Anticoagulation Pharmacology

  1. Drugs that inhibit platelet aggregation:
    • Aspirin
    • IIb-IIIa inhibitors
    • ADP receptor blockers
    • Thrombin receptor blocker
    • Dipyridamole
  2. What are agents of IIb-IIIa inhibitors?
    • Abciximab
    • Tirofiban
    • Eptifibatide
  3. What are agents of ADP receptor blockers?
    • Clopidogrel
    • Prasugrel
    • Ticagrelor
    • Cangrelor
  4. What are agents of thrombin receptor blocker?
  5. Which drug blocks the COX-1 enzyme?
  6. Which drug blocks P2Y12 receptor?
    • Clopidogrel, prasugrel, ticagrelor
    • (ADP receptor blocker)
  7. Which drug block PAR-1?
    Vorapaxar (thrombin receptor blocker)
  8. Which drug increases adenosine level?
  9. Eptifibatide is a _____ receptor blocker
  10. Which drug interferes with the final step of platelet aggregation?
    • Eptifibatide
    • This is a IIb/IIIa receptor blocker which is the final step of platelet aggregation where fibrin cross linking occurs
  11. T/F: inhibitors of platelet aggregation can decrease risk of stroke, MI and colo-rectal cancer
    Si, es verdad
  12. What is the secondary prevention for platelet aggregation inhibitor use?
  13. What are agents of fibrinolytics?
    • Alteplase
    • Urokinase
    • Reteplase
    • Tenecteplase
  14. Which drug is a recombinant- tPA (r-tPA)?
  15. What are therapeutic indications for fibrinolytics?
    • Catheter occlusion
    • DVT
    • MI
    • Peripheral arterial occlusion
    • PE
    • Stroke
  16. T/F: Older clots are resistance to t-PA, that is why stroke treatment is very time sensitive
    True; older clots are more resistance perhaps due to more fibrin cross-linking
  17. What are agents of fibrinolysis inhibitors?
    • Aminocaproic acid
    • Tranexamic acid
  18. What do aminocaproic acid and tranexamic acid do?
    They stop fibrinolysis meaning that it prevents the breakdown of the clot and blood continues to coagulate
  19. What is the MOA of aminocaproic acid/ tranexamic acid?
    Bind to plasminogen and prevents its conversion to plasmin
  20. T/F: Unfractionated heparin, LMWH and Indirect Factor Xa inhibitor all have similar MOA
    True; which is to inactivate thrombin and factor Xa
  21. Heparin molecule must be at least ___ saccharides in length to inactivate thrombin
  22. Heparin binds to _____ to speed up the inactivation of these clotting factors:___,___,____,___,____.
    • Antithrombin
    • Factor IIa (thrombin)
    • Factor IXa
    • Factor Xa
    • Factor XIa
    • Factor XIIa
  23. T/F: unfractionated heparin is taken orally
    False; parenteral administration: SubQ, IV bolus, constant IV infusion
  24. What is the average elimination half life for heparin?
    1.5 hours
  25. Time to steady state with constant IV infusion of heparin is ____ hours
    6 (4x the half-life which is 1.5 hours)
  26. Reversal agent for heparin and LMWH is:
    Protamine – obtained from sperm of salmon
  27. T/F: when administered alone, protamine has an anticoagulant effect
    True; even though when used as a reversal for heparin it losses its anticoagulant activity
  28. T/F: Heparin, LMWH and fondaparinux are safe for pregnant lady
    True; these are safe for baby
  29. MOA of Heparin-induced thrombocytopenia: ____ binds onto heparin which binds onto Ig____. The immune complex then bind onto Fc region of_____ which results in removal of it by _____ in the spleen. Can also result in platelet aggregation leading to ____
    • PF4 (platelet factor 4)
    • IgG
    • Platelet
    • macrophage
    • thrombosis
  30. If HIT occurs in a patient, use ________, do not use___
    • IV direct thrombin inhibitor – ie Argatroban
    • Do not use heparin or LMWH
  31. Which anticoagulant interfere with Vitamin K oxide reductase
  32. Warfarin use would lead to decreased production of which clotting factors? Why?
    • Factors 7,9,10 and thrombin (IIa) [as well as anticoagulant proteins C and S]
    • Because these are vitamin K dependent
  33. T/F: Warfarin has effect on already-synthesized clotting factors (2, 7, 9, 10)
    False; it cannot affect already synthesized clotting factors that is why therapeutic effects for heparin are not seen until those factors are depleted (usually 3-4 days)
  34. Elimination half lives of Factor II is ___ hours, and Factor X is ____ hours
    • 60
    • 48-72
  35. T/F: Drop in concentration from warfarin action potentially can cause clotting early in therapy
    True; warfarin is freaking weird. Early on is prothrombotic which means it can cause blood clots
