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Heme / Onc > SM_260b: Anticoagulant Therapy for VTE > Flashcards

SM_260b: Anticoagulant Therapy for VTE Flashcards

1
Q

Describe indirect anticoagulants

A

Indirect anticoagulants

  • Antagonize Vitamin K: warfarin
  • Require antithrombin: heparin, LMWH (dalteparin, enoxaparin), fondaparinux
  • Direct: factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), thrombin inhibitors (dabigatran, argatroban)
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2
Q

Describe synthesis of Vitamin K dependent clotting factors

A

Synthesis of Vitamin K dependent clotting factors

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3
Q

Describe clotting cascade

A

Clotting cascade

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4
Q

____ is the main regulator of the carboxylation reaction

A

Vitamin K epoxide reductase is the main regulator of the carboxylation reaction

  • Carboxylated proteins: II, VII, IX, X, C, S, Z are Vitamin K dependent clotting factors
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5
Q

Warfarin causes ____ deficiency in all Vitamin K dependent clotting factors

A

Warfarin causes acquired deficiency in all Vitamin K dependent clotting factors

  • Vitamin K epoxide reductase is main modulator of warfarin response
  • Vitamin K epoxide reductase mutations either increase sensitivity to warfarin or cause hereditary warfarin resistance
  • Homozygosity for missense mutation results in inherited combined deficiency of II, VII, IX, and X
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6
Q

____ increases resistance to warfarin

A

VKORC1 increases resistance to warfarin

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7
Q

____ increases sensitivity to warfarin by decreasing warfarin clearance

A

CYP2C9 increases sensitivity to warfarin by decreasing warfarin clearance

  • Genetic polymorphisms
  • Drug inhibitors / enhancers
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8
Q

Describe drugs that increase sensitivity to warfarin

A

Increase sensitivity to warfarin

  • Antibiotics: erythromycin, fluconazole, INH
  • Cardiac: amiodarone, propranolol
  • Anti-inflammatories: piroxicam
  • GI: cimetidine, omeprazole
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9
Q

Describe drugs that increase resistance to warfarin

A

Increase resistance to warfarin

  • Antibiotics: nafcillin, rifampin
  • Anticonvulsants: most
  • Other: sucralfate, cholestyramine
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10
Q

Ginkgo and garlic interactions with warfarin can cause ___

A

Ginkgo and garlic interactions with warfarin can cause bleeding

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11
Q

St. John’s wort interaction with warfarin can cause ____

A

St. John’s wort interaction with warfarin can cause thrombosis

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12
Q

Warfarin is ___-acting and requires ___ to achieve therapeutic levels

A

Warfarin is slow-acting and requires 5 days of dosing to achieve therapeutic levels

  • Full anticoagulation effect occurs when prothrombin levels are reduced to 20%
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13
Q

Warfarin is monitored using ___ and ___

A

Warfarin is monitored using PT and iNR

  • INR standardizes PT results
  • INR = (patient PT / control PT) ISI
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14
Q

Goal INR is ___

A

Goal INR is 2-3

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15
Q

____, ____, and ____ are adverse effects of warfarin

A

Bleeding, teratogenic, and warfarin necrosis are adverse effects of warfarin

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16
Q

____ reverses effects of warfarin

A

Vitamin K reverses effects of warfarin

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17
Q

Describe how to manage elevated INR but no bleeding

A

Elevated INR but no bleeding

  • INR > 3-10: hold warfarin
  • INR > 10: hold warfarin, give oral Vitamin K if possible or IV Vitamin K if not
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18
Q

Describe how to manage bleeding while on warfarin

A

Bleeding while on warfarin

  • Hold warfarin, give Vitamin K IV
  • Give 4 factor prothrombin complex concentrate or FFP if unavailable
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19
Q

Describe heparin

A

Heparin

  • Polymeric, highly sulfated glycosaminoglycan
  • 30-50 saccharide units
  • Pentasaccharide sequence binds antithrombin
  • Longer chains also bind thrombin
  • Inhibits factor Xa and thrombin
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20
Q

Describe unfractionated heparin

A

Unfractionated heparin

  • Inactivated in gut and given IV or SQ
  • Metabolized in liver and kidney
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21
Q

Describe mechanism of unfractionated heparin

A

Unfractionated heparin

  1. Binds antithrombin to activate it and enhance its effects
  2. Heparin-antithrombin complex inhibits thrombin
  • Thrombin bound to fibrin is protected from heparin - prevents further clot formation but doesn’t dissolve clot
  • Inhibits smooth muscle proliferation and angiogenesis
  • Bound form usually inactive
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22
Q

Unfractionated heparin acts ___

A

Unfractionated heparin acts immediately

  • aPTT and/or UFH anti-Xa levels are used to monitor dose
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23
Q
A
24
Q

____, ____, and ____ are adverse reactions of unfractionated heparin

A

Bleeding, heparin-induced thrombocytopenia, and osteoporosis are adverse reactions of unfractionated heparin

  • Mild inhibition of aldosterone may increase potassium
25
Q

Heparin-induced thrombocytopenia occurs when ___

A

Heparin-induced thrombocytopenia occurs when antibodes bind heparin-platelet factor 4 complex and agglutinate platelets, leading to paradoxical thrombosis despite low platelets

  • Discontinue heparin immediately and start alternative anticoagulants (direc thrombin inhibitors)
26
Q

Describe advantages and disadvantages of unfractioned heparin

A

Unfractioned heparin

  • Advantages: effect immediate, 5000 U sc q8-12h is safe and effective thromboprophylaxis for low risk patient, reversed by protamine
  • Disadvantages: protein binding so effect must be monitored, heparin-induced thrombocytopenia
27
Q

