Oral anticoagulants
The major oral
anticoagulant used in the United States is the coumarin compound warfarin.
Warfarin is absorbed rapidly and almost completely
when it’s tak-en orally. It binds extensively to plasma albumin and is
metabo-lized in the liver and excreted in urine. Although warfarin is ab-sorbed
quickly, its effects don’t occur for about 48 hours, with the full effect
taking 3 to 4 days.
Because warfarin is highly plasma-protein-bound and
is metab-olized by the liver, administration of warfarin with other
medica-tions may alter the amount of warfarin in the body. This may in-crease
the risk of bleeding or clotting, depending upon the med-ications administered.
Oral anticoagulants alter the ability of the liver
to synthesize vita-min K–dependent clotting factors, including prothrombin and
fac-tors VII, IX, and X. However, clotting factors already in the blood-stream
continue to coagulate blood until they become depleted, so anticoagulation
doesn’t begin immediately. (See Monitoringwarfarin
levels.)
Oral anticoagulants are prescribed to treat or
prevent thromboem-bolism. Patients with this disorder begin taking the
medication while still receiving heparin. However, outpatients at high risk for
thromboembolism may begin oral anticoagulants without first re-ceiving heparin.
Oral anticoagulants are also the drugs of choice to
prevent DVT and for patients with prosthetic heart valves or diseased mitral
valves. To decrease the risk of arterial clotting, oral anticoagulants are
sometimes combined with an antiplatelet drug, such as as-pirin, clopidogrel, or
dipyridamole.
Many patients who take oral anticoagulants also receive other drugs,
placing them at risk for serious drug interactions.
·
Many drugs, such as
highly protein-bound medications, increase the effects of warfarin, resulting
in an increased risk of bleeding. Examples include acetaminophen, allopurinol,
amiodarone, cephalosporins, cimetidine, ciprofloxacin, clofibrate, danazol,
dia-zoxide, disulfiram, erythromycin, fluoroquinolones, glucagon, he-parin,
ibuprofen, isoniazid, ketoprofen, methylthiouracil, metron-idazole, miconazole,
neomycin, propafenone, propylthiouracil, quinidine, streptokinase,
sulfonamides, tamoxifen, tetracyclines, thiazides, thyroid drugs, tricyclic
antidepressants, urokinase, and vitamin E.
·
Drugs metabolized by the liver may increase or decrease the
ef-fectiveness of warfarin. Examples include barbiturates, carba-mazepine,
corticosteroids, corticotropin, mercaptopurine, naf-cillin, hormonal
contraceptives containing estrogen, rifampin, spironolactone, sucralfate, and
trazodone.
·
The risk of phenytoin toxicity increases when phenytoin is tak-en with
warfarin, and phenytoin may increase or decrease the ef-fects of warfarin.
Other interactions include the following:
§ A diet high in vitamin K reduces the
effectiveness of warfarin.
§ Chronic alcohol abuse increases the patient’s
risk of clotting while taking warfarin. Acute alcohol intoxication increases
the risk of bleeding.
§ Vitamin K and fresh frozen plasma reduce the
effects of war-farin. (See Adverse
reactions to oral anticoagulants.)
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