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Pharm 7 > lipids > Flashcards

lipids Flashcards

1
Q

drugs that decrease cholesterol

A

HMG-CoA reductase inhibitors (statins)
cholesterol absorption inhibitors
bile acid sequestrants
nicotinic acid

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2
Q

drugs that decrease triglycerides

A

fibric acid derivatives
omega-3 fatty acids
nicotinic acid

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3
Q

main MOA statins

A
  • inhibits 3-hydroxy-3-methylglutaryl (HMG) coenzyme A conversion to mevalonate, the rate limiting step preventing intracellular cholesterol biosynthesis
  • causes up-regulation of LDL-Rs and inc removal of LDL chol from plasma (main effect)
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4
Q

other effects of statins

A

inhibits vascular SM proliferation, inhibits platelet-thrombus formation, anti-tumor effect, endothelial protection
*secondary prevention of MI, CAD, etc (they’ve had one before) but no primary prevention

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5
Q

absorption of statins with food

A

must give lovastatin with food

others have no or slight decrease in absorption with food

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6
Q

half lives and time of administration of statins

A

most have short half-lives, give at night (HMG-CoA activity highest from midnight-3 am)
EXCEPT atorva- (12 h t1/2) and rosuva (18 h)

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7
Q

metabolism of statins

A

hepatic

CYP3A4 for atorva, lova, simva

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8
Q

ADRs of statins

A

worst: myopathy
frequent: abd cramps, heartburn, diarrhea
less freq: elevated liver enzmyes, fatigue (? dec protein prenylation and ubiquinone production), dec in cognition
pregnancy: cat X (also in kids)

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9
Q

stages of statin myopathy and tx

A

earliest: mm ache, weakness (may be a/w inc CK levels)
mid: myositis, inflammation, acute pain
late: rhabdo, myoglobinuria, acute renal failure
may be related to low vit D levels, so vit D supplementation may reverse (even w statin continuation)

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10
Q

risk factors for statin toxicity

A

endogenous: age >65, low BMI/frailty, multisystem dz, thyroid d/o, metabolic mm dz, fam hx of mm sx, personal hx elevated CK
exogenous: heavy exercise, EtOH, drugs affecting CYP 450 system, consuming grapefruit juice

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11
Q

statin drug interactions

A

CYP 3A4 inhibitors inc levels of lova-, atorva-, and simvastatin: macrolides (not azithro), azole antifungals, CCBs, grapefruit juice
fibric acid derivatives (mostly gemfibrozil): inc serum level statin and risk of myopathy

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12
Q

statins and fibrates with non-CYP metabolism

A

rosuvastatin (90% non-CYP), pravastatin, pitavastatin

fenofibrate

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13
Q

ezetimibe

A

cholesterol-absorption inhibitor
metabolized to active glucuronide metabolite that localizes in intestinal brush border cells and inhibits absorption of dietary and biliary cholesterol (blocks transporter)
*may be inc risk myopathy when used w statins

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14
Q

cholestyramine

A

bile acid sequestrant - granules

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15
Q

colestipol

A

bile acid sequestrant - granules and tablet

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16
Q

colesevalam

A

bile acid sequestrant - hydrophilic polymer

17
Q

MOA and effects of bile acid sequestrants

A

anion exchange in bowel removes bile acids from circulation, stimulates liver to convert chol to bile acid and up-regulate LDL-R

  • reduces LDL by 10-25% (dose-dep), but can raise TG by 5-10%
  • works best when combined w statin
18
Q

ADR of bile acid sequestrants

A

constipation, pain, bloating, nausea

can reduce absorption of fat-soluble vitamins too

19
Q

when to use fibric acid derivatives

A

may reduce risk of pancreatitis if elevated TGs and VLDL in absence of elevated LDL
hypertriglyceridemia

20
Q

fibric acid use with statins

A

gemfibrozil C/I with statins - inc risk myopathy

fenofibrate may be used w statins

21
Q

MOA of fibric acid derivatives

A

reduce hepatic synthesis of VLDL, inc LPL activity (breaks down VLDL)

22
Q

ADR of fibric acid derivatives

A

may cause cholelithiasis d/t inc secretion of cholesterol in bile acids

23
Q

types of omega-3 FAs

A

marine: EPA, DHA
plant: alpha-linoleic acid (walnut, soybean, canola oil)

24
Q

omega-3-FA effect

A

polyunsaturated fats that can lower TGs (marine > plant) and increase HDL (modestly)

25
Q

niaspan

A

extended-release form of nicotinic acid

26
Q

nicotinic acid MOA and effect

A

inhibits mobilization of FFA from adipose tissue, decreasing synthesis and secretion of VLDL in liver
*most potent drug for raising HDL

27
Q

ADRs of nicotinic acid

A

flushing, itching, rash, HA, GI distress (d/t PG release)

hepatoxicity, hyperglycemia, hyperuricemia

28
Q

how to prevent GI distress with nicotinic acid use

A

pre-medicate with ASA or ibuprofen

29
Q

meds to use for hypercholesterolemia

A

bile acid seqs, niacin, statins

30
Q

meds to use for mixed hyperlipidemia

A

niacin, statins

limited use of fibrates

31
Q

meds to use for hypertriglyceridemia

A

niacin, fibrates

32
Q

patient groups who may benefit from statin use

A

1- hx of clinical ASCVD
2- LDL > 190
3- 40-75 yo w DM
4- 40-75 yo w/o clinical ASCVD or DM but estimated 10-year ASCVD risk >7.5%

Pharm 7 (7 decks)

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