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class="vector-toc-numb">2</span> <span>Physiology</span> </div> </a> <button aria-controls="toc-Physiology-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Physiology subsection</span> </button> <ul id="toc-Physiology-sublist" class="vector-toc-list"> <li id="toc-Vasoconstriction" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Vasoconstriction"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.1</span> <span>Vasoconstriction</span> </div> </a> <ul id="toc-Vasoconstriction-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Platelet_activation_and_platelet_plug_formation" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Platelet_activation_and_platelet_plug_formation"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.2</span> <span>Platelet activation and platelet plug formation</span> </div> </a> <ul id="toc-Platelet_activation_and_platelet_plug_formation-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Coagulation_cascade" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Coagulation_cascade"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.3</span> <span>Coagulation cascade</span> </div> </a> <ul id="toc-Coagulation_cascade-sublist" class="vector-toc-list"> <li id="toc-Tissue_factor_pathway_(extrinsic)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Tissue_factor_pathway_(extrinsic)"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.3.1</span> <span>Tissue factor pathway (extrinsic)</span> </div> </a> <ul id="toc-Tissue_factor_pathway_(extrinsic)-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Contact_activation_pathway_(intrinsic)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Contact_activation_pathway_(intrinsic)"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.3.2</span> <span>Contact activation pathway (intrinsic)</span> </div> </a> <ul id="toc-Contact_activation_pathway_(intrinsic)-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Final_common_pathway" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Final_common_pathway"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.3.3</span> <span>Final common pathway</span> </div> </a> <ul id="toc-Final_common_pathway-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Cell-based_scheme_of_coagulation" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Cell-based_scheme_of_coagulation"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.3.4</span> <span>Cell-based scheme of coagulation</span> </div> </a> <ul id="toc-Cell-based_scheme_of_coagulation-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Fibrinolysis" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Fibrinolysis"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.4</span> <span>Fibrinolysis</span> </div> </a> <ul id="toc-Fibrinolysis-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Role_in_immune_system" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Role_in_immune_system"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.5</span> <span>Role in immune system</span> </div> </a> <ul id="toc-Role_in_immune_system-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Cofactors" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Cofactors"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.6</span> <span>Cofactors</span> </div> </a> <ul id="toc-Cofactors-sublist" class="vector-toc-list"> <li id="toc-Calcium_and_phospholipids" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Calcium_and_phospholipids"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.6.1</span> <span>Calcium and phospholipids</span> </div> </a> <ul id="toc-Calcium_and_phospholipids-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Vitamin_K" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Vitamin_K"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.6.2</span> <span>Vitamin K</span> </div> </a> <ul id="toc-Vitamin_K-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Regulators" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Regulators"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7</span> <span>Regulators</span> </div> </a> <ul id="toc-Regulators-sublist" class="vector-toc-list"> <li id="toc-Protein_C_and_Protein_S" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Protein_C_and_Protein_S"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7.1</span> <span>Protein C and Protein S</span> </div> </a> <ul id="toc-Protein_C_and_Protein_S-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Antithrombin" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Antithrombin"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7.2</span> <span>Antithrombin</span> </div> </a> <ul id="toc-Antithrombin-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Tissue_factor_pathway_inhibitor_(TFPI)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Tissue_factor_pathway_inhibitor_(TFPI)"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7.3</span> <span>Tissue factor pathway inhibitor (TFPI)</span> </div> </a> <ul id="toc-Tissue_factor_pathway_inhibitor_(TFPI)-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Plasmin" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Plasmin"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7.4</span> <span>Plasmin</span> </div> </a> <ul id="toc-Plasmin-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Prostacyclin" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Prostacyclin"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.7.5</span> <span>Prostacyclin</span> </div> </a> <ul id="toc-Prostacyclin-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> </ul> </li> <li id="toc-Medical_assessment" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Medical_assessment"> <div class="vector-toc-text"> <span class="vector-toc-numb">3</span> <span>Medical assessment</span> </div> </a> <ul id="toc-Medical_assessment-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Role_in_disease" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Role_in_disease"> <div class="vector-toc-text"> <span class="vector-toc-numb">4</span> <span>Role in disease</span> </div> </a> <button aria-controls="toc-Role_in_disease-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Role in disease subsection</span> </button> <ul id="toc-Role_in_disease-sublist" class="vector-toc-list"> <li id="toc-Platelet_disorders" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Platelet_disorders"> <div class="vector-toc-text"> <span class="vector-toc-numb">4.1</span> <span>Platelet disorders</span> </div> </a> <ul id="toc-Platelet_disorders-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Coagulation_factor_disorders" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Coagulation_factor_disorders"> <div class="vector-toc-text"> <span class="vector-toc-numb">4.2</span> <span>Coagulation factor disorders</span> </div> </a> <ul id="toc-Coagulation_factor_disorders-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Pharmacology" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Pharmacology"> <div class="vector-toc-text"> <span class="vector-toc-numb">5</span> <span>Pharmacology</span> </div> </a> <button aria-controls="toc-Pharmacology-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Pharmacology subsection</span> </button> <ul id="toc-Pharmacology-sublist" class="vector-toc-list"> <li id="toc-Procoagulants" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Procoagulants"> <div class="vector-toc-text"> <span class="vector-toc-numb">5.1</span> <span>Procoagulants</span> </div> </a> <ul id="toc-Procoagulants-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Anticoagulants" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Anticoagulants"> <div class="vector-toc-text"> <span class="vector-toc-numb">5.2</span> <span>Anticoagulants</span> </div> </a> <ul id="toc-Anticoagulants-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-History" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#History"> <div class="vector-toc-text"> <span class="vector-toc-numb">6</span> <span>History</span> </div> </a> <button aria-controls="toc-History-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle History subsection</span> </button> <ul id="toc-History-sublist" class="vector-toc-list"> <li id="toc-Initial_discoveries" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Initial_discoveries"> <div class="vector-toc-text"> <span class="vector-toc-numb">6.1</span> <span>Initial discoveries</span> </div> </a> <ul id="toc-Initial_discoveries-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Coagulation_factors" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Coagulation_factors"> <div class="vector-toc-text"> <span class="vector-toc-numb">6.2</span> <span>Coagulation factors</span> </div> </a> <ul id="toc-Coagulation_factors-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Nomenclature" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Nomenclature"> <div class="vector-toc-text"> <span class="vector-toc-numb">6.3</span> <span>Nomenclature</span> </div> </a> <ul id="toc-Nomenclature-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Other_species" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Other_species"> <div class="vector-toc-text"> <span class="vector-toc-numb">7</span> <span>Other species</span> </div> </a> <ul id="toc-Other_species-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-See_also" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#See_also"> <div class="vector-toc-text"> <span class="vector-toc-numb">8</span> <span>See also</span> </div> </a> <ul id="toc-See_also-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-References" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#References"> <div class="vector-toc-text"> <span class="vector-toc-numb">9</span> <span>References</span> </div> </a> <ul id="toc-References-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Further_reading" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Further_reading"> <div class="vector-toc-text"> <span class="vector-toc-numb">10</span> <span>Further reading</span> </div> </a> <ul id="toc-Further_reading-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-External_links" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#External_links"> <div class="vector-toc-text"> <span class="vector-toc-numb">11</span> <span>External links</span> </div> </a> <ul id="toc-External_links-sublist" class="vector-toc-list"> </ul> </li> </ul> </div> </div> </nav> </div> </div> <div class="mw-content-container"> <main id="content" class="mw-body"> <header class="mw-body-header vector-page-titlebar"> <nav aria-label="Contents" class="vector-toc-landmark"> <div id="vector-page-titlebar-toc" class="vector-dropdown vector-page-titlebar-toc vector-button-flush-left" title="Table of Contents" > <input type="checkbox" id="vector-page-titlebar-toc-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-vector-page-titlebar-toc" class="vector-dropdown-checkbox " aria-label="Toggle the table of contents" > <label id="vector-page-titlebar-toc-label" for="vector-page-titlebar-toc-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--icon-only " aria-hidden="true" ><span class="vector-icon mw-ui-icon-listBullet mw-ui-icon-wikimedia-listBullet"></span> <span class="vector-dropdown-label-text">Toggle the table of contents</span> </label> <div class="vector-dropdown-content"> <div id="vector-page-titlebar-toc-unpinned-container" class="vector-unpinned-container"> </div> </div> </div> </nav> <h1 id="firstHeading" class="firstHeading mw-first-heading"><span class="mw-page-title-main">Coagulation</span></h1> <div id="p-lang-btn" class="vector-dropdown mw-portlet mw-portlet-lang" > <input type="checkbox" id="p-lang-btn-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-p-lang-btn" class="vector-dropdown-checkbox mw-interlanguage-selector" aria-label="Go to an article in another language. Available in 64 languages" > <label id="p-lang-btn-label" for="p-lang-btn-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--action-progressive mw-portlet-lang-heading-64" aria-hidden="true" ><span class="vector-icon mw-ui-icon-language-progressive mw-ui-icon-wikimedia-language-progressive"></span> <span class="vector-dropdown-label-text">64 languages</span> </label> <div class="vector-dropdown-content"> <div class="vector-menu-content"> <ul class="vector-menu-content-list"> <li class="interlanguage-link interwiki-ang mw-list-item"><a href="https://ang.wikipedia.org/wiki/Gerinnung" title="Gerinnung – Old English" lang="ang" hreflang="ang" data-title="Gerinnung" data-language-autonym="Ænglisc" data-language-local-name="Old English" class="interlanguage-link-target"><span>Ænglisc</span></a></li><li class="interlanguage-link interwiki-ar mw-list-item"><a href="https://ar.wikipedia.org/wiki/%D8%AA%D8%AC%D9%84%D8%B7_%D8%A7%D9%84%D8%AF%D9%85" title="تجلط الدم – Arabic" lang="ar" hreflang="ar" data-title="تجلط الدم" data-language-autonym="العربية" data-language-local-name="Arabic" class="interlanguage-link-target"><span>العربية</span></a></li><li class="interlanguage-link interwiki-az mw-list-item"><a href="https://az.wikipedia.org/wiki/Laxtalanma" title="Laxtalanma – Azerbaijani" lang="az" hreflang="az" data-title="Laxtalanma" data-language-autonym="Azərbaycanca" data-language-local-name="Azerbaijani" class="interlanguage-link-target"><span>Azərbaycanca</span></a></li><li class="interlanguage-link interwiki-bn mw-list-item"><a href="https://bn.wikipedia.org/wiki/%E0%A6%B0%E0%A6%95%E0%A7%8D%E0%A6%A4_%E0%A6%A4%E0%A6%9E%E0%A7%8D%E0%A6%9A%E0%A6%A8" title="রক্ত তঞ্চন – Bangla" lang="bn" hreflang="bn" data-title="রক্ত তঞ্চন" data-language-autonym="বাংলা" data-language-local-name="Bangla" class="interlanguage-link-target"><span>বাংলা</span></a></li><li class="interlanguage-link interwiki-be mw-list-item"><a href="https://be.wikipedia.org/wiki/%D0%97%D0%B3%D1%83%D1%81%D0%B0%D0%BD%D0%BD%D0%B5_%D0%BA%D1%80%D1%8B%D0%B2%D1%96" title="Згусанне крыві – Belarusian" lang="be" hreflang="be" data-title="Згусанне крыві" data-language-autonym="Беларуская" data-language-local-name="Belarusian" class="interlanguage-link-target"><span>Беларуская</span></a></li><li class="interlanguage-link interwiki-bg mw-list-item"><a href="https://bg.wikipedia.org/wiki/%D0%9A%D1%80%D1%8A%D0%B2%D0%BE%D1%81%D1%8A%D1%81%D0%B8%D1%80%D0%B2%D0%B0%D0%BD%D0%B5" title="Кръвосъсирване – Bulgarian" lang="bg" hreflang="bg" data-title="Кръвосъсирване" data-language-autonym="Български" data-language-local-name="Bulgarian" class="interlanguage-link-target"><span>Български</span></a></li><li class="interlanguage-link interwiki-bs mw-list-item"><a href="https://bs.wikipedia.org/wiki/Koagulacija_(krv)" title="Koagulacija (krv) – Bosnian" lang="bs" hreflang="bs" data-title="Koagulacija (krv)" data-language-autonym="Bosanski" data-language-local-name="Bosnian" class="interlanguage-link-target"><span>Bosanski</span></a></li><li class="interlanguage-link interwiki-ca mw-list-item"><a href="https://ca.wikipedia.org/wiki/Coagulaci%C3%B3" title="Coagulació – Catalan" lang="ca" hreflang="ca" data-title="Coagulació" data-language-autonym="Català" data-language-local-name="Catalan" class="interlanguage-link-target"><span>Català</span></a></li><li class="interlanguage-link interwiki-cs mw-list-item"><a href="https://cs.wikipedia.org/wiki/Sr%C3%A1%C5%BEen%C3%AD_krve" title="Srážení krve – Czech" lang="cs" hreflang="cs" data-title="Srážení krve" data-language-autonym="Čeština" data-language-local-name="Czech" class="interlanguage-link-target"><span>Čeština</span></a></li><li class="interlanguage-link interwiki-da mw-list-item"><a href="https://da.wikipedia.org/wiki/Koagulation" title="Koagulation – Danish" lang="da" hreflang="da" data-title="Koagulation" data-language-autonym="Dansk" data-language-local-name="Danish" class="interlanguage-link-target"><span>Dansk</span></a></li><li class="interlanguage-link interwiki-de mw-list-item"><a href="https://de.wikipedia.org/wiki/Blutstillung" title="Blutstillung – German" lang="de" hreflang="de" data-title="Blutstillung" data-language-autonym="Deutsch" data-language-local-name="German" class="interlanguage-link-target"><span>Deutsch</span></a></li><li class="interlanguage-link interwiki-et mw-list-item"><a href="https://et.wikipedia.org/wiki/Vere_h%C3%BC%C3%BCbimine" title="Vere hüübimine – Estonian" lang="et" hreflang="et" data-title="Vere hüübimine" data-language-autonym="Eesti" data-language-local-name="Estonian" class="interlanguage-link-target"><span>Eesti</span></a></li><li class="interlanguage-link interwiki-el mw-list-item"><a href="https://el.wikipedia.org/wiki/%CE%A0%CE%AE%CE%BE%CE%B7_%CF%84%CE%BF%CF%85_%CE%B1%CE%AF%CE%BC%CE%B1%CF%84%CE%BF%CF%82" title="Πήξη του αίματος – Greek" lang="el" hreflang="el" data-title="Πήξη του αίματος" data-language-autonym="Ελληνικά" data-language-local-name="Greek" class="interlanguage-link-target"><span>Ελληνικά</span></a></li><li class="interlanguage-link interwiki-es mw-list-item"><a href="https://es.wikipedia.org/wiki/Coagulaci%C3%B3n" title="Coagulación – Spanish" lang="es" hreflang="es" data-title="Coagulación" data-language-autonym="Español" data-language-local-name="Spanish" class="interlanguage-link-target"><span>Español</span></a></li><li class="interlanguage-link interwiki-eo mw-list-item"><a href="https://eo.wikipedia.org/wiki/Koagulado" title="Koagulado – Esperanto" lang="eo" hreflang="eo" data-title="Koagulado" data-language-autonym="Esperanto" data-language-local-name="Esperanto" class="interlanguage-link-target"><span>Esperanto</span></a></li><li class="interlanguage-link interwiki-eu mw-list-item"><a href="https://eu.wikipedia.org/wiki/Gatzapen" title="Gatzapen – Basque" lang="eu" hreflang="eu" data-title="Gatzapen" data-language-autonym="Euskara" data-language-local-name="Basque" class="interlanguage-link-target"><span>Euskara</span></a></li><li class="interlanguage-link interwiki-fa mw-list-item"><a href="https://fa.wikipedia.org/wiki/%D9%84%D8%AE%D8%AA%D9%87_%D8%B4%D8%AF%D9%86_%D8%AE%D9%88%D9%86" title="لخته شدن خون – Persian" lang="fa" hreflang="fa" data-title="لخته شدن خون" data-language-autonym="فارسی" data-language-local-name="Persian" class="interlanguage-link-target"><span>فارسی</span></a></li><li class="interlanguage-link interwiki-fr mw-list-item"><a href="https://fr.wikipedia.org/wiki/Coagulation_sanguine" title="Coagulation sanguine – French" lang="fr" hreflang="fr" data-title="Coagulation sanguine" data-language-autonym="Français" data-language-local-name="French" class="interlanguage-link-target"><span>Français</span></a></li><li class="interlanguage-link interwiki-ga mw-list-item"><a href="https://ga.wikipedia.org/wiki/T%C3%A9achtadh" title="Téachtadh – Irish" lang="ga" hreflang="ga" data-title="Téachtadh" data-language-autonym="Gaeilge" data-language-local-name="Irish" class="interlanguage-link-target"><span>Gaeilge</span></a></li><li class="interlanguage-link interwiki-gl