Antithrombin
Fibrin and control · Serpin Heparin cofactor
A serpin made in the liver that irreversibly traps the active site of thrombin and factor Xa, and to a lesser degree factors IXa, XIa and XIIa. Endothelial heparan sulfate accelerates it physiologically; pharmacological heparin does the same thing more than a thousand-fold, and that is the entire mechanism of heparin.
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 XaFactor VaProthrombin (factor II)
- Thrombin (factor IIa)
- Antithrombin
Detail
- Inhibits
- Thrombin and factor Xa principally, and also factors IXa, XIa and XIIa
- Accelerated by
- Endothelial heparan sulfate; heparin, LMWH and fondaparinux by more than 1000-fold
- Formerly called
- Antithrombin III
- Depleted in
- Nephrotic syndrome (urinary loss), hepatic failure (reduced synthesis), DIC (consumption), and asparaginase therapy
When it goes wrong
Inherited antithrombin deficiency, autosomal dominant and the most thrombogenic of the common inherited thrombophilias
Venous thromboembolism from young adulthood, and apparent heparin resistance — the APTT fails to prolong despite escalating heparin doses; give antithrombin concentrate or switch to a direct thrombin inhibitor
Antithrombin lost in the urine in nephrotic syndrome
Hypercoagulable state with a characteristic predilection for renal vein thrombosis
Practise this structure
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