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Cardio II: Exam 2 > Pharm - Hyperlipidemics > Flashcards

Pharm - Hyperlipidemics Flashcards

1
Q

Atorvastatin

A

Lipitor
HMG-CoA reductase inhibitor, Statin

14 hours

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2
Q

Niacin

A

nicotinic acid, vitamin B3

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3
Q

fenofibrate

A

fibric acid derivative

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4
Q

gemfibrozil

A

fibric acid derivative

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5
Q

fluvastatin

A

Lescol, HMG-CoA reductase inhibitor, Statin

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6
Q

lovastatin

A

Mevacor, HMG-CoA reductase inhibitor, Statin

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7
Q

Pitavastatin

A

Livalo - HMG-CoA reductase inhibitor, Statin

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8
Q

Pravastatin

A

Pravachol - HMG-CoA reductase inhibitor, Statin

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9
Q

Rosuvastatin

A

Crestor - HMG-CoA reductase inhibitor, Statin

19 hours

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10
Q

Simvastatin

A

Zocor - HMG-CoA reductase inhibitor, Statin

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11
Q

cholestyramine

A

Bile acid seqestrant, resin

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12
Q

colesevelam

A

Bile acid seqestrant, resin

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13
Q

colestipol

A

Bile acid seqestrant, resin

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14
Q

Ezetimibe

A

cholesterol absorption inhibitor

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15
Q

lomitapide

A

new tx. for homozygous familial
hypercholesterolemia

  • Once daily oral dose
    MOA: binds and inhibits microsomal triglyceride transfer proteins and prevents assembly of apoB

ADR’s: GI diarrhea and nausea, increased liver transmainases, hepatic fat accumulation

CI’s: DON’T USE PREGNANCY

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16
Q

mipomersen

A

new tx. for homozygous familial hypercholesterolemia

  • Once weekly injection
  • adjunct to diet and other lipid lowering therapy

MOA: inhibits apo B-100 synthesis (Apo B is the main component of LDL and VLDL). Binds mRNA if apoB thus reducing formation

ADRs: flu like sx, h/a, elevation of liver transaminases

CI’s: moderate or severe hepatic impairment, active liver disease

17
Q

what is optimal target for therpay?

A

optimal = <160

18
Q

HMG-CoA Reductase inhibitors

A
  • Statin: decreased LDL levels
  • inhibit the rate limiting enzyme in cholesterol synthesis –> decreased cholesterol synth –> increased LDL receptor production –> pulls more LDLS out of the blood
  • Pravastatin is only drug not metabolized by CYP’s (good for pt. already taking a lot of drugs)
    CI: DON’T USE for pregnant women

ADRs: LFT elevation, CPK elevation, rhabdomyolysis, myopathy

  • Combination not shown to be beneficial, rather maximizing statin intesnsity reduceds ASCVD events
19
Q

Nicotinic Acid

A
  • Niacin: inhibits lipolysis of triglycerides in adipose tissue, thus reduces circulation of FFA’s
  • results in increased HDL levels, decreased LDL levels
  • ADR’s: cutaneous flush, pruritis, acanthosis nigricans, hepatotoxicity
  • CIs: hepatic disease, active PUD, caution with DM
20
Q

Fibric Acid

A
  • MOA: results in decreasing pt. triglyceride levels - PPARalpha agonists, increase expression of LPL
  • Gemfibrozil, fenofibrate
  • useful in management of hypertriglyceridemias where VLDL predominates
  • ADR’s: GI, lithiasis, myositis, myopathy
  • CI’s: hepatic or renal dysfunction, pregnancy
  • DI’s: warfarin increases risk of rhabdomyolysis in combo with statins
21
Q

Resins

A

= Bile Acid Sequestrants, result in cholesterol conversion being increased into bile acids –> greater chance of LDL clearance

  • (bind bile acids increasing excretion 10x, increased LDL clearance)
  • Colestipol, cholestyramine, colesevelam
  • ADR’s: GI constipation and nausea, impaired ADEK
  • CI’s: caution in divertibulitis, bowel disease, cholestasis
  • ***DI’s: impairs drug absorption - need seperate administration
22
Q

Cholesterol Absorption inhibitor

A
  • Agent: ezetimibe
  • : inhibits NPC1L1, inhibits absorption of cholesterol and plant sterols
  • ADR’s: diarrhea
  • DI’s: avoid administration with bile acid sequestrants
23
Q

what decreases LDL most?

A

statins, bile acid sequesterants second

24
Q

what decreases TG’s most?

A

Fibrates

25
Q

what increases HDL most?

A

Niacin

26
Q

when to prescribe statins?

A
  1. Clinical ASCVD
  2. Primary elevation of LDL-C ≥ 190 mg/dL
  3. Age 40-75 years with diabetes and LDL-C 70-189 mg/dL
  4. No clinical ASCVD or diabetes who are 40-75 years and LDL-C 70-189 mg/dL with ASCVD risk of ≥ 7.5%
27
Q

Two high intensity statins?

A

atorvastatin: 40-80mg

Rosuvastatin 20 mg

28
Q

metabolized by CYP3A4?

A

lovastatin, simvastatin, atorvastatin

29
Q

metabolized by CYP2C9?

A

fluvastatin rosuvastatin

30
Q

CYP450?

A

pitavastatin

31
Q

what are statins used for?

A

plaque stabilization, improvement of coronary endothelial fn, inhibition of platelet thormbus formation, anti-inflamm. effects

Can reduce LDL levels by 20-50%

32
Q

potency of statins

A

rosuvastatin > atorvastatin&raquo_space;simvastatin >pitavastatin = lovastatin = pravastatin >fluvastatin

statins should be given in evening as cholesterol synth occurs mainly at night

33
Q

adverse effects of statins?

A

elevation of serum animotransferase in liver (don’t use with alcoholics or liver disease)

muscle: CK activity may increase in patients with high level of physical activity

rhabdomyolysis –> myoglobinuria can occur and sometimes lead to renal injury

Statins increase warfarin levels

contraindicated in pregnancy, liver disease, skeletal myopathies

34
Q

adverse effects of Niacin?

A

intense cutaneous flush, pruritis, rashes, acanthosis nigricans, hepatotoxicity

CI: hepatic disease, active peptic ulcer
use with caution in pt. w/ DM

35
Q

adverse effects of fibrates?

A

GI disturbances, lithiasis, myositis, myopathy

avoid use in pt w/ hepatic or renal dysfunction

can increase the risk of cholesterol gallstones - don’t use in pt. with biliary tract disease

36
Q

what used to tx. pt. with primary hypercholesterolemia?

A

bile acid sequesterins = resins

37
Q

adverse effects of resins?

A

GI effects, impaired absorption of fat-soluble vitamins at high doses

avoid use in pt. w/ diverticulitis, bowel disease, cholestasis

Cardio II: Exam 2 (7 decks)

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