LMWH works primarily through ___

A

LMWH works primarily through potentiation of antithrombin effect on factor Xa

(lacks tail to bind thrombin)

28
Q

____, ____, and ____ are examples of LMWH

A

Dalteparin, enoxaparin, and tizaparin are examples of LMWH

29
Q

LMWH has ___ subcutaneous absorption than heparin

A

LMWH has better subcutaneous absorption than heparin

30
Q

Describe advantages and disadvantages of LMWH

A

LMWH

  • Advantages: better subcutaneous absorption than heparin, less binding to plasma proteins, more predictable effect so monitoring not routinely needed; outpatient use feasible; infrequently causes heparin-induced thrombocytopenia or osteoporosis
  • Disadvantages: renally cleared, expensive, subcutaneous injection
31
Q

Fondaparinux is a ____ that only has ____ activity

A

Fondaparinux is a synthetic 5 saccharide binding site of antithrombin that only has anti-Xa activity activity

  • Given subcutaneously and has high bioavailability
  • Minimal protein binding and no monitoring needed
  • Once daily subcutaneous injection because half-life of 17 hours
  • Minimal interaction with platelets
32
Q

Describe advantages and disadvantages of fondaparinux

A

Fondaparinux

  • Advantages: once daily dosing, no monitoring required, equivalent in efficacy
  • Disadvantages: not used in renal failure and low body weight due to risk of bleeding, no reversal agent, expensive
33
Q

Direct thrombin inhibitors ___ and ___

A

Direct thrombin inhibitors inactive clot-bound and soluble thrombin and do not require antithrombin as a co-factor

  • Derived from medicinal leech
  • Not inactivated by platelet factor 4 or heparinase
34
Q

____, ____, and ____ are direct thrombin inhibitors

A

Bivalirudin, argatroban, and dabigatran are direct thrombin inhibitors

35
Q

Bivalirudin is used for ___ and has a ___ half-life

A

Bivalirudin is used for thrombus prevention in coronary interventions and has a very short half-life (25 minutes)

36
Q

Argatrobin reversibly binds to ___ and is used primarily in ___

A

Argatrobin reversibly binds to catalytic site of thrombin and is used primarily in treatment of heparin-induced thrombocytopenia

  • IV infusion
  • Monitor with aPTT
  • Conversion to warfarin problematic because argatroban prolongs PT
37
Q

Direct acting oral anticoagulants are ___ and have ___

A

Direct acting oral anticoagulants are oral and have more predictable pharmacokinetics that obviate the need for routine monitoring

  • All approved for prevention of thrombosis in atrial fibrillation, treatment, and prevention of DVT and PE
38
Q

Direct acting oral anticoagulants are ____, ____, ____, ____, and ____

A

Direct acting oral anticoagulants are rivaroxaban, apixaban, edoxaban, betrixaban, and dabigatran etexilate

39
Q

Anti-Xa DOACs are ____, ____, ____, and ____

A

Anti-Xa DOACs are rivaroxaban, apixaban, edoxaban, and betrixaban

40
Q

Direct thrombin inhibitor DOAC is ___

A

Direct thrombin inhibitor DOAC is dabigatran etexilate

41
Q

Compare DOACs

A

DOACs

42
Q

Compare DOACs and warfarin

A

DOACs and warfarin

43
Q

____ is used for reversal of dabigatran

A

Idarucizumab is used for reversal of dabigatran

  • Humanized monoclonal antibody fragment (Fab) that binds specifically to dabigatran
  • Much higher affinity for dabigatran than thrombin
44
Q

___ is used for reversal of rivaroxaban and apixaban

A

Andexanet alpha is used for reversal of rivaroxaban and apixaban

  • Acts as a factor Xa decoy and retains high affinity for all direct FXa inhibitors
  • Change of serin to alanine to eliminate catalytic activity and prevent prothrombin cleavage
45
Q

Thrombolytics ___

A

Thrombolytics activate plasminogen to form plasmin in order to accelerate thrombus breakdown

  • Indications: acute coronary thrombosis, massive PE, thrombotic stroke
46
Q

tPA is a ___

A

tPA is a thrombolytic

47
Q

Cullen’s sign is ___

A

Cullen’s sign is periumbilical bleeding with anticoagulation

48
Q

Turner’s sign is ___

A

Turner’s sign is flank bleeding with anticoagulation

49
Q

If bleeding occurs with anticoagulation, ___ and ___

A

If bleeding occurs with anticoagulation, stop anticoagulant and other offending agents contributing to bleeding (aspirin, NSAIDs) and use a reversal agent

50
Q

Protamine is a reversal agent for ___

A

Protamine is a reversal agent for UFH

  • Partly reverses LMWH
51
Q

Vitamin K and 4-factor prothrombin complex concentrate are reversal agents for ___

A

Vitamin K and 4-factor prothrombin complex concentrate are reversal agents for warfarin

52
Q

Idarucuzimab is a reversal agent for ___

A

Idarucuzimab is a reversal agent for dabigatran

53
Q

Andexanet alpha is a reversal agent for ____

A

Andexanet alpha is a reversal agent for anti-Xa inhibitors

54
Q

Acute management of thrombosis involves ___

A

Acute management of thrombosis involves beginning anticoagulant when thrombosis is suspected or diagnosed

55
Q

Describe long-term management of VTE

A

Long-term management of VTE

  • Everyone with acute VTE needs 3 months of anticoagulation
  • After 3 months
    • If provoked VTE: stop
    • If unprovoked: indefinitely as long as risk of recurrent clot outweighs risk of bleeding
56
Q

Summarize the anticoagulants

A

Anticoagulants

Heme / Onc (41 decks)

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