When we injure ourselves how does blood clot?

Armstrong

Active member
When we injure ourselves how does blood clot?
There's what we call Hemostasis..it is a precisely orchestrated process involving platelets, clotting factors and endothelium that occurs at the site of injury and culminates in the formation of a blood clot.
 

Armstrong

Active member
There's what we call Hemostasis..it is a precisely orchestrated process involving platelets, clotting factors and endothelium that occurs at the site of injury and culminates in the formation of a blood clot.
It consist of four steps: arteriolar vasoconstriction, primary hemostasis, secondary hemostasis and clot stabilization and clot resorption.
 

Armstrong

Active member
It consist of four steps: arteriolar vasoconstriction, primary hemostasis, secondary hemostasis and clot stabilization and clot resorption.
Vasoconstriction occurs immediately and markedly reduces blood flow to the injured area. It is mediated by neurogenic mechanism and by Endothelin. This effect is transient.
 

Armstrong

Active member
It consist of four steps: arteriolar vasoconstriction, primary hemostasis, secondary hemostasis and clot stabilization and clot resorption.
Primary hemostasis is the next.
This involves the formation of primary platelet plug. Disruption of the endothelium exposes von willibrand factor and collagen which promote platelet adherence and activation as well as secretion o granules. Within minutes they undergo aggregation to form primary hemostatic plug.
 

Armstrong

Active member
It consist of four steps: arteriolar vasoconstriction, primary hemostasis, secondary hemostasis and clot stabilization and clot resorption.
Secondary hemostatic plug.
Tissue factor is also exposed. It binds and activates factor VII setting in a cascade of reactions that lead to thrombin generation. Thrombin cleaves circulating fibrinogen to fibrin. This consolidates the initial platelet plug.
 

Armstrong

Active member
It consist of four steps: arteriolar vasoconstriction, primary hemostasis, secondary hemostasis and clot stabilization and clot resorption.
Clot stabilization and resorption
Polymerized fibrin and platelet aggregates undergo contraction to form a solid permanent plug that prevents further hemorrhage. Also counter regulatory mechanism are set in to motion that limit clotting to the site of injury and leads to clot resorption and tissue repair.
 

Hannah

Active member
Clot stabilization and resorption
Polymerized fibrin and platelet aggregates undergo contraction to form a solid permanent plug that prevents further hemorrhage. Also counter regulatory mechanism are set in to motion that limit clotting to the site of injury and leads to clot resorption and tissue repair.
Thanks..I understand now
 

Bethany

Well-known member
Primary hemostasis is the next.
This involves the formation of primary platelet plug. Disruption of the endothelium exposes von willibrand factor and collagen which promote platelet adherence and activation as well as secretion o granules. Within minutes they undergo aggregation to form primary hemostatic plug.
Sorry if I may ask, how does this platelet adhere to each other?
 

Armstrong

Active member
Sorry if I may ask, how does this platelet adhere to each other?
Platelet adhesion is mediated largely via interactions with Von willibrand factor which acts as a bridge between the platelet surface receptor glycoprotein 1b and exposed collagen.
 

Armstrong

Active member
Platelet adhesion is mediated largely via interactions with Von willibrand factor which acts as a bridge between the platelet surface receptor glycoprotein 1b and exposed collagen.
If i may add, deficiency of von willibrand factor leads to von willibrand disease or Bernard Soulier syndrome.
 

Casey

Well-known member
Platelet adhesion is mediated largely via interactions with Von willibrand factor which acts as a bridge between the platelet surface receptor glycoprotein 1b and exposed collagen.
I once saw while reading about this that platelet change shape..can you explain it please?
 

Armstrong

Active member
I once saw while reading about this that platelet change shape..can you explain it please?
They do change shape. That is being converted from smooth discs to spiky "Sea Urchins" with greatly increased surface area. This change are accompanied by alterations in glycoprotein 2b/3a that increase its affinity for fibrinogen.
 

Armstrong

Active member
They do change shape. That is being converted from smooth discs to spiky "Sea Urchins" with greatly increased surface area. This change are accompanied by alterations in glycoprotein 2b/3a that increase its affinity for fibrinogen.
Let me also add again that deficiency in glycoprotein 2b/3a results in a bleeding disorder called Glanzmann thrombasthenia.
 

Casey

Well-known member
They do change shape. That is being converted from smooth discs to spiky "Sea Urchins" with greatly increased surface area. This change are accompanied by alterations in glycoprotein 2b/3a that increase its affinity for fibrinogen.
Thank you for this.
 
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