Plasminogen Coagulation factor XII Collagen alpha-1(I) chain Coagulation factor XIIa Plasma kallikrein Coagulation factor XIII A chain Coagulation factor XIII B chain Coagulation factor VII Tissue factor Tissue factor:Coagulation factor VIIa Plasma prekallikrein Coagulation factor XIIa Coagulation factor XI Coagulation factor XIa Coagulation factor IX Coagulation factor IXa Coagulation factor VIII Coagulation factor VIIIa Prothrombin Coagulation factor V Coagulation factor Va Prothrombin Coagulation factor X Coagulation factor Xa Prothrombin Thrombin Fibrinogen alpha chain Fibrinogen beta chain Fibrinogen gamma chain Fibrin (loose) Fibrin (mesh) Coagulation factor XIIIa Fibrin degradation products Plasmin Plasminogen Tissue-type plasminogen activator Coagulation factor X Vitamin K epoxide reductase complex subunit 1 Vitamin K-dependent gamma- carboxylase Tranexamic Acid Vitamin K1 2,3-epoxide Reduced Vitamin K (phylloquinone) Cortexolone Calcium Calcium Cortexolone Calcium Cortexolone Calcium Calcium Calcium Calcium Calcium Calcium Precursors of Prothrombin and coagulation factors VII, IX, ad X Prothrombin and coagulation factors VII, IX and X Platelet Factor 3 Tenase complex Platelet factor 3 Prothrombinase complex ENDOTHELIAL CELL SUBENDOTHELIUM VASCULAR INJURY ENDOTHELIAL CELL SUBENDOTHELIUM COAGULATION
PLG F12 COL1A1 F12 KLKB1 F13A1 Unknown F7 Unknown F7 KLKB1 F12 Unknown Unknown F9 F9 F8 F8 Unknown F5 F5 Unknown F10 F10 Unknown Unknown Unknown Unknown FGG Unknown Unknown F13A1 Unknown PLG PLG PLAT F10 VKORC1 GGCX Tranexamic Acid Vitamin K1 2,3-epoxide Reduced Vitamin K (phylloquinone) Precursors of Prothrombin and coagulation factors VII, IX, ad X Prothrombin and coagulation factors VII, IX and X Created with Snap
PLG F12 COL1A1 F12 KLKB1 F13A1 F7 F7 KLKB1 F12 F9 F9 F8 F8 F5 F5 F10 F10 FGG F13A1 PLG PLG PLAT F10 VKORC1 GGCX TrnxmcA VitKo ReVitK Cortexo Ca2+ Ca2+ Cortexo Ca2+ Cortexo Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ POPACFV PACFVIA Platelet Factor 3 Tenase complex Platelet factor 3 Prothrombinase complex ENDOTHELIAL CELL SUBENDOTHELIUM VASCULAR INJURY ENDOTHELIAL CELL SUBENDOTHELIUM COAGULATION
PLG F12 COL1A1 F12 KLKB1 F13A1 F7 F7 KLKB1 F12 F9 F9 F8 F8 F5 F5 F10 F10 FGG F13A1 PLG PLG PLAT F10 VKORC1 GGCX TrnxmcA VitKo ReVitK POPACFV PACFVIA Created with Snap
Tranexamic Acid Action Pathway
Tranexamic acid is a synthetic version of an amino acid found in the body called lysine that plays a role in antifibrinolytic processes. It is used to stop bleeding and hemorrhaging in patients. Tranexamic acid works by inhibiting the activation of plasminogen, which reduces the amount of plasmin that can be produced, thereby slowing the amount of clot degradation that can occur. Tranexamic acid inhibits plasminogen. Then zooming in even further to the endoplasmic reticulum within the liver, vitamin K1 2,3-epoxide uses vitamin K epoxide reductase complex subunit 1 to become reduced vitamin K (phylloquinone), and then back to vitamin K1 2,3-epoxide continually through vitamin K-dependent gamma-carboxylase. This enzyme also catalyzes precursors of prothrombin and coagulation factors VII, IX and X to prothrombin, and coagulation factors VII, IX and X. From there, these precursors and factors leave the liver cell and enter into the blood capillary bed. Once there, prothrombin is catalyzed into the protein complex prothrombinase complex which is made up of coagulation factor Xa/coagulation factor Va (platelet factor 3). These factors are joined by coagulation factor V. Through the two factors coagulation factor Xa and coagulation factor Va, thrombin is produced, which then uses fibrinogen alpha, beta, and gamma chains to create fibrin (loose). This is then turned into coagulation factor XIIIa, which is activated through coagulation factor XIII A and B chains. From here, fibrin (mesh) is produced which interacts with endothelial cells to cause coagulation. Plasmin is then created from fibrin (mesh), then joined by tissue-type plasminogen activator through plasminogen, at which point tranexamic acid inhibits plasminogen which does not allow fibrin degradation products to be created as a result. These are enzymes that stay in your blood after your body has dissolved a blood clot. Coming back to the factors transported from the liver, coagulation factor X is catalyzed into a group of enzymes called the tenase complex: coagulation factor IX and coagulation factor VIIIa (platelet factor 3). This protein complex is also contributed to by coagulation factor VIII, which through prothrombin is catalyzed into coagulation factor VIIIa. From there, this protein complex is catalyzed into prothrombinase complex, the group of proteins mentioned above, contributing to the above process ending in fibrin degradation products. Another enzyme transported from the liver is coagulation factor IX which becomes coagulation factor IXa, part of the tense complex, through coagulation factor XIa. Coagulation factor XIa is produced through coagulation factor XIIa which converts coagulation XI to become coagulation factor XIa. Coagulation factor XIIa is introduced through chain of activation starting in the endothelial cell with collagen alpha-1 (I) chain, which paired with coagulation factor XII activates coagulation factor XIIa. It is also activated through plasma prekallikrein and coagulation factor XIIa which activate plasma kallikrein, which then pairs with coagulation factor XII simultaneously with the previous collagen chain pairing to activate coagulation XIIa. Lastly, the previously transported coagulation factor VII and tissue factor coming from a vascular injury work together to activate tissue factor: coagulation factor VIIa. This enzyme helps coagulation factor X catalyze into coagulation factor Xa, to contribute to the prothrombinase complex and complete the pathway.
Tranexamic Acid Pathway References
Cyklokapron. (2009). e-CPS (online version of Compendium of Pharmaceuticals and Specialties). Retrieved June 26, 2009.