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Cardio > VTE Therapy > Flashcards

VTE Therapy Flashcards

1
Q

What are the goals of VTE therapy?

A
  1. Relieve symptoms
  2. Arrest the thrombus
  3. Prevent embolization
  4. Prevent recurrence
  5. Prevent complications (PTS, Pulmonary HTN)
  6. Prevent death
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2
Q

What is the acute treatment for VTE?

A

Bridge therapy or non-bridge therapy

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3
Q

What is bridge therapy?

A

Starting a parenteral agent with warfarin for at least five days AND until the INR is greater than or equal to 2

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4
Q

What is the benefit of parenteral agents?

A

They provide immediate anticoagulant activity

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5
Q

What are the three anticoagulant parenteral agents?

A

UFH, LMWH, and Fondaparinux

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6
Q

Which two parenterals anticoagulants are recommended?

A

LMWH and Fondaparinux

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7
Q

What guideline established the recommendation of LMWH and Fondaparinux over UFH?

A

The CHEST guidelines

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8
Q

What is the common oral anticoagulant that gets bridged with parenteral products?

A

Warfarin

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9
Q

What is considered “non-bridge therapy”?

A

Using novel oral anticoagulants (NOAC)

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10
Q

What are the common NOACs?

A

rivaroxaban, dabigatran, apixaban, and edoxaban

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11
Q

What is the mechanism of action for UFH?

A

Binds to antithrombin and and accelerates its interaction and inactivation of thrombin and factor Xa by 1000-fold

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12
Q

What other factors does UFH inactivate?

A

Factors IXa, XIa, and XIIa

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13
Q

What is the minimum amount of heparin chains needed to inactivate thrombin?

A

18

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14
Q

What happens when antithrombin complexes inactivate thrombin and factor Xa?

A

Heparin is released and available to bind again to antithrombin

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15
Q

Since UFH is not absorbed orally, what are the two routes of administration used?

A

Continuous infusion for treatment of VTE and subcutaneous injections for prophylaxis of VTE

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16
Q

What is a negative aspect to UFH and intravascular binding?

A

The variability/unpredictability is high; therefore, the pt has to be monitored with aPTT tests for dose adjustments

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17
Q

How is UFH cleared from the body?

A

Mainly through a rapid saturable process, but also through a slower, nonsaturable clearance through the kidneys

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18
Q

What rate order is UFH?

A

1st order rate (non-linear, dose-dependent)

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19
Q

What is the 1/2 life of UFH?

A

30-60 minutes

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20
Q

What are the monitoring parameters for UFH?

A
  1. aPTT
  2. Platelet counts, hemoglobin/hematocrit
  3. Signs/symptoms of bleeding
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21
Q

What is the dosing for UFH in VTE treatment?

A

IV bolus of 80 units/kg followed by 18 units/kg/hr continuous IV infusion

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22
Q

What is the dosing for UFH in VTE prophylaxis?

A

5000 units SC every 8 hours

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23
Q

What are the common adverse effects of UFH?

A
  1. bleeding
  2. heparin-induced thrombocytopenia
  3. heparin-induced osteoporosis
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24
Q

How do you stop bleeding in patients on UFH?

A

An IV bolus of protamine sulfate will bind to heparin and form a stable salt

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25
Q

How many mg of protamine sulfate will neutralize 100 units of UFH?

A

1 mg

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26
Q

What is type 1 heparin-induced thrombocytopenia?

A

A transient fall in platelet count due to heparin

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27
Q

What is type 2 heparin-induced thrombocytopenia?

A

an immune-mediated reaction where IgG antibodies are directed at heparin-platelet factor 4 complexes

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28
Q

How can you diagnose type 2 heparin-induced thrombocytopenia?

A

The onset is 5-14 days and the platelet count will fall greater than 50%

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29
Q

How do you treat type 2 heparin-induced thrombocytopenia?

A

Direct thrombin inhibitors: argatroban or bivalirudin

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30
Q

What drug can you use if a patient has a history of heparin-induced thrombocytopenia?

A

Fondaparinux

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31
Q

When does heparin-induced osteoporosis occur?

A

It’s rare, but occurs in infusions lasting greater than 6 months

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32
Q

What is the mechanism of action of LMWH?

A

It binds to antithrombin with a unique pentasaccharide sequence and accelerates the inactivation of factor Xa

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33
Q

What is LMWH’s effect on thrombin?

A

Only 25-50% of LMWH molecules inactivate thrombin

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34
Q

How is LMWH administered?

A

via subcutaneous injections

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35
Q

How does the intravascular binding of LMWH compare to UFH?

A

It’s much less than UFH; therefore, there is a more predictable dose-response relationship

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36
Q

What are the two LMWH products available in the US?

