Warfarin
An oral anticoagulant that inhibits vitamin K-dependent clotting factors; used to prevent thromboembolic events.
Warfarin blocks hepatic synthesis of clotting factors II, VII, IX, and X by competitively inhibiting vitamin K epoxide reductase. Its effect is measured by the INR, with a typical therapeutic target of 2–3. Onset is delayed 2–5 days; the antidote is vitamin K (phytonadione); urgent reversal uses 4-factor prothrombin complex concentrate (PCC), with fresh frozen plasma as the alternative.
On the NCLEX, warfarin questions hinge on matching the right lab to the right antidote: warfarin is followed by PT/INR, whereas heparin is followed by aPTT and reversed with protamine sulfate — swapping these pairs is the single most common trap. The classic “tell” is a bridging scenario: because warfarin’s effect is delayed, a patient is started on heparin or enoxaparin and the parenteral agent is stopped only once the INR has been therapeutic. Expect to act on a critical value — an INR above 4–5 with no bleeding usually means simply holding the dose, while active hemorrhage demands vitamin K plus 4-factor PCC (or FFP).
Unlike furosemide (hypokalemia) and lisinopril (hyperkalemia), where the watched lab is potassium, warfarin’s watched parameters are INR and signs of bleeding — don’t carry over electrolyte thinking. Flag warfarin as historically pregnancy category X (teratogenic, contraindicated), and remember the mantra “green = vitamin K = clotting” — so more greens blunt warfarin’s effect, which is why intake must stay steady, not zero.
Source: ATI Pharmacology for Nursing Care, 10th ed.
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