Editing Coagulation (section)

====Final common pathway====
{{Anchor|Common pathway}}
The division of coagulation in two pathways is arbitrary, originating from laboratory tests in which clotting times were measured either after the clotting was initiated by glass, the intrinsic pathway; or clotting was initiated by thromboplastin (a mix of tissue factor and phospholipids), the extrinsic pathway.<ref name="troisi">{{Cite journal |vauthors=Troisi R, Balasco N, Autiero I, Sica F, Vitagliano L |date=August 2023 |title=New insight into the traditional model of the coagulation cascade and its regulation: illustrated review of a three-dimensional view |journal=Research and Practice in Thrombosis and Haemostasis |volume=7 |issue=6 |page=102160 |doi=10.1016/j.rpth.2023.102160 |pmc=10506138 |pmid=37727847}}</ref>

Further, the final common pathway scheme implies that prothrombin is converted to thrombin only when acted upon by the intrinsic or extrinsic pathways, which is an oversimplification. In fact, thrombin is generated by activated platelets at the initiation of the platelet plug, which in turn promotes more platelet activation.<ref>{{Cite journal |vauthors=Hoffman M |date=September 2003 |title=A cell-based model of coagulation and the role of factor VIIa |journal=Blood Rev |volume=17 |issue=Suppl 1 |pages=S1–5 |doi=10.1016/s0268-960x(03)90000-2 |pmid=14697207}}</ref>

Thrombin functions not only to convert [[fibrinogen]] to fibrin, it also activates Factors VIII and V and their inhibitor [[protein C]] (in the presence of [[thrombomodulin]]). By activating Factor XIII, [[covalent bond]]s are formed that crosslink the fibrin polymers that form from activated monomers.<ref name="Pallister1" /> This stabilizes the fibrin network.<ref>{{Cite journal |vauthors=Moroi M, Induruwa I, Farndale RW, Jung SM |date=March 2022 |title=Factor XIII is a newly identified binding partner for platelet collagen receptor GPVI-dimer-An interaction that may modulate fibrin crosslinking |journal=Res Pract Thromb Haemost |volume=6 |issue=3 |page=e12697 |doi=10.1002/rth2.12697 |pmc=9035508 |pmid=35494504}}</ref>

The coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the [[tenase]] complex until it is down-regulated by the anticoagulant pathways.<ref name="Pallister1" />