As kids we've all cut ourselves, injured ourselves falling off from bicycles or maybe that sliding tackle on your opponent to prevent that precious goal! One way or other, we've seen blood coming out! 

But did you ever wonder, once the blood starts coming out, why don't we eventually completely bleed out to death? How is it that after a while the bleeding stops?

![image.png](https://files.steempeak.com/file/steempeak/simplifylife/Su73Xb8Q-image.png)

_[public domain CC0 image](https://www.rawpixel.com/image/519909/free-photo-image-wound-wounded-blood)_

Let's find out, shall we!

# Initial Response to Vessel Injury
Whenever there is injury to a blood vessel, the protective covering _(aka, endothelium)_ is damaged and stuff that were once hidden beneath/protected by the endothelium now gets exposed.

One such molecule that gets exposed is called _von Willebrand Factor, vWF._ We know we have platelets floating around in the blood, right? _(Platelets are a type of blood cell, tiny in size)._

These platelets have receptors _(GpIb)_ that can bind to vWF.

![1.png](https://files.steempeak.com/file/steempeak/simplifylife/DPEgWfeR-1.png)

_Image Illustration done by @simplifylife_

After this happens, this is a signal for platelets to release two substances : **_ADP_** and **_Thromboxane A2, TXA2._**

- TXA2 is a vasoconstrictor. It constricts the injured vessel, thus reducing blood flow through that injured place. Kind of like when there's a leakage in water pipes, we try to squeeze the pipe to reduce leakage of water flow. Smart!


- What ADP does is a bit more interesting. We have a lot of things floating in our blood, just floating around, doing nothing, waiting for the right command! One such molecule is **_Fibrinogen._** There's a receptor called **_GpIIb-IIIa_** on fibrinogen and ADP changes it's shape in such a way that now it can bind to platelets!

![2.png](https://files.steempeak.com/file/steempeak/simplifylife/PfwgmUnL-2.png)

_Image Illustration done by @simplifylife_

As you can see from the image above, fibrinogen with it's activated receptor now binds to multiple platelets. What this does is brings and binds together a lot of platelets. This process is known as **_Platelet Aggregation._**

Numerous platelets come together and aggregate and bound together by fibrinogen. This collection on platelets and fibrinogen forms a **_temporary_** plug which initially seals the leak and stops the bleeding. What this does is give the body time to produce a stronger, more stable clot.

# Forming a Stronger and More Stable Clot
Remember earlier, damage to the endothelium exposes a lot of stuff which were hidden. Another molecule that gets exposed is subendothelial collagen. This activates another floating substance in the blood, **_Factor XII, aka the Hageman Factor._**

The damaged tissue also release a substance called **_Tissue Thromboplastin.**_ This activates another factor, **_Factor VII._**

Okay I know this is getting too complicated with all these numbers, so i'll skip a few numbers and jump straight to the important one. Both of these activated factors, after a series of steps eventually activates **_Factor X._**

Factor X forms part of a complex structure called the **_Prothrombin Complex,_** and as everything else we have seen so far, it activates something else too! Kill me now LOL!

Prothrombin complex activates prothtombin into **_Thrombin._**

# Converting Unstable Plug into a Stable Clot
Remember the fibrinogen molecules holding the platelet aggregates. That fibrinogen is a soluble molecule and this is sort of why that plug is unstable. If the fibrinogen dissolves, there's nothing to hold the platelets together and they'll wander away, causing the injury to re-bleed.

In comes **Thrombin.**

Thrombin converts fibrinogen into fibrin monomers. Fibrin monomers are still soluble. 

![4.png](https://files.steempeak.com/file/steempeak/simplifylife/TWRMRSYV-4.png)

_Image Illustration done by @simplifylife_

So Thrombin does one final act! It activates _yet another factor!_ Kill me now! Please kill me now!

Thrombin activates Factor XIII and activated factor XIII add the final touch to this mess! It cross links many many fibrin monomers together and this cross-linked fibrin now forms a complex that is now insoluble. Cross linking makes it insoluble because instead of many different fibrin monomers, this is now virtually one single, large complex molecule.

![4.png](https://files.steempeak.com/file/steempeak/simplifylife/vn8zyDVO-4.png)

_Image Illustration done by @simplifylife_

After this stable clot has stopped the bleeding, the injured vessel has enough time to slowly heal itself, regenerate the damaged endothelium and once the need of the clot is over, the clot will be dissolved by the body's intrinsic fibrinolytic pathway. As you can imagine from the name, the cross links are broken down, making the fibrin soluble and it dissolves away.

And that, ladies and gentlemen, is how you do not bleed to death after every single minor cuts! Be thankful for this amazing human body we have!

## **References :**

_Goljan Rapid Review Pathology, 4th ed_
_Guyton and Hall, Textbook of Medical Physiology, 13th ed_
_[How Blood Clots](https://www.sciencedirect.com/topics/medicine-and-dentistry/blood-clotting)_
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