Prab: CSV import

2025-02-20T00:52:39Z

CSV import

← Older revision		Revision as of 00:52, 20 February 2025
Line 32:		Line 32:

	[[Category:Coagulation system]]		[[Category:Coagulation system]]
			<gallery>
			File:Coagulation in vivo.png\|Factor X
			</gallery>

Prab: /* In Vivo Coagulation */

2025-02-18T19:13:01Z

In Vivo Coagulation

← Older revision		Revision as of 19:13, 18 February 2025
Line 22:		Line 22:

	== In Vivo Coagulation ==		== In Vivo Coagulation ==
	~~[[File:Factor_X_Coagulation_in_vivo.png\|thumb\|right\|Diagram of Factor X in the coagulation cascade]]~~
	In vivo, the regulation of Factor X activation is tightly controlled to maintain a balance between bleeding and clotting. The [[endothelial cells]] and [[antithrombin]] play roles in modulating its activity.		In vivo, the regulation of Factor X activation is tightly controlled to maintain a balance between bleeding and clotting. The [[endothelial cells]] and [[antithrombin]] play roles in modulating its activity.

Prab: CSV import

2025-02-15T10:58:35Z

CSV import

New page

{{DISPLAYTITLE:Factor X}}

== Overview ==
[[Factor X]], also known as Stuart-Prower factor, is an essential [[enzyme]] in the [[coagulation]] cascade, which is crucial for [[hemostasis]]. It is a [[serine protease]] that plays a pivotal role in the conversion of [[prothrombin]] to [[thrombin]], a key step in the formation of a [[blood clot]].

== Structure ==
Factor X is synthesized in the [[liver]] and requires [[vitamin K]] for its activation. It circulates in the [[blood]] as an inactive [[zymogen]]. Upon activation, it becomes Factor Xa, which is the active form of the enzyme.

== Activation ==
Factor X can be activated via two pathways:

* The [[intrinsic pathway]], which is initiated by damage to the [[endothelium]] and involves several other clotting factors.
* The [[extrinsic pathway]], which is triggered by external trauma that causes blood to escape from the [[vascular system]].

Both pathways converge at the activation of Factor X, leading to the common pathway of coagulation.

== Function ==
Once activated to Factor Xa, it forms a complex with [[Factor V]], [[calcium ions]], and [[phospholipids]] on the surface of [[platelets]]. This complex, known as the prothrombinase complex, catalyzes the conversion of prothrombin to thrombin. Thrombin then converts [[fibrinogen]] to [[fibrin]], which forms the mesh that stabilizes the blood clot.

== Clinical Significance ==
Deficiency or dysfunction of Factor X can lead to bleeding disorders. Conversely, excessive activity can result in [[thrombosis]]. Factor X inhibitors, such as [[rivaroxaban]] and [[apixaban]], are used as [[anticoagulants]] to prevent and treat thromboembolic disorders.

== In Vivo Coagulation ==
[[File:Factor_X_Coagulation_in_vivo.png|thumb|right|Diagram of Factor X in the coagulation cascade]]
In vivo, the regulation of Factor X activation is tightly controlled to maintain a balance between bleeding and clotting. The [[endothelial cells]] and [[antithrombin]] play roles in modulating its activity.

== Related Pages ==
* [[Coagulation]]
* [[Thrombin]]
* [[Hemostasis]]
* [[Vitamin K]]
* [[Anticoagulant]]

[[Category:Coagulation system]]

Factor X - Revision history

Prab: CSV import

Prab: /* In Vivo Coagulation */

Prab: CSV import