The extrinsic pathway is triggered by external trauma or injury that causes blood to escape the circulation[1][3]. This exposes blood to tissue factor (factor III), which is present on cells outside the blood vessels.
## Key Components
- Tissue factor (factor III): Released by damaged cells outside the circulation[3]
- Factor VII: Exits the circulation into surrounding tissues when blood vessels are damaged[3]
## Process
1. Tissue factor and factor VII form a complex called TF-VIIa[3].
2. The TF-VIIa complex activates factor X, converting it to factor Xa[1][3].
3. Factor Xa, along with factor Va, triggers the formation of thrombin[3].
4. Thrombin then converts fibrinogen (factor I) into fibrin strands, forming the basis of the blood clot[1].
## Role in Coagulation
The extrinsic pathway is believed to be responsible for the initial generation of activated factor X (factor Xa)[3]. It provides a rapid response to vessel injury, initiating clotting faster than the intrinsic pathway.
## Regulation
The extrinsic pathway is regulated by various factors to prevent excessive clotting:
- Protein C and Protein S provide negative feedback[3]
- Antithrombin degrades several activated clotting factors[3]
## Clinical Significance
Understanding the extrinsic pathway is crucial for developing hemostatic agents and antithrombotic drugs[4]. Abnormalities in this pathway can lead to bleeding disorders or increased risk of thrombosis.
The extrinsic pathway ultimately converges with the intrinsic pathway at the common pathway, leading to the formation of a stable fibrin clot[1][2].
Citations:
[1] https://www.osmosis.org/answers/coagulation-cascade
[2] https://www.ncbi.nlm.nih.gov/books/NBK507850/
[3] https://teachmephysiology.com/immune-system/haematology/coagulation/
[4] https://www.ahajournals.org/doi/10.1161/ATVBAHA.107.141911
[5] https://www.britannica.com/science/bleeding/The-extrinsic-pathway-of-blood-coagulation
- Intrinsic pathway: Activated by contact with damaged vessel surfaces
These pathways converge into a common pathway, resulting in the conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin[5].
[Extrinsic Pathway]
{Intrinsic Pathway]