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Do you remember tripping over as a kid and cutting your knee? And then like magic the bleeding suddenly stops? Have you ever wondered why this happens?

Our body is very clever and produces substances to seal off the open wound.

In this video we are going to look at how and why blood clots.

Clotting prevents us from bleeding to death, and also protects us from nasty disease-causing organisms, called pathogens, entering our body.

When we injure ourselves, we can damage the blood vessels just below our skin. This can cause blood to either leak into our tissue and form a bruise, or, if the skin is broken to openly bleed.

To prevent these horrible things happening, blood clotting occurs.

So let’s have a look at how this happens.

Starting with platelets. These are tiny cell fragments that float around in our blood.

When a blood vessel is damaged, collagen is exposed. This collagen exposure attracts platelets to the injured area. The platelets then stick together to form a plug.

They’ve quickly built a little barrier that stops us from losing too much blood. However, this platelet plug isn’t that strong. So it needs to be made stronger.
A protein called fibrin does exactly that.

In our blood there are soluble fibrinogen proteins. At a wound, these soluble fibrinogen proteins are exposed to outside chemicals that aren’t normally found in blood vessels. Like with the collagen and platelets, this exposure causes the fibrinogen proteins to turn into sticky fibrin fibres.

The fibrin fibres form a mesh, holding all the platelets together and making a much stronger clot.

More platelets, red blood cells and other components in our blood, all get stuck in the mesh making it even stronger. This clot stops more blood escaping the body. And also prevents nasty pathogens entering our body from the outside.

The clot develops into a scab, which protects the wound as it heals and new layers of skin form underneath. So really, all a scab is is just platelets trapped in the fibrin mesh!

When the new skin is fully formed, the scab will fall off, revealing the lovely brand new skin underneath.

Remember that I said the exposure to collagen causes the platelets to stick together? And the exposure to outside chemicals causes the fibrinogen to turn into sticky fibrin?

Both the platelets and the fibrin only become sticky AFTER the exposure. This means that in a normal, healthy blood vessel they won’t randomly cause clots.

So from this video, you should understand the magic of blood clotting. Platelets are first to the scene closely followed by fibrin fibres. Our blood clots so that we don’t lose a lot of blood and don’t let lots of nasty pathogens into our body if we cut ourselves.

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(USMLE topics) The 3 stages of hemostasis, blood clotting, bleeding disorders and formation of unwanted blood clots (thrombosis).

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Hemostasis is the process that controls bleeding at the site of injury. Blood loss is stopped by formation of blood clots that seal the breaks in blood vessels. Hemostatic mechanisms involve small cell fragments known as platelets and a dozen of soluble clotting factors. These elements are always present in the blood in their inactive form, ready to activate, typically within seconds of an injury. When blood vessels are damaged, blood is exposed to components of the surrounding tissue. Some of these components bind to and activate platelets. Activated platelets are involved in all stages of hemostasis:
– First, they secrete chemicals that induce blood vessels to constrict, thereby reducing blood loss. This is known as vascular spasm, the most immediate response to tissue injury. Vascular spasm is also triggered by local pain receptors, and by substances released by endothelial cells.
– Second, activated platelets become adhesive to each other and to the endothelium; they clump together, forming a platelet plug. They also secrete substances that attract other nearby platelets, activating them in a positive feedback loop, speeding up the formation and propagation of the plug.
– Third, the surface of activated platelets serves as the site for coagulation – the formation of blood clots. A clot is essentially a platelet plug reinforced with strands of a protein called fibrin – the final product of the coagulation cascade. Coagulation is a complex chain reaction where one clotting factor activates the next in the multi-step pathway.
There are 2 activation pathways for coagulation:
– The extrinsic pathway starts with the exposure of blood clotting factors to the tissue factor, TF, in the extravascular tissue. This pathway is induced by injuries to blood vessels.
– The intrinsic pathway, which involves only factors within blood vessels, is thought to serve as a positive feedback loop, amplifying coagulation.
The 2 pathways converge into a common pathway producing thrombin and ultimately fibrin. Thrombin has the central role in the coagulation cascade. It cleaves soluble fibrinogen to generate insoluble fibrin. Thrombin also further activates platelets, and initiates a positive feedback loop that is essential for clot propagation.
Blood clots prevent blood loss during wound healing, but once the vessels are repaired, they must be dissolved to restore blood flow. This process, called fibrinolysis, is a small cascade that produces the enzyme plasmin. Plasmin cleaves fibrin and dissolves the clot.
Because most clotting factors are produced in the liver and their production requires vitamin-K, liver diseases such as cirrhosis, and vitamin-K deficiency may cause excessive bleeding. The main bleeding disorders, however, are inherited. These conditions are caused by gene mutations that lead to deficiency of a certain clotting factor. They are usually treated with replacement therapy, using purified factors produced by recombinant technology, or frozen platelets.
While formation of blood clots is critical to control bleeding, inappropriate coagulation can be dangerous. In fact, far more people die from unwanted blood clotting than from clotting failure. Unwanted blood clot formation, known as thrombosis, is the most common cause of blocked arteries in heart attacks, strokes and pulmonary embolism.
Factors that prevent inappropriate coagulation include:
– Platelet-repellent property of the endothelium,
– Anticoagulant factors – enzymes that prevent clot formation,
– and the fibrinolysis cascade that dissolves blood clots after they are formed,
Fluidity of normal blood flow also helps dilute the small amount of thrombin that forms spontaneously. Decreased flow or stagnation of blood may increase risks for thrombosis.
People with high risks of unwanted blood clotting are treated with drugs that inhibit platelet aggregation, such as aspirin; or drugs that inhibit coagulation, such as heparin or warfarin.
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“The classic coagulation cascade is divided into the extrinsic and intrinsic pathways which both lead to what is called the common pathway. The hallmark of both intrinsic and extrinsic pathway of coagulation is the sequential activation of a series of clotting factors. Clotting factors are shown as Roman numerals, and numerals followed by the alphabet represents an active clotting factor. For example X –: Xa (Xa being the active factor)

The classical view of coagulation is very useful to interpret coagulation tests and identifying bleeding disorders based on coagulation factors. However physiologically the coagulation cascade is much more confusing. There is a cell based model of coagulation which involves 3 steps: initiation, amplification and propagation.”

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During this lecture Professor Zach Murphy will be teaching you about Hemostasis. We will be discussing the coagulation cascade including the intrinsic and extrinsic clotting mechanisms.

This video will cover the following topics:
1. Vascular Spasm
2. Platelet Plug Formation
3. Coagulation
4. Clot Retraction and Repair
5. Fibrinolysis

References:
● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ: Pearson; 2020.
● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB, Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison’s Principles of Internal Medicine. New York etc.: McGraw-Hill Education; 2018.
● Sabatine MS. Pocket Medicine: the Massachusetts General Hospital Handbook of Internal Medicine. Philadelphia: Wolters Kluwer; 2020

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Coagulation Cascade: description of the physiological process of hemostasis including platelet plug formation and about the intrinsic and extrinsic pathways. More details about the coagulation cascade: https://www.thrombosisadviser.com/en/understanding-thrombosis/the-coagulation-cascade/

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