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U4 Drug table > Hypolipidemics > Flashcards

Hypolipidemics Flashcards

1
Q

What is the class for Niacin (Niaspan)

A

Nicotinic acid

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2
Q

What is the mechanism for Niacin (Niaspan)

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

What are the therapeutics for Niacin (Niaspan)

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

What are the important side effects for Niacin (Niaspan)

A

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

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5
Q

What are the other side effects for Niacin (Niaspan)

A

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

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6
Q

What are the miscellaneous for Niacin (Niaspan)

A

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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7
Q

What is the class for Clofibrate (Atromid-S)

A

Fibric Acid Derivatives (Fibrates)

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8
Q

What is the mechanism for Clofibrate (Atromid-S)

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPAR?) 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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9
Q

What are the therapeutics for Clofibrate (Atromid-S)

A

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

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10
Q

What are the important side effects for Clofibrate (Atromid-S)

A

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

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11
Q

What are the miscellaneous for Clofibrate (Atromid-S)

A

Combination w/statin inadvisable due to higher myositis risk

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12
Q

What is the class for Gemfibrozil (Lopid)

A

Fibric Acid Derivatives (Fibrates)

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13
Q

What is the mechanism for Gemfibrozil (Lopid)

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPAR?) 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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14
Q

What are the therapeutics for Gemfibrozil (Lopid)

A

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

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15
Q

What are the important side effects for Gemfibrozil (Lopid)

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)

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16
Q

What are the miscellaneous for Gemfibrozil (Lopid)

A

Combination w/statin inadvisable due to higher myositis risk

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17
Q

What is the class for Fenofibrate (Tricor)

A

Fibric Acid Derivatives (Fibrates)

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18
Q

What is the mechanism for Fenofibrate (Tricor)

A

Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPAR?) 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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19
Q

What are the therapeutics for Fenofibrate (Tricor)

A

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

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20
Q

What are the important side effects for Fenofibrate (Tricor)

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)

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21
Q

What are the miscellaneous for Fenofibrate (Tricor)

A

Combination w/statin inadvisable due to higher myositis risk

22
Q

What is the class for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

A

Bile acid sequestrants

23
Q

What is the mechanism for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

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

24
Q

What are the therapeutics for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

A

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

25
Q

What are the important side effects for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

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)

26
Q

What are the other side effects for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

A

Bloating, dyspepsia, constipation, gritty/unpleasant taste

27
Q

What are the miscellaneous for Colestipol (Colestid); Cholestyramine (Questran); Colesevelam (Welchol)

A

Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia

28
Q

What is the class for Lovastatin (Mevacor)

A

HMG-CoA reductase Inhibitors (statins)

29
Q

What is the mechanism for Lovastatin (Mevacor)

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

30
Q

What are the therapeutics for Lovastatin (Mevacor)

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%)

31
Q

What are the important side effects for Lovastatin (Mevacor)

A

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

32
Q

What are the miscellaneous for Lovastatin (Mevacor)

A

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

33
Q

What is the class for Simvastatin (Zocor)

A

HMG-CoA reductase Inhibitors (statins)

34
Q

What is the mechanism for Simvastatin (Zocor)

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

35
Q

What are the therapeutics for Simvastatin (Zocor)

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%)

36
Q

What are the important side effects for Simvastatin (Zocor)

A

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

37
Q

What are the miscellaneous for Simvastatin (Zocor)

A

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

38
Q

What is the class for Pravastatin (Pravachol); Fluvastatin (Lescol)

A

HMG-CoA reductase Inhibitors (statins)

39
Q

What is the mechanism for Pravastatin (Pravachol); Fluvastatin (Lescol)

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

40
Q

What are the therapeutics for Pravastatin (Pravachol); Fluvastatin (Lescol)

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%)

41
Q

What are the important side effects for Pravastatin (Pravachol); Fluvastatin (Lescol)

A

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

42
Q

What are the miscellaneous for Pravastatin (Pravachol); Fluvastatin (Lescol)

A

Must be taken in evening

43
Q

What is the class for Atorvastatin (Lipitor); Rosuvastatin (Crestor); Pitavastatin (Livalo)

A

HMG-CoA reductase Inhibitors (statins)

44
Q

What is the mechanism for Atorvastatin (Lipitor); Rosuvastatin (Crestor); Pitavastatin (Livalo)

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

45
Q

What are the therapeutics for Atorvastatin (Lipitor); Rosuvastatin (Crestor); Pitavastatin (Livalo)

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%)

46
Q

What are the important side effects for Atorvastatin (Lipitor); Rosuvastatin (Crestor); Pitavastatin (Livalo)

A

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

47
Q

What are the miscellaneous for Atorvastatin (Lipitor); Rosuvastatin (Crestor); Pitavastatin (Livalo)

A

Due to longer half-life, can be taken anytime per day

48
Q

What is the class for Ezetimbe (Zetia)

A

Inhibits enterocyte absorption of cholesterol in intestine

49
Q

What is the mechanism for Ezetimbe (Zetia)

A

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

50
Q

What are the therapeutics for Ezetimbe (Zetia)

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)

51
Q

What are the important side effects for Ezetimbe (Zetia)

A

None (rare allergies)

52
Q

What are the miscellaneous for Ezetimbe (Zetia)

A

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

U4 Drug table (7 decks)

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