Intrinsic pathway of Hemostasis :a summary

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intrinsic pathway of hemostasis

The intrinsic pathway of hemostasis is the long and slow pathway that occurs when there is a trauma to the blood vessel .  It’s usually common when the trauma doesn’t go deep into the flesh.

It would be tantamount to state that the intrinsic pathway of hemostasis isn’t completely separated from the external pathway of hemostasis, because they can both occur at the same time, and they can both reinforce each other too

When there is a cut to the blood vessel, blood clotting begins immediately.

Hemostasis is the process of ceasing the fluidity of blood at the region of the body exposure so as to prevent blood loss.

If the body injury isn’t deep(at the vessel) , the intrinsic pathway of hemostasis is followed, but if the injury is deep into the flesh, the extrinsic pathway is followed. The extrinsic pathway is very short and fast because it involves quite few factor like the factor X,V,VII and III and the injury is very dangerous which needs urgent attention.

Let’s start with the longer and slower pathway, the intrinsic pathway which involves factor XII,XI,IX,VIII,X and V.

When there is damage to a tiny blood vessel, the collagen underlying the endothelium of the vessel is exposed.

The moment there is trauma to the blood vessel, spasm of the blood vessel occurs, this is due to the contraction of the smooth muscle of the blood vessel. This contraction of the blood vessel is so marked that it sometimes obliterate the lumen of the vessel temporarily enough to reduce blood flow to the injured area thereby contributing to the reduction of blood lose.

After this vessel spasm, and after some platelets have been attached to the exposed collagen of the damaged blood vessel, the attached platelets release some substances from their granules, substances like serotonin and thromboxane A2 both of which are vasoconstrictors released from the attached platelets, platelets also release ADP. ADP and thromoboxane A2 are attractant for other platelets to recruit to the forming platelet plug.

Once the vessel get damaged, the first factor that is affected by this is factor XII(contact factor). Factor XII comes in contact with the collagen and it becomes activated as a result of this contact, platelet also comes in contact with the collagen and thereby releases its phospholipids due to its plasma membrane damage.

Activated factor XII then activates factor XI (PTA) in the presence of HMW kininogen and accelerated by prekallikrein

Activated factor XI then activates factor IX(PTC)

Factor X is the most demanding to be activated, it requires, activated factor IX , activated factor VIII(Antihemophilic F), platelet phospholipids and factor 3 from lipoprotein from platelets’ phospholipids, all in the name of activating factor X.

Activated factor X and Factor V(proaccelerin) and platelet phospholipids and tissue phospholipids all together form the complex called prothrombin activator.

Once prothrombin activator has been formed, it does it work by converting prothrombin to thrombin.

Once some thrombin has been formed they activate factor V(proaccelerin) in the prothrombin activator complex which further makes the complex function faster.

Thrombin then split fibrinogen to fibrin monomer by removing 4 peptides from fibrinogen.

Fibrin monomers automatically polymerise to form weak fibrin fibers(fibrin reticulum).

Little factor XIII(fibrin stabilising factor) in the blood then strengthen the fibrin fiber by creating covalent bonds between fibrin monomers and cross linking fibrin fibers. Some factor XIII are also produced by the platelets too. This process continues to form really strong blood clot.
And that’s it, the complex process of the intrinsic pathway of hemostasis.

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