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VTE Flashcards

1
Q

What is a DVT?

A

a blood clot within a deep vein

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2
Q

What is a PE?

A

a blockage caused by a blood in clot in the pulmonary arteries

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3
Q

What is Virchow’s triad?

A

3 primary factors influencing formation of a pathogenic clot

  • damage to the vessel wall
  • venous stasis -hypercoagulable state
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4
Q

What is the function of antithrombin?

A

inhibits thrombin (IIa), factor IXa, and factor Xa

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5
Q

What is the function of protein S?

A

cofactor for activation of protein C

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6
Q

What is the function of protein C?

A

inactivates factors Va and VIIa

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7
Q

What is the function of tissue factor pathway inhibitor (TFPI)?

A

binds to factor VIIa-tissue factor complex and inhibits activation of factor X

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8
Q

What is the function of plasminogen?

A

converted to plasmin via tissue plasminogen activator (t-PA)

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9
Q

What is the function of plasmin?

A

lyses fibrin to form fibrin degradation products

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10
Q

Where are the most common locations of clot formation?

A
  • muscular veins of the calf
  • valve cusp pockets of the deep calf veins
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11
Q

DVT once formed can:

A
  • spontaneously lyse
  • extend into more proximal veins
  • embolize to the lungs causing PE
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12
Q

What are the clinical presentation/symptoms of DVT?

A
  • unilateral calf or leg swelling
  • calf pain or tenderness
  • erythema
  • warmth
  • palpable cord
    • Homan’s sign
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13
Q

What are the clinical presentation/symptoms of PE?

A
  • dyspnea
  • pleuritic chest pain
  • anxiety
  • tachypnea (>20 breaths/min)
  • tachycardia
  • cough
  • hemoptysis
  • diaphoresis
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14
Q

What is a D-dimer?

A

cross linked fibrin degradation fragment produced during clot dissolution that has a negative predictive value of

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15
Q

What are some non-invasive tests used to diagnose DVT?

A
  • Doppler ultrasonography
  • B-mode compression ultrasound
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16
Q

What are some invasive tests used to diagnose DVT?

A

Contrast venography-radiographic visualization of the involved vessels with injection of radiocontrast material

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17
Q

What diagnostic test is the gold standard for diagnosing DVT?

A

contrast venography

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18
Q

What is the most commonly used diagnostic test used for diagnosing a PE?

A

Chest CT with contrast

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19
Q

What diagnostic test is the gold standard for diagnosing PE?

A

pulmonary angiography

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20
Q

What is the most invasive test used to diagnose PE?

A

pulmonary angiography

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21
Q

What are ancillary tests used to diagnose PE?

A
  • arterial blood gas
  • EKG
  • CXR
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22
Q

What is bridge therapy?

A

When a parenteral agent and warfarin are given together for a minimum of 5 days and until the INR is less than or equal to 2 for at least 24 hours

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23
Q

What are the parenteral agents?

A
  • UFH
  • LMWH
  • Fondaparinux
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24
Q

Per CHEST guidelines, what parenteral agents are recommended over the other?

A

LMWH and Fondaparinux are recommended over UFH

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25
Q

What is the structure of UFH?

A

heterogenous mixture of glycosaminoglycan polysaccharide chains

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26
Q

What is the MOA of UFH?

A

binds to antithrombin via a unique pentasaccharide sequence and accelerates its interaction and inactivation of thrombin and factor Xa by 1000-fold

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27
Q

What other factors does UFH inhibit?

A

IXa, XIa, XIIa

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28
Q

Inhibition of thrombin requires a heparin chain that is at least _________ in length

A

18 saccharide units

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29
Q

What is the route of administration for the treatment of VTE?

A

continuous infusion

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30
Q

What is the route of administration for the prophylaxis of VTE?

A

subcutaneous injection, NOT intramuscular

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31
Q

What is intravascular binding?

A

creates variability and unpredictability in patient response

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32
Q

What do you monitor when a patient is on UFH?

A
  • aPTT (activated partial thromboplastin time)
  • platelet counts, Hgb, Hct
  • signs/symptoms of bleeding
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33
Q

What is the dosing of UFH for VTE treatment?

