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Pharmacology > Lipid Lowering Drugs > Flashcards

Lipid Lowering Drugs Flashcards

1
Q

Cholestyramine pharm class

A

bile acid sequestrant

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2
Q

Cholestyramine therapeutic class

A

lipid lowering

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3
Q

Cholestyramine pharmdynamics

A
  • forms non-absorbable complex w/ bile acids in small bowel and inhibits enterohepatic reuptakeof intestinal bile salts
  • increseases expression of LDL receptor
  • reduces cholesterol by 10-20%
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4
Q

Cholestyramine absorbtion

A

virtually none

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5
Q

Cholestyramine peak

A

3 weeks

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6
Q

Cholestyramine 3 toxicity issues

A

Gi issues
decreased vitamin absorption
interferes w/ statin, steroid, dig, warfarin, and thyroxine absorption

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7
Q

Cholestyramine route

A

powder/ oral

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8
Q

Niacin pharm class

A

vitamin

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9
Q

Niacin therapeutic class

A

lipid lowering

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10
Q

Niacin pharmacodynamics

A

lowers TG and LDL
decreases production of bad lipoproteins
can increases LDL receptor

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11
Q

Niacin absorption (qualitative)

A

good

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12
Q

niacin relationship w/ liver

A

large 1st pass effect to nicotinamide

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13
Q

niacin tmax

A

45 minutes

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14
Q

how is niacin excreted

A

urinary excretion of drug and metabolite

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15
Q

niacin toxicity (2)

A

skin flushing

hepatitis

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16
Q

avoid niacin in

A

CAD and heavy ETOH use

17
Q

Gemfibrozil pharm class

A

fibric acid derivative

18
Q

what is Gemfibrozil most usefulf or?

A

treating hypertriglyceridemia in type IV and V hypertriglyceridemia

19
Q

how is Gemfibrozil absorbed (qualitiatively)

A

well

20
Q

where is Gemfibrozil metabolized

A

liver

21
Q

Gemfibrozil half life

A

1-2 hours

22
Q

Gemfibrozil interactions

A

increases liver and muscle toxicity when combined with statins

23
Q

Gemfibrozil contraindications

A

liver and renal disease

24
Q

Atorvastatin cost

A

$10

25
Q

Atorvastatin pharm class

A

HMG-coA reductase inhibitor

26
Q

Atorvastatin therapeutic class

A

lipid lowering and prevention of CAD

27
Q

Atorvastatin pharm dynamics

A
  • inhibits HMG-COA reductase which is regulatory step in cholesterol synthesis
  • increases LDL receptors
  • leads to 10-65% reduction in cholesterol and small increaes in HDL
28
Q

Atorvastatin metabolized where

A

liver

29
Q

Atorvastatin metabolized by what enzyme

A

CYP3A4

30
Q

what is more active Atorvastatin or metabolites

A

metabolites

31
Q

Atorvastatin half life

A

20-30 hours

32
Q

What do you have to monitor for Atorvastatin

A

LFT and CPK ie liver and kidneys

33
Q

effects of Atorvastatin toxicity

A

hepatitis, myopathy, myositis, rhabdomyolysis

34
Q

avoid Atorvastatin in which situation

A

hepatitis, muscle disease, and pregnancy class (x)

35
Q

How does Ezetimibe work ie pharmacodynamics?

A

blocks intestinal uptake of choelsterol which leads to increased blood clearance of cholesterol

36
Q

how is Ezetimibe absorbed (qualitatively()

A

bad

37
Q

how is Ezetimibe used

A

only in addition to statins

38
Q

what is Ezetimibe’s effect on outcomes

A

doesn’t reduce MI, stroke, or CV outcomes

Pharmacology (9 decks)

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