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CV II Exam 2 > 9-2 Anticoagulant, Antithrombotic,& Thrombolytic Agents > Flashcards

9-2 Anticoagulant, Antithrombotic,& Thrombolytic Agents Flashcards

1
Q

Low Molecular Weight Heparins (LMWH) include:

A

Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Tinzaparin (Innohep)

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2
Q

What are some Factor Xa inhibitors?

A

Fondaparinux (Arixtra)

Rivaroxaban (Xarelto)

Apixaban (Eliquis)

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3
Q

What factor is eventually made by both extrinsic and intrinsic clotting pathways?

A

active proteolytic enzyme:

Xa

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4
Q

What does Xa do in the final common pathway?

A

combines with other factors (V, Ca++, and phospholipids)

converts an inactive proenzyme, prothrombin, into its active enzyme product, thrombin

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5
Q

What does thrombin do in the clotting cascade?

A

Thrombin clips fragments from the protein fibrinogen releasing fibrin monomers

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6
Q

What does fibrin do in the clotting cascade?

A

fibrin monomers

  • polymerize into a meshwork that stabilizes the initial platelet plug
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7
Q

Fibrin monomers have formed an initial plug for a leak. What stabilizes this?

A

Factor XIII, activated by thrombin to XIIIa,

covalently cross‑links adjacent fibrin monomers to form an insoluble fibrin clot

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8
Q

What is a direct thrombin inhibitor?

A

dabigatran

rivaroxaban,

apixaban,

edoxapan

  • all oral
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9
Q

What is an inhibitor of Factor Xa?

A

Rivoroxaban

Apixaban

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10
Q

What are the therapeutic objectives in thromboembolic disease?

A

To prevent formation of pathological thrombi in patients at risk.

To prevent clot extension and/or embolization in patients who have developed thrombosis.

To rapidly dissolve thrombi causing life-threatening or severe ischemia.

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11
Q

What anticoagulant drugs do?

A

slow clotting time and suppress coagulation

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12
Q

What works for rapid parenteral (IV, SQ) anticoagulation?

A

Heparin,

Low Molecular Weight Heparin, and

Fondaparinux

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13
Q

What works well for slow, prolonged, oral anticoagulation?

A

warfarin

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14
Q

What can be given via IV during PCI and for treatment of HIT syndrome ?

A

PCI = percutaneous coronary intervention = angioplasty

lepirudin,

bivalirudin,

argatroban

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15
Q

What do antiplatelet drugs do?

A

inhibit platelet adhesion and aggregation

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16
Q

What are some antiplatelet drugs?

A

aspirin

clopidogrel and prasugrel

cilostazol

abciximab, eptifibatide, tirofiban

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17
Q

How does aspirin work, pharmacologically?

A

inhibit TXA2 formation

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18
Q

How do Clopidogrel and Prasugrel work, pharmacologically?

A

– inhibit platelet ADP receptor and platelet aggregation

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19
Q

How does cilostazol work, pharmacologically?

A

Cilostazol –

cAMP PDE inhibitor, blocks platelet aggregation and stimulates vasodilation

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20
Q

What are the pharmacological effects of abciximab, eptifibatide, and tirofiban?

A

– blockers of glycoprotein IIb/IIIa complex used exclusively during PCI procedures.

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21
Q

When are thrombolytics used?

A

Fibrinolytic (Thrombolytic) Drugs used under emergency situations to dissolve formed fibrin clots

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22
Q

What are some examples of some thrombolytics?

A

t-PA = tissue plasminogen activator

Alteplase (t-PA), reteplase, tenecteplase, streptokinase

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23
Q

What is the structure of heparin?

A

made up of complex linear polysaccharide (glycosaminoglycan) chains

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24
Q

What is the mechanism for heparin?

A

Inhibition of thrombin and factor Xa are most important in the anticoagulant effect

Heparin increases the rate of the thrombin‑antithrombin reaction by serving as a catalytic template to which both the antithrombin and thrombin (or other protease) bind

  • antithrombin III is endogenous, and rapidly inhibits thrombin but only in presence of heparin or naturally occuring heparin-like molecules

Heparin inhibits activated coagulation factors of the intrinsic and common pathways, including thrombin, Xa, IXa, XIa, XIIa, and kallikrein

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25
Q

What is the effect of heparin on plasma clotting times?

A

Heparin prolongs:

aPTT and the thrombin time;

the PT is less effected by UFH,

  • but at high plasma concentrations will also prolong the PT
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26
Q

How is heparin administered? What route of administration is contraindicated and why?

