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Coagulation Tests (view source)

Revision as of 13:26, 25 August 2010

1,594 bytes removed ,  13:26, 25 August 2010
→‎Prothrombin Time
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The contact activator used in the ACT test triggers the intrinsic pathway, and so ACT allows assessment of the intrinsic and common pathways. ACT will therefore be prolonged when factors I, II, V, VIII, IX, X, XI or XII are deficient or abnormal, such as in DIC, liver disease, vitamin K antagonist toxicosis or haemophilia A or B<sup>2</sup>. Thrombocytopenia may also increase ACT.
 
The contact activator used in the ACT test triggers the intrinsic pathway, and so ACT allows assessment of the intrinsic and common pathways. ACT will therefore be prolonged when factors I, II, V, VIII, IX, X, XI or XII are deficient or abnormal, such as in DIC, liver disease, vitamin K antagonist toxicosis or haemophilia A or B<sup>2</sup>. Thrombocytopenia may also increase ACT.
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===Prothrombin Time===
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Prothrombin time (PT) gives an assessment of the extrinsic and common pathways by measuring the time necessary to generate fibrin after activation of factor VII<sup>3</sup>. It is performed by an automated analyser<sup>2</sup> using citrated plasma<sup>1, 3</sup>. Blood should therefore be collected into a sodium citrate tube if prothrombin time is to be performed. In basic terms, the test procedure involves adding thromoplastin to the patient's plasma, warming, adding calcium and recording the time taken to clot<sup>1</sup>.
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A prolonged PT may reflect either factor deficiency or a circulating inhibitor of coagulation. Repeating the test using a mix of test plasma and "normal" plasma can help differentiate these possibilities<sup>3</sup>. PT is more sensitive than APTT for factor deficiencies.
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It will be prolonged by deficiency or
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abnormalities in coagulation factors VII, X, II or I. Disease processes expected to prolong the PT include Vitamin
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K antagonists, liver disease and DIC.
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Inherited deficiency of factor VII is a rare bleeding disorder characterized by a prolonged PT and a normal aPTT. The PT completely corrects when mixed with normal plasma. Acquired deficiencies are usually related to liver disease, warfarin therapy, or depletion secondary to consumptive coagulopathy, severe bleeding, or massive transfusion.
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Circulating inhibitors are most often directed at factor X or thrombin. Most common are heparin or products of fibrinolysis. In their presence the prolonged PT cannot be completely corrected to normal in a 1:1 mixing study.
      
===(A)PTT===
 
===(A)PTT===
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