A

IV bolus of 80 units/kg followed by 18 units/kg/hr continuous IV infusion with no renal adjustment

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34
Q

What is the dosing of UFH for VTE prophylaxis?

A

5000 units SC q8h with no renal adjustment

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35
Q

What are some adverse effects of UFH?

A
  • bleeding
  • Heparin-induced thrombocytopenia (HIT)
  • Heparin-induced osteoporosis
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36
Q

How can bleeding be reversed when on UFH?

A

reversed with IV bolus of protamine sulfate which binds to heparin to form a table salt

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37
Q

What is type 1 HIT?

A

transient fall in platelets due to a direct effect of heparin

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38
Q

What is type 2 HIT?

A

immune-mediated reaction

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39
Q

What is the mechanism of type 2 HIT?

A

IgG antibodies directed at heparin-platelet factor 4 complexes

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40
Q

What is the treatment of type 2 HIT?

A

direct thrombin inhibitors Argatroban and Bivalirudin

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41
Q

What is the mechanism of heparin-induced osteoporosis?

A

binding of heparin to osteoblasts

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42
Q

What is the structure of LMWH?

A

heterogenous mixture of of glycosaminoglycans derived from chemical or enzymatic degradation of UFH (~1/3 of molecular weight of UFH)

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43
Q

What is the MOA of LMWH?

A

binds to antithrombin via a unique pentasaccharide sequence. Accelerates inactivation of factor Xa

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44
Q

What is the route of administration of LMWH?

A

subcutaneous injection

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45
Q

What is a product of LMWH?

A

Enoxaparin (Lovenox)

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46
Q

Is routine anticoagulation testing necessary in patients taking LMWH?

A

It is not recommended

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47
Q

What test could you perform to monitor patients on LMWH?

A

anti-factor Xa levels

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48
Q

When are anti-factor Xa levels drawn?

A

4 hours after steady state is reached (after 3rd dose)

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49
Q

When should anti-factor Xa levels be drawn?

A
  • patients with a total body weight of >150 kg or BMI >50 kg/m2
  • if LMWH are used in patients with renal dysfunction
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50
Q

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

A

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

Renal adjustment: 1 mg/kg SC q24h (CrCl <30 mL/min)

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51
Q

What is the dosing of enoxaparin for the prophylaxis of VTE?

A

40 mg SC q24h

Renal adjustment: 30 mg SC q24h (CrCl <30 mL/min)

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52
Q

What is the preferred parenteral anticoagulant if a patient is obese and CrCl <30 mL/min?

A

UFH

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53
Q

What are some adverse effects of LMWH?

A
  • bleeding
  • heparin-induced thrombocytopenia (HIT)
  • perispinal hematoma
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54
Q

What is the antidote used to reverse the effects of LMWH and what is its dose?

A
  • Protamine sulfate
  • LMWH administered within 8 hours: 1 mg protamine per 100 anti-factor Xa units (this is 1 mg of enoxaparin)
  • a second dose of 0.5 mg protamine per 100 anti-factor Xa units if bleeding continues
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55
Q

What is a perispinal hematoma?

A

increased risk when antithrombotic medications are administered concomitantly with neuraxial blockade

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56
Q

What is the MOA/structure of Fondaparinux?

A

a synthetic analog of the pentasaccharide sequence that binds to antithrombin

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57
Q

What is the half-life of UFH?

A

30-60 min

58
Q

What should you monitor when a patient is on LMWH?

A
  • anti-factor Xa levels
  • assess baseline renal function
  • signs and symptoms of bleeding
  • platelet counts, Hgb, Hct
59
Q

What is the half-life of fondaparinux?

A

17 hours

60
Q

What is the route of administration of fondaparinux?

A

subcutaneous injection

61
Q

Where does excretion occur with fondaparinux?

A

excreted in the urine

62
Q

What should you monitor in patients taking fondaparinux?

A
  • routine anticoagulation testing not required
  • assess baseline kidney function
  • signs and symptoms of bleeding
  • platelet counts/ Hgb/ Hct
63
Q

Do not use fondaparinux in patients with ___________

A

CrCl <30 mL/min

64
Q

What is the dosing of fondaparinux for the treatment of VTE?

