PHARM

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mherzy
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94682
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PHARM
Updated:
2011-07-20 14:20:10
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ANTILIPEMIC AGENTS
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ANTILIPEMIC AGENTSh
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  1. Hyperlipidemia
    • -Elevated blood levels of lipoproteins ( cholesterol, triglycerides, phospholipids)
    • -Lipoprotein abnormalities: greater than or less than 1 of the following: Elevated total cholesterol (TC),Elevated low-density lipoprotein (LDL) bad ones, Elevated triglycerides (TG) should not be elevated, Reduced high-density lipoprotein (HDL) you want high, greater than 68
    • -National guidline- The National Education Program (NCEP) Adult Treatment Panel III (ATP III)
  2. Hyperlipidemia
    • -CHD risk directly correlates with TC & LDL levels in continuous fashion
    • - > 50% of American adults: TC greater or less than 200 mg/dL
    • -Lipid lowering therapy reduces risk of cardiovascular/cerebrovascular even related death
    • -LDL level are significant predictor of morbidity/mortality
  3. Coronary Heart Disease
    -The risk of CHD in patients with cholesterol levels of 300mg/dL is three to four time greater than that in patients with levels less than 200mg/dL
  4. Background & Pathophysiology
    • -Cholesterol: essential for cell membrane formation & hormone synthesis
    • -Lipids not present in free form in plasma; circulate as lipoproteins
  5. Triglycerides & Cholesterol
    • -Two primary forms of lipids in the blood
    • -Water-insoluble fats that must be bound to apolipoproteins, specialized lipid-carrying proteins
    • -Lipoproteins is the combination of triglyceride or cholesterol with apolipoprotein
    • -3 major plasma lipoproteins
  6. Lipoproteins
    -Very-low-density lipoprotein (VLDL) <-BAD - Carries ~10 to 15% of total serum cholesterol; carried in circulation as TG; VLDL= TG/5, produced by the liver, Transports endogenous lipids to the cells

    -Low-density lipoprotein (HDL) GOOD - Carries 20 to 30% of total serum cholesterol; reverse transportation of cholesterol, responsible for "recycling" of cholesterol, also known as "good cholesterol
  7. Lipoprotein Classification
  8. Background & Pathphysiology
    • -VLDL secreted from the liver - converted to IDL then LDL
    • -Plasma LDL taken up by receptors on liver, adrenal, & peripheral cells
    • -LDL internalized & degraded by these cells
    • -Increased intracellular cholesterol level inhibits HMG-CoA reductase & decreases LDL receptor synthesis
    • -Decreases in LDL receptors: plasma LDL not as readily taken up & broken down by cells
    • -LDL also excreted in bile
  9. Cholesterol homeostasis
  10. Background & Pathophysiology
    • -Oxidized LDL in artery walls provokes inflammatory response
    • -Monocytes recruited & transformed into macrophages- results in cholesterol laden foam cell accumulation
    • -Foam cells: beginning of arterial fatty streak
    • -If processes continue: angina, stroke,MI,peripheral artery disease, arrhythmias, death
  11. LIPID GOALS
    -LDL- < 100 optimal, 100-129 near optimal, 130-159 borderline high, 160-189 high, greater than or less than 190 very high

    -Triglycerides- < 150 normal, 150-199 borderline high, 200-499 high, greater or less than 500 very high

    -HDL - MEN greater or less than 40, women greater or less than 50

    -Total cholesterol- <200 desirable, 200-239 borderline high, greater than or less than 240 high
  12. RISK FACTORS
    • -Men: 45 yrs
    • -Women: 55 yrs or premature menopause without estrogen replacement therapy
    • -Family history of premature CHD (definite myocardial infarction or sudden death before age 55 yrs in father or other male first-degree relative, or before age 65 yrs in mother or other female first degree relative)
    • -Ciggarette smoking
    • -Hypertension (140/90 mm hg or taking antihypertensive medication)
    • -Low HDL cholesterol ( <40 mg/dL) b
  13. Goals and Cutpoints

    • Risk

    • Category
    • LDL

    • Goal (mg/dL)
    • Initiate TLC

    • (LDL:

    • mg/dL)
    • Consider

    • Drug Therapy (LDL: mg/dL)
    • High

    • risk: CHD or CHD risk equivalents (10-year risk >20%)
    • <100

    • (optional

    • goal: <70)
    • 100

    • 100

    • (<100

    • mg/dL;
    • consider

    • drug options)
    • Moderately

    • high risk: 2+ risk factors (10-year risk >10%–20%)
    • <130

    • 130

    • 130

    • (100–129:

