Factor Xa
Common pathway · Convergence PT and APTT Vitamin K dep.
Factor X is the point of convergence: it is activated by TF-VIIa and, far more efficiently, by the IXa-VIIIa intrinsic tenase. With factor Va, calcium and phospholipid it forms prothrombinase. A defect here prolongs both the PT and the APTT, which is exactly how the common pathway is recognised on a coagulation screen.
Traced from the start
- Tissue factor and the extrinsic triggerVitamin K cycle and gamma-carboxylation
- Contact activation system (factor XII, prekallikrein, high-molecular-weight kininogen)
- Subendothelial collagen and von Willebrand factor
- Tissue factor-factor VIIa complex (extrinsic tenase)Factor IXaFactor VIIIa and its von Willebrand factor carrierActivated platelet phospholipid surface
- Factor Xa
Detail
- Vitamin K dependent
- Yes
- Activated by
- TF-VIIa, and by intrinsic tenase (IXa-VIIIa-Ca2+-phospholipid), which is one to two orders of magnitude more efficient
- Forms
- Prothrombinase: Xa + Va + Ca2+ + phospholipid; assembly accelerates prothrombin activation roughly 300,000-fold over free Xa
- Inhibited by
- Antithrombin (accelerated over 1000-fold by heparin), tissue factor pathway inhibitor, and the direct inhibitors rivaroxaban, apixaban and edoxaban
- Assays
- Deficiency prolongs both PT and APTT; the anti-Xa assay monitors LMWH, fondaparinux and the Xa inhibitors
When it goes wrong
Acquired factor X deficiency in AL amyloidosis, where factor X adsorbs onto amyloid fibrils
Both PT and APTT prolonged, with periorbital purpura after minimal pressure such as coughing — a classic AL amyloidosis presentation
Both PT and APTT prolonged with a normal thrombin time
Localises the defect to the common pathway above fibrinogen: factor X, factor V or prothrombin deficiency, or a multi-factor process such as DIC or liver failure
Practise this structure
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