A

it can only be administered intravenously or subcutaneously

  • Because heparin is a large molecule and is destroyed in the GI tract

Intramuscular injection is contraindicated because of the likelihood of hematoma formation.

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27
Q

How is heparin’s onset of action started?

A

onset of action is dictated primarily by its rate of appearance in the plasma

  • heparin’s anticoagulant effects occur through a simple binding reaction with antithrombin III and clotting factors
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28
Q

Considering heparin’s onset of action, how would you administer the drug for rapid therapy versus a prophylactic therapy?

A

when rapid anticoagulation is required:

therapy is initiated with a bolus IV injection followed by a continuous IV infusion

slower onset is sufficient, i.e., prophylaxis prior to surgery:

subcutaneous injection of heparin or LMWH is typically used

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29
Q

How is heparin titrated for adults in continuous intravenous infusion?

A

a bolus dose is injected into the tubing after the infusion is started

continuous infusion rate is maintained (infusion pump)

  • rate is subsequently adjusted according to the results of the aPTT performed 4 hours later
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30
Q

What are the advantages and disadvantages of continuous IV infusion of heparin?

A

Advantages:

immediate onset of anticoagulant effect, stable blood concentrations.

Disadvantages:

infusion pump required for long‑term therapy, may cause hypervolemia, patient discomfort, pump must be carefully monitored.

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31
Q

How is intermittent IV dosing done for heparin?

A

(not recommended)

Adults: 5,000 units initially, followed by 5,000 to 10,000 units every four to six hours.

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32
Q

What are the advantages and disadvantages of intermittent IV dosing done for heparin?

A

Advantages:

avoids fluid infusion.

Disadvantages:

greater variation in blood concentrations and requires frequent laboratory tests to regulate the dose

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33
Q

How are minidoses of heparin administered?

A

Subcutaneous low dose prophylaxis (“minidose”)

5,000 units two hours before surgery and every 8 or 12 hours thereafter until the patient is discharged or is fully ambulatory

For full‑dose effects give 10,000 - 12,000 units every eight hours or 15,000 - 17,500 units every 12 hours

The drug should be injected in the smallest volume possible at different sites around the iliac crest, over the lower abdomen, or thigh. A small needle should be used to prevent massive hematoma.

(Note that different protocols may be necessary in varying clinical situations. The trend is now shifting to the use of LMWH SQ injections (replacing UFH) for prophylaxis)

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34
Q

What are some extracorporeal uses of heparin?

A

Extracorpeal (“out of body”) Uses:

Heparin Sodium Lock Solution (Hep-LockÔ) Heparin is used to flush out IV lines, etc.

Sometimes tubes and pipettes used in blood work are “heparinized” to prevent coagulation. These solutions are not for therapeutic use.

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35
Q

What is used to monitor heparin therapy?

A

Monitoring Therapy:

aPTT = 1.5 to 2.5 times control.

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36
Q

How is heparin metabolized out of the body?

A

Termination:

up to 50% of dose is excreted unchanged in urine

‑ remainder metabolized in liver to a weakly active derivative.

Elimination half-life is dose-dependent principally because UFH binds to plasma proteins and endothelial cells in a saturable process. This binding also limits the bioavailability of UFH after subcutaneous injection.

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37
Q

What are some major effects from heparin toxicity?

A

hemorrhage

hematoma

heparin-induced thrombocytopenia (HIT syndromes)

less common stuff - who cares

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38
Q

How does hemorrhage from heparin happen?

A

from inadvertent overdose,

bleeding from undiagnosed disease site (ulcer, carcinoma).

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39
Q

What is HIT syndrome?

A

Heparin induces transient thrombocytopenia in as many as 25% of patients but this usually resolves spontaneously.

However, in approximately 5% of patients (this is a lot of patients!) a severe thrombocytopenia can evolve days after the initiation of therapy.

This heparin-induced thrombocytopenia or HIT syndrome is due to the formation of antibodies directed against the heparin- platelet factor 4 complexes. These antigen-antibody complexes bind to Fc receptors on adjacent platelets causing aggregation, platelet activation and paradoxical thrombosis.

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40
Q

How is HIT syndrome with thrombosis treatred?

A

with direct thrombin inhibitors

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41
Q

What are the less commo side-effects of heparin?

