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Therapeutics > Therapy of Venous Thromboembolism > Flashcards

Therapy of Venous Thromboembolism Flashcards

1
Q

Venous thromboembolism (VTE) results from:

A

Clot formation within the venous circulation

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2
Q

Venous thromboembolism (VTE) is manifested as:

A

1) Deep vein thrombosis (DVT)
2) Pulmonary embolism (PE)

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3
Q

Pharmacologic prevention significantly reduces the risk of VTE following:

A

1) Hip and knee replacement
2) Hip fracture repair
3) Major general surgery
4) Myocardial infarction
5) Ischemic stroke

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4
Q

Hospitalized and acutely ill medical patients at high-VTE-risk and low-bleeding-risk should receive pharmacologic prophylaxis with __, __, or __ during hospitalization or until fully ambulatory

A

1) Low dose unfractionated heparin (UFH)
2) Low molecular weight heparin (LMWH)
3) Fondaparinux

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5
Q

Routine pharmacologic prophylaxis is NOT indicated in which patients?

A

Low-VTE-risk medical patients

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6
Q

How should you prevent VTE following non-orthopedic surgery?

A

1) Low dose UFH
2) LMWH

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7
Q

How should you prevent VTE following following high risk orthopedic surgery (such as joint replacement surgery)?

A

1) Aspirin
2) Adjusted-dose warfarin
3) UFH
4) LMWH
5) Fondaparinux
6) Dabigatran
7) Apixaban
8) Rivaroxaban

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8
Q

How long should patients take VTE prophylactics following high risk orthopedic surgery (such as joint replacement surgery)?

A

At least 10 days post-surgery

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9
Q

What is the mainstay of VTE
(DVT & PE) treatment?

A

Anticoagulation therapy (Rapid-acting)

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10
Q

We should establish an accurate VTE diagnosis in order to avoid:

A

Bleeding

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11
Q

Traditionally, specific VTE therapy is started with:

A

LMWH or UFH overlapped with warfarin for 5 days, then the patient is maintained on warfarin

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12
Q

The appropriate initial duration of therapy to effectively treat an acute first episode of VTE for all patients is:

A

3 months

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13
Q

Which factors determine extending post-VTE anticoagulation therapy beyond 3 months?

A

1) Circumstances surrounding the initial thromboembolic event
2) Presence of ongoing thromboembolic risk factors
3) Bleeding risk
4) Patient preference

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14
Q

What are some clinically important bleeding risk factors?

A

1) Age more than 75 years
2) Previous non-cardioembolic stroke
3) History of GI bleeding
4) Renal or hepatic impairment
5) Anemia
6) Thrombocytopenia
7) Concurrent antiplatelet administration
8) Noncompliance
9) Poor anticoagulant control (for patients on warfarin)
10) Serious acute or chronic illness
11) The presence of structural lesions (tumor, recent surgery) that could bleed

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15
Q

How may Unfractionated Heparin (UFH) be given?

A

1) Subcutaneous injection
2) Continuous IV infusion

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16
Q

Response to UFH is:

A

Highly variable

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17
Q

UFH dose should be adjusted based on:

A

Activated partial thromboplastin time (aPTT)

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18
Q

Both __ and __ produce similar clinical outcomes.

A

Weight-based and Fixed-UFH-dosing

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19
Q

Traditional IV UFH in the acute treatment of VTE may be replaced by:

A

1) LMWH
2) Fondaparinux

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20
Q

Elimination of LMWH and fondaparinux is dependent on:

A

Renal function

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21
Q

Can you give UFH to acute VTE patients with CrCL < 30 mL/min?

A

YES

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22
Q

Why did Low-Molecular-Weight Heparin (LMWH) replace UFH for initial VTE treatment?

A

1) Improved pharmacokinetic and pharmacodynamic profiles
2) Ease of use

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23
Q

How is LMWH given?

A

Subcutaneously in fixed or weight-based doses

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24
Q

Is LMWH given subcutaneously in fixed or weight-based doses as effective as UFH given
intravenously for the treatment of VTE?

