St. Petersburg College
As our population ages, patients are living longer as a result of advances in medical technology, surgical procedures, and drug development(Bressler MD & Bahl PhD, 2003). The average older person is taking two to five prescription medications daily and one in five of this age group has a medication related hospitalization annually (McLean & LeCouteur, 2004). In my eighteen years of nursing, I have taken care of many patients being treated with anticoagulant medications for various reasons, and I have found that most of these patients are not educated about the risks, benefits, and adverse reactions associated with anticoagulants. In this paper, I will focus on Warfarin (Coumadin) the most commonly prescribed anticoagulant. I will discuss the mechanism of Warfarin in the body, therapeutic uses, monitoring treatment, and adverse reactions. I will also explain the therapeutic effects, risks, and benefits of taking Warfarin in a patient that has a mechanical heart valve. “Anticoagulants are drugs that reduce formation of fibrin”(Lehne, 2010, p. 597). The first anticoagulant used to prevent clotting during open-heart surgery in individuals with disseminated intravascular coagulation (DIC) was heparin (Kee & Hayes, 2003). Heparin works by binding with antithrombin III causing inactivation of thrombin. When thrombin is inactivated, the conversion of fibrin to fibrinogen does not take place, preventing clot formation (Kee & Hayes, 2003). Low-molecular-weight heparins (LMWH) are the most commonly used heparin therapy. They are derivatives of the standard heparin, but they have a lower risk for bleeding (Kee & Hayes, 2003). There are five low-molecular-weight heparins namely enoxaparin sodium, dalteparin sodium, ardeparin, danaparoid, and tinzaparin sodium (Kee & Hayes, 2003). Oral anticoagulants are also widely used today. Examples of these are warfarin, dicumarol, and anisindione (Kee & Hayes, 2003). Mechanism
Warfarin suppresses coagulation by decreasing production of four clotting factors, namely, factors VII, IX, X, and prothrombin (Lehne, 2010). These factors are called vitamin K-dependent clotting factors, because an active form of vitamin K is needed to produce them. Warfarin inhibits the enzyme needed to convert vitamin K to the active form. Because of this action, Warfarin is referred to as a vitamin K antagonist (Lehne, 2010). “In therapeutic doses, warfarin reduces production of vitamin K-dependent clotting factors by 30% to 50%.”(Lehne, 2010, p. 604). Warfarin doses taken by mouth, are readily absorbed into the bloodstream where it binds to albumin. Noticeable anticoagulant effects are delayed even though warfarin acts quickly to inhibit clotting factor production.(Lehne, 2010). Because the delayed effects, warfarin is not used in emergent treatment. When rapid action is indicated for treatment, anticoagulant therapy can be initiated with heparin (Lehne, 2010). Adverse Reactions
Bleeding or hemorrhage is the major adverse effect of warfarin and individuals taking this medication should be closely monitored for signs of bleeding (Kee & Hayes, 2003). These include petechiae, ecchymosis, and hematemesis among many others. Due to the oral anticoagulants being highly protein – bound, drug-to-drug interactions are also common. The patient should know and discuss other drugs that he or she is taking with any physician rendering treatment. Aspirin, non-steroidal anti-inflammatory drugs, sulfonamides, allopurinol, phenytoin, and oral hypoglycemic agents for diabetes can cause interactions with warfarin and can enhance bleeding (Kee & Hayes, 2003). Acetaminophen should be used as a substitute for aspirin when taking warfarin (Kee & Hayes, 2003). In addition, there are antidotes in case warfarin or heparin has been taken in toxic amounts. Vitamin K or phytonadione is...
Please join StudyMode to read the full document