After 5 days of heparin therapy, T.M was prescribed warfarin 5 mg PO daily.
Why was T.M changed to warfarin? What is the pharmacologic action of warfarin? (USLO 5.2, 5.3, 5.4)
What laboratory test(s) would be monitored for patients taking warfarin? Explain your answer. (USLO 5.3, 5.6, 5.8)
Explain the half-life and protein-binding of warfarin. What additional concerns do you have? How does this knowledge impact teaching for patient’s taking warfarin? Explain. (USLO 5.2, 5.3, 5.6, 5.8)
What assessments should be performed before starting anticoagulant therapy? (USLO 5.3, 5.8)
Case Context
Patient: T.M
Condition: Thrombophlebitis
Therapy Transition: After 5 days of heparin, switched to warfarin 5 mg PO daily
1. Why T.M Was Changed to Warfarin & Pharmacologic Action (USLO 5.2, 5.3, 5.4)
Reason for Change:
Heparin is used initially for rapid anticoagulation because of its immediate onset.
Warfarin is introduced for long-term anticoagulation since it can be taken orally and is more practical for outpatient management.
Transition occurs after several days because warfarin requires time to reach therapeutic effect (delayed onset).
Pharmacologic Action of Warfarin:
Warfarin is a vitamin K antagonist.
It inhibits vitamin K epoxide reductase, an enzyme needed to recycle vitamin K.
This prevents activation of vitamin K–dependent clotting factors: II (prothrombin), VII, IX, and X, as well as proteins C and S.
Result: reduced synthesis of functional clotting factors → anticoagulation.
2. Laboratory Tests Monitored for Patients Taking Warfarin (USLO 5.3, 5.6, 5.8)
Prothrombin Time (PT):
Measures activity of the extrinsic pathway (factor VII and common pathway).
Warfarin prolongs PT because it reduces vitamin K–dependent factors.
International Normalized Ratio (INR):
Standardized version of PT used worldwide.
Therapeutic range for most indications: INR 2.0–3.0 (higher for mechanical heart valves, e.g., 2.5–3.5).
Ensures effective anticoagulation while minimizing bleeding risk.
Additional Monitoring:
Hemoglobin/hematocrit for occult bleeding.
Liver function tests (since warfarin is metabolized hepatically).
3. Half-Life and Protein-Binding of Warfarin; Concerns & Patient Teaching (USLO 5.2, 5.3, 5.6, 5.8)
Half-Life:
Warfarin has a long half-life (~36–42 hours).
Full anticoagulant effect is delayed because existing clotting factors must degrade before warfarin’s effect is seen.
This is why heparin is overlapped with warfarin for several days (“bridging therapy”).
Protein-Binding:
Warfarin is highly protein-bound (~99% to albumin).
Only the unbound fraction is active.
Drugs that displace warfarin from albumin (e.g., sulfonamides, NSAIDs) can increase bleeding risk.
Additional Concerns:
Drug interactions: Warfarin interacts with many medications (antibiotics, antifungals, anticonvulsants).
Dietary interactions: Foods high in vitamin K (leafy greens) can reduce effectiveness.
Bleeding risk: Patients must be educated to recognize signs of bleeding (bruising, hematuria, GI bleeding).
Impact on Patient Teaching:
Stress importance of consistent vitamin K intake (not avoidance, but consistency).
Emphasize adherence to dosing schedule.
Educate about need for regular INR monitoring.
Warn about drug interactions and advise consulting healthcare provider before starting new medications.
Teach patients to report unusual bleeding or bruising promptly.
4. Assessments Before Starting Anticoagulant Therapy (USLO 5.3, 5.8)
Baseline Laboratory Tests:
PT/INR, aPTT, CBC (hemoglobin, hematocrit, platelet count).
Liver and kidney function tests.
Medical History:
History of bleeding disorders, liver disease, alcohol use, or recent surgery.
Current medications (to identify potential drug interactions).
Physical Assessment:
Signs of active bleeding (e.g., GI bleeding, hematuria, bruising).
Blood pressure and cardiovascular status.
Patient Factors:
Ability to adhere to therapy and monitoring.
Dietary habits (vitamin K intake).
Risk factors for falls or trauma (which increase bleeding risk).
Summary
T.M was transitioned from heparin to warfarin for long-term oral anticoagulation.
Warfarin acts by inhibiting vitamin K–dependent clotting factors.
PT/INR is the key monitoring test, with therapeutic INR ranges tailored to indication.
Warfarin’s long half-life and high protein binding create risks for drug and dietary interactions, requiring careful patient education.
Before starting anticoagulants, clinicians assess labs, history, physical findings, and patient-specific risks
