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Cardio > VTE/PE > Flashcards

VTE/PE Flashcards

1
Q

Risk Factors for VTE/PE

A 
Fractures/trauma
Valvular disease or replacement
Indwelling catheters
Previous DVT/PE
Malignancy
Surgery (especially orthopedic)
Immobility/bed rest/paralysis*
Pregnancy
Increasing age (> 40)
Obesity
Protein C deficiency or resistance (factor V Leiden)
Protein S deficiency
Antiphospholipid antibodies
Antithrombin deficiency Pregnancy
Estrogen therapy
Malignancy
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2
Q

• Virchow’s triad: 3 primary factors influencing formation of a pathologic clot

A

o Damage to the vessel wall
o Venous stasis
o Hypercoagulable state

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3
Q

• Damage to the endothelium initiates two processes

A

o Platelet adhesion, activation and aggregation

o Activation of the coagulation cascade

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4
Q

Describe Blood Clot Formation

A

 Platelet adhesion to the surface of the vessel occurs when blood is exposed to subendothelial collagen and von Willebrand factor (vWF)
Platelets become activated and release adenosine diphosphate (ADP), serotonin and thromboxane A2 (TXA2) which stimulate platelet aggregation
 Platelet aggregation: glycoprotein IIb/IIIa receptor on platelet surface binds to fibrinogen (binding ligand)

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5
Q

Describe the Extrinsic pathway

A
  • Tissue factor is released from subendothelial cells present in many organs extrinsic to blood
  • Factor VII is activated and converted to factor VIIa when tissue factor binds
  • Factor VIIa-tissue factor complex activates factor X at the beginning of the common pathway
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6
Q

Describe Intrinsic pathway

A
  • Factor XII is activated when it comes into contact with the subendothelial membrane during vessel injury
  • A series of reactions leads to activation of factor IXa which activates factor X at the beginning of the common pathway
  • Alternatively, the factor VIIa-tissue factor complex activates factor IX in the intrinsic pathway
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7
Q

Describe Common pathway

A

• Factor Xa converts prothrombin (factor II) to thrombin (factor IIa)

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8
Q

Thrombin plays a central role in clot formation by

A

o Converting fibrinogen to fibrin monomers which begin to precipitate and polymerize to form a fibrin clot
o Activating platelets
o Enhances prothrombin activation on platelets by converting factor V to Va and factor VIII to VIIIa which accelerate the activity of factors Xa and IXa respectively

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9
Q

Natural inhibitors of clot formation

A 
o	Antithrombin
o      Protein S
o      Protein C 
o	Tissue factor pathway inhibitor (TFPI)
o	Plasminogen
o	Plasmin
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10
Q

inhibits thrombin (IIa), factor IXa and factor Xa

A

o Antithrombin

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11
Q

cofactor for activation of protein C

A

o Protein S

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12
Q

inactivates factors Va and VIIIa

A

o Protein C

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13
Q

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

A

o Tissue factor pathway inhibitor (TFPI)

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14
Q

Plasminogen is converted to plasmin via:

A

tissue plasminogen activator (t-PA

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15
Q

lyses fibrin to form fibrin degradation products

A

o Plasmin

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16
Q

Location of clot formation:

A

o Can form in any part of the venous circulation but the muscular veins of the calf or the valve cusp pockets of the deep calf veins are the most common locations

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17
Q

Deep vein thrombosis once formed can potentially do what 3 things

A
  • Spontaneously lyse
  • Extend into more proximal veins
  • Embolize to the lungs causing pulmonary embolus
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18
Q

Clinical Presentation/symptoms of VTE

A 
Unilateral calf or leg swelling
Calf pain or tenderness
Erythema
Warmth
Palpable cord
\+Homan’s sign
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19
Q

Clinical Presentation/symptoms of PE

A 
Dyspnea
Pleuritic chest pain
Anxiety
Tachypnea (>20 breaths/min)
Tachycardia (>100 beats/min)
Cough
Hemoptysis
Diaphoresis
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20
Q

Diagnosis of VTE/PE include

A
  • Clinical Presentation/symptoms
  • Risk factor assessment
  • D-dimer
  • Diagnostic testing
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21
Q

