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951 Block 3 > 5. Oral Anticoagulants > Flashcards

5. Oral Anticoagulants Flashcards

1
Q

What is the MOA of warfarin?

A

inhibits the synthesis of vitamin-K dependent coagulation factors by interfering with the cyclic interconversion of Vit K epoxide to the active form of Vit K

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2
Q

What are the vitamin-K dependent coagulation factors?

A
  • prothrombin
  • VII
  • IX
  • X
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3
Q

________ is a cofactor for the carboxylation of glutamate residues to gamma-carboxyglutamic acid.

A

Vit K

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4
Q

What process allows the coagulation proteins to undergo a conformational change that is necessary for their activation?

A

carboxylation

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5
Q

Warfarin depletes the _______ form of Vitamin K.

A

reduced

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6
Q

What is the reduced form of Vitamin K?

A

vitamin KH2

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7
Q

Therapeutic doses of warfarin decrease the total amount of active Vit K-dependent clotting factors by _____%

A

30-50%

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8
Q

Warfarin affects the activity of already synthesized coagulation factors. (T/F)

A

False: does not affect the activity of already synthesized clotting factors

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9
Q

What is the degradation half-life of prothrombin?

A

60 hours

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10
Q

What is the degradation half-life of factor VII?

A

4-6 hours

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11
Q

What is the degradation half-life of factor IX?

A

24 hours

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12
Q

What is the degradation half-life of factor X?

A

48-72 hours

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13
Q

How many days of warfarin therapy are required before a clinical response occurs?

A

~ 5 days

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14
Q

Warfarin reduces the activity of anticoagulant proteins __ and __.

A

C and S

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15
Q

What is the half-life of protein C?

A

8 hours

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16
Q

What is the half-life of protein S?

A

30 hours

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17
Q

___________ may be induced after treatment with warfarin is started.

A

hyper-coagulation

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18
Q

Why can hyper-coagulation occur at the initiation of warfarin therapy?

A

The rapid loss of protein C temporarily shifts the balance in favor of clotting until sufficient time has passed for warfarin to decrease the activity of the clotting factors.

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19
Q

PT is prolonged by ______.

A

warfarin

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20
Q

Factors reduced by warfarin at a rate proportional to their ________.

A

half-life

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21
Q

During the first few days of warfarin therapy, the PT primarily reflects the depression of factor ____.

A

VII

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22
Q

With subsequent warfarin treatment, the PT is prolonged by depression of _______ and _______.

A

prothrombin and factor X

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23
Q

PT is a reliable measure of anticoagulation throughout the duration of warfarin therapy. (T/F)

A

False: not reliable in the early course

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24
Q

What is the route of administration of warfarin?

A

oral

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25
Q

Orally administered warfarin is well absorbed from the GI tract. (T/F)

A

True

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26
Q

The effect of warfarin is greatly amplified when administered IV compared to oral. (T/F)

A

False: no difference

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27
Q

Plasma concentrations of warfarin are detectable within ______ of administration.

A

1 hour

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28
Q

The clinical effects of warfarin can be seen in _______.

A

5-7 days

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29
Q

A loading dose of 25 mg of warfarin is recommended to achieve clinical effects more quickly. (T/F)

A

False: loading doses > 10 mg do not provide quicker effects and may be associated with hyper-coagulation

30
Q

Warfarin is ______ protein bound.

31
Q

Where is warfarin eliminated?

A

hepatic metabolism (CYP450)

32
Q

Name 3 drugs that increase warfarin levels.

A
  • erythromycin : abx
  • isoniazid : abx
  • fluconazole : antifungal
  • cimetidine : H2RA
  • amiodarone : antiarrhythmic
  • clofibrate : lipid-lowering
  • propranolol : β blocker
33
Q

Name 3 drugs that decrease warfarin levels.

A
  • cholestyramine : lipid-lowering
  • barbiturates : CNS depressant
  • rifampin : abx
  • sucralfate : GI protectant
34
Q

What does INR stand for?