mw-list-item"><a href="https://gl.wikipedia.org/wiki/Coagulaci%C3%B3n_do_sangue" title="Coagulación do sangue – Galician" lang="gl" hreflang="gl" data-title="Coagulación do sangue" data-language-autonym="Galego" data-language-local-name="Galician" class="interlanguage-link-target"><span>Galego</span></a></li><li class="interlanguage-link interwiki-ko mw-list-item"><a href="https://ko.wikipedia.org/wiki/%ED%98%88%EC%95%A1%EC%9D%91%EA%B3%A0" title="혈액응고 – Korean" lang="ko" hreflang="ko" data-title="혈액응고" data-language-autonym="한국어" data-language-local-name="Korean" class="interlanguage-link-target"><span>한국어</span></a></li><li class="interlanguage-link interwiki-hy mw-list-item"><a href="https://hy.wikipedia.org/wiki/%D4%B1%D6%80%D5%B5%D5%A1%D5%B6_%D5%B4%D5%A1%D5%AF%D5%A1%D6%80%D5%A4%D5%B8%D6%82%D5%B4" title="Արյան մակարդում – Armenian" lang="hy" hreflang="hy" data-title="Արյան մակարդում" data-language-autonym="Հայերեն" data-language-local-name="Armenian" class="interlanguage-link-target"><span>Հայերեն</span></a></li><li class="interlanguage-link interwiki-hi mw-list-item"><a href="https://hi.wikipedia.org/wiki/%E0%A4%B0%E0%A4%95%E0%A5%8D%E0%A4%A4_%E0%A4%B8%E0%A5%8D%E0%A4%95%E0%A4%82%E0%A4%A6%E0%A4%A8" title="रक्त स्कंदन – Hindi" lang="hi" hreflang="hi" data-title="रक्त स्कंदन" data-language-autonym="हिन्दी" data-language-local-name="Hindi" class="interlanguage-link-target"><span>हिन्दी</span></a></li><li class="interlanguage-link interwiki-hr mw-list-item"><a href="https://hr.wikipedia.org/wiki/Zgru%C5%A1avanje_krvi" title="Zgrušavanje krvi – Croatian" lang="hr" hreflang="hr" data-title="Zgrušavanje krvi" data-language-autonym="Hrvatski" data-language-local-name="Croatian" class="interlanguage-link-target"><span>Hrvatski</span></a></li><li class="interlanguage-link interwiki-id mw-list-item"><a href="https://id.wikipedia.org/wiki/Penggumpalan_darah" title="Penggumpalan darah – Indonesian" lang="id" hreflang="id" data-title="Penggumpalan darah" data-language-autonym="Bahasa Indonesia" data-language-local-name="Indonesian" class="interlanguage-link-target"><span>Bahasa Indonesia</span></a></li><li class="interlanguage-link interwiki-it mw-list-item"><a href="https://it.wikipedia.org/wiki/Coagulazione" title="Coagulazione – Italian" lang="it" hreflang="it" data-title="Coagulazione" data-language-autonym="Italiano" data-language-local-name="Italian" class="interlanguage-link-target"><span>Italiano</span></a></li><li class="interlanguage-link interwiki-he mw-list-item"><a href="https://he.wikipedia.org/wiki/%D7%A7%D7%A8%D7%99%D7%A9%D7%AA_%D7%93%D7%9D" title="קרישת דם – Hebrew" lang="he" hreflang="he" data-title="קרישת דם" data-language-autonym="עברית" data-language-local-name="Hebrew" class="interlanguage-link-target"><span>עברית</span></a></li><li class="interlanguage-link interwiki-kn mw-list-item"><a href="https://kn.wikipedia.org/wiki/%E0%B2%B0%E0%B2%95%E0%B3%8D%E0%B2%A4_%E0%B2%97%E0%B2%B0%E0%B2%A3%E0%B3%86%E0%B2%97%E0%B2%9F%E0%B3%8D%E0%B2%9F%E0%B3%81%E0%B2%B5%E0%B2%BF%E0%B2%95%E0%B3%86" title="ರಕ್ತ ಗರಣೆಗಟ್ಟುವಿಕೆ – Kannada" lang="kn" hreflang="kn" data-title="ರಕ್ತ ಗರಣೆಗಟ್ಟುವಿಕೆ" data-language-autonym="ಕನ್ನಡ" data-language-local-name="Kannada" class="interlanguage-link-target"><span>ಕನ್ನಡ</span></a></li><li class="interlanguage-link interwiki-kk mw-list-item"><a href="https://kk.wikipedia.org/wiki/%D2%9A%D0%B0%D0%BD_%D2%B1%D1%8E%D1%8B" title="Қан ұюы – Kazakh" lang="kk" hreflang="kk" data-title="Қан ұюы" data-language-autonym="Қазақша" data-language-local-name="Kazakh" class="interlanguage-link-target"><span>Қазақша</span></a></li><li class="interlanguage-link interwiki-la mw-list-item"><a href="https://la.wikipedia.org/wiki/Coagulatio_sanguinea" title="Coagulatio sanguinea – Latin" lang="la" hreflang="la" data-title="Coagulatio sanguinea" data-language-autonym="Latina" data-language-local-name="Latin" class="interlanguage-link-target"><span>Latina</span></a></li><li class="interlanguage-link interwiki-lt badge-Q70893996 mw-list-item" title=""><a href="https://lt.wikipedia.org/wiki/Kraujo_kre%C5%A1%C4%97jimas" title="Kraujo krešėjimas – Lithuanian" lang="lt" hreflang="lt" data-title="Kraujo krešėjimas" data-language-autonym="Lietuvių" data-language-local-name="Lithuanian" class="interlanguage-link-target"><span>Lietuvių</span></a></li><li class="interlanguage-link interwiki-hu mw-list-item"><a href="https://hu.wikipedia.org/wiki/V%C3%A9ralvad%C3%A1s" title="Véralvadás – Hungarian" lang="hu" hreflang="hu" data-title="Véralvadás" data-language-autonym="Magyar" data-language-local-name="Hungarian" class="interlanguage-link-target"><span>Magyar</span></a></li><li class="interlanguage-link interwiki-mk mw-list-item"><a href="https://mk.wikipedia.org/wiki/%D0%97%D0%B3%D1%80%D1%83%D1%82%D1%87%D1%83%D0%B2%D0%B0%D1%9A%D0%B5_%D0%BD%D0%B0_%D0%BA%D1%80%D0%B2%D1%82%D0%B0" title="Згрутчување на крвта – Macedonian" lang="mk" hreflang="mk" data-title="Згрутчување на крвта" data-language-autonym="Македонски" data-language-local-name="Macedonian" class="interlanguage-link-target"><span>Македонски</span></a></li><li class="interlanguage-link interwiki-ml mw-list-item"><a href="https://ml.wikipedia.org/wiki/%E0%B4%B0%E0%B4%95%E0%B5%8D%E0%B4%A4%E0%B4%82_%E0%B4%95%E0%B4%9F%E0%B5%8D%E0%B4%9F%E0%B4%AA%E0%B4%BF%E0%B4%9F%E0%B4%BF%E0%B4%95%E0%B5%8D%E0%B4%95%E0%B5%BD" title="രക്തം കട്ടപിടിക്കൽ – Malayalam" lang="ml" hreflang="ml" data-title="രക്തം കട്ടപിടിക്കൽ" data-language-autonym="മലയാളം" data-language-local-name="Malayalam" class="interlanguage-link-target"><span>മലയാളം</span></a></li><li class="interlanguage-link interwiki-ms mw-list-item"><a href="https://ms.wikipedia.org/wiki/Penggumpalan" title="Penggumpalan – Malay" lang="ms" hreflang="ms" data-title="Penggumpalan" data-language-autonym="Bahasa Melayu" data-language-local-name="Malay" class="interlanguage-link-target"><span>Bahasa Melayu</span></a></li><li class="interlanguage-link interwiki-nl mw-list-item"><a href="https://nl.wikipedia.org/wiki/Bloedstolling" title="Bloedstolling – Dutch" lang="nl" hreflang="nl" data-title="Bloedstolling" data-language-autonym="Nederlands" data-language-local-name="Dutch" class="interlanguage-link-target"><span>Nederlands</span></a></li><li class="interlanguage-link interwiki-ja mw-list-item"><a href="https://ja.wikipedia.org/wiki/%E5%87%9D%E5%9B%BA%E3%83%BB%E7%B7%9A%E6%BA%B6%E7%B3%BB" title="凝固・線溶系 – Japanese" lang="ja" hreflang="ja" data-title="凝固・線溶系" data-language-autonym="日本語" data-language-local-name="Japanese" class="interlanguage-link-target"><span>日本語</span></a></li><li class="interlanguage-link interwiki-no mw-list-item"><a href="https://no.wikipedia.org/wiki/Koagulasjon" title="Koagulasjon – Norwegian Bokmål" lang="nb" hreflang="nb" data-title="Koagulasjon" data-language-autonym="Norsk bokmål" data-language-local-name="Norwegian Bokmål" class="interlanguage-link-target"><span>Norsk bokmål</span></a></li><li class="interlanguage-link interwiki-nn mw-list-item"><a href="https://nn.wikipedia.org/wiki/Koagulasjon" title="Koagulasjon – Norwegian Nynorsk" lang="nn" hreflang="nn" data-title="Koagulasjon" data-language-autonym="Norsk nynorsk" data-language-local-name="Norwegian Nynorsk" class="interlanguage-link-target"><span>Norsk nynorsk</span></a></li><li class="interlanguage-link interwiki-om mw-list-item"><a href="https://om.wikipedia.org/wiki/Itita_Dhiigaa" title="Itita Dhiigaa – Oromo" lang="om" hreflang="om" data-title="Itita Dhiigaa" data-language-autonym="Oromoo" data-language-local-name="Oromo" class="interlanguage-link-target"><span>Oromoo</span></a></li><li class="interlanguage-link interwiki-uz mw-list-item"><a href="https://uz.wikipedia.org/wiki/Koagulyatsiya" title="Koagulyatsiya – Uzbek" lang="uz" hreflang="uz" data-title="Koagulyatsiya" data-language-autonym="Oʻzbekcha / ўзбекча" data-language-local-name="Uzbek" class="interlanguage-link-target"><span>Oʻzbekcha / ўзбекча</span></a></li><li class="interlanguage-link interwiki-pl mw-list-item"><a href="https://pl.wikipedia.org/wiki/Krzepni%C4%99cie_krwi" title="Krzepnięcie krwi – Polish" lang="pl" hreflang="pl" data-title="Krzepnięcie krwi" data-language-autonym="Polski" data-language-local-name="Polish" class="interlanguage-link-target"><span>Polski</span></a></li><li class="interlanguage-link interwiki-pt mw-list-item"><a href="https://pt.wikipedia.org/wiki/Coagula%C3%A7%C3%A3o_sangu%C3%ADnea" title="Coagulação sanguínea – Portuguese" lang="pt" hreflang="pt" data-title="Coagulação sanguínea" data-language-autonym="Português" data-language-local-name="Portuguese" class="interlanguage-link-target"><span>Português</span></a></li><li class="interlanguage-link interwiki-ro mw-list-item"><a href="https://ro.wikipedia.org/wiki/Coagulare" title="Coagulare – Romanian" lang="ro" hreflang="ro" data-title="Coagulare" data-language-autonym="Română" data-language-local-name="Romanian" class="interlanguage-link-target"><span>Română</span></a></li><li class="interlanguage-link interwiki-qu mw-list-item"><a href="https://qu.wikipedia.org/wiki/Yawar_tikayay" title="Yawar tikayay – Quechua" lang="qu" hreflang="qu" data-title="Yawar tikayay" data-language-autonym="Runa Simi" data-language-local-name="Quechua" class="interlanguage-link-target"><span>Runa Simi</span></a></li><li class="interlanguage-link interwiki-ru mw-list-item"><a href="https://ru.wikipedia.org/wiki/%D0%A1%D0%B2%D1%91%D1%80%D1%82%D1%8B%D0%B2%D0%B0%D0%BD%D0%B8%D0%B5_%D0%BA%D1%80%D0%BE%D0%B2%D0%B8" title="Свёртывание крови – Russian" lang="ru" hreflang="ru" data-title="Свёртывание крови" data-language-autonym="Русский" data-language-local-name="Russian" class="interlanguage-link-target"><span>Русский</span></a></li><li class="interlanguage-link interwiki-sq mw-list-item"><a href="https://sq.wikipedia.org/wiki/Koagulimi" title="Koagulimi – Albanian" lang="sq" hreflang="sq" data-title="Koagulimi" data-language-autonym="Shqip" data-language-local-name="Albanian" class="interlanguage-link-target"><span>Shqip</span></a></li><li class="interlanguage-link interwiki-simple mw-list-item"><a href="https://simple.wikipedia.org/wiki/Coagulation" title="Coagulation – Simple English" lang="en-simple" hreflang="en-simple" data-title="Coagulation" data-language-autonym="Simple English" data-language-local-name="Simple English" class="interlanguage-link-target"><span>Simple English</span></a></li><li class="interlanguage-link interwiki-sk mw-list-item"><a href="https://sk.wikipedia.org/wiki/Zr%C3%A1%C5%BEanie_krvi" title="Zrážanie krvi – Slovak" lang="sk" hreflang="sk" data-title="Zrážanie krvi" data-language-autonym="Slovenčina" data-language-local-name="Slovak" class="interlanguage-link-target"><span>Slovenčina</span></a></li><li class="interlanguage-link interwiki-sl mw-list-item"><a href="https://sl.wikipedia.org/wiki/Strjevanje_krvi" title="Strjevanje krvi – Slovenian" lang="sl" hreflang="sl" data-title="Strjevanje krvi" data-language-autonym="Slovenščina" data-language-local-name="Slovenian" class="interlanguage-link-target"><span>Slovenščina</span></a></li><li class="interlanguage-link interwiki-sr mw-list-item"><a href="https://sr.wikipedia.org/wiki/%D0%97%D0%B3%D1%80%D1%83%D1%88%D0%B0%D0%B2%D0%B0%D1%9A%D0%B5_%D0%BA%D1%80%D0%B2%D0%B8" title="Згрушавање крви – Serbian" lang="sr" hreflang="sr" data-title="Згрушавање крви" data-language-autonym="Српски / srpski" data-language-local-name="Serbian" class="interlanguage-link-target"><span>Српски / srpski</span></a></li><li class="interlanguage-link interwiki-sh mw-list-item"><a href="https://sh.wikipedia.org/wiki/Zgru%C5%A1avanje_krvi" title="Zgrušavanje krvi – Serbo-Croatian" lang="sh" hreflang="sh" data-title="Zgrušavanje krvi" data-language-autonym="Srpskohrvatski / српскохрватски" data-language-local-name="Serbo-Croatian" class="interlanguage-link-target"><span>Srpskohrvatski / српскохрватски</span></a></li><li class="interlanguage-link interwiki-fi mw-list-item"><a href="https://fi.wikipedia.org/wiki/Veren_hyytyminen" title="Veren hyytyminen – Finnish" lang="fi" hreflang="fi" data-title="Veren hyytyminen" data-language-autonym="Suomi" data-language-local-name="Finnish" class="interlanguage-link-target"><span>Suomi</span></a></li><li class="interlanguage-link interwiki-sv mw-list-item"><a href="https://sv.wikipedia.org/wiki/Blodkoagulering" title="Blodkoagulering – Swedish" lang="sv" hreflang="sv" data-title="Blodkoagulering" data-language-autonym="Svenska" data-language-local-name="Swedish" class="interlanguage-link-target"><span>Svenska</span></a></li><li class="interlanguage-link interwiki-ta mw-list-item"><a href="https://ta.wikipedia.org/wiki/%E0%AE%95%E0%AF%81%E0%AE%B0%E0%AF%81%E0%AE%A4%E0%AE%BF_%E0%AE%89%E0%AE%B1%E0%AF%88%E0%AE%A4%E0%AE%B2%E0%AF%8D" title="குருதி உறைதல் – Tamil" lang="ta" hreflang="ta" data-title="குருதி உறைதல்" data-language-autonym="தமிழ்" data-language-local-name="Tamil" class="interlanguage-link-target"><span>தமிழ்</span></a></li><li class="interlanguage-link interwiki-th mw-list-item"><a href="https://th.wikipedia.org/wiki/%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B8%88%E0%B8%B1%E0%B8%9A%E0%B8%A5%E0%B8%B4%E0%B9%88%E0%B8%A1%E0%B8%82%E0%B8%AD%E0%B8%87%E0%B9%80%E0%B8%A5%E0%B8%B7%E0%B8%AD%E0%B8%94" title="การจับลิ่มของเลือด – Thai" lang="th" hreflang="th" data-title="การจับลิ่มของเลือด" data-language-autonym="ไทย" data-language-local-name="Thai" class="interlanguage-link-target"><span>ไทย</span></a></li><li class="interlanguage-link interwiki-tr mw-list-item"><a href="https://tr.wikipedia.org/wiki/Koag%C3%BClasyon" title="Koagülasyon – Turkish" lang="tr" hreflang="tr" data-title="Koagülasyon" data-language-autonym="Türkçe" data-language-local-name="Turkish" class="interlanguage-link-target"><span>Türkçe</span></a></li><li class="interlanguage-link interwiki-uk mw-list-item"><a href="https://uk.wikipedia.org/wiki/%D0%97%D1%81%D1%96%D0%B4%D0%B0%D0%BD%D0%BD%D1%8F_%D0%BA%D1%80%D0%BE%D0%B2%D1%96" title="Зсідання крові – Ukrainian" lang="uk" hreflang="uk" data-title="Зсідання крові" data-language-autonym="Українська" data-language-local-name="Ukrainian" class="interlanguage-link-target"><span>Українська</span></a></li><li class="interlanguage-link interwiki-vi mw-list-item"><a href="https://vi.wikipedia.org/wiki/S%E1%BB%B1_%C4%91%C3%B4ng_m%C3%A1u" title="Sự đông máu – Vietnamese" lang="vi" hreflang="vi" data-title="Sự đông máu" data-language-autonym="Tiếng Việt" data-language-local-name="Vietnamese" class="interlanguage-link-target"><span>Tiếng Việt</span></a></li><li class="interlanguage-link interwiki-wuu mw-list-item"><a href="https://wuu.wikipedia.org/wiki/%E5%87%9D%E8%A1%80" title="凝血 – Wu" lang="wuu" hreflang="wuu" data-title="凝血" data-language-autonym="吴语" data-language-local-name="Wu" class="interlanguage-link-target"><span>吴语</span></a></li><li class="interlanguage-link interwiki-yi mw-list-item"><a href="https://yi.wikipedia.org/wiki/%D7%91%D7%9C%D7%95%D7%98_%D7%A4%D7%90%D7%A8%D7%92%D7%9C%D7%99%D7%95%D7%95%D7%A2%D7%A8%D7%95%D7%A0%D7%92" title="בלוט פארגליווערונג – Yiddish" lang="yi" hreflang="yi" data-title="בלוט פארגליווערונג" data-language-autonym="ייִדיש" data-language-local-name="Yiddish" class="interlanguage-link-target"><span>ייִדיש</span></a></li><li class="interlanguage-link interwiki-zh-yue mw-list-item"><a href="https://zh-yue.wikipedia.org/wiki/%E8%A1%80%E6%B6%B2%E5%87%9D%E5%9B%BA" title="血液凝固 – Cantonese" lang="yue" hreflang="yue" data-title="血液凝固" data-language-autonym="粵語" data-language-local-name="Cantonese" class="interlanguage-link-target"><span>粵語</span></a></li><li class="interlanguage-link interwiki-zh mw-list-item"><a href="https://zh.wikipedia.org/wiki/%E5%87%9D%E8%A1%80" title="凝血 – Chinese" lang="zh" hreflang="zh" data-title="凝血" data-language-autonym="中文" data-language-local-name="Chinese" class="interlanguage-link-target"><span>中文</span></a></li><li class="interlanguage-link interwiki-bew mw-list-item"><a href="https://bew.wikipedia.org/wiki/Penggantingan_dara" title="Penggantingan dara – Betawi" lang="bew" hreflang="bew" data-title="Penggantingan dara" data-language-autonym="Betawi" data-language-local-name="Betawi" 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class="mw-content-ltr mw-parser-output" lang="en" dir="ltr"><div class="shortdescription nomobile noexcerpt noprint searchaux" style="display:none">Process of formation of blood clots</div> <style data-mw-deduplicate="TemplateStyles:r1236090951">.mw-parser-output .hatnote{font-style:italic}.mw-parser-output div.hatnote{padding-left:1.6em;margin-bottom:0.5em}.mw-parser-output .hatnote i{font-style:normal}.mw-parser-output .hatnote+link+.hatnote{margin-top:-0.5em}@media print{body.ns-0 .mw-parser-output .hatnote{display:none!important}}</style><div role="note" class="hatnote navigation-not-searchable">This article is about blood clotting. For other uses, see <a href="/wiki/Coagulation_(disambiguation)" class="mw-disambig" title="Coagulation (disambiguation)">Coagulation (disambiguation)</a>.</div> <p class="mw-empty-elt"> </p> <style data-mw-deduplicate="TemplateStyles:r1257001546">.mw-parser-output .infobox-subbox{padding:0;border:none;margin:-3px;width:auto;min-width:100%;font-size:100%;clear:none;float:none;background-color:transparent}.mw-parser-output .infobox-3cols-child{margin:auto}.mw-parser-output .infobox .navbar{font-size:100%}@media screen{html.skin-theme-clientpref-night .mw-parser-output .infobox-full-data:not(.notheme)>div:not(.notheme)[style]{background:#1f1f23!important;color:#f8f9fa}}@media screen and (prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .infobox-full-data:not(.notheme) div:not(.notheme){background:#1f1f23!important;color:#f8f9fa}}@media(min-width:640px){body.skin--responsive .mw-parser-output .infobox-table{display:table!important}body.skin--responsive .mw-parser-output .infobox-table>caption{display:table-caption!important}body.skin--responsive .mw-parser-output .infobox-table>tbody{display:table-row-group}body.skin--responsive .mw-parser-output .infobox-table tr{display:table-row!important}body.skin--responsive .mw-parser-output .infobox-table th,body.skin--responsive .mw-parser-output .infobox-table td{padding-left:inherit;padding-right:inherit}}</style><table class="infobox"><tbody><tr><th colspan="2" class="infobox-above" style="background-color: skyblue">Coagulation</th></tr><tr><td colspan="2" class="infobox-image"><span class="mw-default-size" typeof="mw:File/Frameless"><a href="/wiki/File:Coagulation_in_vivo.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/4/4f/Coagulation_in_vivo.png/220px-Coagulation_in_vivo.png" decoding="async" width="220" height="184" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/4/4f/Coagulation_in_vivo.png/330px-Coagulation_in_vivo.