Glanzmann's thrombasthenia pathophysiology: Difference between revisions
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==Pathophysiology == | ==Pathophysiology == | ||
The [[GpIIb/IIIa]] is an adhesion receptor and is expressed in [[thrombocytes]]. This receptor is activated when the thrombocyte is stimulated by [[Adenosine diphosphate|ADP]], [[epinephrine]], [[collagen]] and [[thrombin]]. The [[GpIIb/IIIa]] [[integrin]] is essential to the [[blood coagulation]] since it has the ability to bind [[fibrinogen]], the [[von Willebrand factor]], [[fibronectin]] and [[vitronectin]]. This enables the platelet to be activated by contact with the collagen-von Willebrand-complex that is exposed when the endothelial blood vessel lining is damaged and then aggregate with other [[thrombocytes]] via [[fibrinogen]]. | |||
Patients suffering from Glanzmann's thrombasthenia thus have platelets less able to adhere to each other and to the underlying tissue of damaged blood vessels. | |||
The understanding of its pathophysiology led to the development of [[GpIIb/IIIa inhibitors]], a class of powerful [[antiplatelet agent]]s.<ref name=seligsohn>Seligsohn U. Glanzmann thrombasthenia: a model disease which paved the way to powerful therapeutic agents. Pathophysiol Haemost Thromb. 2002 Sep-Dec;32(5-6):216-7. PMID 13679645. [http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=73569&ProduktNr=224034&Ausgabe=229381&filename=73569.pdf Free Full Text].</ref> | |||
==References== | ==References== | ||
Revision as of 22:19, 6 June 2016
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Glanzmann's thrombasthenia |
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Overview
Pathophysiology
The GpIIb/IIIa is an adhesion receptor and is expressed in thrombocytes. This receptor is activated when the thrombocyte is stimulated by ADP, epinephrine, collagen and thrombin. The GpIIb/IIIa integrin is essential to the blood coagulation since it has the ability to bind fibrinogen, the von Willebrand factor, fibronectin and vitronectin. This enables the platelet to be activated by contact with the collagen-von Willebrand-complex that is exposed when the endothelial blood vessel lining is damaged and then aggregate with other thrombocytes via fibrinogen.
Patients suffering from Glanzmann's thrombasthenia thus have platelets less able to adhere to each other and to the underlying tissue of damaged blood vessels.
The understanding of its pathophysiology led to the development of GpIIb/IIIa inhibitors, a class of powerful antiplatelet agents.[1]
References
- ↑ Seligsohn U. Glanzmann thrombasthenia: a model disease which paved the way to powerful therapeutic agents. Pathophysiol Haemost Thromb. 2002 Sep-Dec;32(5-6):216-7. PMID 13679645. Free Full Text.