Schematic diagram representing the procoagulant and anticoagulant properties of activated platelets. The crescentic forms represent the activated platelet membrane, except in the case of the form labeled “TF•PL,” which represents tissue factor expressed on a phospholipid membrane surface. The roman numerals represent coagulation proteins including zymogens or substrates (in circles), enzymes (in circles with segmental excisions), and cofactors (in ellipses). The curved arrows represent conversions from zymogens (eg, prothrombin, shown as II) to active enzymes (eg, thrombin, shown as IIa), whereas the left-pointing arrows represent the inhibition of these active enzymes (eg, factor Xa, shown as Xa) to their inactivated forms (eg, inactivated factor Xa, shown as Xi). Shown in boxes are the Kunitz-type inhibitors, protease nexin-2 (PN-2) and tissue factor pathway inhibitor (TFPI), and the serpin, protease nexin-1 (PN-1). The initiation of the coagulation mechanism occurs as the consequence of the assembly of the FVIIa/FX/TF/PL complex and is regulated by TFPI, whereas the consolidation phase of coagulation, regulated by PN-2 and PN-1, is activated by the resulting generation of low concentrations of thrombin sufficient to activate platelets, FXI, FVIII, and FV to produce thrombin in sufficient quantities to form a fibrin clot.

Schematic diagram representing the procoagulant and anticoagulant properties of activated platelets. The crescentic forms represent the activated platelet membrane, except in the case of the form labeled “TFPL,” which represents tissue factor expressed on a phospholipid membrane surface. The roman numerals represent coagulation proteins including zymogens or substrates (in circles), enzymes (in circles with segmental excisions), and cofactors (in ellipses). The curved arrows represent conversions from zymogens (eg, prothrombin, shown as II) to active enzymes (eg, thrombin, shown as IIa), whereas the left-pointing arrows represent the inhibition of these active enzymes (eg, factor Xa, shown as Xa) to their inactivated forms (eg, inactivated factor Xa, shown as Xi). Shown in boxes are the Kunitz-type inhibitors, protease nexin-2 (PN-2) and tissue factor pathway inhibitor (TFPI), and the serpin, protease nexin-1 (PN-1). The initiation of the coagulation mechanism occurs as the consequence of the assembly of the FVIIa/FX/TF/PL complex and is regulated by TFPI, whereas the consolidation phase of coagulation, regulated by PN-2 and PN-1, is activated by the resulting generation of low concentrations of thrombin sufficient to activate platelets, FXI, FVIII, and FV to produce thrombin in sufficient quantities to form a fibrin clot.

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