A
  • for PTs <50 kg: 5 mg SC q24h
  • for PTs 50-100 kg: 7.5 mg SC q24h
  • for PTs >100 kg: 10 mg SC q24h
65
Q

What is the dosing of fondaparinux for prophylaxis of VTE?

A

2.5 mg SC q24h

66
Q

What are some adverse effects with fondaparinux?

A

bleeding (increased risk in patients with smaller weights)

  • contraindicated for prophylaxis in patients who weight <50 kg
  • no antidote for reversal
67
Q

What is the relationship between fondaparinux and HIT?

A

can use fondaparinux in patients with a history of HIT

68
Q

What is the MOA of warfarin?

A

inhibits the activation of coagulation factors by inhibiting vitamin K dependent carboxylation of the factors

-warfain inhibits vitamin K oxide reducatse enzyme complex (VKORC) therefore inhibiting vitamin K activation which then stops carboxylation

69
Q

What coagulation factors are affected with the use of warfarin?

A

Factors VII, IX, X, and II

70
Q

What anticoagulation factors are affected with the use of warfarin?

A

Protein C and S

71
Q

What is the structure of warfarin?

A

racemic mixture of S- and R- enantiomers

72
Q

Which enantiomer of warfarin is more potent?

A

S- enantiomer

73
Q

True or False: warfarin has a high bioavailibility and is highly bound to plasma proteins (primarily albumin)?

A

true

74
Q

What is the onset of anticoagulation action of warfarin?

A

takes 5-7 days to obtain peak anticoagulant effects

75
Q

What is the half-life of warfarin?

A

36-42 hours (takes 3-5 days to reach steady state)

76
Q

Where is warfarin metabolized?

A

in the liver

77
Q

What 2 nucleotide polymorphisms account for up to 50% of the interindividual variability of warfarin response?

A

VKORC1 and CYp450 2C9

78
Q

Mutation of CYP 2C9 leads to _________

A

poor metabolism of warfarin (will require lower doses)

79
Q

Which genetic variations of CYP 2C9 have shown the highest risk of bleeding?

A

CYP 2C9*2 and CYP 2C9*3 (*2 and *3 refers to the alleles)

80
Q

VKORC1 genotype determines ________ and what dose AA, GG, and AG mean?

A

sensitivity to warfarin

  • AA: sensitive= need lower dose of warfarin
  • GG: resistant= need higher doses of warfarin
  • AG= usual dose
81
Q

What should be monitored if a patient is taking warfarin?

A
  • Prothrombin time (PT)
  • INR
  • signs/symptoms of bleeding
82
Q

What is the goal INR range for patients?

A

2-3

83
Q

What is the goal INR range for patients with mechanical heart vavles?

A

2.5-3.5

84
Q

What is the frequency monitoring for INR goals? (hospitalized patients, outpatients, and stable patients)

A
  • Hospitalized patients: daily
  • Outpatients: within 3 days of hospital discharge and then weekly

Once a stable response achieved: every 4 weeks and some patients every 12 weeks

85
Q

What is the normal starting dose of warfarin?

A

5 mg

86
Q

How can warfarin be reveresed?

A
  • Vitamin K
  • Kcentra
87
Q

What Kcentra, what is it indicated for, and how is dosing based?

A
  • Prothrombin complex concentrate
  • indicated for acute major bledding or when patient needs urgent surgery/invasive procedure
  • dosing based on patient’s current INR and body weight
88
Q

True or False: Kcentra does not need to give with vitamin K?

A

false

89
Q

What is Kcentra contraindicated with?

A

contraindicated in patients with a history of HIT because it contains heparin

90
Q

What is the dosing of Kcentra?

A

Pre-treatment INR

2 - <4

4-6

>6

Dose of Kcentra/kg body weight

25

35

50

Maximum dose

2500

3500

5000

91
Q

What is the MOA of rivaroxaban?