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/4/4f/Coagulation_in_vivo.png/440px-Coagulation_in_vivo.png 2x" data-file-width="829" data-file-height="695" /></a></span><div class="infobox-caption">Blood coagulation pathways <i>in vivo</i> showing the central role played by <a href="/wiki/Thrombin" title="Thrombin">thrombin</a></div></td></tr><tr><th scope="row" class="infobox-label">Health</th><td class="infobox-data">Beneficial</td></tr></tbody></table> <p><b>Coagulation</b>, also known as <b>clotting</b>, is the process by which <a href="/wiki/Blood" title="Blood">blood</a> changes from a <a href="/wiki/Liquid" title="Liquid">liquid</a> to a <a href="/wiki/Gel" title="Gel">gel</a>, forming a <a href="/wiki/Thrombus" title="Thrombus">blood clot</a>. It results in <a href="/wiki/Hemostasis" title="Hemostasis">hemostasis</a>, the cessation of blood loss from a damaged vessel, followed by repair. The process of coagulation involves <a href="/wiki/Platelet-activating_factor" title="Platelet-activating factor">activation</a>, <a href="/wiki/Cell_adhesion" title="Cell adhesion">adhesion</a> and aggregation of <a href="/wiki/Platelet" title="Platelet">platelets</a>, as well as deposition and maturation of <a href="/wiki/Fibrin" title="Fibrin">fibrin</a>. </p><p>Coagulation begins almost instantly after an injury to the <a href="/wiki/Endothelium" title="Endothelium">endothelium</a> that lines a <a href="/wiki/Blood_vessel" title="Blood vessel">blood vessel</a>. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial <a href="/wiki/Tissue_factor" title="Tissue factor">platelet tissue factor</a> to <a href="/wiki/Coagulation_factor_VII" class="mw-redirect" title="Coagulation factor VII">coagulation factor VII</a>, which ultimately leads to cross-linked <a href="/wiki/Fibrin" title="Fibrin">fibrin</a> formation. Platelets immediately form a plug at the site of injury; this is called <i>primary hemostasis. Secondary hemostasis</i> occurs simultaneously: additional coagulation factors beyond factor VII (<a href="#Coagulation_factors">listed below</a>) respond in a cascade to form fibrin strands, which strengthen the <a href="/wiki/Platelet_plug" title="Platelet plug">platelet plug</a>.<sup id="cite_ref-Furie_1-0" class="reference"><a href="#cite_note-Furie-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup> </p><p>Coagulation is highly <a href="/wiki/Conserved_sequence" title="Conserved sequence">conserved</a> throughout biology. In all <a href="/wiki/Mammal" title="Mammal">mammals</a>, coagulation involves both cellular components (platelets) and <a href="/wiki/Protein" title="Protein">proteinaceous</a> components (coagulation or clotting factors).<sup id="cite_ref-Michelson2006_2-0" class="reference"><a href="#cite_note-Michelson2006-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-medline2024_3-0" class="reference"><a href="#cite_note-medline2024-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup> The pathway in humans has been the most extensively researched and is the best understood.<sup id="cite_ref-4" class="reference"><a href="#cite_note-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup> Disorders of coagulation can result in problems with <a href="/wiki/Bleeding" title="Bleeding">hemorrhage</a>, <a href="/wiki/Bruise" title="Bruise">bruising</a>, or <a href="/wiki/Thrombosis" title="Thrombosis">thrombosis</a>.<sup id="cite_ref-isbn1-4051-8460-4_5-0" class="reference"><a href="#cite_note-isbn1-4051-8460-4-5"><span class="cite-bracket">[</span>5<span class="cite-bracket">]</span></a></sup> </p> <meta property="mw:PageProp/toc" /> <div class="mw-heading mw-heading2"><h2 id="List_of_coagulation_factors">List of coagulation factors</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=1" title="Edit section: List of coagulation factors"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>There are 13 traditional clotting factors, as named below,<sup id="cite_ref-Openstax_Anatomy_&_Physiology_attribution_6-0" class="reference"><a href="#cite_note-Openstax_Anatomy_&_Physiology_attribution-6"><span class="cite-bracket">[</span>6<span class="cite-bracket">]</span></a></sup> and other substances necessary for coagulation: </p> <table class="wikitable"> <caption>Coagulation factors and related substances </caption> <tbody><tr> <th>Number/Name</th> <th>Synonym(s)</th> <th>Function</th> <th>Associated genetic disorders</th> <th>Type of molecule</th> <th>Source</th> <th>Pathway(s) </th></tr> <tr> <td>Factor I</td> <td><a href="/wiki/Fibrinogen" title="Fibrinogen">Fibrinogen</a></td> <td>Forms fibrin threads in blood clots</td> <td><div><ul><li><a href="/wiki/Congenital_afibrinogenemia" title="Congenital afibrinogenemia">Congenital afibrinogenemia</a></li><li><a href="/wiki/Familial_renal_amyloidosis" title="Familial renal amyloidosis">Familial renal amyloidosis</a></li></ul></div></td> <td><a href="/wiki/Plasma_protein" title="Plasma protein">Plasma protein</a></td> <td>Liver</td> <td>Common pathway; converted into fibrin </td></tr> <tr> <td>Factor II*</td> <td><a href="/wiki/Prothrombin" class="mw-redirect" title="Prothrombin">Prothrombin</a></td> <td>Its active form (IIa) activates <a href="/wiki/Platelet" title="Platelet">platelets</a>, factors I, V, VII, VIII, XI, XIII, <a href="/wiki/Protein_C" title="Protein C">protein C</a></td> <td><div><ul><li><a href="/wiki/Thrombophilia" title="Thrombophilia">Thrombophilia</a></li><li><a href="/wiki/Prothrombin_thrombophilia" class="mw-redirect" title="Prothrombin thrombophilia">Prothrombin thrombophilia</a> (Prothrombin G20210A)<sup id="cite_ref-GHR2018_7-0" class="reference"><a href="#cite_note-GHR2018-7"><span class="cite-bracket">[</span>7<span class="cite-bracket">]</span></a></sup></li></ul></div> </td> <td>Plasma protein</td> <td>Liver</td> <td>Common pathway; converted into thrombin </td></tr> <tr> <td>Factor III</td> <td><div><ul><li><a href="/wiki/Tissue_factor" title="Tissue factor">Tissue factor</a></li><li>tissue thromboplastin</li></ul></div></td> <td>Co-factor of factor VIIa, which was formerly known as factor III</td> <td></td> <td>Lipoprotein mixture</td> <td>Damaged cells and platelets</td> <td>Extrinsic </td></tr> <tr> <td>Factor IV</td> <td><div><ul><li>Calcium</li><li>Calcium ions</li><li>Ca<sup>2+</sup> ions</li></ul></div></td> <td>Required for coagulation factors to bind to phospholipids, which were formerly known as factor IV</td> <td></td> <td>Inorganic ions in plasma</td> <td>Diet, platelets, bone matrix</td> <td>Entire process of coagulation </td></tr> <tr> <td><a href="/wiki/Factor_V" title="Factor V">Factor V</a></td> <td><div><ul><li>Proaccelerin</li><li>labile factor</li><li>Ac-globulin</li></ul></div></td> <td>Co-factor of factor X with which it forms the <a href="/wiki/Prothrombinase" title="Prothrombinase">prothrombinase</a> complex</td> <td><a href="/wiki/Activated_protein_C_resistance" title="Activated protein C resistance">Activated protein C resistance</a></td> <td>Plasma protein</td> <td>Liver, platelets</td> <td>Extrinsic and intrinsic </td></tr> <tr> <td>Factor VI</td> <td><div><ul><li><i>Unassigned</i> –<br />old name of factor Va<br />(activated form of factor V)</li><li>accelerin (formerly)</li></ul></div></td> <td>N/A</td> <td>N/A</td> <td>N/A</td> <td> </td></tr> <tr> <td><a href="/wiki/Factor_VII" title="Factor VII">Factor VII</a>*</td> <td><div><ul><li>Proconvertin</li><li>Serum Prothrombin Conversion Accelerator (SPCA)</li><li>Stable factor</li></ul></div></td> <td>Activates factors IX, X; increases rate of catalytic conversion of prothrombin into thrombin</td> <td>Congenital <a href="/wiki/Factor_VII_deficiency" title="Factor VII deficiency">factor VII deficiency</a></td> <td>Plasma protein</td> <td>Liver</td> <td>Extrinsic </td></tr> <tr> <td><a href="/wiki/Factor_VIII" title="Factor VIII">Factor VIII</a></td> <td><div><ul><li>Antihemophilic factor A</li><li>Antihemophilic factor (AHF)</li><li>Antihemophilic globulin (AHG)</li></ul></div></td> <td>Co-factor of factor IX with which it forms the <a href="/wiki/Tenase" title="Tenase">tenase</a> complex</td> <td><a href="/wiki/Hemophilia_A" class="mw-redirect" title="Hemophilia A">Hemophilia A</a></td> <td>Plasma protein factor</td> <td>Platelets and endothelial cells</td> <td>Intrinsic </td></tr> <tr> <td><a href="/wiki/Factor_IX" title="Factor IX">Factor IX</a>*</td> <td><div><ul><li>Antihemophilic factor B</li><li>Christmas factor</li><li>plasma thromboplastin component (PTC)</li></ul></div></td> <td>Activates factor X, forms <a href="/wiki/Tenase" title="Tenase">tenase</a> complex with factor VIII</td> <td><a href="/wiki/Hemophilia_B" class="mw-redirect" title="Hemophilia B">Hemophilia B</a></td> <td>Plasma protein</td> <td>Liver</td> <td>Intrinsic </td></tr> <tr> <td><a href="/wiki/Factor_X" title="Factor X">Factor X</a>*</td> <td><div><ul><li>Stuart-Prower factor</li><li>Stuart factor</li></ul></div></td> <td>Activates factor II, forms <a href="/wiki/Prothrombinase" title="Prothrombinase">prothrombinase</a> complex with factor V</td> <td>Congenital Factor X deficiency</td> <td>Protein</td> <td>Liver</td> <td>Extrinsic and intrinsic </td></tr> <tr> <td><a href="/wiki/Factor_XI" title="Factor XI">Factor XI</a></td> <td><div><ul><li>Plasma thromboplastin antecedent (PTA)</li><li>Antihemophilic factor C</li></ul></div></td> <td>Activates factor IX</td> <td><a href="/wiki/Hemophilia_C" class="mw-redirect" title="Hemophilia C">Hemophilia C</a></td> <td>Plasma protein</td> <td>Liver</td> <td>Intrinsic </td></tr> <tr> <td><a href="/wiki/Factor_XII" title="Factor XII">Factor XII</a></td> <td>Hageman factor</td> <td>Activates XI, VII, prekallikrein and plasminogen</td> <td><span class="nowrap"><a href="/wiki/Hereditary_angioedema" title="Hereditary angioedema">Hereditary angioedema</a> type III</span></td> <td>Plasma protein</td> <td>Liver</td> <td>Intrinsic; initiates clotting in vitro; also activates plasmin </td></tr> <tr> <td><a href="/wiki/Factor_XIII" title="Factor XIII">Factor XIII</a></td> <td>Fibrin-stabilizing factor</td> <td>Crosslinks fibrin threads</td> <td>Congenital factor XIIIa/b deficiency</td> <td>Plasma protein</td> <td>Liver, platelets</td> <td>Common pathway; stabilizes fibrin; slows down fibrinolysis </td></tr> <tr> <td><a href="/wiki/Vitamin_K" title="Vitamin K">Vitamin K</a></td> <td>Clotting vitamin</td> <td>Essential factor to the hepatic <a href="/wiki/Gamma-glutamyl_carboxylase" title="Gamma-glutamyl carboxylase">gamma-glutamyl carboxylase</a> that adds a <a href="/wiki/Carboxyl" class="mw-redirect" title="Carboxyl">carboxyl</a> group to <a href="/wiki/Glutamic_acid" title="Glutamic acid">glutamic acid</a> residues on factors II, VII, IX and X, as well as <a href="/wiki/Protein_S" title="Protein S">Protein S</a>, <a href="/wiki/Protein_C" title="Protein C">Protein C</a> and <a href="/wiki/Protein_Z" title="Protein Z">Protein Z</a><sup id="cite_ref-Vitamin_K_8-0" class="reference"><a href="#cite_note-Vitamin_K-8"><span class="cite-bracket">[</span>8<span class="cite-bracket">]</span></a></sup></td> <td><a href="/wiki/Vitamin_K_deficiency" title="Vitamin K deficiency">Vitamin K deficiency</a></td> <td>Phytyl-substituted naphthoquinone derivative</td> <td><a href="/wiki/Gut_microbiota" title="Gut microbiota">Gut microbiota</a><br />(e.g. <a href="/wiki/Escherichia_coli" title="Escherichia coli">E. coli</a><sup id="cite_ref-9" class="reference"><a href="#cite_note-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup>),<br />dietary sources</td> <td>Extrinsic<sup id="cite_ref-10" class="reference"><a href="#cite_note-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> </td></tr> <tr> <td><a href="/wiki/Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor</a></td> <td></td> <td>Binds to VIII, mediates platelet adhesion</td> <td><a href="/wiki/Von_Willebrand_disease" title="Von Willebrand disease">von Willebrand disease</a></td> <td>Blood glycoprotein</td> <td>Blood vessels' <a href="/wiki/Endothelia" class="mw-redirect" title="Endothelia">endothelia</a>,<br /> bone marrow<sup id="cite_ref-11" class="reference"><a href="#cite_note-11"><span class="cite-bracket">[</span>11<span class="cite-bracket">]</span></a></sup></td> <td> </td></tr> <tr> <td><a href="/wiki/Prekallikrein" title="Prekallikrein">Prekallikrein</a></td> <td>Fletcher factor</td> <td>Activates XII and prekallikrein; cleaves HMWK</td> <td>Prekallikrein/Fletcher factor deficiency </td></tr> <tr> <td><a href="/wiki/Kallikrein" title="Kallikrein">Kallikrein</a></td> <td></td> <td>Activates plasminogen</td> <td> </td></tr> <tr> <td><a href="/wiki/High-molecular-weight_kininogen" title="High-molecular-weight kininogen">High-molecular-weight kininogen</a></td> <td><div><ul><li>Fitzgerald factor</li><li>HMWK</li></ul></div></td> <td>Supports reciprocal activation of factors XII, XI, and prekallikrein</td> <td><a href="/w/index.php?title=Kininogen_deficiency&action=edit&redlink=1" class="new" title="Kininogen deficiency (page does not exist)">Kininogen deficiency</a> </td></tr> <tr> <td><a href="/wiki/Fibronectin" title="Fibronectin">Fibronectin</a></td> <td></td> <td>Mediates cell adhesion</td> <td><a href="/wiki/Glomerulopathy" title="Glomerulopathy">Glomerulopathy</a> with fibronectin deposits </td></tr> <tr> <td><a href="/wiki/Antithrombin" title="Antithrombin">Antithrombin</a> III</td> <td></td> <td>Inhibits factors IIa, Xa, IXa, XIa, and XIIa</td> <td><a href="/wiki/Antithrombin_III_deficiency" title="Antithrombin III deficiency">Antithrombin III deficiency</a> </td></tr> <tr> <td><a href="/wiki/Heparin_cofactor_II" title="Heparin cofactor II">Heparin cofactor II</a></td> <td></td> <td>Inhibits factor IIa, cofactor for heparin and <a href="/wiki/Dermatan_sulfate" title="Dermatan sulfate">dermatan sulfate</a> ("minor antithrombin")</td> <td>Heparin cofactor II deficiency </td></tr> <tr> <td><a href="/wiki/Protein_C" title="Protein C">Protein C</a></td> <td></td> <td>Inactivates factors Va and VIIIa</td> <td><a href="/wiki/Protein_C_deficiency" title="Protein C deficiency">Protein C deficiency</a> </td></tr> <tr> <td><a href="/wiki/Protein_S" title="Protein S">Protein S</a></td> <td></td> <td>Cofactor for activated protein C (APC, inactive when bound to C4b-binding protein</td> <td><a href="/wiki/Protein_S_deficiency" title="Protein S deficiency">Protein S deficiency</a> </td></tr> <tr> <td><a href="/wiki/Protein_Z" title="Protein Z">Protein Z</a></td> <td></td> <td>Mediates thrombin adhesion to phospholipids and stimulates degradation of factor X by ZPI</td> <td><a href="/w/index.php?title=Protein_Z_deficiency&action=edit&redlink=1" class="new" title="Protein Z deficiency (page does not exist)">Protein Z deficiency</a> </td></tr> <tr> <td><a href="/wiki/Protein_Z-related_protease_inhibitor" title="Protein Z-related protease inhibitor">Protein Z-related protease inhibitor</a></td> <td>ZPI</td> <td>Degrades factors X (in presence of protein Z) and XI (independently</td> <td> </td></tr> <tr> <td><a href="/wiki/Plasminogen" class="mw-redirect" title="Plasminogen">Plasminogen</a></td> <td></td> <td>Converts to plasmin, lyses fibrin and other proteins</td> <td>Plasminogen deficiency type I (ligneous conjunctivitis) </td></tr> <tr> <td><a href="/wiki/Alpha_2-antiplasmin" title="Alpha 2-antiplasmin">α<sub>2</sub>-Antiplasmin</a></td> <td></td> <td>Inhibits plasmin</td> <td>Antiplasmin deficiency </td></tr> <tr> <td><a href="/wiki/Alpha-2-Macroglobulin" title="Alpha-2-Macroglobulin">α<sub>2</sub>-Macroglobulin</a></td> <td></td> <td>Inhibits plasmin, kallikrein, and thrombin</td> <td> </td></tr> <tr> <td><a href="/wiki/Tissue_plasminogen_activator" class="mw-redirect" title="Tissue plasminogen activator">Tissue plasminogen activator</a></td> <td>t-PA or TPA</td> <td>Activates plasminogen</td> <td><div><ul><li>Familial <a href="/wiki/Hyperfibrinolysis" title="Hyperfibrinolysis">hyperfibrinolysis</a></li><li><a href="/wiki/Thrombophilia" title="Thrombophilia">Thrombophilia</a></li></ul></div> </td></tr> <tr> <td><a href="/wiki/Urokinase" title="Urokinase">Urokinase</a></td> <td></td> <td>Activates plasminogen</td> <td><a href="/wiki/Quebec_platelet_disorder" title="Quebec platelet disorder">Quebec platelet disorder</a> </td></tr> <tr> <td><a href="/wiki/Plasminogen_activator_inhibitor-1" title="Plasminogen activator inhibitor-1">Plasminogen activator inhibitor-1</a></td> <td>PAI-1</td> <td>Inactivates tPA and urokinase (endothelial PAI</td> <td>Plasminogen activator inhibitor-1 deficiency </td></tr> <tr> <td><a href="/wiki/Plasminogen_activator_inhibitor-2" title="Plasminogen activator inhibitor-2">Plasminogen activator inhibitor-2</a></td> <td>PAI-2</td> <td>Inactivates tPA and urokinase</td> <td>Plasminogen activator inhibitor-1 deficiency </td></tr> <tr> <td><a href="/wiki/Cancer_procoagulant" title="Cancer procoagulant">Cancer procoagulant</a></td> <td></td> <td>Pathological activator of <a href="/wiki/Factor_X" title="Factor X">factor X</a>; linked to thrombosis in various <a href="/wiki/Cancer" title="Cancer">cancers</a><sup id="cite_ref-12" class="reference"><a href="#cite_note-12"><span class="cite-bracket">[</span>12<span class="cite-bracket">]</span></a></sup></td> <td> </td></tr> <tr> <th colspan="7">* Vitamin K is required for biosynthesis of these clotting factors<sup id="cite_ref-Vitamin_K_8-1" class="reference"><a href="#cite_note-Vitamin_K-8"><span class="cite-bracket">[</span>8<span class="cite-bracket">]</span></a></sup> </th></tr></tbody></table> <div class="mw-heading mw-heading2"><h2 id="Physiology">Physiology</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=2" title="Edit section: Physiology"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <figure class="mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:VWF-GP1ba.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/a/ab/VWF-GP1ba.png/300px-VWF-GP1ba.png" decoding="async" width="300" height="262" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/a/ab/VWF-GP1ba.png/450px-VWF-GP1ba.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/a/ab/VWF-GP1ba.png/600px-VWF-GP1ba.png 2x" data-file-width="3000" data-file-height="2615" /></a><figcaption>The interaction of vWF and GP1b alpha. The GP1b receptor on the surface of platelets allows the platelet to bind to vWF, which is exposed upon damage to vasculature. The vWF A1 domain (yellow) interacts with the extracellular domain of GP1ba (blue).</figcaption></figure> <p>Physiology of blood coagulation is based on <a href="/wiki/Hemostasis" title="Hemostasis">hemostasis</a>, the normal bodily process that stops bleeding. Coagulation is a part of an integrated series of haemostatic reactions, involving plasma, platelet, and vascular components.<sup id="cite_ref-13" class="reference"><a href="#cite_note-13"><span class="cite-bracket">[</span>13<span class="cite-bracket">]</span></a></sup> </p><p>Hemostasis consists of four main stages: </p> <ul><li><a href="/wiki/Vasoconstriction" title="Vasoconstriction">Vasoconstriction</a> (vasospasm or vascular spasm): Here, this refers to contraction of smooth muscles in the <a href="/wiki/Tunica_media" title="Tunica media">tunica media</a> layer of <a href="/wiki/Endothelium" title="Endothelium">endothelium</a> (blood vessel wall).