A

YES

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25
Q

LMWHs have reduced need for:

A

Laboratory monitoring

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26
Q

LMWH monitoring is indicated in:

A

1) Obesity
2) Pregnancy
3) Children

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27
Q

How is LMWH monitored?

A

By anti–factor Xa activity

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28
Q

Anti–factor Xa goal levels are 0.5 - 1.0 unit/mL __-__ hours following subcutaneous LMWH injection.

A

4 - 6 hours

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29
Q

Can LMWH be used on an outpatient basis for stable low-risk patients?

A

YES

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30
Q

In patients without cancer, acute treatment with LMWH is generally transitioned to long-term warfarin therapy after about:

A

5 - 10 days

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31
Q

_____ is preferred if thrombolytic therapy or embolectomy is anticipated.

A

Rapidly reversible UFH

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32
Q

Fondaparinux is dosed ___ via weight-based subcutaneous injection.

A

Once daily

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33
Q

When is Fondaparinux contraindicated?

A

If CrCL < 30 mL/min

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34
Q

Can we give Warfarin monotherapy for acute VTE treatment? Why or why not?

A

NO, because the slow onset of action is associated with high incidence of recurrent thromboembolism.

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35
Q

Warfarin is effective in the long-term VTE management IF:

A

It is started concurrently with rapid-acting parenteral anticoagulant

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36
Q

The initial dose of Warfarin is:

A

5-10 mg for most patients

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37
Q

Warfarin is periodically adjusted to achieve and maintain an INR between:

A

2-3

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38
Q

Which direct oral anticoagulants can be started as single-drug therapy?

A

1) Rivaroxaban
2) Apixaban

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39
Q

How are Rivaroxaban and Apixaban monitored?

A

None, they don’t need to be monitored.

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40
Q

Which direct oral anticoagulants require prior parenteral anticoagulation?

A

1) Dabigatran
2) Edoxaban

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41
Q

Can patients with CrCL < 30 mL/min take Edoxaban?

A

Yes, at half the dose.

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42
Q

Can patients with CrCL < 30 mL/min receive Dabigatran?

A

NO

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43
Q

Most VTE cases require only ___ therapy.

A

Anticoagulation

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44
Q

What are Thrombolytic agents?

A

Proteolytic enzymes

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45
Q

What do Thrombolytic agents do?

A

Enhance conversion of plasminogen to plasmin, which lyses the thrombus.

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46
Q

Thrombolytic therapy improves:

A

Early venous patency

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47
Q

Does Thrombolytic therapy improve long-term outcomes?

A

NO

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48
Q

How should you adjust anticoagulation therapy duration and intensity for DVT patients receiving thrombolysis?

A

No change

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49
Q

Patients with DVT involving the iliac and common femoral veins are at highest risk of:

A

Post-thrombotic syndrome

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50
Q

Patients at high risk for post-thrombotic syndrome may benefit from:

A

Thrombus removal

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51
Q

Which patients are at highest risk for post-thrombotic syndrome?

A

Patients with DVT involving the iliac and common femoral veins

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52
Q

In acute PE management, successful clot dissolution with thrombolytic therapy:

A

1) Reduces elevated pulmonary artery pressure
2) Improves right ventricular dysfunction

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53
Q

For thrombolytic therapy to be used, the risk of ___ should outweigh the risk of ___ from thrombolytic therapy.

A

Death from PE; Serious bleeding

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54
Q

Prior to initiating Thrombolytic therapy, what should patients be screened carefully for?

A

Contraindications related to bleeding risk

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55
Q

Which anticoagulant crosses the placenta?

A

Warfarin

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55
Q

Which anticoagulants are preferred in pregnancy?

A

1) UFH
2) LMWH

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56
Q

What are the complications of taking Warfarin during pregnancy?

A

1) Fetal bleeding
2) CNS abnormalities
3) embryopathy

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57
Q

Pregnant women with a history of VTE should receive VTE prophylaxis for how long after
delivery?

A

6-12 weeks

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58
Q

Which anticoagulants are safe during breast-feeding?