A

selectively blocks the active site of factor Xa without requiring a cofactor

  • inhibits factor Xa in both the intrinsic and extrinsic pathways
  • inhibition of clot bound factor Xa
92
Q

What is the half-life of rivaroxaban?

A

5-9 hours

93
Q

True or false: rivaroxaban is 90% bound to plasma proteins?

A

true

94
Q

Where is rivaroxaban metabolized and excreted?

A

hepatic metabolism and excreted in urine and feces

95
Q

What drug-drug interactions does rivaroxaban have?

A

strong 3a4 and P-glycoprotein inhibitors

96
Q

What is the dosing of rivaroxaban for the treatment of VTE?

A

15 mg bid with food for the first 21 days, then 20 mg once daily with food

(avoid use in patients with CrCl <30 mL/min (for VTE treatment, VTE prevention, and hip/knee surgery))

97
Q

What is the conversion from warfarin to rivaroxaban?

A

discontinue warfarin and start INR is <3.0

98
Q

What is the conversion from other anticoagulants (besides warfarin) to rivaroxaban?

A

discontinue agen and start rivaroxaban 0-2 hours prior to the next scheduled dose of previous agent

99
Q

State the clinical trials for rivaroxaban

A
  • Einstein DVT
  • Einsten PE
100
Q

What is the MOA/structure of Dabigatran?

A

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

101
Q

How is dabigatran absorbed and how is eliminated?

A
  • rapid absorption: peak concentration reached within 2 hours
  • renal elimation (~80% of total clearance)
102
Q

What is the half-life of dabigatran?

A

12-17 hours

103
Q

What drug-drug interactions does dabigatran have?

A

P-glycoprotein inhibitors (may increase concentration of dabigatran)

104
Q

When should treatment of dabigatran begin?

A

VTE treatment after the aptient has received a parenteral anticoagulant for 5-10 days

105
Q

What is the dosing of dabigatran?

A

150 mg bid for CrCl >30 mL/min

(CrCl <30 mL/min, no dosing recommendations)

106
Q

When should a patient avoid use of dabigatran?

A

in patients with CrCl <50 mL/min and use of P-gp inhibitors

107
Q

What is the conversion from warfarin to dabigatran?

A

discontinue warfarin and start dabigatran when INR <2.0

108
Q

What is the conversion from a parenteral anticoagulant to dabigatran?

A

start dabigatran 0-2 hours before the time that the next dose of the parenteral drug would be administered or at the time of the discontinuation of IV heparin

109
Q

What are some adverse effects of dabigatran?

A
  • bleeding (dose dependent increase in the incidence of major GI bleeding, no available antidote)
  • GI effects: dyspepsia
110
Q

State the clinical trials for dabigatran

A

RECOVER, RECOVER II, RE-MEDY, AND RE-SONATE

111
Q

What is the MOA/structure of apixaban?

A

direct factor Xa inhibitor, inhibits both free and clot-associated factor Xa activity

112
Q

What is the route of administration for apixaban and how is metabolized and excreted?

A
  • oral administration (not affected by food)
  • metabolized by CYP enzymes (mainly 3A4)- avoid strong 3A4 inhibitors
  • eliminated in the urine (25%) and feces
113
Q

What is the half-life of apixaban?

A

prolonged abosorption therefore half-life is ~12 hours with repeat dosing (onset 3-4 hours)

114
Q

What are some drug-drug interactions with apixaban?

A
  • 5 mg dose should be reduced to 2.5 mg bid when co-administered with strong CYP3A4 and P-gp inhibitors
  • if patient already on 2.5 mg bid dose and started on a strong CYP3A4 and P-gp inhibitor, avoid use
115
Q

What should be monitored when on apixaban?

A
  • Hgb, Hct, platelets
  • signs and symptoms of bleeding
  • drug-drug interactions
  • renal function, body weight
116
Q

What is the dosing for apixaban?

A

10 mg bid for 7 days, then 5 mg bid

117
Q

What is the conversion from warfarin to apixaban?

A

start apixaban when INR <2.0

118
Q

What is the conversion between apixaban and other anticoagulants (other than warfarin)?