</li> <li>Activation of platelets and <a href="/wiki/Platelet_plug" title="Platelet plug">platelet plug</a> formation: <ul><li>Platelet activation: <a href="/w/index.php?title=Platelet_activator&action=edit&redlink=1" class="new" title="Platelet activator (page does not exist)">Platelet activators</a>, such as <a href="/wiki/Platelet_activating_factor" class="mw-redirect" title="Platelet activating factor">platelet activating factor</a> and <a href="/wiki/Thromboxane_A2" title="Thromboxane A2">thromboxane A2</a>,<sup id="cite_ref-14" class="reference"><a href="#cite_note-14"><span class="cite-bracket">[</span>14<span class="cite-bracket">]</span></a></sup> activate platelets in the bloodstream, leading to attachment of platelets' membrane receptors (e.g. <a href="/wiki/Glycoprotein_IIb/IIIa" title="Glycoprotein IIb/IIIa">glycoprotein IIb/IIIa</a><sup id="cite_ref-15" class="reference"><a href="#cite_note-15"><span class="cite-bracket">[</span>15<span class="cite-bracket">]</span></a></sup>) to <a href="/wiki/Extracellular_matrix" title="Extracellular matrix">extracellular matrix</a><sup id="cite_ref-16" class="reference"><a href="#cite_note-16"><span class="cite-bracket">[</span>16<span class="cite-bracket">]</span></a></sup> proteins (e.g. von Willebrand factor<sup id="cite_ref-17" class="reference"><a href="#cite_note-17"><span class="cite-bracket">[</span>17<span class="cite-bracket">]</span></a></sup>) on cell membranes of damaged endothelial cells and exposed <a href="/wiki/Collagen" title="Collagen">collagen</a> at the site of injury.<sup id="cite_ref-18" class="reference"><a href="#cite_note-18"><span class="cite-bracket">[</span>18<span class="cite-bracket">]</span></a></sup></li> <li>Platelet plug formation: The adhered platelets aggregate and form a temporary plug to stop bleeding. This process is often called "primary hemostasis".<sup id="cite_ref-19" class="reference"><a href="#cite_note-19"><span class="cite-bracket">[</span>19<span class="cite-bracket">]</span></a></sup></li></ul></li> <li><a href="/wiki/Coagulation_cascade" class="mw-redirect" title="Coagulation cascade">Coagulation cascade</a>: It is a series of enzymatic reactions that lead to the formation of a stable blood clot. The endothelial cells release substances like tissue factor, which triggers the extrinsic pathway of the coagulation cascade. This is called as "secondary hemostasis".<sup id="cite_ref-20" class="reference"><a href="#cite_note-20"><span class="cite-bracket">[</span>20<span class="cite-bracket">]</span></a></sup></li> <li><a href="/w/index.php?title=Fibrin_clot&action=edit&redlink=1" class="new" title="Fibrin clot (page does not exist)">Fibrin clot</a> formation: Near the end of the extrinsic pathway, after <a href="/wiki/Thrombin" title="Thrombin">thrombin</a> completes conversion of fibrinogen into fibrin,<sup id="cite_ref-Weisel2017_21-0" class="reference"><a href="#cite_note-Weisel2017-21"><span class="cite-bracket">[</span>21<span class="cite-bracket">]</span></a></sup> <a href="/wiki/Factor_XIIIa" class="mw-redirect" title="Factor XIIIa">factor XIIIa</a> (plasma transglutaminase;<sup id="cite_ref-Weisel2017_21-1" class="reference"><a href="#cite_note-Weisel2017-21"><span class="cite-bracket">[</span>21<span class="cite-bracket">]</span></a></sup> activated form of fibrin-stabilizing factor) promotes fibrin cross-linking, and subsequent stabilization of fibrin, leading to the formation of a fibrin clot (final blood clot), which temporarily seals the wound to allow <a href="/wiki/Wound_healing" title="Wound healing">wound healing</a> until its inner part is dissolved by <a href="/w/index.php?title=Fibrinolytic_enzyme&action=edit&redlink=1" class="new" title="Fibrinolytic enzyme (page does not exist)">fibrinolytic enzymes</a>, while the clot's outer part is shed off.</li></ul> <p>After the fibrin clot is formed, <a href="/wiki/Clot_retraction" title="Clot retraction">clot retraction</a> occurs and then <a href="/w/index.php?title=Clot_resolution&action=edit&redlink=1" class="new" title="Clot resolution (page does not exist)">clot resolution</a> starts, and these two process are together called "tertiary hemostasis". Activated platelets contract their internal actin and myosin fibrils in their cytoskeleton, which leads to shrinkage of the clot volume. <a href="/wiki/Plasminogen_activator" title="Plasminogen activator">Plasminogen activators</a>, such as <a href="/wiki/Tissue_plasminogen_activator" class="mw-redirect" title="Tissue plasminogen activator">tissue plasminogen activator</a> (t-PA), activate <a href="/wiki/Plasminogen" class="mw-redirect" title="Plasminogen">plasminogen</a> into plasmin, which promotes lysis of the fibrin clot; this restores the flow of blood in the damaged/obstructed blood vessels.<sup id="cite_ref-22" class="reference"><a href="#cite_note-22"><span class="cite-bracket">[</span>22<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Vasoconstriction">Vasoconstriction</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=3" title="Edit section: Vasoconstriction"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Vasoconstriction" title="Vasoconstriction">Vasoconstriction</a></div> <p>When there is an injury to a blood vessel, the endothelial cells can release various vasoconstrictor substances, such as endothelin<sup id="cite_ref-23" class="reference"><a href="#cite_note-23"><span class="cite-bracket">[</span>23<span class="cite-bracket">]</span></a></sup> and thromboxane,<sup id="cite_ref-24" class="reference"><a href="#cite_note-24"><span class="cite-bracket">[</span>24<span class="cite-bracket">]</span></a></sup> to induce the constriction of the smooth muscles in the vessel wall. This helps reduce blood flow to the site of injury and limits bleeding. </p> <div class="mw-heading mw-heading3"><h3 id="Platelet_activation_and_platelet_plug_formation">Platelet activation and platelet plug formation</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=4" title="Edit section: Platelet activation and platelet plug formation"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>When the endothelium is damaged, the normally isolated underlying collagen is exposed to circulating platelets, which bind directly to collagen with collagen-specific <a href="/wiki/Glycoprotein_Ia/IIa" class="mw-redirect" title="Glycoprotein Ia/IIa">glycoprotein Ia/IIa</a> surface receptors. This adhesion is strengthened further by <a href="/wiki/Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor</a> (vWF), which is released from the endothelium and from platelets; vWF forms additional links between the platelets' <a href="/wiki/Glycoprotein_Ib/IX/V" class="mw-redirect" title="Glycoprotein Ib/IX/V">glycoprotein Ib/IX/V</a> and A1 domain. This localization of platelets to the extracellular matrix promotes collagen interaction with platelet <a href="/wiki/Glycoprotein_VI" class="mw-redirect" title="Glycoprotein VI">glycoprotein VI</a>. Binding of collagen to <a href="/wiki/Glycoprotein_VI" class="mw-redirect" title="Glycoprotein VI">glycoprotein VI</a> triggers a signaling cascade that results in activation of platelet integrins. Activated integrins mediate tight binding of platelets to the extracellular matrix. This process adheres platelets to the site of injury.<sup id="cite_ref-PracticalH1_25-0" class="reference"><a href="#cite_note-PracticalH1-25"><span class="cite-bracket">[</span>25<span class="cite-bracket">]</span></a></sup> </p><p>Activated platelets release the contents of stored granules into the blood plasma. The granules include <a href="/wiki/Adenosine_diphosphate" title="Adenosine diphosphate">ADP</a>, <a href="/wiki/Serotonin" title="Serotonin">serotonin</a>, <a href="/wiki/Platelet-activating_factor" title="Platelet-activating factor">platelet-activating factor</a> (PAF), <a href="/wiki/Von_Willebrand_factor" title="Von Willebrand factor">vWF</a>, <a href="/wiki/Platelet_factor_4" title="Platelet factor 4">platelet factor 4</a>, and <a href="/wiki/Thromboxane_A2" title="Thromboxane A2">thromboxane A<sub>2</sub></a> (TXA<sub>2</sub>), which, in turn, activate additional platelets. The granules' contents activate a <a href="/wiki/G_protein-coupled_receptor" title="G protein-coupled receptor">G<sub>q</sub>-linked protein receptor</a> cascade, resulting in increased calcium concentration in the platelets' cytosol. The calcium activates <a href="/wiki/Protein_kinase_C" title="Protein kinase C">protein kinase C</a>, which, in turn, activates <a href="/wiki/Phospholipase_A2" title="Phospholipase A2">phospholipase A<sub>2</sub></a> (PLA<sub>2</sub>). PLA<sub>2</sub> then modifies the <a href="/wiki/Integrin" title="Integrin">integrin</a> membrane <a href="/wiki/Glycoprotein_IIb/IIIa" title="Glycoprotein IIb/IIIa">glycoprotein IIb/IIIa</a>, increasing its affinity to bind <a href="/wiki/Fibrinogen" title="Fibrinogen">fibrinogen</a>. The activated platelets change shape from spherical to stellate, and the <a href="/wiki/Fibrinogen" title="Fibrinogen">fibrinogen</a> cross-links with <a href="/wiki/Glycoprotein_IIb/IIIa" title="Glycoprotein IIb/IIIa">glycoprotein IIb/IIIa</a> aid in aggregation of adjacent platelets, forming a platelet plug and thereby completing primary hemostasis).<sup id="cite_ref-Pallister1b_26-0" class="reference"><a href="#cite_note-Pallister1b-26"><span class="cite-bracket">[</span>26<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Coagulation_cascade">Coagulation cascade</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=5" title="Edit section: Coagulation cascade"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><span class="anchor" id="The_coagulation_cascade"></span> </p> <figure class="mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:Classical_blood_coagulation_pathway.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/4/42/Classical_blood_coagulation_pathway.png/350px-Classical_blood_coagulation_pathway.png" decoding="async" width="350" height="263" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/4/42/Classical_blood_coagulation_pathway.png/525px-Classical_blood_coagulation_pathway.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/4/42/Classical_blood_coagulation_pathway.png/700px-Classical_blood_coagulation_pathway.png 2x" data-file-width="960" data-file-height="720" /></a><figcaption>The classical blood coagulation pathway<sup id="cite_ref-Pallister1_27-0" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup></figcaption></figure> <figure class="mw-default-size" typeof="mw:File/Thumb"><a href="/wiki/File:Rapaport_Coagulation_Cascade.svg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/5/55/Rapaport_Coagulation_Cascade.svg/220px-Rapaport_Coagulation_Cascade.svg.png" decoding="async" width="220" height="170" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/5/55/Rapaport_Coagulation_Cascade.svg/330px-Rapaport_Coagulation_Cascade.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/5/55/Rapaport_Coagulation_Cascade.svg/440px-Rapaport_Coagulation_Cascade.svg.png 2x" data-file-width="990" data-file-height="765" /></a><figcaption>Modern coagulation pathway. Hand-drawn composite from similar drawings presented by Professor Dzung Le, MD, PhD, at UCSD Clinical Chemistry conferences on 14 and 21 October 2014. Original schema from Introduction to Hematology by Samuel I. Rapaport. 2nd ed.; Lippencott: 1987. Dr Le added the factor XI portion based on a paper from about year 2000. Dr. Le's similar drawings presented the development of this cascade over 6 frames, like a comic.</figcaption></figure> <p>The coagulation cascade of secondary hemostasis has two initial pathways which lead to <i><a href="/wiki/Fibrin" title="Fibrin">fibrin</a></i> formation. These are the <i>contact activation pathway</i> (also known as the intrinsic pathway), and the <i>tissue factor pathway</i> (also known as the extrinsic pathway), which both lead to the same fundamental reactions that produce fibrin. It was previously thought that the two pathways of coagulation cascade were of equal importance, but it is now known that the primary pathway for the initiation of blood coagulation is the <i>tissue factor</i> (extrinsic) pathway. The pathways are a series of reactions, in which a <a href="/wiki/Zymogen" title="Zymogen">zymogen</a> (inactive enzyme precursor) of a <a href="/wiki/Serine_protease" title="Serine protease">serine protease</a> and its <a href="/wiki/Glycoprotein" title="Glycoprotein">glycoprotein</a> co-factor are activated to become active components that then catalyze the next reaction in the cascade, ultimately resulting in cross-linked fibrin. Coagulation factors are generally indicated by <a href="/wiki/Roman_numeral" class="mw-redirect" title="Roman numeral">Roman numerals</a>, with a lowercase <i>a</i> appended to indicate an active form.<sup id="cite_ref-Pallister1_27-1" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> </p><p>The coagulation factors are generally <a href="/wiki/Enzyme" title="Enzyme">enzymes</a> called <a href="/wiki/Serine_protease" title="Serine protease">serine proteases</a>, which act by cleaving downstream proteins. The exceptions are tissue factor, FV, FVIII, FXIII.<sup id="cite_ref-28" class="reference"><a href="#cite_note-28"><span class="cite-bracket">[</span>28<span class="cite-bracket">]</span></a></sup> Tissue factor, FV and FVIII are glycoproteins, and Factor XIII is a <a href="/wiki/Transglutaminase" title="Transglutaminase">transglutaminase</a>.<sup id="cite_ref-Pallister1_27-2" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> The coagulation factors circulate as inactive <a href="/wiki/Zymogens" class="mw-redirect" title="Zymogens">zymogens</a>. The coagulation cascade is therefore classically divided into three pathways. The <i>tissue factor</i> and <i>contact activation</i> pathways both activate the "final common pathway" of factor X, thrombin and fibrin.<sup id="cite_ref-Hoffbrand2_29-0" class="reference"><a href="#cite_note-Hoffbrand2-29"><span class="cite-bracket">[</span>29<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Tissue_factor_pathway_(extrinsic)"><span id="Tissue_factor_pathway_.28extrinsic.29"></span>Tissue factor pathway (extrinsic)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=6" title="Edit section: Tissue factor pathway (extrinsic)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><span class="anchor" id="Extrinsic_pathway"></span> The main role of the <a href="/wiki/Tissue_factor" title="Tissue factor">tissue factor</a> (TF) pathway is to generate a "thrombin burst", a process by which <a href="/wiki/Thrombin" title="Thrombin">thrombin</a>, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly. FVIIa circulates in a higher amount than any other activated coagulation factor. The process includes the following steps:<sup id="cite_ref-Pallister1_27-3" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> </p> <ol><li>Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor expressed on tissue-factor-bearing cells (<a href="/wiki/Stromal_cell" title="Stromal cell">stromal</a> fibroblasts and leukocytes), forming an activated complex (TF-FVIIa).</li> <li>TF-FVIIa activates FIX and FX.</li> <li>FVII is itself activated by thrombin, FXIa, FXII, and FXa.</li> <li>The activation of FX (to form FXa) by TF-FVIIa is almost immediately inhibited by <a href="/wiki/Tissue_factor_pathway_inhibitor" title="Tissue factor pathway inhibitor">tissue factor pathway inhibitor</a> (TFPI).</li> <li>FXa and its co-factor FVa form the <a href="/wiki/Prothrombinase" title="Prothrombinase">prothrombinase</a> complex, which activates <a href="/wiki/Prothrombin" class="mw-redirect" title="Prothrombin">prothrombin</a> to thrombin.</li> <li>Thrombin then activates other components of the coagulation cascade, including FV and FVIII (which forms a complex with FIX), and activates and releases FVIII from being bound to vWF.</li> <li>FVIIIa is the co-factor of FIXa, and together they form the "<a href="/wiki/Tenase" title="Tenase">tenase</a>" complex, which activates FX; and so the cycle continues. ("Tenase" is a contraction of "ten" and the suffix "-ase" used for enzymes.)</li></ol> <div class="mw-heading mw-heading4"><h4 id="Contact_activation_pathway_(intrinsic)"><span id="Contact_activation_pathway_.28intrinsic.29"></span>Contact activation pathway (intrinsic)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=7" title="Edit section: Contact activation pathway (intrinsic)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><span class="anchor" id="Intrinsic_pathway"></span> The <a href="/wiki/Contact_activation_system" title="Contact activation system">contact activation pathway</a> begins with formation of the primary complex on <a href="/wiki/Collagen" title="Collagen">collagen</a> by <a href="/wiki/High-molecular-weight_kininogen" title="High-molecular-weight kininogen">high-molecular-weight kininogen</a> (HMWK), <a href="/wiki/Prekallikrein" title="Prekallikrein">prekallikrein</a>, and <a href="/wiki/Hageman_factor" class="mw-redirect" title="Hageman factor">FXII (Hageman factor)</a>. <a href="/wiki/Prekallikrein" title="Prekallikrein">Prekallikrein</a> is converted to <a href="/wiki/Kallikrein" title="Kallikrein">kallikrein</a> and FXII becomes FXIIa. FXIIa converts FXI into FXIa. Factor XIa activates FIX, which with its co-factor FVIIIa form the <a href="/wiki/Tenase" title="Tenase">tenase</a> complex, which activates FX to FXa. The minor role that the contact activation pathway has in initiating blood clot formation (or more specifically, physiological <a href="/wiki/Hemostasis" title="Hemostasis">hemostasis</a>) can be illustrated by the fact that individuals with severe deficiencies of FXII, HMWK, and <a href="/wiki/Prekallikrein" title="Prekallikrein">prekallikrein</a> do not have a bleeding disorder. Instead, contact activation system seems to be more involved in inflammation,<sup id="cite_ref-Pallister1_27-4" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> and innate immunity.<sup id="cite_ref-Long2016_30-0" class="reference"><a href="#cite_note-Long2016-30"><span class="cite-bracket">[</span>30<span class="cite-bracket">]</span></a></sup> Interference with the pathway may confer protection against thrombosis without a significant bleeding risk.<sup id="cite_ref-Long2016_30-1" class="reference"><a href="#cite_note-Long2016-30"><span class="cite-bracket">[</span>30<span class="cite-bracket">]</span></a></sup> </p><p>Inhibition of factor XII and PK interferes with innate immunity in animal models.<sup id="cite_ref-Long2016_30-2" class="reference"><a href="#cite_note-Long2016-30"><span class="cite-bracket">[</span>30<span class="cite-bracket">]</span></a></sup> More promising is <a href="/wiki/Factor_XI#Inhibition" title="Factor XI">inhibition of factor XI</a>, which in early clinical trials have shown the expected effect.