

25
Q

Simvastatin

Drug class

A

HMG-CoA reductase Inhibitors (statins)

26
Q

Simvastatin

Mechanism

A

Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG

27
Q

Simvastatin

Uses

A

Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)

28
Q

Simvastatin

Side effects

A

Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)

Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Vytorin = ezetemibe + simvastatin

29
Q

Pravastatin (Pravachol); Fluvastatin (Lescol)

Drug class

A

HMG-CoA reductase Inhibitors (statins)

30
Q

Pravastatin (Pravachol); Fluvastatin (Lescol)

Mechanism

A

Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG

31
Q

Pravastatin (Pravachol); Fluvastatin (Lescol)

Uses

A

Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)

32
Q

Pravastatin (Pravachol); Fluvastatin (Lescol)

Side effects

A

Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)

Must be taken in evening

33
Q

Ezetimibe

Drug class

A

Inhibits enterocyte absorption of cholesterol in intestine

34
Q

Ezetimibe

Mechanism

A

Decreases LDL-C alone (15-20%) or in combination w/statin (60%)

35
Q

Ezetimibe

Uses

A

Inhibits cholesterol absorption by enterocytes in jejunum (70% in mice), leading to less cholesterol in chylomicrons; reduction in chylomicron remnant cholesterol delivery to liver; may also decrease atherogenesis directly (remnants very atherogenic)

36
Q

Ezetimibe

Side effects

A

None (rare allergies)

Long-term decrease in endpoints not seen yet (questionable effectiveness)

37
Q

Alirocumab; Evolucumab

Drug class

A

PCSK9 inhibitors

38
Q

Alirocumab; Evolucumab

Mechanism

A

Inhibits an endopeptidase (PCSK9) responsible for LDL-R degradation, resulting in higher numbers of LDL-Rs on hepatocytes

39
Q

Alirocumab; Evolucumab

Uses

A

2nd line therapy for hypercholesterolemia not controlled by diet and statins

40
Q

Alirocumab; Evolucumab

Side effects

A

Injection site reactions; flu-like symptoms; nose and throat irritation; muscle pain; diarrhea

Pharmacology (26 decks)

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