A

1) Warfarin
2) UFH
3) LMWH

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59
Q

VTE in pediatric patients is increasing secondary to:

A

1) Prematurity
2) Cancer
3) Trauma
4) Surgery
5) Congenital heart disease
6) SLE

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60
Q

Pediatric patients rarely experience ___(provoked/unprovoked) VTE

A

Unprovoked

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61
Q

Pediatric patients often develop DVT associated with:

A

Indwelling central venous catheters

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62
Q

How do you give pediatric patients anticoagulation with UFH and warfarin?

A

Similar to that of adults

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63
Q

Why is obtaining blood from pediatric patients for coagulation monitoring tests problematic?

A

Because of poor venous access

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64
Q

Which anticoagulant is preferred in pediatric patients?

A

LMWH

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65
Q

Why is LMWH preferred in pediatric patients?

A

1) Low drug interaction potential
2) Less frequent lab testing

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66
Q

Warfarin should be continued in pediatric patients for at least ____ for provoked VTE.

A

3 months

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67
Q

Warfarin should be continued in pediatric patients for at least ____ for unprovoked VTE.

A

6 months

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68
Q

Is routine use of thrombolysis and thrombectomy recommended in children?

A

NO

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69
Q

Cancer-related VTE is associated with:

A

1) Higher rates of recurrent VTE
2) Higher rates of bleeding
3) More resistance to standard warfarin-based therapy

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70
Q

Warfarin therapy in cancer patients is often complicated by:

A

1) Drug interactions (chemotherapy and antibiotics)
2) The need to interrupt therapy for invasive procedures

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71
Q

Why is maintaining a stable INR difficult in cancer patients?

A

1) Nausea
2) Anorexia
3) Vomiting

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72
Q

________ for cancer-related VTE decreases recurrent VTE rates without increasing bleeding risks compared with warfarin-based therapy.

A

Long-term LMWH monotherapy

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73
Q

LMWH therapy for cancer-related VTE should be used for at least the first ___ of long-term treatment

A

3 - 6 months

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74
Q

Anticoagulation therapy for cancer-related VTE should continue for as long as:

A

1) The cancer is “active”
2) While the patient is receiving chemotherapy

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75
Q

__ is preferred for acute VTE treatment in renal dysfunction.

A

UFH

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76
Q

Why can’t LMWH, fondaparinux, and direct-acting anticoagulants (DOACs) be used in renal dysfunction?

A

Because they accumulate

77
Q

Patients with chronic kidney disease are at increased risk of __ from other causes.

A

Bleeding

78
Q

Unfractionated heparin is a heterogeneous mixture of ___ of variable lengths.

A

Sulfated mucopolysaccharides

79
Q

How is the anticoagulant effect of UFH mediated?

A

Through a specific pentasaccharide sequence that binds to antithrombin.

80
Q

UFH accelerates the anticoagulant action of ___ 100 - 1,000 times.

A

Antithrombin

81
Q

Antithrombin inhibits factors:

A

2, 9, 10, 12

82
Q

UFH prevents:

A

Thrombus growth and propagation

83
Q

UFH prevents thrombus growth and propagation allowing:

A

Endogenous thrombolytic systems to dissolve the clot.

84
Q

Which 2 factors are most sensitive to UFH–antithrombin complex inhibition?

A

2 (Thrombin) and 10

85
Q

In order to inactivate thrombin (IIa), the heparin molecule must first form what?

A

A ternary complex bridging between antithrombin and thrombin

86
Q

The inactivation of factor Xa requires UFH binding to antithrombin via:

A

The specific pentasaccharide sequence

87
Q

The onset of action of UFH after SC injection is:

A

1-2 hours

88
Q

The action of UFH peaks at:

A

3 hours

89
Q

Why should intramuscular UFH be avoided?

A

Because of the risk of bleeding and hematomas

90
Q

UFH has a dose-dependent half-life of:

A

30-90 minutes

91
Q

UFH’s elimination follows __(zero/first) order kinetics.

A

Zero

92
Q

What are the Adverse Effects of UFH?

A

1) Bleeding
2) Heparin-induced thrombocytopenia (HIT)
3) Significant bone loss and osteoporosis

93
Q

What can you give to reverse the anticoagulant effects of UFH?