<sup id="cite_ref-31" class="reference"><a href="#cite_note-31"><span class="cite-bracket">[</span>31<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Final_common_pathway">Final common pathway</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=8" title="Edit section: Final common pathway"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><span class="anchor" id="Common_pathway"></span> 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.<sup id="cite_ref-troisi_32-0" class="reference"><a href="#cite_note-troisi-32"><span class="cite-bracket">[</span>32<span class="cite-bracket">]</span></a></sup> </p><p>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.<sup id="cite_ref-33" class="reference"><a href="#cite_note-33"><span class="cite-bracket">[</span>33<span class="cite-bracket">]</span></a></sup> </p><p>Thrombin functions not only to convert <a href="/wiki/Fibrinogen" title="Fibrinogen">fibrinogen</a> to fibrin, it also activates Factors VIII and V and their inhibitor <a href="/wiki/Protein_C" title="Protein C">protein C</a> (in the presence of <a href="/wiki/Thrombomodulin" title="Thrombomodulin">thrombomodulin</a>). By activating Factor XIII, <a href="/wiki/Covalent_bond" title="Covalent bond">covalent bonds</a> are formed that crosslink the fibrin polymers that form from activated monomers.<sup id="cite_ref-Pallister1_27-5" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> This stabilizes the fibrin network.<sup id="cite_ref-34" class="reference"><a href="#cite_note-34"><span class="cite-bracket">[</span>34<span class="cite-bracket">]</span></a></sup> </p><p>The coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the <a href="/wiki/Tenase" title="Tenase">tenase</a> complex until it is down-regulated by the anticoagulant pathways.<sup id="cite_ref-Pallister1_27-6" class="reference"><a href="#cite_note-Pallister1-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Cell-based_scheme_of_coagulation">Cell-based scheme of coagulation</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=9" title="Edit section: Cell-based scheme of coagulation"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>A newer model of coagulation mechanism explains the intricate combination of cellular and biochemical events that occur during the coagulation process <i><a href="/wiki/In_vivo" title="In vivo">in vivo</a></i>. Along with the procoagulant and anticoagulant plasma proteins, normal physiologic coagulation requires the presence of two cell types for formation of coagulation complexes: cells that express tissue factor (usually extravascular) and platelets.<sup id="cite_ref-35" class="reference"><a href="#cite_note-35"><span class="cite-bracket">[</span>35<span class="cite-bracket">]</span></a></sup> </p><p>The coagulation process occurs in two phases. First is the initiation phase, which occurs in tissue-factor-expressing cells. This is followed by the propagation phase, which occurs on activated <a href="/wiki/Platelet" title="Platelet">platelets</a>. The initiation phase, mediated by the tissue factor exposure, proceeds via the classic extrinsic pathway and contributes to about 5% of thrombin production. The amplified production of thrombin occurs via the classic intrinsic pathway in the propagation phase; about 95% of thrombin generated will be during this second phase.<sup id="cite_ref-Hoffman-2003_36-0" class="reference"><a href="#cite_note-Hoffman-2003-36"><span class="cite-bracket">[</span>36<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Fibrinolysis">Fibrinolysis</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=10" title="Edit section: Fibrinolysis"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Fibrinolysis" title="Fibrinolysis">Fibrinolysis</a></div> <p>Eventually, blood clots are reorganized and resorbed by a process termed <i><a href="/wiki/Fibrinolysis" title="Fibrinolysis">fibrinolysis</a></i>. The main enzyme responsible for this process is <a href="/wiki/Plasmin" title="Plasmin">plasmin</a>, which is regulated by <a href="/w/index.php?title=Plasmin_activator&action=edit&redlink=1" class="new" title="Plasmin activator (page does not exist)">plasmin activators</a> and <a href="/wiki/Plasmin_inhibitor" class="mw-redirect" title="Plasmin inhibitor">plasmin inhibitors</a>.<sup id="cite_ref-Hoffbrand_37-0" class="reference"><a href="#cite_note-Hoffbrand-37"><span class="cite-bracket">[</span>37<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Role_in_immune_system">Role in immune system</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=11" title="Edit section: Role in immune system"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The coagulation system overlaps with the <a href="/wiki/Immune_system" title="Immune system">immune system</a>. Coagulation can physically trap invading microbes in blood clots. Also, some products of the coagulation system can contribute to the <a href="/wiki/Innate_immune_system" title="Innate immune system">innate immune system</a> by their ability to increase vascular permeability and act as <a href="/wiki/Chemotactic_agent" class="mw-redirect" title="Chemotactic agent">chemotactic agents</a> for <a href="/wiki/Phagocytic_cell" class="mw-redirect" title="Phagocytic cell">phagocytic cells</a>. In addition, some of the products of the coagulation system are directly <a href="/wiki/Antimicrobial" title="Antimicrobial">antimicrobial</a>. For example, <a href="/wiki/Beta-lysine" class="mw-redirect" title="Beta-lysine">beta-lysine</a>, an amino acid produced by platelets during coagulation, can cause <a href="/wiki/Lysis" title="Lysis">lysis</a> of many <a href="/wiki/Gram-positive_bacteria" title="Gram-positive bacteria">Gram-positive bacteria</a> by acting as a cationic detergent.<sup id="cite_ref-Mayer_38-0" class="reference"><a href="#cite_note-Mayer-38"><span class="cite-bracket">[</span>38<span class="cite-bracket">]</span></a></sup> Many <a href="/wiki/Acute-phase_protein" title="Acute-phase protein">acute-phase proteins</a> of <a href="/wiki/Inflammation" title="Inflammation">inflammation</a> are involved in the coagulation system. In addition, pathogenic bacteria may secrete agents that alter the coagulation system, e.g. <a href="/wiki/Coagulase" title="Coagulase">coagulase</a> and <a href="/wiki/Streptokinase" title="Streptokinase">streptokinase</a>.<sup id="cite_ref-39" class="reference"><a href="#cite_note-39"><span class="cite-bracket">[</span>39<span class="cite-bracket">]</span></a></sup> </p><p>Immunohemostasis is the integration of immune activation into adaptive clot formation. Immunothrombosis is the pathological result of crosstalk between immunity, inflammation, and coagulation. Mediators of this process include <a href="/wiki/Damage-associated_molecular_pattern" title="Damage-associated molecular pattern">damage-associated molecular patterns</a> and <a href="/wiki/Pathogen-associated_molecular_pattern" title="Pathogen-associated molecular pattern">pathogen-associated molecular patterns</a>, which are recognized by <a href="/wiki/Toll-like_receptor" title="Toll-like receptor">toll-like receptors</a>, triggering procoagulant and proinflammatory responses such as formation of <a href="/wiki/Neutrophil_extracellular_traps" title="Neutrophil extracellular traps">neutrophil extracellular traps</a>.<sup id="cite_ref-Yong23_40-0" class="reference"><a href="#cite_note-Yong23-40"><span class="cite-bracket">[</span>40<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Cofactors">Cofactors</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=12" title="Edit section: Cofactors"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Various substances are required for the proper functioning of the coagulation cascade: </p> <div class="mw-heading mw-heading4"><h4 id="Calcium_and_phospholipids">Calcium and phospholipids</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=13" title="Edit section: Calcium and phospholipids"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Calcium" title="Calcium">Calcium</a> and <a href="/wiki/Phospholipid" title="Phospholipid">phospholipids</a> (constituents of <a href="/wiki/Platelet" title="Platelet">platelet</a> membrane) are required for the <a href="/wiki/Tenase" title="Tenase">tenase</a> and prothrombinase complexes to function.<sup id="cite_ref-41" class="reference"><a href="#cite_note-41"><span class="cite-bracket">[</span>41<span class="cite-bracket">]</span></a></sup> Calcium mediates the binding of the complexes via the terminal gamma-carboxy residues on Factor Xa and Factor IXa to the phospholipid surfaces expressed by platelets, as well as procoagulant microparticles or <a href="/wiki/Microvesicles" class="mw-redirect" title="Microvesicles">microvesicles</a> shed from them.<sup id="cite_ref-42" class="reference"><a href="#cite_note-42"><span class="cite-bracket">[</span>42<span class="cite-bracket">]</span></a></sup> Calcium is also required at other points in the coagulation cascade. Calcium ions play a major role in the regulation of coagulation cascade that is paramount in the maintenance of hemostasis. Other than platelet activation, calcium ions are responsible for complete activation of several coagulation factors, including coagulation Factor XIII.<sup id="cite_ref-43" class="reference"><a href="#cite_note-43"><span class="cite-bracket">[</span>43<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Vitamin_K">Vitamin K</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=14" title="Edit section: Vitamin K"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Vitamin_K" title="Vitamin K">Vitamin K</a> is an essential factor to the hepatic <a href="/wiki/Gamma-glutamyl_carboxylase" title="Gamma-glutamyl carboxylase">gamma-glutamyl carboxylase</a> that adds a <a href="/wiki/Carboxyl" class="mw-redirect" title="Carboxyl">carboxyl</a> group to <a href="/wiki/Glutamic_acid" title="Glutamic acid">glutamic acid</a> residues on factors II, VII, IX and X, as well as <a href="/wiki/Protein_S" title="Protein S">Protein S</a>, <a href="/wiki/Protein_C" title="Protein C">Protein C</a> and <a href="/wiki/Protein_Z" title="Protein Z">Protein Z</a>. In adding the gamma-carboxyl group to glutamate residues on the immature clotting factors, Vitamin K is itself oxidized. Another enzyme, <i><a href="/wiki/Vitamin_K_epoxide_reductase" title="Vitamin K epoxide reductase">Vitamin K epoxide reductase</a></i> (VKORC), reduces vitamin K back to its active form. Vitamin K epoxide reductase is pharmacologically important as a target of anticoagulant drugs <a href="/wiki/Warfarin" title="Warfarin">warfarin</a> and related <a href="/wiki/Coumarin" title="Coumarin">coumarins</a> such as <a href="/wiki/Acenocoumarol" title="Acenocoumarol">acenocoumarol</a>, <a href="/wiki/Phenprocoumon" title="Phenprocoumon">phenprocoumon</a>, and <a href="/wiki/Dicumarol" class="mw-redirect" title="Dicumarol">dicumarol</a>. These drugs create a deficiency of reduced vitamin K by blocking VKORC, thereby inhibiting maturation of clotting factors. Vitamin K deficiency from other causes (e.g., in <a href="/wiki/Malabsorption" title="Malabsorption">malabsorption</a>) or impaired vitamin K metabolism in disease (e.g., in <a href="/wiki/Liver_failure" title="Liver failure">liver failure</a>) lead to the formation of PIVKAs (proteins formed in vitamin K absence), which are partially or totally non-gamma carboxylated, affecting the coagulation factors' ability to bind to phospholipid.<sup id="cite_ref-Paulus_44-0" class="reference"><a href="#cite_note-Paulus-44"><span class="cite-bracket">[</span>44<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Regulators">Regulators</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=15" title="Edit section: Regulators"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <figure class="mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:Coagulation_full.svg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Coagulation_full.svg/400px-Coagulation_full.svg.png" decoding="async" width="400" height="320" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Coagulation_full.svg/600px-Coagulation_full.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Coagulation_full.svg/800px-Coagulation_full.svg.png 2x" data-file-width="1000" data-file-height="800" /></a><figcaption>Coagulation with arrows for negative and positive feedback.</figcaption></figure> <p>Several mechanisms keep platelet activation and the coagulation cascade in check.<sup id="cite_ref-Dicks24_45-0" class="reference"><a href="#cite_note-Dicks24-45"><span class="cite-bracket">[</span>45<span class="cite-bracket">]</span></a></sup> Abnormalities can lead to an increased tendency toward thrombosis: </p> <div class="mw-heading mw-heading4"><h4 id="Protein_C_and_Protein_S">Protein C and Protein S</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=16" title="Edit section: Protein C and Protein S"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Protein_C" title="Protein C">Protein C</a> is a major physiological anticoagulant. It is a vitamin K-dependent <a href="/wiki/Serine_protease" title="Serine protease">serine protease enzyme</a> that is activated by thrombin into activated protein C (APC). Protein C is activated in a sequence that starts with Protein C and thrombin binding to a cell surface protein <a href="/wiki/Thrombomodulin" title="Thrombomodulin">thrombomodulin</a>. Thrombomodulin binds these proteins in such a way that it activates Protein C. The activated form, along with <a href="/wiki/Protein_S" title="Protein S">protein S</a> and a phospholipid as cofactors, degrades FVa and FVIIIa. Quantitative or qualitative deficiency of either (protein C or protein S) may lead to <a href="/wiki/Thrombophilia" title="Thrombophilia">thrombophilia</a> (a tendency to develop thrombosis). Impaired action of Protein C (activated Protein C resistance), for example by <a href="/wiki/Factor_V_Leiden" title="Factor V Leiden">having the "Leiden" variant of Factor V</a> or high levels of FVIII, also may lead to a thrombotic tendency.<sup id="cite_ref-Dicks24_45-1" class="reference"><a href="#cite_note-Dicks24-45"><span class="cite-bracket">[</span>45<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Antithrombin">Antithrombin</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=17" title="Edit section: Antithrombin"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Antithrombin" title="Antithrombin">Antithrombin</a> is a <a href="/wiki/Serine_protease_inhibitor" class="mw-redirect" title="Serine protease inhibitor">serine protease inhibitor</a> (<a href="/wiki/Serpin" title="Serpin">serpin</a>) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa. It is constantly active, but its adhesion to these factors is increased by the presence of <a href="/wiki/Heparan_sulfate" title="Heparan sulfate">heparan sulfate</a> (a <a href="/wiki/Glycosaminoglycan" title="Glycosaminoglycan">glycosaminoglycan</a>) or the administration of <a href="/wiki/Heparin" title="Heparin">heparins</a> (different heparinoids increase affinity to FXa, thrombin, or both). Quantitative or qualitative deficiency of antithrombin (inborn or acquired, e.g., in <a href="/wiki/Proteinuria" title="Proteinuria">proteinuria</a>) leads to thrombophilia.<sup id="cite_ref-Dicks24_45-2" class="reference"><a href="#cite_note-Dicks24-45"><span class="cite-bracket">[</span>45<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Tissue_factor_pathway_inhibitor_(TFPI)"><span id="Tissue_factor_pathway_inhibitor_.28TFPI.29"></span>Tissue factor pathway inhibitor (TFPI)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=18" title="Edit section: Tissue factor pathway inhibitor (TFPI)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Tissue_factor_pathway_inhibitor" title="Tissue factor pathway inhibitor">Tissue factor pathway inhibitor</a> (TFPI) limits the action of tissue factor (TF). It also inhibits excessive TF-mediated activation of FVII and FX.<sup id="cite_ref-46" class="reference"><a href="#cite_note-46"><span class="cite-bracket">[</span>46<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Plasmin">Plasmin</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=19" title="Edit section: Plasmin"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Plasmin" title="Plasmin">Plasmin</a> is generated by proteolytic cleavage of plasminogen, a plasma protein synthesized in the liver. This cleavage is catalyzed by <a href="/wiki/Tissue_plasminogen_activator" class="mw-redirect" title="Tissue plasminogen activator">tissue plasminogen activator</a> (t-PA), which is synthesized and secreted by endothelium. Plasmin proteolytically cleaves fibrin into fibrin degradation products that inhibit excessive fibrin formation.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (June 2022)">citation needed</span></a></i>]</sup> </p> <div class="mw-heading mw-heading4"><h4 id="Prostacyclin">Prostacyclin</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=20" title="Edit section: Prostacyclin"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Prostacyclin" title="Prostacyclin">Prostacyclin</a> (PGI<sub>2</sub>) is released by endothelium and activates platelet G<sub>s</sub> protein-linked receptors. This, in turn, activates <a href="/wiki/Adenylyl_cyclase" title="Adenylyl cyclase">adenylyl cyclase</a>, which synthesizes cAMP. cAMP inhibits platelet activation by decreasing cytosolic levels of calcium and, by doing so, inhibits the release of granules that would lead to activation of additional platelets and the coagulation cascade.<sup id="cite_ref-Hoffbrand_37-1" class="reference"><a href="#cite_note-Hoffbrand-37"><span class="cite-bracket">[</span>37<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="Medical_assessment">Medical assessment</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=21" title="Edit section: Medical assessment"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Numerous medical tests are used to assess the function of the coagulation system:<sup id="cite_ref-medline2024_3-1" class="reference"><a href="#cite_note-medline2024-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Lillicrap_47-0" class="reference"><a href="#cite_note-Lillicrap-47"><span class="cite-bracket">[</span>47<span class="cite-bracket">]</span></a></sup> </p> <ul><li>Common: <a href="/wiki/Partial_thromboplastin_time" title="Partial thromboplastin time">aPTT</a>, <a href="/wiki/Prothrombin_time" title="Prothrombin time">PT</a> (also used to determine <a href="/wiki/International_normalized_ratio" class="mw-redirect" title="International normalized ratio">INR</a>), <a href="/wiki/Fibrinogen" title="Fibrinogen">fibrinogen</a> testing (often by the <i>Clauss fibrinogen assay</i>),<sup id="cite_ref-Stang_48-0" class="reference"><a href="#cite_note-Stang-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> <a href="/wiki/Platelet" title="Platelet">platelet</a> count, platelet function testing (often by <a href="/wiki/PFA-100" title="PFA-100">PFA-100</a>), <a href="/wiki/Thrombodynamics_test" title="Thrombodynamics test">thrombodynamics test</a>.