A

Enoxaparin (Lovenox) and Dalteparin

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37
Q

What are the monitoring parameters for LMWH?

A
  1. Baseline renal function
  2. Platelet counts and hemoglobin/hematocrit
  3. Signs and symptoms of bleeding
  4. Antifactor Xa levels in pt’s > 150kg or BMI >50 kg/m2
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38
Q

What are the factor Xa target ranges?

A
  1. 6 - 1.0 IU/mL (twice daily)

1. 0-2.0 IU/ml (once daily)

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39
Q

What is the dosing of enoxaparin in the treatment of VTE?

A

1 mg/kg SC q12h or 1.5 mg/kg SC q24h

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40
Q

What is the dosing adjustment of enoxaparin for VTE treatment in patients with a CrCl of less than 30 mL/min?

A

1 mg/kg SC q24h

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41
Q

What is the dosing of enoxaparin in VTE prophylaxis?

A

40 mg SC q 24h

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42
Q

What is the dosing of enoxaparin in VTE prophylaxis in pt with CrCl less than 30 mL/min?

A

30 mg SC q 24h

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43
Q

What medication is preferred in an obese (>190kg) patient with a CrCl less than 30 mL/min?

A

UFH

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44
Q

How do you reverse bleeding associated with LMWH?

A

administer 1 mg of protamine sulfate per 1 mg (100 units) of enoxaparin. A second dose of 0.5 mg of protamine sulfate per 1 mg (100 units) of enoxaparin can be used of bleeding persists

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45
Q

How does the chance of heparin-induced thrombocytopenia compare with UFH?

A

It’s much lower in LMWH due to less intravascular binding

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46
Q

When do you run the risk of a perispinal hematoma?

A

When administering antithrombotic medications with neuraxial blockade

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47
Q

What is the mechanism of action for Fondaparinux?

A

It’s a synthetic analog of the pentasaccharide structure that binds to antithrombin; therefore, it selectively inhibits factor Xa.

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48
Q

What is the half-life of fondaparinux?

A

12 hours

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49
Q

What is the route of administration for Fondaparinux?

A

Subcutaneous injection

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50
Q

What monitoring parameters are needed for Fondaparinux?

A
  1. CrCl can’t be less than 30
  2. Signs and symptoms of bleeding
  3. Platelet counts and hemoglobin/hematocrit
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51
Q

What is the dosing of Fondaparinux for patients less than 50 kg?

A

5 mg SC q 24h

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52
Q

What is the dosing of Fondaparinux for patients 50-100 kg?

A

7.5 mg SC 1 24h

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53
Q

What is the dosing of Fondaparinux for patients greater than 100 kg?

A

10 mg SC q 24h

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54
Q

What is the dosing of Fondaparinux for VTE prophylaxis?

A

2.5 mg SC q 24h

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55
Q

What are the adverse events associated with Fondaparinux?

A

Bleeding and heparin-induced thrombocytopenia

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56
Q

Why is it important to monitor signs and symptoms of bleeding with Fondaparinux?

A

There is no antidote for reversal

57
Q

In what population is Fondaparinux contraindicated?

A

In prophylaxis patients weighing less than 50 kg

58
Q

What is the mechanism of action of Warfarin?

A

It inhibits the vitamin k oxide reductase enzyme from activating vitamin k which is a cofactor for vitamin k-dependent carboxylation of factors II, VII, IX, and X.

59
Q

Why is the onset of action for warfarin 5-6 days?

A

Because it depends on the half-life of factors II, VII, IX, and X

60
Q

What is the half-life of factor VII?

A

6 hours

61
Q

What is the half-life of factor IX?

A

21-30 hours

62
Q

What is the half-life of factor X?

A

27-48 hours

63
Q

What is the half-life of factor II?

A

60-72 hours

64
Q

What is the half-life of protein C?

A

9 hours

65
Q

What is the half-life of protein S?

A

60 hours

66
Q

What type of mixture is warfarin?

A

A racemic mixture of the R and S enantiomers, with the S enantiomer being 2.7 to 3.8 times stronger

67
Q

What is the half-life of warfarin?

A

36-42 hours, and it takes 3-5 days to reach steady state

68
Q

What enzyme metabolizes the S enantiomer, and what effect does this have on drug interactions?

A

CYP4502C9. Since this is the stronger enantiomer, any drug that is also metabolized by this enzyme will increase the drug interactions

69
Q

What two factors are most common in interindividual variability of warfarin response?

A

single nucleotide polymorphisms in VKORC1 and CYP4502C9

70
Q

What effect does a polymorphism in CYP450*2C9 have on a patient?

A

It leads to poor metabolism of warfarin (use lower doses) and increases the risk of bleeding

71
Q

What effect does a polymorphism in VKORC1 have on patients?

