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Pharm N895 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

Types of lipids

A

Low density lipoproteins (LDL)

Very low density lipoproteins (VLDL)

Triglycerides (TG)

High density lipoproteins (HDL)

emerging data on additional lipoproteins

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2
Q

LDL and lipid lowering therapy

A

“bad” cholesterol & primary target of lipid lowering Tx

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3
Q

CV risk and LDL

A

CV risk increases w/increasing LDL

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4
Q

Origin and role of VLDL

A

secreted by liver, some are converted to LDL

Export TGs to peripheral tissues

tend to see w/ingestion of excessive calories

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5
Q

TGs: what is hypertriglyceridemia associated with?

A

pancreatitis

pancreatitis typically at very high levels, e.g., >500mg/dL

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6
Q

Why is a fasting lipid panel recommended?

A

TGs increase after food–

new evidence shows may not change >10%, so not so important

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7
Q

Drugs that may induce hypertriglyceridemia

A

TPN, propofol, cleviprex (clevidipine), protease inhibitors, alcohol

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8
Q

HDL and lipid therapy

A

“good” cholesterol & secondary target for dyslipidemia

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9
Q

HDL and CV risk

A

declines w/higher HDL

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10
Q

Secondary causes of elevated LDL and TG

A

Diet, medications, comorbid conditions, disordered/altered metabolism

altered metabolism is most common

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11
Q

ATP III Guidelines: Total cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable: <200
  • borderline high: 200-239
  • high: > 240
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12
Q

ATP III Guidelines: LDL cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable: <100
  • near optimal: <100-129
  • borderline high: 130-159
  • high: 160-189
  • very high: _>_190
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13
Q

ATP III Guidelines: TGs (mg/dL)

Optimal/desirable, borderline high, high

A
  • Optimal/desirable: <150
  • near optimal
  • borderline high: 150-199
  • high: >/=200
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14
Q

ATP III Guidelines: HDL Cholesterol (mg/dL)

Optimal/desirable, near optimal

A
  • Optimal/desirable: >/=60
  • near optimal: >40 men, >50 women
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15
Q

ATP III Guidelines

A

Former guidelines based on risk factors

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16
Q

Niacin + statin

A

previously what we did but no added benefit so no longer rec’d to combine

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17
Q

2013 ACC/AHA Guidelines

A
  • Replaced ATP III
  • no longer to Tx LDL chol targets
  • Non statin therpay discouraged in most cases
  • Lifestyle modification rec’d for all pts
  • 10yr ASCVD risk calculator - risk category determines what level of statin therapy
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18
Q

Statins: when risk may outweigh benefit / C/Is / avoid in…

A
  • Risk > benefit: NYHA class II-IV HF; Maintenance hemodialysis; LDL-C <70mg/dL
  • **Avoid in: **severe hepatic impairment
  • **C/I: **pregnancy & lactation
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19
Q

Initial evaluation: labs

A
  • Fasting lipid panel: to assess adherence and predicted response
  • ALT
  • CK
  • HbA1c
  • Hx of prior or current muscle Sx
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20
Q

Evaluation: lipid panel

A
  • LDL-D >190mg/dL should assess for secondary cause or screen family for familial hyperlipidemia
  • TG: >500mg/dL should be treated
  • Repeat 4-12 w, then q3-12mths when response established
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21
Q

Evaluation: significance of ALT

A

result >3x ULN is C/I to statin therapy

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22
Q

Pharmacologic therapy for dyslipidemia

A
  • HMG-CoA reductase inhibitors (statins)
  • fibrates
  • bile acid sequestrants
  • sterol absorption inhibitor
  • nicotinic acid
  • omega3 ethyl esters
  • plant sterols/stanols
  • red yeast chinese rice
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23
Q

Statins: Agents

A

Lovastatin/Mevacor

Pravastatin/Pravachol

Simvastatin/Zocor

Fluvastatin/Lescol XL

*Atorvastatin/Liptor

*Rosuvastatin/ Crestor

*can be dosed High intensity

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24
Q

Statins: MOA

A

Inhibits HMG-CoA reductase from converting HMG-CoA to cholesterol,

thereby reducing cholesterol synthesis.

Up-regulates LDL receptors on hepatocytes.

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25
Q

Statins: Adverse Effects

A

rare confusional state or memory impairment, hepatic dysfunction, myopathy, rhabdomyolysis, DM, hemorrhagic stroke

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26
Q

Statins: timing of dose

A

some agents more effective when given in evening when most chol synthesis occurs

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27
Q

Who is at highest risk for AEs from statins?

A

multiple comorbidities including renal or hepatic impairment; Hx statin intolerance or muscle d/os; unexplained ALT >3x ULN; Age >75y; genetic polymorphisms or concomitant drugs that decrease statin metabolism/clearance

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28
Q

Statins: what to do if muscle sx

A

D/C statin. Evaluate factors that may predispose pt to Sx. R/O other causes

Next steps diff depending on severe vs mild/mod

29
Q

what to check in severe muscle sx

A

Check CK, Cr, urinalysis for myoglobinuria

30
Q

What to do if mild-moderate sx on statin, after d/cing dose

A
  • Resolve & no C/Is –> restart same statin at same or lower dose
  • Resolve, statin established as cause –> use low dose of diff statin then increase as tolerated
  • Sx unresolved after 2mth –> consider other causes. If other cause identified, restart original statin at original dose
31
Q

Statins: CYP3A4 substrates

A

Lipitor (atorvastatin)

Zocor (simvastatin)

Mevacor (lovastatin)

32
Q

Statins: CYP2C9

A

Crestor (rosuvastatin) - substrate

Lescol XL (fluvastatin) - inhibitor

33
Q

Statins: which one reduce in renal impairment

A

Crestor (rosuvastatin)

34
Q

Statin w/low potential for drug interactions, low potency (not necessarily low intensity)

A

Pravachol (pravastatin)

35
Q

Anticipated response of High, moderate, low intensity

A

High: >/= 50%

Moderate: 30-50%

Low: <30% (not recommended)

36
Q

Which statin has increased myopathy at 80mg/day?

