Hemostasis
💡 Blood vessels are composed of three main layers: the intima, media, and
adventitia. Each layer plays a crucial role in maintaining vascular integrity
and function. The intima, the innermost layer, is lined with endothelial
cells that form a smooth, non-thrombogenic surface. This endothelial
lining secretes different substances like nitric oxide, Prostacyclin (aka
Prostaglandin I2, it inhibates platelet aggregation), Antithrombin
(inactivates thrombin and factors IXa, Xa, XIa, and XIIa), Thrombin (aka
Factor II ), …
Hemostasis is a complex process that involves multiple physiological mechanisms
that allow the cessation of bleeding following a vascular rupture and prevent
spontaneous hemorrhages. It can be divided into 3 key stages:
Primary hemostasis:
1. Vasoconstriction: After getting damaged, the endothelial tissue secrets
endothelin , a potent vasoconstrictor that causes blood vessels to contract
.This process is a very short defensive element, especially effective for small
caliber vessels (the caliber can decrease by 40% of its initial size). It also
facilitates platelet adhesion to the subendothelial stroma plaquettes.
2. Formation of platlet plug: Platelet adhesion to the subendothelial stroma
occurs thanks to von Willebrand factor (a glycoprotein synthesized by
endothelial cells and megakaryocytes, released into the plasma and binds to
the factor VII in circulation). Platelets bind to this factor through their
membrane receptor GP Ib, leading to platelet activation. This triggers the
release of the platelet granules containing ADP and thromboxane A2 (which
stimulates other platelets to trigger the platelet aggregation), as well as
adrenaline and serotonin. The platelets then bind to each other thanks to
Hemostasis 1
, fibrinogen through their membrane receptor GP IIb/IIIa (this process requires
calcium).
Coagulation:
This phase consists of converting Fibrinogen, a soluble protein, into fibrin, an
insoluble protein, to stabilize the platelet plug. This process is initiated by 2
different pathways:
The intrinsic pathway (activated due to internal damage of the vascular
endothelium) starts by the activation of factor XII and ends by the activation of
factor X.
The extrinsique pathway (activated due to external damage) it is faster than
the intrisic pathway, it starts by the activation of factor VII that can either
directly activate factor X or activate factor IX to undergo the intrinsic pathway.
Now that factor X is activated, the common pathway begins to form fibrin as a
result .
Hemostasis 2
💡 Blood vessels are composed of three main layers: the intima, media, and
adventitia. Each layer plays a crucial role in maintaining vascular integrity
and function. The intima, the innermost layer, is lined with endothelial
cells that form a smooth, non-thrombogenic surface. This endothelial
lining secretes different substances like nitric oxide, Prostacyclin (aka
Prostaglandin I2, it inhibates platelet aggregation), Antithrombin
(inactivates thrombin and factors IXa, Xa, XIa, and XIIa), Thrombin (aka
Factor II ), …
Hemostasis is a complex process that involves multiple physiological mechanisms
that allow the cessation of bleeding following a vascular rupture and prevent
spontaneous hemorrhages. It can be divided into 3 key stages:
Primary hemostasis:
1. Vasoconstriction: After getting damaged, the endothelial tissue secrets
endothelin , a potent vasoconstrictor that causes blood vessels to contract
.This process is a very short defensive element, especially effective for small
caliber vessels (the caliber can decrease by 40% of its initial size). It also
facilitates platelet adhesion to the subendothelial stroma plaquettes.
2. Formation of platlet plug: Platelet adhesion to the subendothelial stroma
occurs thanks to von Willebrand factor (a glycoprotein synthesized by
endothelial cells and megakaryocytes, released into the plasma and binds to
the factor VII in circulation). Platelets bind to this factor through their
membrane receptor GP Ib, leading to platelet activation. This triggers the
release of the platelet granules containing ADP and thromboxane A2 (which
stimulates other platelets to trigger the platelet aggregation), as well as
adrenaline and serotonin. The platelets then bind to each other thanks to
Hemostasis 1
, fibrinogen through their membrane receptor GP IIb/IIIa (this process requires
calcium).
Coagulation:
This phase consists of converting Fibrinogen, a soluble protein, into fibrin, an
insoluble protein, to stabilize the platelet plug. This process is initiated by 2
different pathways:
The intrinsic pathway (activated due to internal damage of the vascular
endothelium) starts by the activation of factor XII and ends by the activation of
factor X.
The extrinsique pathway (activated due to external damage) it is faster than
the intrisic pathway, it starts by the activation of factor VII that can either
directly activate factor X or activate factor IX to undergo the intrinsic pathway.
Now that factor X is activated, the common pathway begins to form fibrin as a
result .
Hemostasis 2