Explain D-dimer testing

A

o Cross linked fibrin degredation fragment produced during clot dissolution
o Negative predictive value
o Negative = <0.5 mg/L

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22
Q

Diagnostic testing for DVT

A 
Doppler ultrasonography and B-mode compression ultrasound
Contrast venography (Gold standard)
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23
Q

Diagnostic testing for PE

A

Ventilation perfusion (V/Q) lung scan
Chest CT with contrast (most commonly used)
Pulmonary angiography (Gold standard but most invasive)
Confirmation of proximal DVT via Doppler or venography

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24
Q

Radiographic visualization of the involved vessels with injection of radiocontrast material

A

Contrast venography

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25
Q

Perfusion evaluated by radiolabeled albumin and ventilation evaluated by inhalation of radiolabeled particles

A

Ventilation perfusion (V/Q) lung scan - V/Q mismatch indicates possible PE

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26
Q

Injection of radiocontrast dye into the pulmonary artery

A

Pulmonary angiography

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27
Q

 Ancillary tests for PE

A

arterial blood gas, EKG, CXR

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28
Q

Acute treatment for DVT/PE

A

Bridge therapy
o Parenteral agent: provides immediate anticoagulant activity
o Oral Therapy: Warfarin
o Bridge oral and parenteral agents for a minimum of 5 days AND until the INR is ≥ 2 for at least 24 hours

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29
Q

Structure of UFH

A

Heterogeneous mixture of glycosaminoglycan polysaccharide chains with molecular weights ranging from 3000 to 30000 kDa (mean = 1500)

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30
Q

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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31
Q

 Inhibition of thrombin requires

A

a heparin chain that is at least 18 saccharide units in length

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32
Q

 Also inhibits Factor IXa, XIa, XIIa

A

UFH

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33
Q

can inhibit factor Xa by binding to antithrombin

A

 Any pentasaccharide-containing heparin

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34
Q

Pharmacokinetics of UFH

A

not absorbed orally
treatment of VTE = continuous infusion, propylaxis of VTE = subcutaneous injection
Clearance: non-linear, dose-dependant
• Rapid saturable binding process
(Intravascular Binding)
• Slower, nonsaturable clearance through the kidneys
• T1/2 = 30-60 min

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35
Q

creates variablity and unpredictability in patient response

A

 Intravascular binding

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36
Q

Monitoring for UFH

A

Activated partial thromboplastin time (aPTT)
Platelet counts, hemoglobin/hematocrit
Signs/symptoms of bleeding

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37
Q

Clotting time reported in seconds- measures activity of thrombin and factor Xa

A

aPTT

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38
Q

Dosing of UFH

A
  • VTE treatment: IV bolus of 80 units/kg, followed by 18 units/kg/hr continous IV infusion
  • VTE prophylaxis: 5000 units SC q 8 hrs
  • No renal adjustment
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39
Q

Adverse effects

A
  •  Bleeding
  •  Heparin-induced thrombocytopenia
  •  Heparin-induced osteoporosis
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40
Q

How is bleeding that is caused by UFH reversed

A

o 1 mg of protamine will neutralize 100 units of UFH
o Short half life of heparin allows neutralization of heparin infused in the previous 60 mins
• Transfusion therapy may be required

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41
Q

2 types of HIT

A
  • Type 1: transient fall in platelets due to a direct effect of heparin
  • Type 2: immune-mediated reaction
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42
Q

MOA and onset of type II HIT

A

o Mechanism: IgG antibodies directed at heparin-platelet factor 4 complexes
o Patients are at an increased risk of thromboembolic events due to excessive thrombin generation, expression of tissue factor by monocytes and endothelial cells and platelet activation
o Onset: 5-14 days
o Platelet counts fall by greater than 50%

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43
Q

Treatment of HIT

A

 Direct thrombin inhibitors: FDA approved
• Argatroban (see drug chart)
• Bivalirudin (see drug chart)
 Fondaparinux

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44
Q

What types of patients are more at risk for Heparin-induced osteoporosis

A

• Usually only occurs with infusions > 6 months (rare)

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45
Q

heterogenous mixture of glycosaminoglycans derived from chemical or enzymatic degradation of UFH - Approximately 1/3 the molecular weight of UFH