A

Protamine sulfate

94
Q

How quickly does Protamine sulfate act?

A

5 minutes

95
Q

What is Heparin-induced thrombocytopenia (HIT) caused by?

A

Pro-thrombotic antibodies that bind to complexes of heparin and platelet factor 4 (PF4)

96
Q

Heparin-induced thrombocytopenia (HIT) leads to:

A

Arterial thromboembolic events

97
Q

Heparin-induced thrombocytopenia (HIT) occurs ____ after initiation of UFH.

A

5-10 days

98
Q

What alternative anticoagulants can be given if the patient experiences Heparin-induced thrombocytopenia (HIT)?

A

Direct thrombin inhibitors

99
Q

What represents vaccine-related variant of HIT?

A

Vaccine-induced immune thrombotic thrombocytopenia (Ex. Thrombosis seen with some Covid-19 vaccines is similar to HIT)

100
Q

When used for more than 6 months, such as in pregnancy, UFH can cause:

A

Significant bone loss and osteoporosis

101
Q

Which drugs can’t be used with UFH out of fear of increased bleeding?

A

1) Anticoagulants
2) Thrombolytics
3) Antiplatelet agents
4) Aspirin
5) NSAIDs

102
Q

How is LMWH produced?

A

By depolymerization of UFH

103
Q

Which is lighter in weight: LMWH or UFH?

A

LMWH

104
Q

Advantages of LMWH?

A

1) Predictable anticoagulation dose response
2) Improved subcutaneous bioavailability
3) Dose-independent elimination (first-order)
4) Longer half-life
5) Reduced need for routine laboratory monitoring

105
Q

Which drugs are LMWH?

A

1) Enoxaparin
2) Dalteparin

106
Q

How does Low-molecular-weight heparin (LMWH) prevent thrombus growth and propagation?

A

By enhancing and accelerating the activity of antithrombin against factor Xa

107
Q

Because of smaller chain lengths, LMWH has limited activity against:

A

Activated thrombin (IIa)

108
Q

The bioavailability of LMWH is __% after SC injection.

A

90%

109
Q

The peak anticoagulation of LMWH is between __-__ hours.

A

3 - 5

110
Q

LMWH is mainly eliminated by:

A

Renal excretion

111
Q

Adverse Effects of LMWH?

A

1) Bleeding
2) HIT
3) Osteoporosis and osteopenia

112
Q

Antidote for LMWH?

A

IV protamine sulfate

113
Q

HIT in LMWH is three times __(higher/lower) than that observed with UFH.

A

Lower

114
Q

LMWH should be avoided in patients with __, because of cross reactivity with antibodies.

A

HIT

115
Q

Which drugs can’t be used with LMWH because of drug-drug interactions (increased bleeding)?

A

1) Anticoagulants
2) Thrombolytics
3) Antiplatelet agents
4) Aspirin
5) NSAIDs
6) Dipyridamole
7) Sulfinpyrazone

116
Q

Fondaparinux is a synthetic molecule consisting of the active pentasaccharide units that bind __(irreversibly/reversibly) to antithrombin.

A

Reversibly

117
Q

Fondaparinux is a synthetic molecule consisting of the active pentasaccharide units that bind reversibly to ___.

A

Antithrombin

118
Q

Fondaparinux inhibits:

A

Factor Xa activity ONLY

119
Q

Fondaparinux is eliminated __(unchanged/changed) in the urine.

A

Unchanged

120
Q

Elimination half-life of Fondaparinux is:

A

19 hours

121
Q

The anticoagulant effect of Fondaparinux persists for ___ following discontinuation of the drug in patients with normal renal function.

A

2 to 4 days

122
Q

Adverse Effects of Fondaparinux?

A

1) Bleeding
2) Rare cause of HIT

123
Q

Fondaparinux antidote?

A

NONE

124
Q

Which drugs can’t be used with Fondaparinux because of drug-drug interactions (increased bleeding)?

A

1) Anticoagulant
2) Fibrinolytics
3) Antiplatelets

125
Q

Hirudin is derived from ___.