A

discontinue one and start the other at the time of the next scheduled dose

119
Q

Stat the clinical trials for apixaban

A

AMPLIFY, AMPLIFY-EXT

120
Q

What is the MOA/structure of edoxaban?

A

factor Xa inhibitor

121
Q

What is the route of administration, metabolism, and excreted for edoxaban?

A
  • oral administration (food dose not affect it, peak plasma concentration 1-2 hours)
  • Metabolism: mostly in the unchanged form in plasma; minimal metabolism by hydrolysis, conjugation, oxidation by CYP3A4
  • Elimination: unchanged in urine (50%) also biliary/intestinal excretion
122
Q

What is the half-life of edoxaban?

A

10-14 hours

123
Q

What should be monitored when on edoxaban?

A
  • Hbg, Hct, platelets
  • signs/symptoms of bleeding
  • renal function and body weight
124
Q

What is the dosing of edoxaban?

A
  • 60 mg qd after 5-10 days of treatment with a parenteral anticoagulant
  • reduce dose to 30 mg qd for patients with CrCl 15-50 mL/min, weight less than 60 kg, or take concomitatn P-gp inhbitors
125
Q

What is the conversion from warfarin to edoxaban?

A

discontinue warfarin and start edoxaban when INR <2.5

126
Q

What is the conversion from UFH to edoxaban?

A

discontinue UFH and start edoxaban 4 hours later

127
Q

What is the conversion from other anticoagulants (not warfarin) to edoxaban (and vice-versa)?

A

discontinue one and start the new drug at the time of the next dose of the previous agent

128
Q

State the clinical trial for edoxaban

A

Hokusai VTE study

129
Q

What is the duration of therapy for the 1st episode of DVT or PE secondary to a reversible risk factor?

A

treatment for 3 months

130
Q

What is the duration of therapy for the 1st episode of idiopathic (unprovoked) DVT or PE?

A

treatment for at least 3 months (then evaluate risk-benefit ratio or extended therapy)

131
Q

What is the duration of therapy for two or more episodes of DVT or PE?

A

indefinite treatment

132
Q

What are some additional therapy options for treatment of VTE?

A
  • thrombolysis
  • inferior vena cava filter
133
Q

When should a patient be considered for thrombolysis therapy?

A
  • risk of limb gangrene secondary to venous occlusion
  • massive PE in hemodynamically unstable patients
  • administered systemically or locally via catheter
134
Q

When should a patient be considered for inferior vena cava treatment?

A
  • patients with contraindications to anticoagulation
  • patients with recurrent thromboembolism despite adequate anticoagulation
135
Q

What are some mechanical methods for the prevention/prophylaxis of VTE?

A
  • ambulation and physical therapy
  • graduated compression stockings (GCS) or elastic stockings (ES)
  • intermittent pneumatic compression (IPC) devices
  • venous foot pump (VFP)
136
Q

When should mechanical methods for the prevention/prophylaxis of VTE be used?

A
  • in patients who are at high risk of bleeding
  • as an adjunct to anticoagulant-based prophylaxis
137
Q

What are some pharmacological methods to prevention/prophylaxis of VTE?

A
  • general surgery for acutely ill medical patients
  • orthopedic surgery
138
Q

What are the medications and doses for total hip replacement?

A

DOC: enoxaparin 40 mg SC q 24 hr or enoxaparin 30 mg SC q 12 hr (crcl <30 use enoxaparin 30 SC q 24 hr)

Other agents: fondaparinux 2.5 mg SC q 24 hr, rivaroxaban 10 mg po q 24 hr, or warfarin (INR goal 2-3), apixaban 2.5 mg po twice daily, dabigatran (recommended in CHEST but not FDA approved), aspirin

139
Q

What are the medications and doses for total knee replacement?

A

DOC: enoxaparin 30 mg SC q 12 hr (crcl <30 enoxaparin 30 mg SC q 24 hr)

Other agents: fondaparinux 2.5 mg SC q 24 hr, rivaroxaban 10 mg po q 24 hr, warfarin (INR goal 2-3), apixaban 2.5 mg po twice daily, dabigatran (recommended in CHEST but not FDA approved), aspirin

140
Q
A

Cardio (4 decks)

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