A

• Low Molecular Weight Heparins (LMWH)

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46
Q

MOA of LMWHs

A

Binds to antithrombin via a unique pentasaccharide sequence

  •  Accelerates inactivation of factor Xa
  •  Only 25-50% of LMWH molecules inactivate thrombin
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47
Q

Pharmacokinetics of LMWHs

A

SC injection

- Intravascular binding: much less than UFH = more predictable dose-response relationship

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48
Q

2 LMWHs

A
  • Enoxaparin (Lovenox)

* Dalteparin (Fragmin)

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49
Q

Monitoring of LMWHs

A

Antifactor Xa levels
 Assess baseline renal function
 Signs and symptoms of bleeding
 Platelet counts, hemoglobin/hematocrit

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50
Q

Dosing (enoxaparin)

A

 Treatment of VTE: 1 mg/kg SC q 12 hr or 1.5 mg/kg SC q 24 hr
• Renal adjustment: 1 mg/kg SC q 24 hr (CrCl < 30 mL/min)

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51
Q

Adverse events of LMWHs

A

 Bleeding
 Heparin-induced thrombocytopenia
 Perispinal hematoma

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52
Q

How is bleeding that is caused by LMWHs reversed

A

o LMWH administered within 8 hours: 1 mg protamine per 100 antifactor Xa units of LMWH (this is 1 mg of enoxaparin)
o A second dose of 0.5 mg protamine per 100 antifactor Xa units if bleeding continues
o Smaller doses can be used if the LMWH was administered more than 8 hours before the bleeding event

53
Q

When is a patient at an increased risk for perispinal hematoma

A

when antithrombotic medications are administered concomitantly with neuraxial blockade

54
Q

Dosing of LMWHs in patients with renal dysfunction

A
  • Clinical trials have demonstrated increased exposure to anti-Xa activity with CrCl <30 mL/min
  • Measurement of anti-factor Xa levels is reasonable if LMWHs are used in patients with renal dysfunction
55
Q

Dosing adjustments of LMWHs based on weight

A
  • Prescribing information now includes doses for patients up to 190 kg
  • Risk of overdosing since intravascular volume does not have a linear relationship with total body weight
  • Testing of anti-factor Xa levels is reasonable in patients with a total body weight >150 kg or BMI >50 kg/m2
56
Q

When may UFH be preferred over LMWH

A

• If patient is obese and Crcl <30 ml/min then UFH may be preferred

57
Q

 A synthetic analog of the pentasaccharide sequence that binds to antithrombin - Selectively inhibits factor Xa

A

• Fondaparinux (Arixtra)

58
Q

Pharmacokinetics of fondaparinux

A

 Subcutaneous injections
 Mimimal intravascular binding
 Half life = 17 hours
 Excreted unchanged in the urine

59
Q

Monitoring of fondaparinux

A

 Assess baseline kidney function
 Signs and symptoms of bleeding
 Platelet counts and hemoglobin/hematocrit

60
Q

In what patients would you not want to use fondaparinux

A

Do not use in patients with CrCl <50 kg

61
Q

Dosing of fondaparinux

A 
	Treatment
•	For patients < 50 kg: 5 mg SC q 24 hr
•	For patients 50-100 kg: 7.5 mg SC q 24 hr
•	For patients >100 kg: 10 mg SC q 24 hr
	Prophylaxis: 2.5 mg SC q 24 hr
62
Q

Adverse events of fondaparinux

A

 Bleeding (increased risk in patients with smaller weights)

63
Q

inhibits the activation of coagulation factors by inhibiting the vitamin K dependent carboxylation of the factors - inhibits vitamin K oxide reductase enzyme complex (VKORC) therefore inhibiting vitamin K activation (from its inactive form: vitamin K epoxide) which then stops carboxylation

A

• Warfarin

64
Q

 Coagulation factors affected by warfarin

A
  • Factor VII (t1/2 = 6 hours)
  • Factor IX ( t1/2 = 21-30 hours)
  • Factor X (t1/2 = 27-48 hours)
  • Factor II (t1/2 = 60-72)
65
Q