</li> <li>Other: <a href="/wiki/Thrombin_clotting_time" class="mw-redirect" title="Thrombin clotting time">TCT</a>, <a href="/wiki/Bleeding_time" title="Bleeding time">bleeding time</a>, <a href="/wiki/Mixing_test" class="mw-redirect" title="Mixing test">mixing test</a> (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), coagulation factor assays, <a href="/wiki/Antiphospholipid_antibody" class="mw-redirect" title="Antiphospholipid antibody">antiphospholipid antibodies</a>, <a href="/wiki/D-dimer" title="D-dimer">D-dimer</a>, genetic tests (e.g. <a href="/wiki/Factor_V_Leiden" title="Factor V Leiden">factor V Leiden</a>, <a href="/wiki/Prothrombin" class="mw-redirect" title="Prothrombin">prothrombin</a> mutation G20210A), <a href="/wiki/Dilute_Russell%27s_viper_venom_time" title="Dilute Russell's viper venom time">dilute Russell's viper venom time</a> (dRVVT), miscellaneous platelet function tests, <a href="/wiki/Thromboelastography" title="Thromboelastography">thromboelastography</a> (TEG or Sonoclot), <a href="/wiki/Euglobulin_lysis_time" title="Euglobulin lysis time">euglobulin lysis time</a> (ELT).</li></ul> <p>The contact activation (intrinsic) pathway is initiated by activation of the <a href="/wiki/Contact_activation_system" title="Contact activation system">contact activation system</a>, and can be measured by the <a href="/wiki/Partial_thromboplastin_time" title="Partial thromboplastin time">activated partial thromboplastin</a> time (aPTT) test.<sup id="cite_ref-49" class="reference"><a href="#cite_note-49"><span class="cite-bracket">[</span>49<span class="cite-bracket">]</span></a></sup> </p><p>The tissue factor (extrinsic) pathway is initiated by release of <a href="/wiki/Tissue_factor" title="Tissue factor">tissue factor</a> (a specific cellular lipoprotein), and can be measured by the <a href="/wiki/Prothrombin_time" title="Prothrombin time">prothrombin time</a> (PT) test.<sup id="cite_ref-medline_50-0" class="reference"><a href="#cite_note-medline-50"><span class="cite-bracket">[</span>50<span class="cite-bracket">]</span></a></sup> PT results are often reported as ratio (<a href="/wiki/International_normalized_ratio" class="mw-redirect" title="International normalized ratio">INR</a> value) to monitor dosing of oral anticoagulants such as <a href="/wiki/Warfarin" title="Warfarin">warfarin</a>.<sup id="cite_ref-51" class="reference"><a href="#cite_note-51"><span class="cite-bracket">[</span>51<span class="cite-bracket">]</span></a></sup> </p><p>The quantitative and qualitative screening of fibrinogen is measured by the <a href="/wiki/Thrombin_clotting_time" class="mw-redirect" title="Thrombin clotting time">thrombin clotting time</a> (TCT). Measurement of the exact amount of fibrinogen present in the blood is generally done using the <i>Clauss fibrinogen assay</i>.<sup id="cite_ref-Stang_48-1" class="reference"><a href="#cite_note-Stang-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> Many analysers are capable of measuring a "derived fibrinogen" level from the graph of the Prothrombin time clot. </p><p>If a coagulation factor is part of the contact activation or tissue factor pathway, a deficiency of that factor will affect only one of the tests: Thus <a href="/wiki/Hemophilia_A" class="mw-redirect" title="Hemophilia A">hemophilia A</a>, a deficiency of factor VIII, which is part of the contact activation pathway, results in an abnormally prolonged aPTT test but a normal PT test. Deficiencies of common pathway factors prothrombin, fibrinogen, FX, and FV will prolong both aPTT and PT. If an abnormal PT or aPTT is present, additional testing will occur to determine which (if any) factor is present as aberrant concentrations. </p><p>Deficiencies of fibrinogen (quantitative or qualitative) will prolong PT, aPTT, thrombin time, and <a href="/wiki/Reptilase_time" title="Reptilase time">reptilase time</a>. </p> <div class="mw-heading mw-heading2"><h2 id="Role_in_disease">Role in disease</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=22" title="Edit section: Role in disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Coagulation defects may cause hemorrhage or thrombosis, and occasionally both, depending on the nature of the defect.<sup id="cite_ref-isbn1-4051-8050-1_52-0" class="reference"><a href="#cite_note-isbn1-4051-8050-1-52"><span class="cite-bracket">[</span>52<span class="cite-bracket">]</span></a></sup> </p> <figure class="mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:Gp1brec3.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/9/9b/Gp1brec3.png/160px-Gp1brec3.png" decoding="async" width="160" height="358" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/9/9b/Gp1brec3.png/240px-Gp1brec3.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/9/9b/Gp1brec3.png/320px-Gp1brec3.png 2x" data-file-width="966" data-file-height="2160" /></a><figcaption>The GP1b-IX receptor complex. This protein receptor complex is found on the surface of platelets, and in conjunction with <a href="/wiki/GP5_(gene)" title="GP5 (gene)">GPV</a> allows for platelets to adhere to the site of injury. Mutations in the genes associated with the glycoprotein Ib-IX-V complex are characteristic of <a href="/wiki/Bernard%E2%80%93Soulier_syndrome" title="Bernard–Soulier syndrome">Bernard–Soulier syndrome</a>.</figcaption></figure> <div class="mw-heading mw-heading3"><h3 id="Platelet_disorders">Platelet disorders</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=23" title="Edit section: Platelet disorders"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Platelet disorders are either congenital or acquired. Examples of congenital platelet disorders are <a href="/wiki/Glanzmann%27s_thrombasthenia" title="Glanzmann's thrombasthenia">Glanzmann's thrombasthenia</a>, <a href="/wiki/Bernard%E2%80%93Soulier_syndrome" title="Bernard–Soulier syndrome">Bernard–Soulier syndrome</a> (abnormal <a href="/wiki/Glycoprotein_Ib-IX-V_Receptor_Complex" class="mw-redirect" title="Glycoprotein Ib-IX-V Receptor Complex">glycoprotein Ib-IX-V complex</a>), <a href="/wiki/Gray_platelet_syndrome" title="Gray platelet syndrome">gray platelet syndrome</a> (deficient <a href="/wiki/Alpha_granules" class="mw-redirect" title="Alpha granules">alpha granules</a>), and <a href="/wiki/Delta_storage_pool_deficiency" class="mw-redirect" title="Delta storage pool deficiency">delta storage pool deficiency</a> (deficient <a href="/wiki/Dense_granules" class="mw-redirect" title="Dense granules">dense granules</a>). Most are rare. They predispose to hemorrhage. <a href="/wiki/Von_Willebrand_disease" title="Von Willebrand disease">Von Willebrand disease</a> is due to deficiency or abnormal function of <a href="/wiki/Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor</a>, and leads to a similar bleeding pattern; its milder forms are relatively common.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (November 2021)">citation needed</span></a></i>]</sup> </p><p>Decreased platelet numbers (thrombocytopenia) is due to insufficient production (e.g., <a href="/wiki/Myelodysplastic_syndrome" title="Myelodysplastic syndrome">myelodysplastic syndrome</a> or other bone marrow disorders), destruction by the immune system (<a href="/wiki/Immune_thrombocytopenic_purpura" title="Immune thrombocytopenic purpura">immune thrombocytopenic purpura</a>), or consumption (e.g., <a href="/wiki/Thrombotic_thrombocytopenic_purpura" title="Thrombotic thrombocytopenic purpura">thrombotic thrombocytopenic purpura</a>, <a href="/wiki/Hemolytic-uremic_syndrome" class="mw-redirect" title="Hemolytic-uremic syndrome">hemolytic-uremic syndrome</a>, <a href="/wiki/Paroxysmal_nocturnal_hemoglobinuria" title="Paroxysmal nocturnal hemoglobinuria">paroxysmal nocturnal hemoglobinuria</a>, <a href="/wiki/Disseminated_intravascular_coagulation" title="Disseminated intravascular coagulation">disseminated intravascular coagulation</a>, <a href="/wiki/Heparin-induced_thrombocytopenia" title="Heparin-induced thrombocytopenia">heparin-induced thrombocytopenia</a>).<sup id="cite_ref-53" class="reference"><a href="#cite_note-53"><span class="cite-bracket">[</span>53<span class="cite-bracket">]</span></a></sup> An increase in platelet count is called <a href="/wiki/Thrombocytosis" class="mw-redirect" title="Thrombocytosis">thrombocytosis</a>, which may lead to formation of <a href="/wiki/Thrombosis" title="Thrombosis">thromboembolisms</a>; however, thrombocytosis may be associated with increased risk of either thrombosis or hemorrhage in patients with <a href="/wiki/Myeloproliferative_neoplasm" title="Myeloproliferative neoplasm">myeloproliferative neoplasm</a>.<sup id="cite_ref-54" class="reference"><a href="#cite_note-54"><span class="cite-bracket">[</span>54<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Coagulation_factor_disorders">Coagulation factor disorders</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=24" title="Edit section: Coagulation factor disorders"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The best-known coagulation factor disorders are the <a href="/wiki/Hemophilia" class="mw-redirect" title="Hemophilia">hemophilias</a>. The three main forms are <a href="/wiki/Hemophilia_A" class="mw-redirect" title="Hemophilia A">hemophilia A</a> (factor VIII deficiency), <a href="/wiki/Hemophilia_B" class="mw-redirect" title="Hemophilia B">hemophilia B</a> (factor IX deficiency or "Christmas disease") and <a href="/wiki/Hemophilia_C" class="mw-redirect" title="Hemophilia C">hemophilia C</a> (factor XI deficiency, mild bleeding tendency).<sup id="cite_ref-55" class="reference"><a href="#cite_note-55"><span class="cite-bracket">[</span>55<span class="cite-bracket">]</span></a></sup> </p><p><a href="/wiki/Von_Willebrand_disease" title="Von Willebrand disease">Von Willebrand disease</a> (which behaves more like a platelet disorder except in severe cases), is the most common hereditary bleeding disorder and is characterized as being inherited autosomal recessive or dominant. In this disease, there is a defect in von Willebrand factor (vWF), which mediates the binding of glycoprotein Ib (GPIb) to collagen. This binding helps mediate the activation of platelets and formation of primary hemostasis.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Identifying_reliable_sources_(medicine)" title="Wikipedia:Identifying reliable sources (medicine)"><span title="Material near this tag needs references to reliable medical sources. (August 2020)">medical citation needed</span></a></i>]</sup> </p><p>In acute or chronic <a href="/wiki/Liver_failure" title="Liver failure">liver failure</a>, there is insufficient production of coagulation factors, possibly increasing risk of bleeding during surgery.<sup id="cite_ref-56" class="reference"><a href="#cite_note-56"><span class="cite-bracket">[</span>56<span class="cite-bracket">]</span></a></sup> </p><p><a href="/wiki/Thrombosis" title="Thrombosis">Thrombosis</a> is the pathological development of blood clots. These clots may break free and become mobile, forming an <a href="/wiki/Embolism" title="Embolism">embolus</a> or grow to such a size that occludes the vessel in which it developed. An <a href="/wiki/Embolism" title="Embolism">embolism</a> is said to occur when the <a href="/wiki/Thrombus" title="Thrombus">thrombus</a> (blood clot) becomes a mobile embolus and migrates to another part of the body, interfering with blood circulation and hence impairing organ function downstream of the occlusion. This causes <a href="/wiki/Ischemia" title="Ischemia">ischemia</a> and often leads to ischemic <a href="/wiki/Necrosis" title="Necrosis">necrosis</a> of tissue. Most cases of <a href="/wiki/Venous_thrombosis" title="Venous thrombosis">venous thrombosis</a> are due to acquired states (older age, surgery, cancer, immobility). Unprovoked venous thrombosis may be related to inherited <a href="/wiki/Thrombophilia" title="Thrombophilia">thrombophilias</a> (e.g., <a href="/wiki/Factor_V_Leiden" title="Factor V Leiden">factor V Leiden</a>, antithrombin deficiency, and various other genetic deficiencies or variants), particularly in younger patients with family history of thrombosis; however, thrombotic events are more likely when acquired risk factors are superimposed on the inherited state.<sup id="cite_ref-57" class="reference"><a href="#cite_note-57"><span class="cite-bracket">[</span>57<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="Pharmacology">Pharmacology</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=25" title="Edit section: Pharmacology"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <div class="mw-heading mw-heading3"><h3 id="Procoagulants">Procoagulants</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=26" title="Edit section: Procoagulants"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><span class="anchor" id="Procoagulants"></span> </p> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">"Coagulant (drug)" redirects here. For other uses, see <a href="/w/index.php?title=Coagulant_(drug)_(disambiguation)&action=edit&redlink=1" class="new" title="Coagulant (drug) (disambiguation) (page does not exist)">Coagulant (drug) (disambiguation)</a>.</div> <p>The use of <a href="/wiki/Adsorption" title="Adsorption">adsorbent</a> chemicals, such as <a href="/wiki/Zeolite" title="Zeolite">zeolites</a>, and other <a href="/wiki/Hemostatic_agent" class="mw-redirect" title="Hemostatic agent">hemostatic agents</a> are also used for sealing severe injuries quickly (such as in traumatic bleeding secondary to gunshot wounds). Thrombin and fibrin <a href="/wiki/Glue" class="mw-redirect" title="Glue">glue</a> are used surgically to treat bleeding and to thrombose aneurysms. <a href="/wiki/Hemostatic_Powder_Spray_TC-325" title="Hemostatic Powder Spray TC-325">Hemostatic Powder Spray TC-325</a> is used to treated gastrointestinal bleeding.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (May 2023)">citation needed</span></a></i>]</sup> </p><p><a href="/wiki/Desmopressin" title="Desmopressin">Desmopressin</a> is used to improve platelet function by activating <a href="/wiki/Arginine_vasopressin_receptor_1A" class="mw-redirect" title="Arginine vasopressin receptor 1A">arginine vasopressin receptor 1A</a>.<sup id="cite_ref-58" class="reference"><a href="#cite_note-58"><span class="cite-bracket">[</span>58<span class="cite-bracket">]</span></a></sup> </p><p>Coagulation factor concentrates are used to treat <a href="/wiki/Hemophilia" class="mw-redirect" title="Hemophilia">hemophilia</a>, to reverse the effects of anticoagulants, and to treat bleeding in people with impaired coagulation factor synthesis or increased consumption. <a href="/wiki/Prothrombin_complex_concentrate" title="Prothrombin complex concentrate">Prothrombin complex concentrate</a>, <a href="/wiki/Cryoprecipitate" title="Cryoprecipitate">cryoprecipitate</a> and <a href="/wiki/Fresh_frozen_plasma" title="Fresh frozen plasma">fresh frozen plasma</a> are commonly used coagulation factor products. <a href="/wiki/Factor_VII" title="Factor VII">Recombinant activated human factor VII</a> is sometimes used in the treatment of major bleeding. </p><p><a href="/wiki/Tranexamic_acid" title="Tranexamic acid">Tranexamic acid</a> and <a href="/wiki/Aminocaproic_acid" title="Aminocaproic acid">aminocaproic acid</a> inhibit fibrinolysis and lead to a <i>de facto</i> reduced bleeding rate. Before its withdrawal, <a href="/wiki/Aprotinin" title="Aprotinin">aprotinin</a> was used in some forms of major surgery to decrease bleeding risk and the need for blood products. </p> <figure class="mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:FXa-rivaroxaban.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/a/a8/FXa-rivaroxaban.png/300px-FXa-rivaroxaban.png" decoding="async" width="300" height="203" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/a/a8/FXa-rivaroxaban.png/450px-FXa-rivaroxaban.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/a/a8/FXa-rivaroxaban.png/600px-FXa-rivaroxaban.png 2x" data-file-width="3000" data-file-height="2034" /></a><figcaption><a href="/wiki/Rivaroxaban" title="Rivaroxaban">Rivaroxaban</a> drug bound to the <a href="/wiki/Coagulation_factor_Xa" class="mw-redirect" title="Coagulation factor Xa">coagulation factor Xa</a>. The drug prevents this protein from activating the coagulation pathway by inhibiting its <a href="/wiki/Enzyme" title="Enzyme">enzymatic activity</a>.</figcaption></figure> <div class="mw-heading mw-heading3"><h3 id="Anticoagulants">Anticoagulants</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=27" title="Edit section: Anticoagulants"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main articles: <a href="/wiki/Antiplatelet_drug" title="Antiplatelet drug">Antiplatelet drug</a> and <a href="/wiki/Anticoagulant" title="Anticoagulant">Anticoagulant</a></div> <p>Anticoagulants and anti-platelet agents (together "antithrombotics") are amongst the most commonly used medications. <a href="/wiki/Antiplatelet_drug" title="Antiplatelet drug">Anti-platelet agents</a> include <a href="/wiki/Aspirin" title="Aspirin">aspirin</a>, <a href="/wiki/Dipyridamole" title="Dipyridamole">dipyridamole</a>, <a href="/wiki/Ticlopidine" title="Ticlopidine">ticlopidine</a>, <a href="/wiki/Clopidogrel" title="Clopidogrel">clopidogrel</a>, <a href="/wiki/Ticagrelor" title="Ticagrelor">ticagrelor</a> and <a href="/wiki/Prasugrel" title="Prasugrel">prasugrel</a>; the parenteral <a href="/wiki/Glycoprotein_IIb/IIIa_inhibitors" title="Glycoprotein IIb/IIIa inhibitors">glycoprotein IIb/IIIa inhibitors</a> are used during <a href="/wiki/Angioplasty" title="Angioplasty">angioplasty</a>. Of the anticoagulants, <a href="/wiki/Warfarin" title="Warfarin">warfarin</a> (and related <a href="/wiki/Coumarin" title="Coumarin">coumarins</a>) and <a href="/wiki/Heparin" title="Heparin">heparin</a> are the most commonly used. Warfarin affects the vitamin K-dependent clotting factors (II, VII, IX, X) and protein C and protein S, whereas heparin and related compounds increase the action of antithrombin on thrombin and factor Xa. A newer class of drugs, the <a href="/wiki/Direct_thrombin_inhibitor" title="Direct thrombin inhibitor">direct thrombin inhibitors</a>, is under development; some members are already in clinical use (such as <a href="/wiki/Lepirudin" title="Lepirudin">lepirudin</a>, <a href="/wiki/Argatroban" title="Argatroban">argatroban</a>, <a href="/wiki/Bivalirudin" title="Bivalirudin">bivalirudin</a> and <a href="/wiki/Dabigatran" title="Dabigatran">dabigatran</a>). Also in clinical use are other small molecular compounds that interfere directly with the enzymatic action of particular coagulation factors (the <a href="/wiki/Anticoagulant#Directly_acting_oral_anticoagulants" title="Anticoagulant">directly acting oral anticoagulants</a>: <a href="/wiki/Dabigatran" title="Dabigatran">dabigatran</a>, <a href="/wiki/Rivaroxaban" title="Rivaroxaban">rivaroxaban</a>, <a href="/wiki/Apixaban" title="Apixaban">apixaban</a>, and <a href="/wiki/Edoxaban" title="Edoxaban">edoxaban</a>).