A

Leech

126
Q

Lepirudin is from:

A

Recombinant DNA technology

127
Q

What is Lepirudin?

A

Irreversible inhibitor, inactivates fibrin-bound thrombin.

128
Q

How is Lepirudin given?

A

1) IV
2) SC

129
Q

Lepirudin is monitored by:

A

aPTT

130
Q

How is Lepirudin eliminated?

A

1) Hepatic metabolism
2) Renal excretion

131
Q

Lepirudin should not be given in:

A

Renal failure

132
Q

Lepirudin is used for:

A

Thrombosis related to HIT

133
Q

Antidote for Lepirudin?

A

NONE

134
Q

What is Bivalirudin?

A

Direct thrombin inhibitor

135
Q

Bivalirudin is a synthetic congener of the naturally occurring anticoagulant ___.

A

Hirudin

136
Q

How is Bivalirudin given?

A

IV bolus followed by infusion

137
Q

How is Bivalirudin eliminated?

A

1) Hepatic elimination
2) Renal elimination
3) Proteolytic cleavage

138
Q

Bivalirudin __(reversibly/irreversibly) inhibits both circulating and clot-bound thrombin.

A

Reversibly

139
Q

Bivalirudin inhibits:

A

1) Circulating thrombin
2) Clot-bound thrombin
3) Thrombin-mediated platelet activation and aggregation

140
Q

Does Bivalirudin have a higher or lower bleeding risk than r-hirudins?

A

Lower

141
Q

Bivalirudin is used in:

A

1) Percutaneous coronary intervention (PCI)
2) HIT

142
Q

How is Bivalirudin monitored?

A

Thrombin Inhibitor Assay

143
Q

Why is Thrombin Inhibitor Assay better than aPTT?

A

Because it is NOT affected by antiphospholipid antibodies

144
Q

Bivalirudin is contraindicated in:

A

Severe renal impairment

145
Q

Vitamin K in its reduced form is required for vitamin K-dependent carboxylation of:

A

1) Factors 2, 7, 9, and 10
2) Proteins C and S

146
Q

What does Warfarin do?

A

Inhibits the reduction of vitamin K epoxide = Impairs the formation of complete functioning clotting factors

147
Q

How long does it take for Warfarin to achieve its full antithrombotic effect?

A

6 days

148
Q

Why does it take so long for Warfarin to work?

A

Because it has NO effect on pre-formed clotting factors

149
Q

The time required for warfarin to achieve its pharmacologic effect is dependent on:

A

Coagulation protein elimination half-lives (6 hours for factor 7 and 72 hours for prothrombin (2))

150
Q

Half-life of Factor 2? (Two)

A

72 hours (Too long)

151
Q

Half-life of Factor 7? (Seven)

A

6 hours (Short)

152
Q

Half-life of Factor 9?

A

24 hours

153
Q

Half-life of Factor 10?

A

40 hours

154
Q

Half-life of Protein C?

A

8 hours

155
Q

Half-life of Protein S?

A

30 hours

156
Q

Warfarin has a __(wide/narrow) therapeutic index.

A

Narrow

157
Q

Adverse Effects of Warfarin?

A

1) Bleeding
2) Purple Toe Syndrome
3) Warfarin-induced skin necrosis

158
Q

Warfarin antidote?

A

Vitamin K

158
Q

In case of bleeding, warfarin should be:

A

1) Temporarily stopped
2) Dose reduced

158
Q

What causes Purple Toe Syndrome?

A

Cholesterol microembolization into the arterial circulation of the toes

159
Q

Which areas of the body are most commonly affected by Warfarin-induced skin necrosis?

A

Areas rich in subcutaneous fat:
1) Breasts
2) Thighs
3) Buttocks
4) Abdomen

160
Q

How is Warfarin monitored?

A

INR

161
Q

Which drugs cause pharmacodynamic interactions with Warfarin?

A

1) Aspirin/NSAIDs
2) Clopidogrel/Ticlopidine
3) Tramadol
4) Levothyroxine
5) Vitamin K containing foods/supplements

162
Q

What does Tramadol do when given with Warfarin?