 Anticoagulation factors affected by warfarin

A
  • Protein C (t1/2 = 9 hours)

* Protein S (t1/2 = 60 hours)

66
Q

Structure, pharmacokinetics and pharmacodynamics of warfarin

A

 Racemic mixture of S- and R- isomers
 High bioavailability
 Highly bound to plasma proteins (primarily albumin)

67
Q

 Onset of anticoagulant action of warfarin

A

• Takes 5-7 days to obtain peak anticoagulant effects

68
Q

 Half life of warfarin

A

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

69
Q

 warfarin Metabolism

A

 Metabolized in the liver
• S-isomer: CYP 450 2C9
• R-isomer: CYP 450 1A2 and 3A4

70
Q

account for up to 50% of the interindividual variability of warfarin response

A

• VKORC1 and CYP450 2C9

71
Q

leads to poor metabolism of warfarin (will require lower doses)

A

• Mutation of CYP 2C9

72
Q

mutations that have shown the highest risk of bleeding

A

• Mutation of CYP 2C92 and CYP 2C93 (*2 and *3 refers to the alleles) genetic variations

73
Q
  • VKORC1 (vitamin K epoxide reductase complex subunit 1)
  • Genotype AA
  • Genotype GG
  • Genotype AG
A

o AA: sensitive = need lower dose of warfarin
o GG: resistant = need higher doses of wararin
o AG = usual dose

74
Q

Medications/Drugs/Diseases that increase INR

A 
Hepatic dysfunction
Thyroid hormones
Hypermetabolic states (hyperthyroidism, fever)
Broad-spectrum antibiotics
Amiodaroneb,c,d
Isoniazidb
Metronidazolec
Celecoxibc
Grapefruit juiceb,d
Sulfamethoxazolec
Phenytoine
Tobacco smokee
Azole antifungalsb,c
Macrolide antibioticsb 
(erythromycin and clarithromycin)
Heparin
LMWH
Thrombolytic agents
75
Q

Medications/Drugs/Diseases that decrease INR

A 
Vitamin K (drugs/food)a
Methimazole, propylthiouracil
Hypothyroidism
Carbamazepineb
Barbiturateb
Rifampinb
Phenytoine
Tobacco smokee
Cholestyramine
76
Q

Monitoring of warfarin

A

 Prothrombin time (PT)
 International normalized ratio (INR)
Signs/symptoms of bleeding

77
Q

Accounts for variations in sensitivity of thromboplastin reagents to reductions in vitamin k-dependant clotting factors

A

 International normalized ratio (INR)

78
Q

Goal INR range

A

2-3

79
Q

Frequency of monitoring warfarin

A
  • Hospitalized patients = daily
  • Outpatients = within 3 days of hospital discharge then weekly
  • Once a stable response achieved = Every 4 weeks and some patients every 12 weeks
80
Q

Adverse events of warfarin

A

 Bleeding

81
Q

Types of patients initiated on 2.5 mg PO daily of warfarin

A

Patients > 65 y/o
Significant drug interaction that ↑ INR (especially 2C9 inhibitors)
Patients with congestive heart failure (CHF)
Liver disease
Malnourished (low albumin state)
High risk of bleeding
Baseline INR > 1.5

82
Q

Types of patients initiated on 7.5 - 10 mg PO daily of warfarin

A 
Younger patients (< 60 y/o)
 No interacting medications
 Low bleeding risk
83
Q

For patients treated in the outpatient setting what loading dose would be used of warfarin

A

loading dose of 10 mg for the first 2 days of therapy

84
Q 
Goal INR 2.5 (Range 2.0-3.0):
dose adjust for INR < 1.5
or
Goal INR 3.0 (Range 2.5-3.5) (mechanical valves)
dose adjust for INR < 2.0
A

↑ total weekly dose by 10 – 20%

85
Q 
Goal INR 2.5 (Range 2.0-3.0):
dose adjust for INR 1.5 – 1.9
or 
Goal INR 3.0 (Range 2.5-3.5) (mechanical valves)
dose adjust for INR 2.0 – 2.4
A