A

Zocor (simvastatin)

37
Q

Fibrates: MOA

A

peroxisome proliferator-activated receptor alpha agonists, reduced secretion of VLDL, increased lipoprotein lipase activity, increase HDL

(mainly to lower TGs)

38
Q

FIbrates: ADRs

A

dyspepsia, rash, hypokalemia, myopathy, hepatic dysfunction, gallstones, rare blood dyscrasias, rhabdo

39
Q

Fibrates: caution in what populations & why?

A

obese, females, Native Americans due to increased risk of gallstones

40
Q

Fibrates: renal / hepatic

A

Avoid in renal or hepatic impairment

41
Q

Concomitant therapy w/statins and fibrates

A

Avoid! Increased risk myopathy and rhabdo

*may consider adding fenofibrate to a low or moderate intensity statin in select cases if benefits > risks (e.g., TG >500mg/dL)

42
Q

Fibrates: Agents

A

lopid (gemfibrozil), tricor (fenofibrate)

43
Q

Fibrates and CYPs

A

Lopid (gemfibrozil) is CYP2C9 and CYP2C19 inhibitor

44
Q

Zetia (ezetimibe): MOA

A

sterol absorption inhibitor, in bile inhibits resorption of chol, decreases LDL

45
Q

Zetia (ezetimibe): ADRs

A

rare hepatic dysfunction, myositis

46
Q

Zetia (ezetimibe): Monitoring

A

baseline LFTs, discontinue if persistent ALT >3x ULN

47
Q

Zetia (ezetimibe): how are they used?

A

generally in combo w/HMG-CoA reductase inhibitors (statins)

48
Q

Zetia (ezetimibe): contraindications

A

pregnancy and lactation

49
Q

Bile Acid Sequestrants: MOA

A

Prevent reabsorption of bile acis by binding them in the intestinal lumen, increased chol catabolism, upregulate LDL receptors

50
Q

Bile acid sequestrants: AEs

A

constipation, bloating, heartburn, diarrhea, increased VLDL

51
Q

Bile acid sequestrants: monitoring

A

fasting lipid panel at baseine, 3mths, then every 6-12mths

52
Q

Bile acid sequestrants: avoid in

A

diverticulitis, TG >/= 250mg/dL (**C/I >400), **type III hyperlipoproteinemia

53
Q

Bile acid sequestrants:​ effect on nutrient absorption

A

may impair vit K and FA absorption

must take with food to be effective

54
Q

Bile acid sequestrants and drug interaction

A

administer other meds 1 hour prior, or 2 hours after to limit interaction

55
Q

Bile acid sequestrants:​ Agents

A

Colestid (colestipol)

questran (cholestyramine)

Welchol (colesevelam)

56
Q

Niaspan (nicotinic acid): what is it?

57
Q

Niaspan (nicotinic acid): MOA

A

reduced VLDL hepatic secretion and catabolism of apoAl; increased HDL, reduced LDL and TG

58
Q

Niaspan (nicotinic acid): dosing

A

initiate at low dose, then titrate as tolerated over weeks

59
Q

Niaspan (nicotinic acid): Monitoring

A

fasting BG or HbA1c, LFTs, uric acid at baseline, when dose increase and Q6mths

60
Q

Niaspan (nicotinic acid): how to prevent flushing

A

pre-medication w/aspirin 325mg 30min prior to nicotinic acid dose

61
Q

Niaspan (nicotinic acid): contraindications

A

pregnancy and lactation

62
Q

Niaspan (nicotinic acid): ADRs

A

flushing, pruritis, rash, dry skin, nausea, abdominal discomfort, hyperuricemia, rare hepatotoxicity, arrhythmias, macular edema

63
Q

Niaspan (nicotinic acid): discontinue niacin if…

A

persistent severe cutaneous symptoms, persistent hyperglycemia, acute gout, unexplained abdominal pain or GI Sx, new onset afib, new onset weight loss

64
Q

Omega-3 Ethyl Esters: available forms

A

Lovaza by prescription or over-the-counter fish oil capsules; 3-4gm docosahexaenoic and eicosapentaenoic acids/day

65
Q

Omega-3 Ethyl Esters: MOA

A

reduce hepatic synthesis of TGs, increase plasma lipoprotein lipase activity

66
Q

Omega-3 Ethyl Esters:​ Adverse Effects

A

pruritis, rash, dysgeusia, dyspepsia, constipation, LFT abnormalities, may increase LDL levels

67
Q

Omega-3 Ethyl Esters:​ monitoring

A

GI disturbances, skin changes, bleeding

68
Q

When to consider Omega-3 Ethyl Esters?

A

may consider when TG >500mg/dL

Pharm N895 (13 decks)

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