Blood Coagulation

This article deals with specific medical use of the term in connection with the mechanisms of human blood to form clots. For the other directions, to see the article Coagulation.

The coagulation in general is the thickening or the congelation of a liquid in solid clots.

The blood coagulation or coagulation of human blood is a complex process during which the Sang form of the solid clots. It is an important part of the Hémostase where the damaged wall of a Blood-vessel is covered with a clot of Fibrine to stop the Hémorragie and to help to repair the damaged vessel. The disorders of coagulation can involve a greater hemorrhage and/or a Thrombose and Embolie.

In short

Plasmatic coagulation or hémostase secondary is the whole of the biological reactions resulting in transforming a liquid (plasma) into a gel made up of Fibrine. Fibrin comes from the enzymatic cleavage of the Fibrinogène by the Thrombine, which is the enzyme-key of the coagulation.
When a vascular lesion occurs, this breach must be quickly blocked to stop the bleeding and to allow the vessel of réparer.
The vascular lesion lets appear the components of the under-endothelium: Fibroblasts and proteins

the Fibroblastes which carry on their surface the tissue factor which will initiate plasmatic coagulation by connection of the Facteur VII.
Among proteins of the under-endothelium, a certain number allow the adhesion of the plates then their activation and the formation of a plate clot or plate nail which will stop the bleeding. It is the primary hémostase
This clot is fragile and will quickly be reinforced by the production of fibrin on the surface of the clot, making it solid and impermeable. The phenomena leading to the fibrin formation represent the plasmatic coagulation or hémostase secondary
When the clot made it possible to reconstitute an intact endothelium, the clot must be destroyed: it is the fibrinolyse . The fibrinolyse represents the whole of the phenomena leading to the enzymatic destruction of fibrin by the plasmine.

There exists in medicine of the important criteria which define in which moment coagulation is likely to be created, it is the Triade of Virchow. This page explains in fact why they are these criteria.

Primary Hémostase

The primary hémostase comprise two times: a vascular time and a plate time. During this stage intervene the vascular wall, the plasmatic plates and two proteins: the factor Willebrand and the Fibrinogen, these two proteins being present inside the plates. The various stages include/understand:

a vascular time which facilitates the adhesion of the plates with the collagen of the under-endothelium by very short vasoconstriction reflex of the vessel, especially effective for the vessels of gauge lower than 400 micrometers. The reduction in the gauge can reach 40% of its initial size.
Adhesion of the plates thanks to a membrane receiver: the GPIb protein with the under-endothelium which is carried out via the factor Willebrand. This phenomenon is very fast and causes the activation of the plates.
the activated plates change form and release from the substances having an incorporating action: ADP, Adrenalin, Noradrenalin.
These elements will cause the plate aggregation via the fibrinogen molecules, in the presence of Calcium, which set on a receiver of the plate membrane GPIIbllla.
the membranes of the aggregate plates amalgamate. The cluster formed by these amalgamated plates is called the plate nail or hemostatic nail or white thrombus

Secondary Hémostase or coagulation itself

The vascular lesion starts in parallel with the formation of the plate nail, coagulation itself. The final stage of coagulation is the fibrinogen transformation into Fibrine, under the action of the Thrombine

The cascade of coagulation

Cofacteurs and inhibiters

Examination of coagulation

Fibrinolyse

The fibrinolyse is the process by which the Fibrine is degraded by the Plasmine and is dissolved, therefore the plate nail, product of coagulation is destroyed.

The plasmine is produced by the liver, in an inactive form the Plasminogène. The human plasminogene has a molecular mass from approximately 92.000 Dalton and accounts for 0.5% of plasmatic proteins. The plasminogene has an affinity for fibrin and is built-in the clot during its formation (what will make it possible to degrade it later). This recognition is due to particular proteinic reasons the fields pins some which recognizes the lysin and the arginine of fibrin.

The activation of plasminogene in plasmine is done on the level of the clot. This reaction is catalyzed by two activators:

the urokinase which comes from the pro-urokinase, the activation of the urokinase is done thanks to the kallicreïne (enzyme which intervenes at the beginning of coagulation) and with the plasmine (amplification of the fibrinolyse).
the tissue activator of plasminogene (T-Pa) secreted by the vascular wall after a traumatism.

The plasmine is a protease with serine which has a rather broad specificity: it attacks the fibrin and proteins of coagulation. It cuts fibrin in various places releasing in the circulation of the fragments which will be degraded by other proteases and eliminated by the kidney. The proportioning of the breakdown products of fibrin (pdf) soluble in blood makes it possible to follow the activity of the fibrinolyse. The plasmine is inactivated by the antiplasmine α2.

The urokinase and T-Pa are inhibited from the inhibiters of the activator of plasminogene PAI-1 and PAI-2.

Factors of coagulation

Exploration of coagulation by the tests of laboratory

Exploration of the primary hémostase

Time of plate bleeding
Numeration
plate Test of aggregation
Proportioning of the factor Willebrand

Exploration of the secondary hémostase

Time of activated cephalin
Time of cephalin Kaolin
Test of Quick

Exploration of the fibrinolyse

Ordinary: Rate of prothrombine (TP, INR…), Time of cephalin activated (TCA, TCK), Time of thrombin, Time of reptilase.
Others: measure activity of the factors, Anticorps antiphospholipides, tests genetic, proportioning of the pdf, proportioning of D-dimers,…
Test of Von Kaulla

Disorders of the hémostase

Pathology of the primary hémostase

Pathology of the plates

Anomaly of the factor of von Willebrand

Disease of von Willebrand

Pathology of the secondary hémostase

Vitamin deficiency K
Problem hepatic

Pathology of the inhibiters

Pathology of the fibrinolyse

If the fibrinogen rate is lower than 2 g/L: congenital dysfibrinogenemy or CIVD
If the fibrinogen rate is higher than 4 g/L: infectious or inflammatory syndrome

History

References

Simple: Closes

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