A

The genotype determines the sensitivity to warfarin. AA is sensitive and needs a low dose, GG is resistant and needs a high dose, AG is normal

72
Q

What are the monitoring parameters for warfarin?

A
  1. Prothrombin time
  2. INR
  3. Management of non-therapeutic INRS
  4. S/Sx of bleeding
73
Q

What is the goal INR range?

A

2-3

74
Q

What is the goal INR for a patient with mechanical heart valves?

A

2.5-3.5

75
Q

How often do you monitor hospital patients on warfarin?

A

Daily

76
Q

How often do you monitor outpatients?

A

Within three days of hospital discharge and then weekly

77
Q

Once a stable response is achieved with warfarin, how often do you monitor?

A

every 4 weeks and some patients every 12 weeks

78
Q

What adverse event is associated with warfarin?

A

Bleeding

79
Q

What can reverse the bleeding in patients on warfarin?

A

Vitamin K

80
Q

What is the new reversal agent for warfarin?

A

Kcentra

81
Q

When should Kcentra be used?

A

In acute major bleeding or when a patient needs urgent surgery or invasive procedure

82
Q

What patient population is Kcentra contraindicated in?

A

In patients with a history of HIT because the antidote contains heparin

83
Q

What are the 4 non-bridge therapies?

A

Rivaroxaban (Xarelto), Dabigatran (Pradaxa), Apixiban (Eliquis), and Edoxaban (Savaysa)

84
Q

What is the mechanism of action of Rivaroxaban

A

It inhibits the active site of factor Xa without requiring a cofactor like antithrombin

85
Q

Why should rivaroxaban be taken with food?

A

To increase the bioavailability

86
Q

What are the monitoring parameters for rivaroxaban?

A
  1. Baseline kidney and liver function
  2. S/Sx of bleeding
  3. Platelet count and hemoglobin/hematocrit
87
Q

What are the strong drug-drug interactions with rivaroxaban?

A

strong 3A4 and P-glycoprotein inhibitors

88
Q

What is the dosing of rivaroxaban for VTE treatment?

A

15 mg twice daily w/ food for 21 days, then 20 mg once daily w/ food

89
Q

In what patients should you avoid the use of rivaroxaban?

A

In patients with a CrCl less than 30 or if they are on a P-pg and CYP3A4 inhibitor

90
Q

How do you convert from warfarin to rivaroxaban?

A

Discontinue warfarin and start rivaroxaban when the INR is less than 3

91
Q

How do you convert from other anticoagulants and rivaroxaban?

A

Discontinue other anticoagulants and take rivaroxaban 0-2 hours before next scheduled dose

92
Q

What is the antidote for rivaroxaban?

A

ANDEXXA

93
Q

What is the low dose of ANDEXXA?

A

400 mg IV bolus at 30 mg/min followed by 4 mg/min for up to 120 minutes

94
Q

What is a high dose of ANDEXXA?

A

800 mg IV bolus at 30 mg/min followed by 8 mg/min for up to 120 minutes

95
Q

What trial proved that rivaroxaban was noninferior to warfarin for the treatment of DVT and PE, and had no major difference in major or non-major bleeding?

A

EINSTEIN

96
Q

What is the mechanism of action for Dabigatran?

A

It is a direct thrombin inhibitor that inhibits free and clot-bound thrombin and thrombin-induced platelet aggregation

97
Q

What is special about dabigatran and it’s structure?

A

Because it is highly polar, it is not orally bioavailable and is actually a pro-drug

98
Q

What are the monitoring parameters for Dabigatran?

A
  1. Renal function
  2. Platelet count and hemoglobin/hematocrit
  3. S/Sx of bleeding
99
Q

When should dabigatran be used?

A

5-10 days after treatment with a parenteral anticoagulant

100
Q

What is the dosing for VTE treatment with dabigatran?

A

150 mg twice daily (no dosing for CrCl less than 30)

101
Q

How do you convert from warfarin to dabigatran?

A

Stop warfarin and start dabigatran when INR is less than 2

102
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

103
Q

What is the dosing for idarucizumab?

A

5 gram infusion

104
Q

What is the adverse effects of dabigatran?

A

dose-dependent GI bleed and dyspepsia

105
Q

What did the RECOVER I and RECOVER II trials prove?

A

That dabigatran is noninferior to warfarin for VTE treatment, and that there was no major difference in bleeding

106
Q

What did the RE-MEDY and RE-SONATE trials prove?

A

They proved the extended use of dabigatran after completion of a 3 month trials

107
Q

What is the mechanism of action for Apixiban?

A

It’s a direct factor Xa inhibitor that inhibits both free and clot-bound factor Xa

108
Q

What are the monitoring parameters for Apixiban?

