Natural anticoagulants and fibrinolysis
How antithrombin, the protein C pathway and TFPI limit clotting, how plasmin breaks clot down and is controlled, and how these explain thrombophilia, heparin action, D-dimer and tranexamic acid.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Normal endothelium is anticoagulant: it carries thrombomodulin, endothelial protein C receptor (EPCR), heparan sulfate (which activates antithrombin) and TFPI, and releases prostacyclin, nitric oxide and tissue plasminogen activator (tPA).
- Three anticoagulant systems: antithrombin (serine protease inhibitor), the protein C pathway (switches off cofactors Va and VIIIa) and TFPI (switches off initiation).
- Fibrinolysis by plasmin removes fibrin. PAI-1, alpha2-antiplasmin and TAFI restrain it.
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Sources
- Postgraduate Haematology (7th ed.)Wiley-Blackwell (Hoffbrand, Higgs, Keeling and Mehta, 2016), 2016
- Hoffbrand's Essential Haematology (8th ed.)Wiley-Blackwell (Hoffbrand and Steensma, 2019), 2019
- Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE studyJAMA (Righini et al., 2014;311:1117-1124), 2014
- Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2)Lancet (CRASH-2 trial collaborators, 2010;376:23-32), 2010
- The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trialLancet (CRASH-2 collaborators, 2011;377:1096-1101), 2011
- Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT)Lancet (HALT-IT trial collaborators, 2020;395:1927-1936), 2020
- Last updated
- 14 November 2026
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