2.12 Drug Therapy for Dyslipidemias

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xangxelax
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2.12 Drug Therapy for Dyslipidemias
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2014-01-18 05:14:53
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  1. How do cells requiring cholesterol absorb LDLs?
    By receptor mediated endocytosis
  2. What is dyslipidemia?
    • Elevation in total cholesterol
    • Elevation in LDL cholesterol
    • Elevation in triglycerides
    • Low HDL concentration
  3. What is the mechanism of action for Statins?
    • Inhibition of HMG Co-A Reductase which interrupts the conversion of HMG Co-A to mevalonate
    • Rate limiting step in cholesterol biosynthesis
    • Inhibiting HMG Co-A Reductase --> Reducing intracellular concentrations of cholesterol
    • Provoke synthesis of LDL-Receptors on surface of cell type¬†
    • More receptors for LDL, LDL can bind to it and bring them in, into the cell so they reduce LDL concentration in blood
  4. What is the most effective agent in reducing LDL cholesterol?
    Statin
  5. What are common adverse events for statins?
    • Hepatic - Increase in serum transaminases (2-3%)
    • MSK - Myalgia, weakness
  6. What are serious adverse events for statins?
    • Rhabdomyolysis - muscle symptoms w/ increased creatinine kinase (10X more than normal)
    • Increase in serum creatinine and dark urine
  7. What are contraindications for statins?
    • Active liver disease
    • Persistent unexplained elevations in serum transaminases
    • Pregnancy category X
  8. If one type of statins increases LFT 3X, what should you do?
    • Discontinue that particular statin and give a different kind of statin
    • No Class Effect for statins
  9. How is Statins metabolized?
    By CYP3A4
  10. What drug interactions do Statins have?
    • Drugs that interfere with CYP3A4 can increase serum concentrations of statins (ie. Macrolides (antibiotics), Azole antifungals, Amiodarone, HIV protease inhibitors)
    • Drugs that interfere with Hepatic Glucuronidation - another way our body metabolizes neobiotics (ie. Gemfibrozil - Fibric acid derivative)
    • Will all increase concentration of statins
  11. What are monitoring parameters for Statins?
    • Baselines for:¬†
    • Liver Function Tests (LFTs)
    • CK Levels
    • TC, LDL, HDL Levels (6 weeks after initiation or dosage change)
  12. What should you not be eating/ drinking when you're on statins?
    • Grapefruit Juice
    • Red Yeast Rice
  13. When is the optimal time to take statins?
    • In the evening
    • Maximal hepatic cholesterol synthesis from midnight - 2 AM
  14. What is the mechanism of action for Bile Acid Binding Resins?
    • Bind to bile acids to prevent reabsorption
    • Increases hepatic bile acid synthesis ultimately reducing hepatic cholesterol content
    • Stimulates production of hepatic LDL receptors increasing LDL clearance
  15. What are common adverse events for Bile Acid-Binding Resins?
    • GI - Dyspepsia, bloating, abdominal discomfort
    • Hepatic - hypertriglyceridemia, elevated transaminases
  16. What are serious adverse events for Bile Acid-Binding Resins?
    Pancreatitis
  17. What are drug interactions for Bile Acid-Binding Resins?
    • Interference w/ absorption
    • Administer all drugs 1 hour before or 3-4 hours after the admin. of the BARs
  18. What is the mechanism of action for Fibric Acid Derivatives?
    • Activation of the nuclear transcription factor perioxisome proliferator activated receptor-alpha (PPAR-alpha) - regulates genes that control lipid and glucose metabolism
    • Inhibition of lipolysis - reduces hepatic fatty acid uptake
  19. What are some common adverse events for Fibric Acid Derivatives?
    • Hepatic - increases in serum transaminases
    • MSK - Myalgia, weakness
  20. What are some contraindications for Fibric Acid Derivatives?
    • Significant hepatic or renal dysfunction
    • Primarly biliary cirrhosis
    • Pre-existing gall bladder disease
  21. What are drug interactions for Fibric Acid Derivatives?
    Gemfibrozil (due to hepatic metabolism)
  22. What are Monitoring Parameters for Fibric Acid Derivatives?
    • Cholesterol Levels
    • LFT (discontinue if levels remain >3X ULN Normal)
  23. What is the mechanism of action for Niacin?
    • Inhibition triglyceride synthesis
    • Enhancement of LPL activity (promotes clearance of VLDL)
    • Enhancement of HDL synthesis (blocks clearance of apolipoprotein A)
    • Promotes Lipolysis
  24. What are common adverse events for Niacin?
    • Flushing - Prostaglandin-mediated
    • GI - Dyspepsia, peptic ulcer disease, Nausea
    • Endocrine - Hyperuricemia, Glucose intolerance
  25. What are serious adverse events for Niacin?
    Hepatotoxicity - elevations in ALT/AST
  26. What are contraindications for Niacin?
    • Active liver disease
    • Pregnancy
  27. What is the mechanism of action for Cholesterol Absorption Inhibitors (Zetia)?
    Inhibition of cholesterol absorption at the brush border of the small intestine (decreased delivery of cholesterol to liver, reduction of hepatic cholesterol stores and resultant increased clearance of cholesterol from blood)
  28. What are adverse effects for Cholesterol Absorption Inhibitors (Zetia)?
    • Well tolerated
    • Higher incidence of ADEs when combined w/ Statin
  29. What is the mechanism of action for Fish Oil?
    • Reduces hepatic triglyceride synthesis
    • Increases triglyceride clearance
  30. What are the adverse effects for Fish Oil?
    • GI - Dyspepsia, Taste Aversion
    • Hematologic - Prolongation in bleeding time
  31. What do you give pts that have Clinical ASCVD?
    • High intensity statin if <75 yo
    • Moderate intensity statin if >75 yo or can't tolerate high intensity statin
  32. What do you give pts that have LDL >190 mg/dL?
    • High intensity statin
    • Moderate intensity statin if can't tolerate high intensity statin
  33. What do you give pts that have Diabetes (age 40-75 yo) w/ LDL 70-189 mg/dL or no clinical ASCVD?
    • Moderate intensity statin if ASCVD risk <7.5%
    • High intensity statin if ASCVD risk >7.5%?
  34. What do you give pts with no clinical ASCVD or diabetes w/ LDL 70-189 mg/dL estimated 10 year ASCVD risk >7.5%?
    Moderate to high intensity statin

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