Coumadin, whose generic name is Warfarin, and is manufactured by Bristol-Myers Squibb Company, is an anticoagulant medication. It is more commonly known as a “blood thinner”; however it does not actually thin the blood. An anticoagulant helps your body control how fast your blood clots and it prevents clots from forming during certain medical conditions. Medications such as Coumadin may prevent an already present clot from getting any larger and may also prevent a piece of the clot from breaking off and traveling to your heart, brain or lungs. Anticoagulants do not dissolve blood clots but with time, clots may dissolve on their own. (Cleveland Clinic, 2014)
Coumadin works by inhibiting with how your body uses vitamin K. The metabolism of Coumadin, vitamin K and vitamin K dependant clotting factors take place in your liver. “Coumadin prevents the production of the vitamin K dependent clotting factors and this results in a slower clotting rate.” (National Blood Clot Alliance, 2014)
Coumadin most commonly comes in round and scored tablets of many different strengths and colors, although different manufactures may produce the medication in an oval shape. Scored tablets are meant to be easily broken in half to adjust your dose as your doctor may instruct you to do. The dose of medication usually ranges from 1 mg to 10 mg to be taken once daily. The different colors of each tablet represent a different strength that is measured in milligrams.
• 1 mg (pink)
• 2 mg (lavender)
• 2.5 mg (green)
• 3 mg (tan)
• 4 mg (blue)
• 5 mg (peach)
• 6 mg (teal or blue green)
• 7.5 mg (yellow)
• 10 mg (white)
Coumadin in pill form is taken orally. It needs to be stored at a controlled room temperature of 59 – 86 degrees and needs to be protecte...
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In some individuals with severe hemophilia, the factor VIII replacement therapy is identified as a foreign substance by their immune system. If this happens, their immune system will make antibodies against factor VIII. These antibodies will inhibit the ability of the factor to work in the clotting process. The higher the antibody or inhibitor level, the more factor VIII replacement therapy it takes to overcome the inhibition and produce clotting. This can complicate the treatment of a bleed. The good news is that there are different types of therapies available to successfully treat most individuals who develop inhibitors.
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More research should be done on new oral anticoagulants with different study population and similar patients that are seen in everyday clinical practice as well as attempt to define the best pharmacodynamic monitoring tools. Research should be conducted to outline monitoring protocol including timing relative to dosing and frequency as well as therapeutic targets. Using these strategies, future trials could enhance further the efficacy and safety of these new agents and could extend their use to new indications.
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In septic patients, increased levels of PAI-1 inhibit plasminogen activator (t-PA), which converts plasminogen to plasmin. Release of fibrin inhibits fibrinolysis by activation of thrombin-activatable fibrinolysis inhibitor (TAFI). In addition, the release of PAF causes platelet aggregation. This combination of inhibition of fibrinolysis, fibrin strand production and platelet aggregation contribute to a state of coagulopathy. This can lead to microcirculatory dysfunction with isolated or multiple organ dysfunction and cell death. Mr Hertz’s coagulation profile showed a fibrinogen level of 5.6 g/L, indicating that coagulopathies were underway in his system.
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