A

Less common side effects of HFH therapy include acute hypersensitivity reactions, alopecia, platelet aggregation, osteoporosis (1 year therapy), and priapism.

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42
Q

What is the main contraindication for heparin?

A

Active bleeding!!!

  • always know the potential for bleeding before administering heparin (perform blood coagulation test, look for occult bleeding).
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43
Q

What diseases is heparin use contraindicated for?

A

Heparin should not be administered to patients with:

severe hypertension and/or known vascular aneurysm,

hemophilia,

thrombocytopenia,

intracranial hemorrhage,

active tuberculosis,

ulcerative lesions of the GI tract,

threatened abortion,

or visceral carcinoma.

44
Q

With what kinds of surgery should you not give heparin?

A

Heparin should be withheld during and after surgery of the brain, eye, or spinal cord, and should not be given to patients undergoing lumbar puncture or regional anesthetic block

45
Q

What are the guidelines for use of heparin in pregnant women?

A

The drug should be used only where clearly indicated in pregnant women, despite its apparent lack of transfer across the placenta

46
Q

What problems is heparin indicated for?

A

DVT and PE - Tx and prevention

Extra corporeal circulation (hemodialysis and heart-lung machine)

Prophylaxis of postoperative and recumbency thrombosis

Myocardial infarction and unstable angina

Disseminated intravascular coagulation (DIC)

47
Q

Why is heparin indicated for MI treatment? What is the recommended treatment for acute MI?

A

Lessen incidence of secondary peripheral venous thrombosis and pulmonary embolism.

Recommended treatment during acute MI is: aspirin therapy immediately (+O2, nitroglycerin, and morphine), followed by thrombolytic therapy (if percutaneous coronary intervention (PCI) cannot be conducted), followed by heparin IV. Heparin is usually contraindicated if PCI is anticipated.

48
Q

What can you give to treat heparin overdose?

A

Protamine Sulfate

  • also, withdraw heparin
49
Q

How does protamine sulfate work? What are some adverse effects?

A

Protamine sulfate: is a strongly basic protein administered IV that binds and inactivates heparin because of its strong positive charge.

Protamine may cause transient hypotension if given too rapidly. This drug must be used cautiously to avoid thrombotic complications. Occasionally, anaphylactic reactions occur.

Protamine sulfate is not capable of reversing the effects of warfarin.

50
Q

What are some low molecular weight heparins?

A

Enoxaparin Sodium (Lovenox),

Dalteparin (Fragmin),

Tinzaparin (Innohep).

51
Q

How does LMWH differ from heparin in terms of activity?

A

LMWH doesn’t have a binding spot for activated IIa, so it mostly inactivates Xa

  • LMWH anti-IIa activity 2:1 to 4:1, anti-Xa is 1:1

Heparin has binding sites for Xa and IIa, so anti activity for both is 1:1

LMWH has a greater ratio of anti-factor Xa to antithrombin (IIa) activity and less effect on platelet activity

52
Q

What makes LMWH a favorable drug over heparin?

A

developed with the goal of decreasing bleeding episodes while still retaining anticoagulant activity

  • helps prevent DVT in surgical patients
  • greater bioavailability after subcutaneous administration
  • a longer duration of anti-factor Xa activity that allows for less frequent dosing intervals
  • linear pharmacokinetics
  • possibly fewer side effects, i.e., less incidence of HIT syndrome
  • lack of required laboratory monitoring (i.e., no aPTT is required).

The current trend is to substitute LMWH for UFH treatment for well-defined clinical situations.

53
Q

What are the indications for enoxaparin, a type of LMWH?

A

Enoxaparin is indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism:

  • In patients undergoing abdominal surgery who are at risk for thromboembolic complications.
  • In patients undergoing hip replacement surgery, during and following hospitalization.
  • In patients undergoing knee replacement surgery.
  • In medical patients who are at risk for thromboembolic complications due to severely restricted mobility during acute illness
54
Q

What are some additional uses for enoxaparin, in addition to prevention of DVT?

A

unstable angina and non-Q-wave myocardial infarction, when concurrently administered with aspirin

The inpatient treatment of acute DVT with or without PE, when administered in conjunction with warfarin sodium

The outpatient treatment of acute DVT without PE when administered in conjunction with warfarin sodium.

55
Q

When are LMWHs contraindicated?

A

LMWHs are contraindicated during spinal / epidural anesthesia or spinal puncture because of the increased risk of spinal hematomas

56
Q

What is the pharmacological activity of fondaparinux?