<sup id="cite_ref-pmid22345595_59-0" class="reference"><a href="#cite_note-pmid22345595-59"><span class="cite-bracket">[</span>59<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="History">History</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=28" title="Edit section: History"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <div class="mw-heading mw-heading3"><h3 id="Initial_discoveries">Initial discoveries</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=29" title="Edit section: Initial discoveries"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Theories on the coagulation of blood have existed since antiquity. Physiologist <a href="/wiki/Johannes_Peter_M%C3%BCller" title="Johannes Peter Müller">Johannes Müller</a> (1801–1858) described fibrin, the substance of a <a href="/wiki/Thrombus" title="Thrombus">thrombus</a>. Its soluble precursor, <a href="/wiki/Fibrinogen" title="Fibrinogen">fibrinogen</a>, was thus named by <a href="/wiki/Rudolf_Virchow" title="Rudolf Virchow">Rudolf Virchow</a> (1821–1902), and isolated chemically by <a href="/w/index.php?title=Prosper_Sylvain_Denis&action=edit&redlink=1" class="new" title="Prosper Sylvain Denis (page does not exist)">Prosper Sylvain Denis</a> (1799–1863). <a href="/wiki/Alexander_Schmidt_(physiologist)" title="Alexander Schmidt (physiologist)">Alexander Schmidt</a> suggested that the conversion from fibrinogen to fibrin is the result of an <a href="/wiki/Enzyme" title="Enzyme">enzymatic</a> process, and labeled the hypothetical enzyme "<a href="/wiki/Thrombin" title="Thrombin">thrombin</a>" and its precursor "<a href="/wiki/Prothrombin" class="mw-redirect" title="Prothrombin">prothrombin</a>".<sup id="cite_ref-60" class="reference"><a href="#cite_note-60"><span class="cite-bracket">[</span>60<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-61" class="reference"><a href="#cite_note-61"><span class="cite-bracket">[</span>61<span class="cite-bracket">]</span></a></sup> <a href="/wiki/Nicolas_Maurice_Arthus" title="Nicolas Maurice Arthus">Arthus</a> discovered in 1890 that calcium was essential in coagulation.<sup id="cite_ref-62" class="reference"><a href="#cite_note-62"><span class="cite-bracket">[</span>62<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Shapiro_63-0" class="reference"><a href="#cite_note-Shapiro-63"><span class="cite-bracket">[</span>63<span class="cite-bracket">]</span></a></sup> <a href="/wiki/Platelet" title="Platelet">Platelets</a> were identified in 1865, and their function was elucidated by <a href="/wiki/Giulio_Bizzozero" title="Giulio Bizzozero">Giulio Bizzozero</a> in 1882.<sup id="cite_ref-Brewer_64-0" class="reference"><a href="#cite_note-Brewer-64"><span class="cite-bracket">[</span>64<span class="cite-bracket">]</span></a></sup> </p><p>The theory that thrombin is generated by the presence of <a href="/wiki/Tissue_factor" title="Tissue factor">tissue factor</a> was consolidated by <a href="/wiki/Paul_Morawitz" title="Paul Morawitz">Paul Morawitz</a> in 1905.<sup id="cite_ref-65" class="reference"><a href="#cite_note-65"><span class="cite-bracket">[</span>65<span class="cite-bracket">]</span></a></sup> At this stage, it was known that <i>thrombokinase/thromboplastin</i> (factor III) is released by damaged tissues, reacting with <i>prothrombin</i> (II), which, together with <a href="/wiki/Calcium_in_biology" title="Calcium in biology">calcium</a> (IV), forms <i>thrombin</i>, which converts fibrinogen into <i>fibrin</i> (I).<sup id="cite_ref-Giangrande_66-0" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Coagulation_factors">Coagulation factors</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=30" title="Edit section: Coagulation factors"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The remainder of the biochemical factors in the process of coagulation were largely discovered in the 20th century.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (September 2022)">citation needed</span></a></i>]</sup> </p><p>A first clue as to the actual complexity of the system of coagulation was the discovery of <i>proaccelerin</i> (initially and later called Factor V) by <a href="/w/index.php?title=Paul_Owren&action=edit&redlink=1" class="new" title="Paul Owren (page does not exist)">Paul Owren</a><span class="noprint" style="font-size:85%; font-style: normal;"> [<a href="https://no.wikipedia.org/wiki/Paul_Owren" class="extiw" title="no:Paul Owren">no</a>]</span> (1905–1990) in 1947. He also postulated its function to be the generation of accelerin (Factor VI), which later turned out to be the activated form of V (or Va); hence, VI is not now in active use.<sup id="cite_ref-Giangrande_66-1" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>Factor VII (also known as <i>serum prothrombin conversion accelerator</i> or <i>proconvertin</i>, precipitated by barium sulfate) was discovered in a young female patient in 1949 and 1951 by different groups. </p><p><a href="/wiki/Factor_VIII" title="Factor VIII">Factor VIII</a> turned out to be deficient in the clinically recognized but etiologically elusive <a href="/wiki/Haemophilia_A" title="Haemophilia A">hemophilia A</a>; it was identified in the 1950s and is alternatively called <i>antihemophilic globulin</i> due to its capability to correct hemophilia A.<sup id="cite_ref-Giangrande_66-2" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>Factor IX was discovered in 1952 in a young patient with <a href="/wiki/Haemophilia_B" title="Haemophilia B">hemophilia B</a> named <a href="/wiki/Stephen_Christmas" class="mw-redirect" title="Stephen Christmas">Stephen Christmas</a> (1947–1993). His deficiency was described by Dr. Rosemary Biggs and Professor <a href="/wiki/R.G._MacFarlane" class="mw-redirect" title="R.G. MacFarlane">R.G. MacFarlane</a> in Oxford, UK. The factor is, hence, called Christmas Factor. Christmas lived in Canada and campaigned for blood transfusion safety until succumbing to transfusion-related <a href="/wiki/AIDS" class="mw-redirect" title="AIDS">AIDS</a> at age 46. An alternative name for the factor is <i>plasma thromboplastin component</i>, given by an independent group in California.<sup id="cite_ref-Giangrande_66-3" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>Hageman factor, now known as factor XII, was identified in 1955 in an asymptomatic patient with a prolonged bleeding time named of John Hageman. Factor X, or Stuart-Prower factor, followed, in 1956. This protein was identified in a Ms. Audrey Prower of London, who had a lifelong bleeding tendency. In 1957, an American group identified the same factor in a Mr. Rufus Stuart. Factors XI and XIII were identified in 1953 and 1961, respectively.<sup id="cite_ref-Giangrande_66-4" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>The view that the coagulation process is a "cascade" or "waterfall" was enunciated almost simultaneously by MacFarlane<sup id="cite_ref-pmid14167839_67-0" class="reference"><a href="#cite_note-pmid14167839-67"><span class="cite-bracket">[</span>67<span class="cite-bracket">]</span></a></sup> in the UK and by Davie and Ratnoff<sup id="cite_ref-pmid14173416_68-0" class="reference"><a href="#cite_note-pmid14173416-68"><span class="cite-bracket">[</span>68<span class="cite-bracket">]</span></a></sup> in the US, respectively. </p> <div class="mw-heading mw-heading3"><h3 id="Nomenclature">Nomenclature</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=31" title="Edit section: Nomenclature"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The usage of <a href="/wiki/Roman_numeral" class="mw-redirect" title="Roman numeral">Roman numerals</a> rather than eponyms or systematic names was agreed upon during annual conferences (starting in 1955) of hemostasis experts. In 1962, consensus was achieved on the numbering of factors I–XII.<sup id="cite_ref-69" class="reference"><a href="#cite_note-69"><span class="cite-bracket">[</span>69<span class="cite-bracket">]</span></a></sup> This committee evolved into the present-day International Committee on Thrombosis and Hemostasis (ICTH). Assignment of numerals ceased in 1963 after the naming of Factor XIII. The names Fletcher Factor and Fitzgerald Factor were given to further coagulation-related proteins, namely <a href="/wiki/Prekallikrein" title="Prekallikrein">prekallikrein</a> and <a href="/wiki/High-molecular-weight_kininogen" title="High-molecular-weight kininogen">high-molecular-weight kininogen</a>, respectively.<sup id="cite_ref-Giangrande_66-5" class="reference"><a href="#cite_note-Giangrande-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>Factor VI<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (December 2018)">citation needed</span></a></i>]</sup> is unassigned, as accelerin was found to be activated Factor V. </p> <div class="mw-heading mw-heading2"><h2 id="Other_species">Other species</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=32" title="Edit section: Other species"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>All mammals have an extremely closely related blood coagulation process, using a combined cellular and serine protease process.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (October 2012)">citation needed</span></a></i>]</sup> It is possible for any mammalian coagulation factor to "cleave" its equivalent target in any other mammal.<sup class="noprint Inline-Template Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed"><span title="This claim needs references to reliable sources. (October 2012)">citation needed</span></a></i>]</sup> The only non-mammalian animal known to use serine proteases for blood coagulation is the <a href="/wiki/Horseshoe_crab" title="Horseshoe crab">horseshoe crab</a>.<sup id="cite_ref-pmid15170505_70-0" class="reference"><a href="#cite_note-pmid15170505-70"><span class="cite-bracket">[</span>70<span class="cite-bracket">]</span></a></sup> Exemplifying the close links between coagulation and inflammation, the horseshoe crab has a primitive response to injury, carried out by cells known as amoebocytes (or <a href="/wiki/Hemocyte_(invertebrate_immune_system_cell)" title="Hemocyte (invertebrate immune system cell)">hemocytes</a>) which serve both hemostatic and immune functions.<sup id="cite_ref-Yong23_40-1" class="reference"><a href="#cite_note-Yong23-40"><span class="cite-bracket">[</span>40<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Iwanaga_71-0" class="reference"><a href="#cite_note-Iwanaga-71"><span class="cite-bracket">[</span>71<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="See_also">See also</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=33" title="Edit section: See also"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <style data-mw-deduplicate="TemplateStyles:r1266661725">.mw-parser-output .portalbox{padding:0;margin:0.5em 0;display:table;box-sizing:border-box;max-width:175px;list-style:none}.mw-parser-output .portalborder{border:1px solid var(--border-color-base,#a2a9b1);padding:0.1em;background:var(--background-color-neutral-subtle,#f8f9fa)}.mw-parser-output .portalbox-entry{display:table-row;font-size:85%;line-height:110%;height:1.9em;font-style:italic;font-weight:bold}.mw-parser-output .portalbox-image{display:table-cell;padding:0.2em;vertical-align:middle;text-align:center}.mw-parser-output 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portal</a></span></li></ul> <ul><li><a href="/wiki/Agglutination_(biology)" title="Agglutination (biology)">Agglutination (biology)</a></li> <li><a href="/wiki/Antihemorrhagic" title="Antihemorrhagic">Antihemorrhagic</a></li> <li><a href="/wiki/Post-vaccination_embolic_and_thrombotic_events" class="mw-redirect" title="Post-vaccination embolic and thrombotic events">Post-vaccination embolic and thrombotic events</a></li></ul> <div class="mw-heading mw-heading2"><h2 id="References">References</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=34" title="Edit section: References"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <style data-mw-deduplicate="TemplateStyles:r1239543626">.mw-parser-output .reflist{margin-bottom:0.5em;list-style-type:decimal}@media screen{.mw-parser-output .reflist{font-size:90%}}.mw-parser-output .reflist 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data-mw-deduplicate="TemplateStyles:r1238218222">.mw-parser-output cite.citation{font-style:inherit;word-wrap:break-word}.mw-parser-output .citation q{quotes:"\"""\"""'""'"}.mw-parser-output .citation:target{background-color:rgba(0,127,255,0.133)}.mw-parser-output .id-lock-free.id-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/6/65/Lock-green.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-limited.id-lock-limited a,.mw-parser-output .id-lock-registration.id-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/d/d6/Lock-gray-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-subscription.id-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/a/aa/Lock-red-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .cs1-ws-icon a{background:url("//upload.wikimedia.org/wikipedia/commons/4/4c/Wikisource-logo.svg")right 0.1em center/12px 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.cs1-format{font-size:95%}html.skin-theme-clientpref-night .mw-parser-output .cs1-maint{color:#18911f}}@media screen and (prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .cs1-maint{color:#18911f}}</style><cite id="CITEREFFurieFurie2005" class="citation journal cs1">Furie, Barbara C.; Furie, Bruce (December 2005). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297262">"Thrombus formation in vivo"</a>. <i>The Journal of Clinical Investigation</i>. <b>115</b> (12): <span class="nowrap">3355–</span>62. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1172%2FJCI26987">10.1172/JCI26987</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="id-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" 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class="noprint Inline-Template" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:Citing_sources" title="Wikipedia:Citing sources"><span title="This citation requires a reference to the specific page or range of pages in which the material appears. (September 2024)">page needed</span></a></i>]</sup></span> </li> <li id="cite_note-medline2024-3"><span class="mw-cite-backlink">^ <a href="#cite_ref-medline2024_3-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-medline2024_3-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite class="citation web cs1"><a rel="nofollow" class="external text" href="https://medlineplus.gov/lab-tests/coagulation-factor-tests/">"Coagulation Factor Tests"</a>. <i>MedlinePlus Medical Test</i><span class="reference-accessdate">. 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Wiley-Blackwell. pp. <span class="nowrap">1–</span>5. <a href="/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/wiki/Special:BookSources/978-1-4051-8460-1" title="Special:BookSources/978-1-4051-8460-1"><bdi>978-1-4051-8460-1</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Practical+Hemostasis+and+Thrombosis&rft.pages=%3Cspan+class%3D%22nowrap%22%3E1-%3C%2Fspan%3E5&rft.pub=Wiley-Blackwell&rft.date=2009&rft.isbn=978-1-4051-8460-1&rft.aulast=Lillicrap&rft.aufirst=D.&rft.au=Key%2C+Nigel&rft.au=Makris%2C+Michael&rft.au=Denise%2C+O%27Shaughnessy&rft_id=https%3A%2F%2Farchive.org%2Fdetails%2Fpracticalhemosta00keyn&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-Openstax_Anatomy_&_Physiology_attribution-6"><span class="mw-cite-backlink"><b><a href="#cite_ref-Openstax_Anatomy_&_Physiology_attribution_6-0">^</a></b></span> <span class="reference-text"><i><span typeof="mw:File"><a href="//creativecommons.org/licenses/by/4.0/" title="creativecommons:by/4.0/"><img alt="" src="//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Creative_Commons_by_small.svg/80px-Creative_Commons_by_small.svg.png" decoding="async" width="80" height="15" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Creative_Commons_by_small.svg/120px-Creative_Commons_by_small.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/6/65/Creative_Commons_by_small.svg/160px-Creative_Commons_by_small.svg.png 2x" data-file-width="80" data-file-height="15" /></a></span> This article incorporates <a rel="nofollow" class="external text" href="https://openstax.org/books/anatomy-and-physiology/pages/18-5-hemostasis">text</a> available under the <a href="//creativecommons.org/licenses/by/4.0/" class="extiw" title="creativecommons:by/4.0/">CC BY 4.0</a> license.</i> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFBettsDesaixJohnsonJohnson2023" class="citation book cs1">Betts, J Gordon; Desaix, Peter; Johnson, Eddie; Johnson, Jody E; Korol, Oksana; Kruse, Dean; Poe, Brandon; Wise, James; Womble, Mark D; Young, Kelly A (28 July 2023). <a rel="nofollow" class="external text" href="https://openstax.org/books/anatomy-and-physiology/pages/18-5-hemostasis">"§18.5 Homeostasis"</a>. <i>Anatomy & Physiology</i>. Houston: OpenStax CNX. <a href="/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/wiki/Special:BookSources/978-1-947172-04-3" title="Special:BookSources/978-1-947172-04-3"><bdi>978-1-947172-04-3</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=bookitem&rft.atitle=%C2%A718.5+Homeostasis&rft.btitle=Anatomy+%26+Physiology&rft.place=Houston&rft.pub=OpenStax+CNX&rft.date=2023-07-28&rft.isbn=978-1-947172-04-3&rft.aulast=Betts&rft.aufirst=J+Gordon&rft.au=Desaix%2C+Peter&rft.au=Johnson%2C+Eddie&rft.au=Johnson%2C+Jody+E&rft.au=Korol%2C+Oksana&rft.au=Kruse%2C+Dean&rft.au=Poe%2C+Brandon&rft.au=Wise%2C+James&rft.au=Womble%2C+Mark+D&rft.au=Young%2C+Kelly+A&rft_id=https%3A%2F%2Fopenstax.org%2Fbooks%2Fanatomy-and-physiology%2Fpages%2F18-5-hemostasis&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-GHR2018-7"><span class="mw-cite-backlink"><b><a href="#cite_ref-GHR2018_7-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite class="citation web cs1"><a rel="nofollow" class="external text" href="https://medlineplus.gov/genetics/condition/prothrombin-thrombophilia/">"Prothrombin thrombophilia"</a>. <i>MedlinePlus</i>. <a rel="nofollow" class="external text" href="https://web.archive.org/web/20230912225514/https://medlineplus.gov/genetics/condition/prothrombin-thrombophilia/">Archived</a> from the original on 12 September 2023<span class="reference-accessdate">. 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Wiley-Blackwell. p. 2. <a href="/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/wiki/Special:BookSources/978-1-4051-8460-1" title="Special:BookSources/978-1-4051-8460-1"><bdi>978-1-4051-8460-1</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Practical+Hemostasis+and+Thrombosis&rft.pages=2&rft.pub=Wiley-Blackwell&rft.date=2009&rft.isbn=978-1-4051-8460-1&rft.au=Nigel+Key&rft.au=Michael+Makris&rft_id=https%3A%2F%2Farchive.org%2Fdetails%2Fpracticalhemosta00keyn&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-Pallister1b-26"><span class="mw-cite-backlink"><b><a href="#cite_ref-Pallister1b_26-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFWatsonPallister2010" class="citation book cs1">Watson, M. S.; Pallister, C. J. 