Anticoagulant Case Study

• What is the rationale for using warfarin in this patient?

Warfarin is the medicine to used treat blood clots and/or prevent new body clots from developing (like in the deep veins thrombotic DVT or pulmonary embolus PE). Preventing unhealthy blood coagulation helps reduce the risk of heart disease or stroke.

• What is the mechanism of action of warfarin?

Warfarin is an oral anticoagulant, a drug that prevents blood clotting. The development of blood clots is prevented by reducing the production of liver factors that promote coagulation, factors II, VII, IX and X, as well as anticoagulant proteins C and S. The development of these liver factors, depends on ample quantities of vitamin K. Warfarin decreases the development by antagonizing vitamin K. Blood clots in the lower limbs of the veins (deep venous thrombosis [DVT]) will occur frequently following immobility cycles. Those coagulations are prone to split and become trapped in the lung blood vessels (pulmonary embolism), causing breathability, chest pain or even life-threatening shock. During atrial fibrillation and artificial heart valves, a blood clot may also occur in the atria of the heart. These coagulations can also split and block brain arteries, triggering an embolic paralysis stroke. Warfarin is an essential factor in preventing the development of blood coagulants, preventing the expansion of existing coagulations to other vital bodies such as the lungs and brain and reducing the risk of blood coagulation.

Pharmacokinetic model for warfarin absorption, delivery, and disposal. Warfarin is primarily fully absorbed and has a plasma concentration of up to 2 to 6 hours. This is distributed in a small amount (10L/70 kg) and extracted with very low clearance by liver metabolism (0.2L / h/70 kg). The half-life of disposal is around 35 hours.

A pharmacodynamics model for the effect of warfarin on the synthesis of coagulation factors. Prothrombin complex synthesis at a warfarin concentration of about 1.5 mg / L is inhibited at 50 percent. Warfarin levels are close in magnitude to surgical anticoagulation.

• What kinds of laboratory monitoring is required for patients receiving warfarin and why?

The laboratory parameter for evaluating therapeutic warfarin anticoagulation is INR. A blood sample for INR is taken during warfarin therapy. While the patient is in the clinical rehabilitation stage, at least every four weeks the INR is normally obtained. When an INR is supra therapy or sub therapy to the particular patient, an INR must be obtained within 1 to 7 days to ensure a return to the therapeutic area of the patient. An INR can also be obtained if drugs that are known to interfere with warfarin begin or discontinue or change their doses (Holbrook, A. 2012). Since warfarin is an anticoagulant, it is important to check for signs and symptoms of bleeding including black tarry stools, nosebleeds, or hematomas. Previously and every six months during the use of warfarin hemoglobin and hematocrit levels should be obtained. Specific lab examinations, including urinalysis, occult blood, and liver function testing may be demonstrated by the presentation of a patient. Interactions with medications, drug ingredients, medical products, and pharmaceutical disorders are all main factors to be controlled to avoid any adverse effects related to supra therapy or sub-therapeutic anticoagulation.

• What kinds of factors lead to altered anticoagulant therapy?

       Pregnancy: Oral anticoagulants cross the placenta and may produce a standard fetus, defects in the central nervous system or bleeding. The first trimester of pregnancy should not be used with warfarin or prevented during pregnancy, if possible. There is compelling evidence that warfarin is not an anti-contaminant effect for the breastfeeding baby when given to the mom. Anticoagulant therapy is favored when anticoagulants are required in pregnancy.

Rx- Rx interaction: The possible risk of bleeding with individuals in warfarin (Coumadin) can also be potentiated by Rx-Rx Interactions. Warfarin (Coumadin) capacity for analgesic and anti-inflammatory drugs (e.g. salicylates and no steroidal anti-inflammatory drugs), producing greater levels of INR therapeutic. Doses of salicylate above 1.5 g / d can induce anticoagulation. The metabolism of vitamin K or displacement of warfarin (Coumadin) from its bonding point on albumin may lead to anticoagulation by salicylates (Darnell et al., 2014).

• What are the risks and toxicities associated with warfarin therapy?

Bleeding is the main complication of warfarin therapy. During warfarin care, SSRIs can increase the risk of bleeding by hindering aggregation platelet by depleting platelet-serotonin levels. Some SSRIs can also inhibit CYP2C9’s oxidative metabolism. Side effects less common can include tissue damage areas and purple toe syndrome. During pregnancy, use is not recommended.

• What counseling should this patient receive?

The right medication for personalized pharmacotherapy at the right dose is required. If the dosage is less or more, the desired therapeutic effects cannot be created because the smaller dosage is due to therapeutic failure and the higher dose is harmful. The pharmacist is duty-bound to test the dosage for indications. Firstly take 2 to 5 mg once daily orally or intravenously for 1 to 2 days, then change to International Normalized Ratio (INR) or Time of Prothrombin (PT) tests.

Keep Perseveration: the daily maintenance dosage ranges orally or intravenously from 2 to 10 mg once a day.

Advice the patient to take the missing dose when you know that you missing it, do not administer two doses concurrently to take the missed dose. Excessive bleeding may occur due to overdose.

• Are there other oral anticoagulants that this patient might be prescribed instead of warfarin?

Warfarin was used mainly as an anticoagulant for decades (also known as Coumadin). Recent studies have seen and published a variety of other medicines known as the novel oral anticoagulants (NOACs) as alternatives to warfarin. Warfarin treats and avoids blood coagulation by reducing the development of many vitamin K coagulation proteins. Warfarin is administered once in your mouth and the dosage depends on ethnicity, medicine, and diet, while NOACs are used to treat clotting proteins individually. You do not need laboratory testing or dose adaptation because in most patients you hit consistent rates. This is, therefore, shorter than warfarin. A patient may often dilute their blood enough if a dose of warfarin is skipped, as it takes several days to wear off the anticoagulant. By comparison, in the absence of a dose of NOAC, the anticoagulant effect is easily lost and unprotected. NOACs are taken once or twice daily (depending on the usage of NOAC and the condition).