A

Elevates INR

163
Q

What does Levothyroxine do when given with Warfarin?

A

Increases catabolism of clotting factors

164
Q

Which drugs elevate the INR when given with Warfarin?

A

1) Amiodarone
2) Fluoroquinolones
3) Trimethoprim/Sulfamethoxazole
4) Metronidazole
5) Azole antifungals
6) Statins
7) Isoniazid
8) NSAIDs
9) Sertraline
10) Gemfibrozil
11) Ethanol
12) Macrolides
13) Cimetidine
14) Omeprazole
15) Fluorouracil
16) Garlic!!
17) Gingko
18) Vitamin E

165
Q

Which drugs reduce the INR when given with Warfarin?

A

1) Rifampin
2) Barbiturates
3) Carbamazepine
4) Phenytoin
5) St. John’s Wort
6) Smoking
7) Cholestyramine (Bile Binding Resins)
8) OCPs (Estrogen)
9) Ginseng
10) Green tea
11) Avocado
12) Leafy greens

166
Q

Which enzyme metabolizes Warfarin?

A

CYP2C9

167
Q

Why does warfarin exhibit dose variability between patients?

A

Polymorphisms in:
1) CYP2C9
2) The gene coding for VKOR (Vitamin K Epoxide Reductase)

168
Q

Which metabolizer subtypes have been associated with increased risk of bleeding on Warfarin?

A

Poor metabolizers

169
Q

Warfarin resistance can be due to:

A

Mutations in the receptor gene

170
Q

Which drugs are Direct Oral Anticoagulants?

A

1) Rivaroxaban
2) Apixaban
3) Edoxaban
4) Dabigatran

171
Q

What do Rivaroxaban, Apixaban, and Edoxaban do?

A

Selectively inhibit both free and clot-bound factor Xa.

172
Q

True or False: Rivaroxaban, Apixaban, and Edoxaban require antithrombin to exert their anticoagulant effect.

A

FALSE; THEY DO NOT REQUIRE IT.

173
Q

What is Dabigatran?

A

A selective, reversible, prodrug that directly inhibits factor IIa (Thrombin)

174
Q

Direct Oral Anticoagulants should be avoided in:

A

Renal failure (CrCl < 30 mL/min)

175
Q

Which last longer: Factor 10 inhibitors or Dabigatran?

A

Dabigatran

176
Q

Rivaroxaban and apixaban are substrates of:

A

1) Cytochrome CYP3A4
2) P-glycoprotein

177
Q

Indications for using Rivaroxaban and Apixaban?

A

1) Prevent VTE following hip or knee replacement surgery
2) Extended VTE treatment after the first 6 months of anticoagulant therapy

178
Q

Which drugs are substrates of Cytochrome CYP3A4 and P-glycoprotein?

A

1) Rivaroxaban
2) Apixaban

179
Q

Indications for using Dabigatran?

A

Extended VTE treatment after the first 6 months of anticoagulant therapy

180
Q

Adverse Effects of Direct Oral Anticoagulants?

A

1) GI complaints
2) Bleeding

181
Q

Antidote for Dabigatran?

A

1) Idarucizumab
2) Hemodialysis

182
Q

Antidote for Direct Oral Anticoagulants?

A

Activated charcoal within 2 hours of presentation

183
Q

How does Idarucizumab work to stop the effects of Dabigatran?

A

It binds to dabigatran and its acylglucuronide with higher affinity than that of dabigatran to thrombin.

184
Q

When is Idarucizumab used?

A

Dabigatran severe side effects:
1) Life-threatening bleeding
2) When there is need for urgent surgical intervention

185
Q

ALL Direct Oral Anticoagulants should not be given with:

A

1) P-glycoprotein inducers
2) P-glycoprotein inhibitors

186
Q

Rivaroxaban and Apixaban should not be given with:

A

1) CYP3A4 inducers
2) CYP3A4 inhibitors

187
Q

What should we assess when giving Direct Oral Anticoagulants?

A

Renal function

188
Q

___ dosing should be reduced in patients with CrCL 15 - 50 mL/min

A

Edoxaban

Therapeutics (23 decks)

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