    • consider drug options)
    • Moderate

    • risk: 2+ risk factors (10-year risk <10%)
    • <130

    • 130

    • 160

    • Lower

    • risk: 0–1 risk factor
    • <160

    • 160

    • 190

    • (160–189:

    • LDL-lowering drug optional)
  14. Antilipemics
    • -HMG-CoA reuctase inhibitors (HMGs, or statins)
    • -Bile acid sequestrants
    • -Niacin ( nocotinic acid)
    • -Fibric acid derivatives
  15. Antilipemics: HMG-CoA Reductase Inhibitors (HMGs, or statins)
    Most potent LDL reducers
    • -rosuvastatin (Crestor)
    • -atorvastatin (Lipitor)
    • -simvastatin (Zocor)
    • -lovastatin (Mevacor)
    • -pravastatin (Pravachol)
    • -fluvastatin (Lescol)
  16. Statins (cont'd)
    Mechanism of action
    • -Inhibit HMG-CoA reductase, which is used by the liver to produce cholesterol
    • -Lower the rate of cholesterol production
  17. Statins: Indications
    -First-line drug therapy for hypercholesterolemia - Reduce LDL levels by 18% to 55%, Increase HDL levels by 5% to 15%, Reduce triglycerides by 7% to 30%
  18. Statins: side effects
    -Mild, transient GI disturbances, rash, headache, myopathy (muscle pain), Elevations in liver enzymes or liver disease*, Rhabdomyolysis*- muscle breaks down
  19. Bile Acid Sequestrants
    • -Also caled bile acid-binding resins and ion-exchange resins
    • -cholestyramine (Questran)
    • -colestipol hydrochloride (Colestid)
  20. Bile Acid Sequestrants: Mechanisms of action
    • -Prevent resorption of bile acids from small intestine
    • -Bile acids are necessary for absorption of cholesterol
  21. Bile Acid Sequestrants: Indications
    • -Hypercholesterolemia
    • -Relief of pruritus associated with partial biliary obstruction (cholestyramine)
  22. Bile Acid Sequestrants: Side effects
    • -Constipation
    • -Heartburn, nausea, belching, bloating- These adverse effects tend to dissapear over time
  23. Niacin ( Nicotinic Acid)
    • -Vitamin B3
    • -Lipid lowering properties require much higher doses than when used as a vitamin
    • -Effective, inexpensive, often used in combination with other lipid-lowering agents.
  24. Niacin: Mechanism of action
    • -Thought to increase activity of lipase, which breaks down lipids.
    • -Reduces the metabolism or catabolism of cholesterol and triglycerides
  25. Niacin: Indications
    • -Effective in loweing triglyceride, total serum cholesterol, and LDL levels
    • -Increases HDL levels
  26. Niacin:Side effects
    • -Flushing
    • -Pruritus
    • -GI distress
    • -Hyperuricemia (gout)
    • -Hepatotoxicity
  27. Fibric Acid Derivatives
    • -clofibrate
    • -gemfibrozil (Lopid)
    • -fenofibrate (Tricor)
    • *used if triglycerides are high
  28. Fibric Acid Derivatives: Mechanism of action
    • -Believed to work by activiting lipase, which breaks down cholesterol- lower release of free fatty acid from adipose tissue, inhibit synthesis of triglycerides in the liver, higher the secretion of cholesterol in the bile
    • -DRUG EFFECTS
    • -Decrease the triglyceride levels
    • -Increase HDL by as much as 25%
  29. Fibric Acid Derivatives: Side Effects
    • -Abdominal discomfort
    • -Diarrhea
    • -Nausea
    • -Blurred vision
    • - Increased risk of gallstones
    • -Pronlonged prothrombin time
    • -Liver studies may show increased function
  30. Omega 3 fatty acids
    • -Diests rich in omega 3 fatty acids from oily fish decrease TC, TG, increase HDL & decrease CV events
    • -RX fish oil: Lovaza- lowers TG 14-30%, raises HDL ~10%
    • -FDA approved as dietary adjunct for very high TG levels (>500mg/dL)
    • -Thrombocytopenia, bleeding disorders: potential complication of high doses
  31. Omega 3 fatty acids
    • -Greater than or less than 3 grams PO daily generally recognized as safe
    • -Until further research is done on nutraceuticals it is recommended that patients get dietary EPA & DHA- eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA)
    • -2 to 4 g of EPA & DHA may be used for very high TG
    • -Adverse effects: GI disturbances, fishy aftertaste, increased bleeding risk, worsening glycemic control, increased LDL, abnormal LFTs




























