  36. Dosing of warfarin, must follow ____ result. Which is calculated by_____
    • INR
    • INR= (Prothrombin time/ lab normal Prothrombin time)^ISI
    • ISI= international sensitivity index
  37. Warfarin is metabolized by which organ?
  38. Half life of warfarin is:
    36 hours (1.5 days)
  39. Warfarin rescues:
    • Fresh frozen plasma
    • Vitamin K : phytonadione
    • Prothrombin complex concentrate
    • Factor VIIa
  40. T/F: warfarin is safe to use in pregnant women
    False; unlike heparin/LMWH/fondaparinux, warfarin is bad, unless you are a pregnant woman with mechanical heart valves
  41. T/F: vitamin K is fat soluble, so given too much as a warfarin reversal could lead to difficulty to re-anticoagulate for a while
  42. For life-threatening bleed from warfarin, what is the treatment?
    Give Fresh frozen plasma, prothrombin complex concentrate or factor VIIa in addition to IV vitamin K
  43. Rank from greatest molecular weight to least: LMWH, Fondaparinux and heparin (UFH)
    Heparin (greated at 15,000 Da) -> LMWH (5000 Da) -> Fondaparinux (1500 Da)
  44. Clotting factor(s) targeted in: heparin (UFH), LMWH, Fondaparinux
    • UFH: Factors Xa and IIa
    • LMWH: Factors Xa and IIa
    • Fondaparinux: Xa (does not target IIa!)
  45. T/F: Fondaparinux can be administered subcutaneously
    True; an advantage over heparin
  46. Fondaparinux is ____ (direct/ indirect) Xa inhibitor, given _____, and need dose adjustment in ______, and has ____ (high/ low) incidence of thrombocytopenia
    • Indirect
    • Subcutaneously
    • Renal disease
    • Very low to rare
  47. T/F: there is usually no coagulation test monitoring required for LMWH and fondaparinux therapy
    True; PTT not used
  48. T/F: protamine is a reversal agent used for fondaparinux
    False; Factor VIIa is. Protamine is for heparin and most the time for LMWH
  49. What are agents of direct thrombin inhibitors:
    • Bivalirudin
    • Argatroban
    • Dabigatran
  50. What are agents of direct Factor Xa inhibitors:
    • Rivaroxaban
    • Apixaban
    • Edoxaban
    • Betrixaban
  51. The common -xa name stem means it is a ____
    Direct factor Xa inhibitor
  52. T/F: Hirudin is an anticoagulant derived from salmon saliva and it is a direct thrombin inhibitor
    False; it is derived from leech saliva, lol. Salmon sperm is protamine which is a UFH/LMWH reversal
  53. Which direct thrombin inhibitor is used in cardiac cath-labs?
    Bivalirudin (used IV), alternate anticoagulant when pt has heparin allergy or HIT
  54. Argatroban is a_______
    Direct thrombin inhibitor, given IV
  55. Which direct thrombin inhibitor is given orally
  56. What does DOAC stand for?
    • Direct-acting oral anticoagulant
    • Either direct Xa inhibitors or direct thrombin inhibitors
  57. _____ is used to reduce the risk of stroke and systemic embolism in patient with nonvalvular atrial fibrillation
    Rivaroxaban (Xarelto is the trade name)
  58. Therapeutic indications for DOACs:
    • Reduce risk of stroke in nonvalvular a. fib pt
    • Treatment of DVT, PE, and reduction in risk of recurrence
    • Prophylaxis of DVT
  59. PROs of DOACs compared to warfarin:
    • Lower risk of major bleeding
    • No INR monitoring required
    • Fewer drug-diet co-morbidity interactions
  60. CONS of DOAC compared to warfarin:
    • No specific monitoring parament and only dabigatran has reversal agent
    • Renal monitoring and dose adjustment required (warfarin is eliminated via Liver)
    • Higher out-of-pocket costs and copays
  61. What is the reversal agent for dabigatran (a direct thrombin inhibitor)
  62. What is the reversal agent for direct Xa inhibitors?
    Inactivated Factor Xa
  63. What dosage and route of administration of anticoagulant should be given for effective primary prevention of hospital-acquired Venous thromboembolism (VTE)?
    Low dose, given subcutaneously
  64. High risk for venous thromboembolism:
    • Major lower extremity or pelvic orthopedic surgery
    • Neurosurgery
    • Major spine surgery
    • Active cancer
    • Active stroke
  65. If a pt is high risk for VTE, what is the treatment?
    Pharmacologic and mechanical prophylaxis (ie compression hose)
  66. If a patient is hypotensive with PE, what is the primary therapy?
    • Anticoagulation plus thrombolysis
    • Embolectomy: catheter/ surgical
  67. Primary therapy for DVT:
    Clot dissolution with pharmacochemical therapy that usually includes low-dose catheter-directed thrombolysis
  68. What is warfarin INR goal in patient with PE or DVT?
  69. Which has a delayed response: warfarin or heparin
    Warfarin, so use heparin first with warfarin then transition to just warfarin
  70. T/F: DOACs typically have a quick onset of anticoagulant effect and may not require any lead-in or overlap therapy with an additional injectable anticoagulant
  71. First choice of long-term anticoagulant in DVT of leg or PE WITH cancer:
  72. First choice of long-term anticoagulant in DVT of leg or PE without cancer:
  73. Length of anticoagulation treatment in patients with provoked (known cause) DVT:
    3 months
Card Set
Anticoagulation Pharmacology
HemeOnc Final