II. Images
- Overview
- Full Thrombosis Pathway
III. Physiology: Pathway
- Antagonized by Clotting Pathway Inhibition
- Common Clotting Pathway is triggered by two different initiating pathways
- Intrinsic Clotting Pathway
- Initiated by Negatively charged surface of foreign material or from damaged Red Blood Cells
- Pathway is relatively slow (minutes to form blood clot)
- Factor XII to Factor XI to Factor IX and Factor VIII which trigger conversion of Factor X to Xa
- Factor Xa then proceeds into the common pathway, generating Thrombin and then Fibrin
- Extrinsic Clotting Pathway
- Initiated by disrupted cell membranes
- Damaged cells (including vascular endothelial cells) release Tissue Thromboplastin
- Pathway is relatively rapid with Blood Clotting occuring within 15 seconds
- Intrinsic Clotting Pathway
- Common Clotting Pathway
- Factor Xa
- Factor II (Prothrombin) converted to IIa (Thrombin)
- Fibrinogen cleaved (catalyzed by Thrombin)
- Fibrinogen cleaved to Fibrin Monomer
- Fibrin Monomer coalesced into Fibrin Polymer
- Fibrin combines with Platelets, plasma factors and Red Blood Cells to form blood clot
- Factor XIII converted to XIIIa
- Fibrin polymer cross-linked
- Fibrinogen cleaved (catalyzed by Thrombin)
IV. Causes: Abnormal Common Clotting Pathway
- Severe liver disease
- Liver synthesizes Prothrombin, Fibrinogen and other Clotting Factors
-
Vitamin K Deficiency
- Clotting Factors (both pro-coagulant and Anticoagulant, including Prothrombin) are Vitamin K Dependent
- Medications