A

synthetic analog of heparin

increases factor Xa inhibition without neutralizing thrombin

Does not bind to platelet factor 4 and has not caused immune-mediated thrombocytopenia (HIT)

57
Q

What does fondaparinux not affect?

A

PT time,

aPTT time,

bleeding time,

or platelet function

58
Q

What are the indications for fondaparinux?

A

Fondaparinux is indicated for the prevention of deep vein thrombosis after:

hip fracture surgery,

knee or hip replacement surgery,

or abdominal surgery when at risk for thromboembolic complications.

The drug is administered in conjunction with warfarin sodium in the treatment of acute DVT or acute pulmonary embolism (PE) when initial therapy is administered in the hospital.

59
Q

What are 2 direct thrombin inhibitors? How are they administered?

A

hirudin

lepirudin

60
Q

How do direct thrombin modulators work? How are they administered?

A

direct binding to the active site of thrombin; they do not require other binding proteins, such as antithrombin

IV administration only

61
Q

What is bivalirudin? What is it used for?

A

short-acting, synthetic direct thrombin binding inhibitor approved for patients with unstable angina undergoing coronary angioplasty.

Most patients in the USA with acute coronary syndromes undergoing angioplasty are now treated with platelet glycoprotein IIb/IIIa receptor antagonists (eptifibatide, tirofiban, or abciximab) plus aspirin and low doses of unfractionated heparin. This drug is very expensive compared to more conventional treatments. ($456.00 versus $68.00 Lovenox or $1.20 for UFH).

Only administered by IV infusion.

62
Q

What is argatroban?

A

another short-acting, direct thrombin inhibitor that reversibly binds to the thrombin active site

63
Q

What clotting factors does argatroban need to work? How does this make it effective as an anticoagulant?

A

does not require antithrombin III for antithrombotic activity

highly selective for thrombin

  • is capable of inhibiting the action of both free and clot-associated thrombin
64
Q

What is argatroban indicated for? How is it administered?

A

in patients with heparin-induced thrombocytopenia (HIT) and coronary angioplasty in patients with HIT

Only administered by IV infusion.

65
Q

What is an important oral anticoagulant?

A

warfarin - Coumadin

66
Q

What is the action of warfarin? Does it work in vitro?

A

The coumarin-type oral anticoagulants (warfarin) inhibit blood clotting by interfering with the hepatic synthesis of the vitamin K-dependent clotting factors,

prothrombin (II)

factors VII, IX, and X,

and the anticoagulant proteins, Protein C and Protein S, as well.

Warfarin has no in vitro anticoagulant effects

67
Q

What is the mechanism for warfarin?

A

Normally:

A vitamin K‑dependent mechanism converts glutamic acid residues in several clotting factor proteins (II, VII, IX, X and proteins C and S) to gamma carboxyglutamic acid residues (two COO- residues).

This transformation is required to give these clotting proteins high affinity for Ca++ and phospholipid and without undergoing this post-translational modification they are basically inactive. Vitamin K undergoes a cycle of oxidation and reduction in the liver to produce the active form of the vitamin.

Warfarin prevents the reduction of vitamin K once it is oxidized by inhibiting the enzyme vitamin K epoxide reductase.

68
Q

What is the onset and half-life of warfarin?

A

Onset is considerably delayed (36‑72 hours):

  • because of long half‑life of drug, (e.g., 36-48 hours for warfarin) and
  • half‑lives of clotting factors (fastest decay t1/2 approximately 6 hour for Factor VII).
69
Q

How is warfarin absorbed from the GI tract? Availability?

A

The drug is completely absorbed from the G.I. tract, is highly fat soluble, and is 99% bound to albumin

70
Q

What is the duration of action for warfarin?

A

Duration of action: is prolonged (proportional to half‑life of drug), which allows single daily administration of drug

71
Q

How is the effect of warfarin terminated?

A

Termination:

delayed by slow drug elimination rate (t1/2 = 40 hours) and also,

  • prothrombin and other factors must be synthesized in liver and delivered to blood.

Warfarin is converted to inactive metabolites in the liver and kidney which are excreted in urine and stool.

72
Q

What are the toxicities associated with warfarin?

A

Hemorrhage: incidence 2‑4%, serious bleeding approximately 1%

Anorexia nausea, vomiting, diarrhea

Cutaneous lesions ‑ skin necrosis, purpura, dermatitis, urticaria, alopecia.

