지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록· 키워드
오류제보하기
Department of Neurology, KyungPook National University Hospital,
KyungPook National University School of Medicine
Oral anticoagulants (OAC)
OAC is an antagonist of vitamin K, which is a cofactor for a microsomal enzyme that activates coagulation factors II, VII, IX, and X by carboxylation of their glutamic residues. Administration of OAC in therapeutic doses decreases the synthesis of these coagulation factors in the liver by approximately 40 percent, resulting in hypocoagulability of the blood and reducing the propensity towards thrombus formation. As a result, thrombin generation slows, and clot formation becomes
impaired due to decreased biologic activity of the prothrombin complex proteins. The dose of OAC should be closely monitored because anticoagulant response differs from patient to patient. The dose-response is influenced by both pharmacokinetic factors (differences in absorption) and pharmacodynamic factors (differences in the hemostatic response to several concentrations). The effect of vitamin K antagonists is gradual and reversible. It takes several days before an adequate level of anticoagulation is achieved, and for the anticoagulant effect to disappear after drug discontinuation.
The most common agents associated with enhanced anticoagulant effect are allopurinol, common analgesics, antiarrhythmics, antidepressants, antidiabetics, antiplatelets, anxiolytics, disulfiram, levothyroxine, lipid regulating
agents, testosterone, and alcohol. Oral contraceptives, retinoids, and vitamin K have the opposite, reducing effect on anticoagulation. The most common contraindications for OAC include evidence of any active bleeding, uncontrolled severe hypertension, recent brain, eye or spinal cord surgery or injury, propensity for recurrent falling, inability for INR monitoring, and patient non-compliance.
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