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title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Waterfall+sequence+for+intrinsic+blood+clotting&rft.volume=145&rft.issue=3638&rft.pages=%3Cspan+class%3D%22nowrap%22%3E1310-%3C%2Fspan%3E2&rft.date=1964-09&rft_id=info%3Adoi%2F10.1126%2Fscience.145.3638.1310&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A34111840%23id-name%3DS2CID&rft_id=info%3Apmid%2F14173416&rft_id=info%3Abibcode%2F1964Sci...145.1310D&rft.aulast=Davie&rft.aufirst=EW&rft.au=Ratnoff%2C+OD&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-69"><span class="mw-cite-backlink"><b><a href="#cite_ref-69">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFWright1962" class="citation journal cs1">Wright IS (February 1962). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1848865">"The nomenclature of blood clotting factors"</a>. <i>Canadian Medical Association Journal</i>. <b>86</b> (8): <span class="nowrap">373–</span>4. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="id-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1848865">1848865</a></span>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/14008442">14008442</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Canadian+Medical+Association+Journal&rft.atitle=The+nomenclature+of+blood+clotting+factors&rft.volume=86&rft.issue=8&rft.pages=%3Cspan+class%3D%22nowrap%22%3E373-%3C%2Fspan%3E4&rft.date=1962-02&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1848865%23id-name%3DPMC&rft_id=info%3Apmid%2F14008442&rft.aulast=Wright&rft.aufirst=IS&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1848865&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-pmid15170505-70"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15170505_70-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFOsakiKawabata2004" class="citation journal cs1">Osaki T, Kawabata S (June 2004). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11138774">"Structure and function of coagulogen, a clottable protein in horseshoe crabs"</a>. <i>Cellular and Molecular Life Sciences</i>. <b>61</b> (11): <span class="nowrap">1257–</span>65. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1007%2Fs00018-004-3396-5">10.1007/s00018-004-3396-5</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="id-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11138774">11138774</a></span>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/15170505">15170505</a>. <a href="/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:24537601">24537601</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Cellular+and+Molecular+Life+Sciences&rft.atitle=Structure+and+function+of+coagulogen%2C+a+clottable+protein+in+horseshoe+crabs&rft.volume=61&rft.issue=11&rft.pages=%3Cspan+class%3D%22nowrap%22%3E1257-%3C%2Fspan%3E65&rft.date=2004-06&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC11138774%23id-name%3DPMC&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A24537601%23id-name%3DS2CID&rft_id=info%3Apmid%2F15170505&rft_id=info%3Adoi%2F10.1007%2Fs00018-004-3396-5&rft.aulast=Osaki&rft.aufirst=T&rft.au=Kawabata%2C+S&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC11138774&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> <li id="cite_note-Iwanaga-71"><span class="mw-cite-backlink"><b><a href="#cite_ref-Iwanaga_71-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFIwanaga2007" class="citation journal cs1">Iwanaga, S (May 2007). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756735">"Biochemical principle of Limulus test for detecting bacterial endotoxins"</a>. <i>Proceedings of the Japan Academy. Series B, Physical and Biological Sciences</i>. <b>83</b> (4): <span class="nowrap">110–</span>9. <a href="/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/2007PJAB...83..110I">2007PJAB...83..110I</a>. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.2183%2Fpjab.83.110">10.2183/pjab.83.110</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="id-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756735">3756735</a></span>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/24019589">24019589</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Proceedings+of+the+Japan+Academy.+Series+B%2C+Physical+and+Biological+Sciences&rft.atitle=Biochemical+principle+of+Limulus+test+for+detecting+bacterial+endotoxins.&rft.volume=83&rft.issue=4&rft.pages=%3Cspan+class%3D%22nowrap%22%3E110-%3C%2Fspan%3E9&rft.date=2007-05&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3756735%23id-name%3DPMC&rft_id=info%3Apmid%2F24019589&rft_id=info%3Adoi%2F10.2183%2Fpjab.83.110&rft_id=info%3Abibcode%2F2007PJAB...83..110I&rft.aulast=Iwanaga&rft.aufirst=S&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3756735&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></span> </li> </ol></div></div> <div class="mw-heading mw-heading2"><h2 id="Further_reading">Further reading</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=35" title="Edit section: Further reading"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <ul><li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFHoffmanMonroe2001" class="citation journal cs1">Hoffman, Maureane; Monroe, Dougald (2001). "A Cell-based Model of Hemostasis". <i>Thrombosis and Haemostasis</i>. <b>85</b> (6): <span class="nowrap">958–</span>965. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1055%2Fs-0037-1615947">10.1055/s-0037-1615947</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/11434702">11434702</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Thrombosis+and+Haemostasis&rft.atitle=A+Cell-based+Model+of+Hemostasis&rft.volume=85&rft.issue=6&rft.pages=%3Cspan+class%3D%22nowrap%22%3E958-%3C%2Fspan%3E965&rft.date=2001&rft_id=info%3Adoi%2F10.1055%2Fs-0037-1615947&rft_id=info%3Apmid%2F11434702&rft.aulast=Hoffman&rft.aufirst=Maureane&rft.au=Monroe%2C+Dougald&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFHoffmanMonroe2007" class="citation journal cs1">Hoffman M, Monroe DM (February 2007). "Coagulation 2006: a modern view of hemostasis". <i>Hematology/Oncology Clinics of North America</i>. <b>21</b> (1): <span class="nowrap">1–</span>11. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.hoc.2006.11.004">10.1016/j.hoc.2006.11.004</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/17258114">17258114</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Hematology%2FOncology+Clinics+of+North+America&rft.atitle=Coagulation+2006%3A+a+modern+view+of+hemostasis&rft.volume=21&rft.issue=1&rft.pages=%3Cspan+class%3D%22nowrap%22%3E1-%3C%2Fspan%3E11&rft.date=2007-02&rft_id=info%3Adoi%2F10.1016%2Fj.hoc.2006.11.004&rft_id=info%3Apmid%2F17258114&rft.aulast=Hoffman&rft.aufirst=M&rft.au=Monroe%2C+DM&rfr_id=info%3Asid%2Fen.wikipedia.org%3ACoagulation" class="Z3988"></span></li></ul> <div class="mw-heading mw-heading2"><h2 id="External_links">External links</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Coagulation&action=edit&section=36" title="Edit section: External links"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <ul><li><span class="noviewer" typeof="mw:File"><a href="/wiki/File:Commons-logo.svg" class="mw-file-description"><img alt="" src="//upload.wikimedia.org/wikipedia/en/thumb/4/4a/Commons-logo.svg/12px-Commons-logo.svg.png" decoding="async" width="12" height="16" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/en/thumb/4/4a/Commons-logo.svg/18px-Commons-logo.svg.png 1.5x, //upload.wikimedia.org/wikipedia/en/thumb/4/4a/Commons-logo.svg/24px-Commons-logo.svg.png 2x" data-file-width="1024" data-file-height="1376" /></a></span> Media related to <a href="https://commons.wikimedia.org/wiki/Category:Coagulation" class="extiw" title="commons:Category:Coagulation">Coagulation</a> at Wikimedia Commons</li></ul> <div class="navbox-styles"><style data-mw-deduplicate="TemplateStyles:r1129693374">.mw-parser-output .hlist dl,.mw-parser-output .hlist ol,.mw-parser-output .hlist ul{margin:0;padding:0}.mw-parser-output .hlist dd,.mw-parser-output .hlist dt,.mw-parser-output .hlist li{margin:0;display:inline}.mw-parser-output .hlist.inline,.mw-parser-output .hlist.inline dl,.mw-parser-output .hlist.inline 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class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink-fragment" href="#Platelet_activation">Primary hemostasis<br />(platelet activation)</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Von_Willebrand_factor" title="Von Willebrand factor">von Willebrand factor (vWF)</a></li> <li><i><a href="/wiki/Platelet_membrane_glycoprotein" title="Platelet membrane glycoprotein">Platelet membrane glycoproteins</a>:</i> <a href="/wiki/Glycoprotein_Ib" title="Glycoprotein Ib">Glycoprotein Ib (GPIb)</a> (<a href="/wiki/GP1BA" title="GP1BA">GP1BA</a></li> <li><a href="/wiki/GP1BB" title="GP1BB">GP1BB</a></li> <li><a href="/wiki/Glycoprotein_IX" title="Glycoprotein IX">Glycoprotein IX (GP9)</a>)</li> <li><a href="/wiki/Glycoprotein_IIb/IIIa" title="Glycoprotein IIb/IIIa">Glycoprotein IIb/IIIa</a> (<a href="/wiki/ITGA2B" class="mw-redirect" title="ITGA2B">GPIIb</a></li> <li><a href="/wiki/CD61" class="mw-redirect" title="CD61">GPIIIa</a>)</li> <li><a href="/wiki/Glycoprotein_VI" class="mw-redirect" title="Glycoprotein VI">Glycoprotein VI (GPVI)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink-fragment" href="#Contact_activation_pathway_(intrinsic)">Intrinsic pathway<br />(contact activation)</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/High-molecular-weight_kininogen" title="High-molecular-weight kininogen">High-molecular-weight kininogen (HMWK)</a></li> <li><a href="/wiki/Bradykinin" title="Bradykinin">Bradykinin</a></li> <li><a href="/wiki/Prekallikrein" title="Prekallikrein">Prekallikrein</a></li> <li><a href="/wiki/Kallikrein" title="Kallikrein">Kallikrein</a></li> <li><a href="/wiki/Factor_XII" title="Factor XII">Factor XII (Hageman factor)</a></li> <li><a href="/wiki/Factor_XI" title="Factor XI">Factor XI</a></li> <li><a href="/wiki/Factor_IX" title="Factor IX">Factor IX</a></li> <li><a href="/wiki/Factor_VIII" title="Factor VIII">Factor VIII</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink-fragment" href="#Tissue_factor_pathway_(extrinsic)">Extrinsic pathway<br />(tissue factor)</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Tissue_factor" title="Tissue factor">Factor III (tissue factor)</a></li> <li><a href="/wiki/Factor_VII" title="Factor VII">Factor VII</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink-fragment" href="#Final_common_pathway">Common pathway</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Factor_X" title="Factor X">Factor X</a></li> <li><a href="/wiki/Factor_V" title="Factor V">Factor V</a></li> <li><a href="/wiki/Prothrombin" class="mw-redirect" title="Prothrombin">Prothrombin (factor II)</a></li> <li><a href="/wiki/Thrombin" title="Thrombin">Thrombin (factor IIa)</a></li> <li><a href="/wiki/Fibrinogen" title="Fibrinogen">Fibrinogen (factor I)</a> (<a href="/wiki/Fibrinogen_alpha_chain" title="Fibrinogen alpha chain">FGA</a>, <a href="/wiki/Fibrinogen_gamma_chain" title="Fibrinogen gamma chain">FGG</a>)</li> <li><a href="/wiki/Fibrin" title="Fibrin">Fibrin (factor Ia)</a></li> <li><a href="/wiki/Factor_XIII" title="Factor XIII">Factor XIII</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Anticoagulant" title="Anticoagulant">Anticoagulant factors</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Antithrombin" title="Antithrombin">Antithrombin (inhibits FII, FIX, FX, FXI, FXII)</a></li> <li><a href="/wiki/Protein_C" title="Protein C">Protein C (inhibits FV, FVIII)</a></li> <li><a href="/wiki/Protein_S" title="Protein S">Protein S (cofactor for protein C)</a></li> <li><a href="/wiki/Protein_Z" title="Protein Z">Protein Z (inhibits FX)</a></li> <li><a href="/wiki/Protein_Z-related_protease_inhibitor" title="Protein Z-related protease inhibitor">Protein Z-related protease inhibitor (ZPI) (inhibits FX, FXI)</a></li> <li><a href="/wiki/Tissue_factor_pathway_inhibitor" title="Tissue factor pathway inhibitor">Tissue factor pathway inhibitor (TFPI) (inhibits FIII)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Fibrinolysis" title="Fibrinolysis">Fibrinolytic factors</a></th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Plasminogen" class="mw-redirect" title="Plasminogen">Plasminogen</a></li> <li><a href="/wiki/Plasmin" title="Plasmin">Plasmin</a></li> <li><a href="/wiki/Tissue_plasminogen_activator" class="mw-redirect" title="Tissue plasminogen activator">Tissue plasminogen activator (tPA)</a></li> <li><a href="/wiki/Urokinase" title="Urokinase">Urokinase</a></li> <li><a href="/wiki/Plasminogen_activator_inhibitor-1" title="Plasminogen activator inhibitor-1">Plasminogen activator inhibitor-1 (PAI-1)</a></li> <li><a href="/wiki/Plasminogen_activator_inhibitor-2" title="Plasminogen activator inhibitor-2">Plasminogen activator inhibitor-2 (PAI-2)</a></li> <li><a href="/wiki/Alpha_2-antiplasmin" title="Alpha 2-antiplasmin">α<sub>2</sub>-Antiplasmin</a></li> <li><a href="/wiki/Alpha-2-Macroglobulin" title="Alpha-2-Macroglobulin">α<sub>2</sub>-Macroglobulin</a></li> <li><a href="/wiki/Carboxypeptidase_B2" title="Carboxypeptidase B2">Thrombin-activatable fibrinolysis inhibitor (TAFI)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Coagulation_activation_marker" title="Coagulation activation marker">Coagulation markers</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Platelet_activation" class="mw-redirect" title="Platelet activation">Platelet activation</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Platelet_factor_4" title="Platelet factor 4">Platelet factor 4 (PF4)</a></li> <li><a href="/wiki/%CE%92-Thromboglobulin" title="Β-Thromboglobulin">β-Thromboglobulin (β-TG)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Thrombin_generation" class="mw-redirect" title="Thrombin generation">Thrombin generation</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Prothrombin_fragment_1%2B2" title="Prothrombin fragment 1+2">Prothrombin fragment 1+2 (F1+2)</a></li> <li><a href="/wiki/Thrombin%E2%80%93antithrombin_complex" title="Thrombin–antithrombin complex">Thrombin–antithrombin complex (TAT)</a></li> <li><a href="/wiki/Activated_protein_C%E2%80%93protein_C_inhibitor" title="Activated protein C–protein C inhibitor">Activated protein C–protein C inhibitor (APC–PCI)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Fibrin_generation" class="mw-redirect" title="Fibrin generation">Fibrin generation</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Fibrinopeptide_A" class="mw-redirect" title="Fibrinopeptide A">Fibrinopeptide A (FpA)</a></li> <li><a href="/wiki/Fibrinopeptide_B" class="mw-redirect" title="Fibrinopeptide B">Fibrinopeptide B (FpB)</a></li> <li><a href="/wiki/Fibrin_monomer" title="Fibrin monomer">Fibrin monomers (FM)</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Fibrinolysis" title="Fibrinolysis">Fibrinolysis</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Plasmin-%CE%B12-antiplasmin_complex" title="Plasmin-α2-antiplasmin complex">Plasmin-α<sub>2</sub>-antiplasmin complex (PAP)</a></li> <li><a href="/wiki/D-Dimer" class="mw-redirect" title="D-Dimer">D-Dimer (DD)</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr></tbody></table></div> <div 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class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"><style data-mw-deduplicate="TemplateStyles:r1038841319">.mw-parser-output .tooltip-dotted{border-bottom:1px dotted;cursor:help}</style><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1038841319"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1038841319"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1038841319"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1038841319"></div><div role="navigation" class="navbox authority-control" aria-label="Navbox1637" style="padding:3px"><table class="nowraplinks hlist navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Help:Authority_control" title="Help:Authority control">Authority control databases</a>: National <span class="mw-valign-text-top noprint" typeof="mw:File/Frameless"><a href="https://www.wikidata.org/wiki/Q179217#identifiers" title="Edit this at Wikidata"><img alt="Edit this at Wikidata" src="//upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/10px-OOjs_UI_icon_edit-ltr-progressive.svg.png" decoding="async" width="10" height="10" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/15px-OOjs_UI_icon_edit-ltr-progressive.svg.png 1.5x, //upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/20px-OOjs_UI_icon_edit-ltr-progressive.svg.png 2x" data-file-width="20" data-file-height="20" /></a></span></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"><ul><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Blutgerinnung"><a rel="nofollow" class="external text" href="https://d-nb.info/gnd/4007275-7">Germany</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Blood--Coagulation"><a rel="nofollow" class="external text" href="https://id.loc.gov/authorities/sh85014936">United States</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Coagulation du sang"><a rel="nofollow" class="external text" href="https://catalogue.bnf.fr/ark:/12148/cb11978819v">France</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Coagulation du sang"><a rel="nofollow" class="external text" href="https://data.bnf.fr/ark:/12148/cb11978819v">BnF data</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="hemokoagulace"><a rel="nofollow" class="external text" href="https://aleph.nkp.cz/F/?func=find-c&local_base=aut&ccl_term=ica=ph171353&CON_LNG=ENG">Czech Republic</a></span></span></li><li><span class="uid"><a rel="nofollow" class="external text" href="https://www.nli.org.il/en/authorities/987007283116505171">Israel</a></span></li></ul></div></td></tr></tbody></table></div>    </div><noscript><img src="https://login.wikimedia.org/wiki/Special:CentralAutoLogin/start?useformat=desktop&type=1x1&usesul3=0" alt="" width="1" height="1" style="border: none; position: absolute;"></noscript> <div class="printfooter" data-nosnippet="">Retrieved from "<a dir="ltr" href="https://en.wikipedia.org/w/index.php?title=Coagulation&oldid=1275617668">https://en.wikipedia.org/w/index.php?title=Coagulation&oldid=1275617668</a>"</div></div> <div id="catlinks" class="catlinks" data-mw="interface"><div id="mw-normal-catlinks" class="mw-normal-catlinks"><a href="/wiki/Help:Category" title="Help:Category">Categories</a>: <ul><li><a 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