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)

20
Q

where is Gemfibrozil metabolized

21
Q

Gemfibrozil half life

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

25
Atorvastatin pharm class
HMG-coA reductase inhibitor
26
Atorvastatin therapeutic class
lipid lowering and prevention of CAD
27
Atorvastatin pharm dynamics
- 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
Atorvastatin metabolized where
liver
29
Atorvastatin metabolized by what enzyme
CYP3A4
30
what is more active Atorvastatin or metabolites
metabolites
31
Atorvastatin half life
20-30 hours
32
What do you have to monitor for Atorvastatin
LFT and CPK ie liver and kidneys
33
effects of Atorvastatin toxicity
hepatitis, myopathy, myositis, rhabdomyolysis
34
avoid Atorvastatin in which situation
hepatitis, muscle disease, and pregnancy class (x)
35
How does Ezetimibe work ie pharmacodynamics?
blocks intestinal uptake of choelsterol which leads to increased blood clearance of cholesterol
36
how is Ezetimibe absorbed (qualitatively()
bad
37
how is Ezetimibe used
only in addition to statins
38
what is Ezetimibe's effect on outcomes
doesn't reduce MI, stroke, or CV outcomes