A

international normalized ratio

35
Q

Why is INR used?

A

normalization of results using different commercial sources of tissue factor

36
Q

What is ISI?

A

international sensitivity index: sensitivity of each particular thromboplastin to warfarin

37
Q

What is the formula for INR?

A

INR = (PT patient/ PT mean normal) ^ISI

38
Q

Thromboplastin with higher ISI values are more sensitive to anticoagulation effects. (T/F)

A

False: lower ISI = more sensitive

39
Q

For most indications what is the target INR for warfarin therapy?

A

2.0 – 3.0

40
Q

What is the target INR for mechanical heart valves?

A

2.5 – 3.5

41
Q

What is the usual starting dose for warfarin?

A

5 – 10 mg

42
Q

How is anticoagulation therapy managed for an established thrombosis or high risk for thrombosis?

A
  • initial treatment: rapid acting parenteral anticoagulant (heparin or LMWH)
  • long-term: warfarin with INR determined q4 weeks
43
Q

What are the direct factor Xa inhibitors?

A
  • rivaroxaban (Xarelto)
  • edoxaban (Savaysa)
  • apixaban (Eliquis)
44
Q

What are the direct thrombin inhibitors?

A

dabigatran (Pradaxa)

45
Q

Dabigatran is a prodrug. (T/F)

46
Q

Dabigatran is an irreversible competitive inhibitor of thrombin. (T/F)

A

False: reversible

47
Q

Dabigatran inhibits free or clot-bound thrombin?

A

both free and clot-bound

48
Q

Dabigatran inhibits thrombin’s activation of ________.

49
Q

How is dabigatran eliminated?

A

primarily unchanged in urine

substrate of P-glycoprotein

50
Q

Dabigatran is an inducer of CYP450 enzymes. (T/F)

51
Q

Dabigatran is a substrate of CYP450 enzymes. (T/F)

52
Q

Dabigatran is not an inhibitor of CYP450 enzymes. (T/F)

53
Q

What drug will reduce the plasma concentrations of dabigatran?

A

P-glycoprotein inducers: rifampin

54
Q

Dabigatran shows linear PK. (T/F)

55
Q

What is the dose of dabigatran?

A

150 mg BID (may reduce for ↓ CrCl)

56
Q

What is dabigatran approved for?

A

reduction in risk of stroke and systemic embolism in non-valvular a.fib

57
Q

What is the “antidote” for reversing anticoagulation with dabigatran?

A

idarucizumab

58
Q

How is rivaroxaban dosed?

A

once or twice daily depending on indication and CrCl

59
Q

What is the onset of action of rivaroxaban?

60
Q

Rivaroxaban requires no lab monitoring. (T/F)

61
Q

How is rivaroxaban eliminated?

A

metabolized by CYP3A4 and excreted unchanged in urine

62
Q

What is the onset of action of edoxaban?

63
Q

INR must be monitored with edoxaban therapy. (T/F)

A

False: no lab monitoring

64
Q

Edoxaban undergoes minimal liver metabolism. (T/F)

65
Q

How is edoxaban primarily eliminated?

A

unchanged by the kidneys

66
Q

What is the black box warning with edoxaban?

A

Do not administer to non-valvular atrial fibrillation patients with CrCl > 95 mL/min

67
Q

What is the onset of action of apixaban?

68
Q

Apixaban does not require lab monitoring. (T/F)

69
Q

What is the metabolism of apixaban?

A
  • Hepatic: primarily by CYP3A4/5

- ~27% unchanged in urine

70
Q

What are the advantages of using direct thrombin/Xa inhibitors vs. warfarin?

A
  • similar efficacy in preventing clots
  • rapid onset of action
  • less drug interactions / no food interactions
  • wide therapeutic index
  • no lab monitoring
71
Q

What are the disadvantages of using direct thrombin/Xa inhibitors vs. warfarin?

A
  • high cost
  • lack of antidotes
  • difficulty with renal impairment
  • not approved for preventing embolism following MI

951 Block 3 (10 decks)

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