  32. Drug


    Mechanism
    of Action


    Effects
    on Lipids


    Effects
    on Lipoproteins


    Comment


    Cholestyramine,
    colestipol, colesevelam


    LDL
    catabolism

    Cholesterol
    absorption


    Cholesterol




    LDL

    VLDL


    Problem
    with compliance; binds many coadministered acidic drugs


    Niacin




    LDL
    and VLDL synthesis




    Triglyceride

    Cholesterol



    VLDL

    LDL

    HDL


    Problems
    with patient acceptance; good in combination with bile acid resins; ER niacin
    causes less flushing and is less hepatotoxic than SR form


    Gemfibrozil,
    fenofibrate, clofibrate


    VLDL
    clearance

    VLDL
    synthesis


    Triglyceride

    Cholesterol


    VLDL

    LDL

    HDL


    Clofibrate
    causes cholesterol gallstones; modest LDL lowering; raises HDL;
    gemfibrozil
    inhibits
    glucuronidation
    of simvastatin, lovastatin, atorvastatin


    Lovastatin,
    pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin


    LDL
    catabolism; inhibit LDL synthesis



    Cholesterol


    LDL


    Highly
    effective in heterozygous familial hypercholesterolemia and in
    combination with other agents


    Ezetimibe


    Blocks
    cholesterol absorption across the intestinal border


    Cholesterol


    LDL


    Few
    adverse effects; effects additive to other drugs; ENHANCE trial – no change
    in carotid intima media thickness
    (CIMT) compared to simvastatin
    monotherapy
    in patients with familial hypercholesterolemia


    Omega
    3 Fatty Acids


    inhibit
    VLDL and triglyceride synthesis in the liver


    Triglyceride



    LDL

    HDL



    May
    be administered orally with or without food. Administration with food may
    decrease stomach upset















































  33. Class


    Effect


    Side
    Effects


    CI


    Statins


    LDL
    ↓18-55%

    HDL↑
    5-15%

    TG ↓ 7-30%


    Myopathy


    LFTs


    Active/chronic

    liver
    dx


    Bile
    acid

    sequestrant


    LDL
    ↓15-30%

    HDL↑
    3-5%

    TG ßà


    GI
    distress

    Constipation

    ↓Absorption


    TG > 400



    Nicotinic
    acid


    LDL
    ↓5-25%

    HDL↑15-35%

    TG ↓20-50


    Flushing


    BG

    Gout

    Hepatotoxicity


    Chronic
    liver dx

    Severe
    gout


    Fibric
    acid


    LDL
    ↓5-20%

    HDL↑10-20%

    TG ↓20-50%


    Dyspepsia

    Gallstones

    Myopathy


    Severe
    renal dx

    Severe
    hepatic dx


    Omega
    3 Fatty Acids



    LDL
    ↑10-44.5%

    HDL↑ 9%

    TG ↓25-50%




    LDL

    Fishy
    Taste

    Abnormal
    LFTs


    Bleed risks


    Fish hypersensitivity




  34. Nursing Implications
    • -Before beginning therapy, obtain a thorough health and medication history
    • -Assess dietary patterns, exercise level, weight, height, VS, tobacco and alcohol use, family history
    • -Asses for contraindications, conditions that require caustious use, and drug interactions
    • -Contraindications include biliary obstruction, liver dysfunction, active liver disease
    • -Obtain baseline liver function studies
    • -Patients on long term therapy with sequestrants may need fat-soluble vitamins (A,D,E,K)
    • -Take with meals to decrease GI upset
    • -Patient must be counseled concerning diet and nutrition on an ongoing basis
    • -Instruct on proper procedure for taking medications
    • -Powder forms must be taken with a liquid, mixed thoroughly but not stirred, and NEVER taken dry
    • -Other medications should be taken 1 hr before or 4 to 6 hrs after meals to avoid interference with absorption
    • -Clofibrate often causes constipation; instruct patients to increase fiber and fluid intake to offset effect
    • -Instruct patients to report persistant GI upset, constipation, abnormal or unusual bleeding, and yellow discoloration of the skin
    • -Monitor for side effects, including increased lives enzyme studies
    • -Monitor for therapeutic effects- Reduced cholesterol and trglyceride levels
    • -To minimize side effects of niacin, start on low initial dose and gradually increase it, and take with meals
    • -Small doses of aspirin or NSAIDs may be taken 30 mins before niacin to minimize cutaneous flushing
    • -Inform patients that these agents may take several weeks to show effectiveness

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