A
  1. Hemoglobin/hematocrit and platelet counts
  2. S/Sx of bleeding
  3. Renal function/body weight
109
Q

What dose of Apixiban is used to treat VTE?

A

10 mg twice daily for 7 days (no dose adjustments)

110
Q

What is the antidote for Apixiban?

A

ANDEXXA

111
Q

What is the mechanism of action for Edoxaban?

A

It’s a factor Xa inhibitor

112
Q

What are the monitoring parameters for Edoxaban?

A
  1. Hemoglobin/hematocrit and platelet counts
  2. S/Sx of bleeding
  3. Renal function and body weight
113
Q

What is the dosing of Edoxaban used for VTE treatment?

A

60 mg once daily after 5-10 days of treatment with a parenteral anticoagulant

114
Q

When do you adjust the dose of edoxaban down to 30 mg daily?

A

When the patient has a CrCl of 15-50, or weighs less than 60 kg, or is taking verapamil or azithromycin.

115
Q

How do you convert warfarin to Edoxaban?

A

Discontinue warfarin and initiate edoxaban when the INR is less than 2.5

116
Q

How do you convert UFH to edoxaban?

A

Discontinue UFH and start edoxaban 4 hours later

117
Q

When are NOACs recommended over warfarin?

A

In the treatment of VTE in patients without active cancer

118
Q

What should active cancer patients receive to treat VTE?

A

LMWH monotherapy

119
Q

According to ISTH, what medications are not recommended for use in patients with a BMI greater than 40 kg/m^2 or with a weight greater than 120 kg?

A

NOACs

120
Q

How long do you treat a patient with 1st episode of DVT or PE secondary to a provoking transient event?

A

3 months

121
Q

How long do you treat a patient with 1st episode of unprovoked DVT or PE?

A

3 months and then evaluate risk-benefit ratio for extended therapy

122
Q

How long do you treat a patient with second episode of unprovoked DVT or PE?

A

Indefinitely, unless patient is at a high risk of bleeding

123
Q

According to the 2016 CHEST update, what defines a high risk for bleeding?

A

2 or more bleeding risk factors

124
Q

What are the risk factors for bleeding, according to CHEST?

A
  1. greater than 65
  2. previous bleeding
  3. cancer
  4. renal failure
  5. liver failure
  6. thrombocytopenia
  7. diabetes
  8. previous stroke
  9. anemia
  10. recent surgery
  11. frequent falls
  12. alcohol abuse
  13. antiplatelet therapy
  14. poor anticoagulant control
  15. NSAID use
125
Q

What drugs should not be combined with rivaroxaban?

A

carbamazepine, phenytoin, or rifampin

126
Q

What are the drug-drug interactions of dabigatran?

A

A patient with CrCl less than 50 taking dronedarone, amiodarone, or verapamil. Also, do not use with rifampin, no matter the CrCl.

127
Q

When should the dose of apixiban be reduced to 2.5 mg twice daily?

A

When patient is taking ketoconazole, itraconazole, ritonavir, or clarithromycin (If already on 2.5 mg then do not take).

128
Q

When should patients avoid the use of apixiban?

A

When taking rifampin, carbamazepine, or phenytoin

129
Q

How can a patient reduce the risk of recurrent DVT or PE with apixiban?

A

By taking 2.5 mg twice daily after completing VTE treatment dosing, according to AMPLIFY-EXT

130
Q

How do you convert warfarin to apixiban?

A

Start apixiban when INR is less than 2

131
Q

What did the AMPLIFY trial prove?

A

Apixiban was noninferior to warfarin for primary endpoint of recurrent VTE, and it was superior to warfarin for the safety outcome of major bleeding

132
Q

What is the one drug-drug interaction for edoxaban?

A

rifampin

133
Q

When do you avoid the use of edoxaban?

A

If CrCl is less than 15

134
Q

What are the transient risk factors for VTE, according to CHEST?

A
  1. major or minor surgery
  2. estrogen therapy
  3. pregnancy or puerperium
  4. trauma
  5. immobility
  6. active cancer
135
Q

When should you use thrombolysis?

A

When there is a risk of limb gangrene or massive PE

136
Q

How can thrombolytic agents be administered?

A

Systemically or locally via catheter

137
Q

What are the thrombolytic agents?

A

streptokinase, urokinase, and Rt-PA

138
Q

When should you use an inferior vena cava filter?

A

When the patient has contraindications to anticoagulation, according to 2016 CHEST guidelines

139
Q

What drug regimen do you use for total hip replacement surgery?

A

Enoxaparin 40 mg SC q 24 hours or enoxaparin 30 mg SC q 12 hours. If CrCl is less than 30 use enoxaparin 30 mg SC q 24 hours.

Cardio (11 decks)

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