Continue current dose and recheck in 1-2 weeks

86
Q 
Goal INR 2.5 (Range 2.0-3.0):
dose adjust for INR 3.1 – 3.5
or
Goal INR 3.0 (Range 2.5-3.5) (mechanical valves)
dose adjust for INR 3.6 – 4.0
A

Continue current dose and recheck in 1-2 weeks

87
Q 
Goal INR 2.5 (Range 2.0-3.0)
dose adjust for INR 3.6 – 4.5
or
Goal INR 3.0 (Range 2.5-3.5) (mechanical valves)
dose adjust for INR 4.1 – 4.5
A

Hold 1 – 2 doses; when resume ↓ total weekly dose by 10 – 20%

88
Q

Intervention for INR > 4.5, but < 10, no significant bleeding

A

Hold warfarin until INR close to goal
Monitor more frequently and resume therapy at lower dose as above when close to goal INR
-If rapid reversal for surgery required administer vitamin K PO < 5 mg and hold warfarin.
- Expect INR ↓ in 24 hours. If still elevated administer another 1 – 2 mg of vitamin K orally

89
Q

Intervention for INR > 10, no significant bleeding

A

Hold warfarin therapy and administer Vitamin K 2.5 – 5 mg PO. Expect INR ↓ in 24 – 48 hrs. Resume therapy at lower dose as above when close to goal INR.

90
Q

Intervention for Serious bleeding at any elevated INR

A

Hold warfarin therapy and give Vitamin K 10 mg slow IV infusion. May repeat Vitamin K q12h for persistent elevated INR.
-Supplement with fresh frozen plasma, prothrombin complex concentrate, or recombinant factor VIIa in
life threatening situations such as intracranial hemorrhage

91
Q

What would happen if doses of Vitamin K greater than recommended were given

A

could result in warfarin resistance for up to 1 week

92
Q

Non Bridge Therapy

A
  • Rivaroxaban (Xarelto)

* Dabigatran (Pradaxa)

93
Q

Selectively blocks the active site of factor Xa without requiring a cofactor (like AT)
• Inhibits factor Xa in both the intrinsic and extrinsic pathways
• Inhibition of clot bound factor Xa

A

• Rivaroxaban (Xarelto)

94
Q

Pharmacokinetics of rivaroxaban

A

• 15 mg and 20 mg tablets should be taken with food to increase bioavailability 90% bound to plasma proteins
Half life: 5-9 hours
Hepatic metabolism (3A4, 2J2), excreted in urine and feces

95
Q

Monitoring of rivaroxaban

A

Assess baseline kidney function and hepatic function
 Signs and symptoms of bleeding
 Platelet counts and hemoglobin/hematocrit

96
Q

 Drug-drug interactions with rivaroxaban

A

strong 3A4 and P-glycoprotein inhibitors

97
Q

Dosing of rivaroxaban

A

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

98
Q

Rivaroxaban is contraindicated in which patients

A

• Avoid use in patients with Crcl <15 ml/min (for Afib patients)

99
Q

Adverse effects of rivaroxaban

A

 Bleeding

100
Q

Clinical Trials associated with rivaroxaban

A

 VTE: Einstein DVT, Einstein PE

101
Q

not orally bioavailable due to its highly polar structure - is a prodrug

A

• Dabigatran (Pradaxa)

102
Q

MOA of dabigatran

A

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

103
Q

Pharmacokinetics of dabigatran

A

 Rapid absorption: peak concentration reached within 2 hours
 Not metabolized by CYP enzymes to any significant extent
 Renal elimination (~80% of total clearance)
 Half life: 12-17 hours

104
Q

Monitoring of dabigatran

A

 Renal function
 Platelet counts and hemoglobin/hematocrit
 Signs and symptoms of bleeding

105
Q

Drug interactions with dabigatran

A

• P-glycoprotein inhibitors: may increase concentration of dabigatran
o Drugs: amiodarone, dronedarone, verapamil, ketoconazole

106
Q

Indication/dosing of dabigatran

A

 VTE treatment after the patient has received a parenteral anticoagulant for 5-10 days
• Dosing: 150 mg twice daily for CrCl > 30 ml/min, Crcl <30 mL/min no doing recommendations provider per PI
 FDA approval for nonvalvular atrial fibrillation