73
Q

What are some general contraindications for warfarin?

A

similar to heparin, but include pregnancy and unreliable patient

  • hemorrhage, hematoma, HIT syndrome

General contraindications for anticoagulant therapy include:

patients with recent eye, brain, or spinal cord surgery;

head injury;

or uncontrolled bleeding.

Patients with severe hypertension or suspected aneurysm are at high risk for bleeding complications.

74
Q

Can you give warfarin to a pregnant lady?

A

Warfarin is contraindicated in pregnant patients because its use during the first or third trimesters is associated with congenital abnormalities

75
Q

What are the general indications for warfarin?

A

Usually anticoagulant therapy is started with heparin (UFH or LMWH) and followed with warfarin (or increasingly other oral anticoagulant drugs) for long‑term therapy.

76
Q

What conditions/problems is warfarin indicated for?

A

DVT and PE

Atrial fibrillation (valvular heart disease, CHF, mitral stenosis, cardiomyopathy)

Myocardial infarction (to prevent mural thrombosis and systemic embolism).

Rheumatic heart disease (emboli frequently associated with this disorder).

Mechanical prosthetic valves, bioprosthetic mitral valves.

77
Q

How is warfarin dosed?

A

(Warfarin is only given orally.)

Dose

Warfarin: 10-15 mg/day for 3-5 days, then adjust dose appropriately.

Usual maintenance dose is 2-10 mg/daily.

78
Q

What factors will influence the effect of warfarin?

A

considerable variations in response

due to differences in:

absorption,

sensitivity,

elimination, and

drug-drug interactions

79
Q

What are some drug-drug interactions involving warfarin?

A

Warfarin has been implicated in many drug-drug interactions (See Appendix )

Important! Know this fact! Drug-drug interactions involving warfarin are frequently used to test for knowledge of this subject on board exams and other tests! Be aware of common drug-drug interactions.

Move on to further questions.

80
Q

These agents may increase the anticoagulant effect of warfarin. The risk of bleeding may be increased. The mechanism of the interaction is unknown or complicated.

A

Acetaminophen

Influenza virus vaccine

Androgens

Isoniazid

Beta blockers

Ketoconazole

Clofibrate

Phenytoin

Corticosteroids

Propoxyphene

Disulfiram

Sulfonamides

Erythromycin

Tamoxifen

Fluconazole

Thioamides

Glucagon

Thyroid hormones

81
Q

These drugs may increase the anticoagulant effect of warfarin or anisindione due to inhibition of the anticoagulant’s hepatic metabolism. The risk of bleeding may be increased.

A

Amiodarone

Phenylbutazones

Chloramphenicol

Propafenone

Cimetidine

Quinidine

Ifosfamide

Quinine

Lovastatin

SMZ-TMP

Metronidazole

Sulfinpyrazone

Omeprazole

82
Q

These agents may increase the anticoagulant effect of warfarin due to displacement from plasma binding sites. The risk of bleeding may be increased.

A

Choral hydrate

Loop diuretics

Nalidixic acid

83
Q

These drugs may increase the anticoagulant effect of warfarin due to interference with vitamin K. The risk of bleeding may be increased.

A

Aminoglycosides

Mineral Oil

Tetracyclines

Vitamin E

84
Q

These agents may increase the anticoagulant effect of warfarin and increase the risk of bleeding due to effects on platelet function , and, in the case of NSAIDS, GI irritant effects

A

Cephalospoprins

Difunisal

NSAIDS

Penicillins

Salicylates

85
Q

These drugs may decrease the anticoagulant effect of warfarin. The mechanism of action is unknown.

A

Ascorbic acid

Griseofulvin

Dicloxacillin

Nafcillin

Ethanol

Sucralfate

Ethcholrvynol

Trazodone

86
Q

These agents may decrease the anticoagulant effect of warfarin due to induction of hepatic microsomal enzymes and increased metabolism.

A

Aminoglutethimide

Etretinate

Barbiturates

Glutethimide

Carbamazepine

Rifampin

87
Q

These drugs may decrease the anticoagulant effect of warfarin due to reduced absorption, increased synthesis of clotting factors, hemoconcentration of clotting factors, or by bypass of the site of action.

A

Cholestyramine

Thiopurines

Oral contraceptives

Spironolactone

Estrogens

Thiazide diuretics

Vitamin K

88
Q

How is warfarin therapy monitored? Which labs are helpful, and what ranges do you want?

