GU Pharm Anticoag, Lipid-Lowering

  1. How does chloral hydrate effect warfarin?
    • displaces it from albumin
    • enhances effect of Warfarin
  2. Which drugs decrease metabolism of Warfarin by inhibiting p450 enzymes?
    • Amiodarone
    • Clopidogrel
    • Ethanol
    • Fluconazole
    • Fluoxetine
    • Metronidazole
    • Sulfamethoxadole
  3. How do abx effect Warfarin?
    • decrease gut bacteria
    • decrease in vitamin K availability in GI tract
    • enhance effect of Warfarin
  4. How do anabolic steroids (like testosterone) effect Warfarin?
    • inhibit synthesis
    • increase coagulation degradation factors
  5. What coagulation factors are affected by Warfarin and what is their half-life?
    • VII: 4-6 hrs
    • IX: 24 hrs
    • X: 48 hrs
    • II: 60 hrs
  6. Main CYP450 enzyme used to metabolize Warfarin.
  7. How does cholestyramine effect Warfarin?
    inhibits GI absorption (reduces effect)
  8. Which drugs increase metabolism of Warfarin by inducing P450 enzymes (esp 2C9)?
    • Barbituates
    • Carbamazapine
    • Phenytoin
    • Rifampin
    • (all reduce effects of Warfarin)
  9. How does vitamin K effect Warfarin?
    • bypasses its inhibition of epoxide reductase;
    • reduces effect
  10. Warfarin will inhibit _____ before inhibiting ______.
    • protein C
    • Factors II, VII, IX, X
  11. Major AEs of Warfarin.
    • Purple Toe (sm cholesterol deposit breaks off & travels to feet)
    • Osteoporosis (b/c of decreased vitamin K intake & inhibition of vitamin K-mediated bone function)
    • Skin Necrosis (Microvascular thrombosis via inhibition of Proteins C & S)
  12. Goal of INR with Warfarin.
    2-3 or 2.5-3.5
  13. What are Enoxaparin, dalteparin, & tinzaparin? How are they eliminated?
    • LMWH
    • renally
  14. What does heparin bind to?
    • ATIII
    • *ATIII by itself will not inactivate coagulation factors*
  15. Coagulation factors effected by heparin.
    • IIa (Thrombin)
    • Xa
    • *LMWH more selective for Xa than IIa 3:1)
  16. What is a type 1 HIT reaction?
    • (heparin-induced thrombocytopenia)
    • Ab-coated platelets are targeted for removal from circulation
    • 50-75% reduction in platelet counts after 5 days
  17. Which HIT reaction is transient and rapidly reversible?
    Type I
  18. What is a type 2 HIT reaction?
    • platelets are targeted for destruction, AND
    • the ab cause plt activation and aggregation
  19. Which HIT rxn causes FATAL thrombosis? How?
    • type 2
    • ab cause platelet activation and aggregation
  20. What is the antidote for heparin? What is it ineffective against?
    • protamine
    • fondaparinux, a selective factor Xa inhibitor
  21. What is a sign of HIT reaction?
    decreased platelet count (20,000 - 30,000) in just a few days
  22. Fondaparinux—parenteral
    Rivaroxaban (Xarelto) & apixaban (Eliquis)—oral
    Selective Factor Xa Inhibitors
  23. Lepirudin, hirudin, desirudin, bivalirudin, argatroban, dabigatran.
    Direct Thrombin Inhibitors.
  24. Many _______ are for HIT to prevent further reduction of platelet count while preventing thrombosis
    direct thrombin inhibitors
  25. Oral direct thrombin inhibitor.
    Dabigatran (Pradaxa)
  26. Which direct thrombin inhibitor is a prodrug?
    Dabigatran (Pradaxa)
  27. Advantage and disadvantage of Dabigatran (Pradaxa) over Warfarin.
    • advantage: no frequent monitoring
    • disadvantage: no direct reversal agent
  28. How does tPA work?
    • Converts plasminogen to plasmin; 
    • Plasmin degrades fibrin, which is required for formation of stable clot.
  29. Three tPA fibrinolytics.
    • Alteplase (recombinant)
    • Tenecteplase (genetically engineered)
    • Reteplase (genetically engineered)
  30. Two thrombolytics (not tPAs)
    • Streptokinase
    • Urokinase
  31. Cause lysis of EXISTING clots.
  32. How do Thrombolytics/Fibrinolytics prevent distal tissue necrosis?
    • Restore patency of an obstructed tissue
    • cause lysis of existing clots
  33. Clinical indications for thrombolytics.
    • Acute MI
    • Acute ischemic stroke
    • Massive PE
    • Central IV line occlusion
  34. What to administer with acute ischemic stroke?
    Alteplase w/in 3 hours
  35. Most potent statin.
  36. Atorvastatin, simvastatin, & lovastatin are metabolized by _____.
    CYP 3A4
  37. How do HMG CoA Reductase Inhibitors work?
    • Reduce body’s natural production of LDL, which
    • causes upregulation of LDL receptors, which
    • increases uptake of plasma LDL into hepatocytes
    • (takes it out of systemic circulation)
  38. Pharm classes of lipid-lowering agents.
    • HMG CoA reductase inhibitors (statins)
    • Bile acid sequestrants
    • Cholesterol absorption inhibitors
    • Fibrates
    • Niacin
    • Omega-3 fatty acids
  39. Which HMG CoA Reductase Inhibitors are not metabolized by 3A4?
    • Rosuvastatin
    • Pitavastatin
  40. What is Ezetimibe?
    A cholesterol absorption inhibitor that is usually combined with a statin
  41. How are Cholesterol Absorption Inhibitors metabolized? Why is this significant?
    • glucuronidation
    • less drug interactions
  42. Fibrates bind to ______.
    • peroxisome proliferator-activated receptors (PPAR)
    • PPARs play a role in metabolism of macronutrients
  43. How do fibrates work?
    increase plasma HDL & decrease triglyceride synthesis
  44. How do fibrates effect Warfarin?
    displace warfarin from albumin binding sites --- increases free warfarin concentrations
  45. Fibrates increase _____ clearance
  46. Niacin releases _____ and _____ within the skin
    • PGD2
    • PGE2
  47. AE of Niacin.
    • Pruritis
    • Hyperuricemia
    • Impaired insulin sensitivity
    • Myopathy (rare)
Card Set
GU Pharm Anticoag, Lipid-Lowering
Anticoags, Lipid Lowering