107
Q

AE of dabigatran

A

 Bleeding

 GI effects: dyspepsia

108
Q

In patients with CrCl 30-50 mL/min and concomitant use of P-gp inhibitor dronedarone or ketoconazole what would the dose of dabigatran be

A

consider reducing the dose to 75 mg twice daily

109
Q

Converting from parenteral anticoagulant to dabigatran when would dabigatran be started

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 discontinuation of IV heparin

110
Q

Clinical Trials for dabigatran

A

 VTE: RECOVER, RECOVER II, RE-MEDY and RE-SONATE trials

111
Q

Duration of treatment for dabigatran

A

1st episode of DVT or PE secondary to a reversible risk factor = Treatment for 3 months
1st episode of idiopathic (unprovoked) DVT or PE = Treatment for at least 3 months (then evaluate risk-benefit ratio for extended therapy)
DVT or PE in patients with cancer = LMWH for 3 months, continue therapy indefinitely with wafarin or LMWH or until cancer is resolved
Two or more episodes of DVT or PE = Indefinite treatment

112
Q

Risk factors for bleeding

A

age >65, previous bleeding, cancer, renal failure, liver failure, thrombocytopenia, diabetes, previous stroke, anemia, recent surgery, frequent falls, alcohol abuse

113
Q

Additional therapy options for DVT/PE

A 
o	Thrombolysis (Streptokinase, Urokinase, Rt-PA)
o	Inferior vena cava filter
114
Q

 Situations to consider thrombolysis

A
  • Risk of limb gangrene secondary to venous occlusion (seen with massive ileofemoral thrombosis)
  • Massive PE in hemodynamically unstable patients
115
Q

 Situations to consider inferior vena cava filter

A

patients with contraindications to anticoagulation, patients with recurrent thromboembolism despite adequate anticoagulation

116
Q

Risk factors for VTE in hospitalized patients

A
  • previous VTE
  • reduced mobility
  • thromboembolic condition
  • trauma or surgery within 3 months
  • 70 y/o and above
  • heart and/or respiratory failure
  • acute MI or ischemic stroke
  • acute infection or rheumatologic disorder
  • obesity (BMI 30 and greater)
  • ongoing hormonal treatment
117
Q

 Uses of mechanical methods for VTE

A
  • In patients who are at high risk of bleeding

* As an adjunct to anticoagulant-based prophylaxis

118
Q

 Types of mechanical methods

A
  • Ambulation and physical therapy
  • Graduated compression stockings (GCS) or elastic stockings (ES)
  • Intermittent pneumatic compression (IPC) devices
  • Venous foot pump (VFP)
119
Q

Pharmacologic methods for General surgery or acutely ill medical patients

A

• UFH, enoxaparin, or fondaprinux

120
Q

Pharmacologic methods for Orthopedic surgery - Total hip replacement

A

o 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)
o 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

121
Q

Pharmacologic methods for Orthopedic surgery -Total knee replacement

A

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

122
Q

MOA of apixaban

A

 Direct factor Xa inhibitor: inhibits both free and clot-associated factor Xa activity

123
Q

Pharmacokinetics of apixaban

A

 Oral administration
• Absorption not affected by food
 Prolonged absorption therefore half life is ~12 hours with repeat dosing
• Onset 3-4 hours
 Metabolized by CYP enzymes (mainly 3A4)
• Avoid strong 3A4 inhibitors
 Elimination: urine (25%) and feces

124
Q

Monitoring of apixaban

A

 Hemoglobin/hematocrite and platelet counts
 Signs and symptoms of bleeding
 Renal function, body weight (dose adjustment)

125
Q

 Drug-Drug interactions for apixaban

A

• 5 mg dose should be reduced to 2.5 mg twice dialy when coadministrated with strong CYP3A4 and P-gp inhibitors like ketoconazole, itraconazole, ritonavir, or clarithromycin

126
Q

Indication for apixaban

A

 FDA approved for nonvalvular atrial fibrillation

 VTE prophylaxis for post-hip or knee replacement

127
Q

Adverse events of apixaban

A

 Bleeding

128
Q

Clinical Trial for apixaban

A

 VTE: AMPLIFY-EXT

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