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Coags PT & INR

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Explores Anti-Coagulants, What INR Measures

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  • CoagsPT & INR

  • Extrinsic Measure PT(INR)IntrinsicMeasured aPTT

  • What does INR measure?

  • What does INR measure?INR is derived from the measured prothrombin time when compared to a laboratory standard

    The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation

    PT measures factors I, II, V, VII, and X

  • InterpretationThe prothrombin time is the time it takes plasma to clot after addition of tissue factor

    This measures the quality of the extrinsic pathway (as well as the common pathway) of coagulation

    The speed of the extrinsic pathway is greatly affected by levels of functional factor VII in the body.

    Factor VII has a short half-life and the carboxylation of its glutamine residues requires vitamin K.

  • What causes PT to be prolonged?

  • What causes PT to be prolonged?deficiencies in vitamin K warfarin therapymalabsorption, or lack of intestinal colonization by bacteria (such as in newborns). poor factor VII synthesis (due to liver disease) increased consumption (in disseminated intravascular coagulation)

  • INR rangesNormal ranges 0.9-1.3

    Over 5 risk of bleeding

    Under 0.5 risk of clotting

  • How to manage raised INR measurement in warfarinised patient?

  • How to manage raised INR measurement in warfarinised patient?INR 9; no bleeding- if low bleeding risk, cease warfarin and give vitamin K (2.5-5mg orally or 1mg IV). Measure INR in 6-12hrs. Resume warfarin at reduced dose once INR
  • Why do we commence clexane on initial initiation of warfarin for treatment of thrombosis?

  • Action of warfarinInitially it is prothrombotic because it inhibits the synthesis of protein C and S which have shorter half lives than the other factors

    Delayed action 8-12hrs

    Acts on factor VII, IX, X and II (half lives 6, 24, 40, 60hrs)- all Vitamin K dependant

    Warfarin prevents reductive metabolism of the inactive vitamin K epoxide back to its active hydroquinone form