A

Monitor therapy with INR;

PT time (corrected to an INR) should be determined before initial dose and daily thereafter until the response is stabilized.

Weekly monitoring until maintenance dose established.

INR = 2.0‑3.0 is the usual target range for less intense therapy.

89
Q

How is warfarin overdose treated?

A

Anticoagulant effects can be reversed by withdrawal of drug (but remember-effects are quite prolonged),

administration of vitamin K1

if necessary, the infusion of fresh-frozen plasma or plasma concentrates rich in II, VII, X.

90
Q

What are the advantages of oral direct thrombin inhibitors (as a class) instead of warfarin?

A

Warfarin needs close monitoring, dose adjustment to keep INR 2-3

  • high variability in patients with absorption, metabolism and elimination

Oral direct thrombin inhibitors

  • orally active, sage as warfarin
  • stable drug levels & pharmacological effects without dose adjustment/continuous (INR) monitoring
91
Q

What is dabigatran etexilate/Pradaxa? What does it do?

A

synthetic, non-peptide, direct thrombin inhibitor.

It inhibits both clot-bound and circulating thrombin and decreases thrombin-stimulated platelet aggregation.

92
Q

How is dabigatran etexilate absorbed?

A

prodrug that is rapidly absorbed after an oral dose and then converted to the active drug by esterases in the blood

93
Q

How is dabigatran metabolized? What is the half life?

A

The drug is not metabolized by hepatic enzymes and is excreted mainly in urine.

Dabigatran reaches a peak about 1 hour after oral administration and has an elimination half-life of 12-17 hours.

Capsules of the drug should not be chewed, crushed, or emptied prior to swallowing.

The drug is dosed twice per day

94
Q

Why is INR monitoring not required with dabigatran?

A

Dabigatran’s anticoagulant effect is much less variable than that of warfarin

- INR monitoring is not required.

Dabigatran has few drug-drug-interactions (ketoconazole, rifampin).

95
Q

How is dabigatran overdose remedied?

A

Unlike warfarin, there is no effective antidote for dabigatran that could be used in case of bleeding or emergency surgery, but it is dialyzable

96
Q

What are the adverse effects of dabigatran?

A

Adverse effects of dabigatran include bleeding (lower incidence than warfarin); incidence of hemorrhagic stroke is significantly lower with dabigatran compared to warfarin.

Dyspepsia and gastritis are the most common adverse effects

97
Q

What is dabigatran etexilate approved for?

A

prevention of thromboembolic stroke in patients with non-valvular atrial fibrillation

may be approved soon for prevention of thromboembolism in patients undergoing knee and hip replacement surgery

98
Q

What does rivaroxaban/Xarelto do? What is it indicated for?

A

oral direct factor Xa inhibitor

for prevention of deep vein thrombosis in patients undergoing knee or hip replacement surgery

99
Q

How does rivaroxaban compare to enoxaparin? Warfarin?

A

more effective than enoxaparin in preventing DVT and death after elective hip and knee surgery

at least as effective and safe as warfarin in preventing stroke in patients with atrial fibrillation

100
Q

What is an antidote to side effects or overdose of rivaroxaban?

A

There is no specific antidote for rivaroxaban-induced bleeding and, due to the high percentage of drug bound to protein in plasma, rivaroxaban is not dialyzable

101
Q

What are some drug-drug interactions with rivaroxaban?

A

rifampin and ketoconazole

102
Q

What is apixaban/Eliquis? What is it indicated for?

A

oral direct factor Xa inhibitor

for prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation.

103
Q

How does efficacy of apixaban compare to warfarin?

A

apixaban is at least as effective as warfarin in preventing stroke and to cause less bleeding

Comparisons to dabigatran and rivaroxaban remain to be determined.

104
Q

What is a side effect associated with apixaban?

A

The only common adverse effect of apixaban in clinical trials was bleeding,

but apixaban is the only one of the new oral anticoagulants to cause less overall bleeding than warfarin

105
Q

How is overdose on apixaban treated?

A

no specific antidote for apixaban-induced bleeding and,

due to the high percentage of drug bound to protein in plasma, apixaban is not dialyzable.

106
Q

What are some drug-drug interactions with apixaban?

A

Drug-drug interactions with apixaban involve drugs that:

interfere with hemostasis:

aspirin

NSAIDs

SSRIs

or drug metabolism

  • rifampin
  • ketoconazole
107
Q
A

CV II Exam 2 (8 decks)

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