What Is Blood Clotting and How Are Blood Clots Formed?

What Is Blood Clotting And How Are Blood Clots Formed?

The body suffers injury everyday, it could be a minor cut, burns, or bruises on your skin. Sometimes our body can heal all by itself miraculously when there’s an injury, it may take some days and weeks, depending on the condition. Most people have the ability to heal from an injury much faster through a body mechanism but others take much longer.

This mechanism is known as blood clotting.

Blood clotting is initiated in one of two ways. The first, referred to as the internal pathway, it occurs when a clot forms inside of a blood vessel due to an injury to the blood vessel itself.

The second, referred to as the external pathway, it occurs following an injury, such as a cut, when blood is exposed to the outside environment.

No matter how the clotting process is initiated, the clot forms in the same way. This is referred to as the common pathway.

Blood cells called platelets, along with numerous factors including proteins, enzymes, vitamin k, and calcium, found in blood plasma, are involved in the clotting process.

In this post, the main focus is on factors leading to external blood clotting, the processes and mechanisms.

What is blood clotting?

Blood clotting is an important process that prevents excessive bleeding when a blood vessel is injured. Platelets and proteins in plasma work together to stop the bleeding by forming a clot over the injury.

blood platelets

How are blood clots formed?

Blood clots are formed in four different stages and processes:

  1. Vasoconstriction – Narrowing of an injured blood vessel so that blood flows out more slowly and clotting can start right away.
  2. Platelet activation – The cellular components of the clotting mechanism include platelets, endothelial cells.
  3. Thrombus formation – Activity of proteins, enzymes and ions.
  4. Dissolution of the clot.

How long does it take for blood clot to form?

The prothrombin time test measures how long it takes for your blood to clot. Blood clotting takes about 30 seconds to form depending on the injury. It may take longer if you take blood thinners. Other reasons for abnormal results include hemophilia, and liver disease.

Blood Clotting Factors

There are certain factors that helps the blood to clot when there’s injury.

blood clotting factors

These clotting factors in the blood include:

  • Fibrinogen
  • Fibrin
  • Prothrombin
  • Thrombin
  • Thromboplastin
  • Calcium
  • Proaccelerin
  • Accelerin
  • Proconvertin
  • Antihemophilic factor A
  • Antihemophilic factor B
  • Stuart-Prower factor
  • Antihemophilic factor C
  • Hageman factor
  • Fibrinase

Blood Clotting Mechanism

The clotting mechanism is broken into two stages:

  • Primary hemostasis
  • Secondary hemostasis

Primary Hemostasis

The primary hemostasis is the formation of a weak platelet plug which is achieved in four phases: vasoconstriction, platelet
adhesion, platelet activation, and platelet aggregation.

Secondary Hemostasis

The secondary hemostasis is stabilizing the weak platelet plug into a clot by the fibrin network. This involves the clotting factors acting in a cascade to ultimately stabilize the weak platelet plug.

blood clotting mechanism

This is achieved by completing three tasks: triggering activation of clotting factors, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin.

Blood clotting goes through a series of mechanisms, this includes:

  • Vasoconstriction
  • Platelets activation
  • Thrombus formation
  • Dissolution of the clot


Vasoconstriction is used to describe tightening of the muscle in the blood vessel wall. When an injury occurs, nerves in the tissue surrounding the blood vessel stimulates the muscle of the blood vessel wall to constrict, narrowing the lumen of the vessel, thereby temporarily restricting the flow of blood from the wound.

This initial vasoconstriction lasts only about a minute, but then a secondary mechanism takes over, that sustains vasoconstriction at the site of the wound.

The secondary mechanism involves release of chemicals, such as serotonin and epinephrine, from the blood cells called platelets that have started to gather at the site of the injury.

blood clotting formation

Platelets continue to stimulate the nerves, which causes contraction of the muscle of the vessel for several more minutes.

Platelet activation

Following damage, such as an accidental cut, blood is exposed to collagen from the nearby tissues. At the time of injury, two things happen almost instantly and simultaneously.

First, two substances, fibrinogen, found in collagen, and prothrombin, found on the surface of the platelets are activated.

The platelets begins to stick to the exposed collagen. This initial step in blood clotting is called platelet activation.

As the platelets begin to assemble at the site of the injury, several factors are released from the platelets. One of them is the von willebrand factor (vWF), binds the platelets to the collagen fibers.

platelet activation

Several substances are also released from the platelets, including adenosine diphosphate (ADP), which attracts more platelets until a seal is formed over the opening in the blood vessel wall.

The clump of platelets is known as the platelet plug. The platelet plug may be sufficient to seal a small vessel. However, in larger vessels, the platelet plug is temporary and will be replaced by a thrombus. The platelet plug does not contain red blood cells, and it is referred to as the white thrombus.

Thrombus formation

A more stable clot, called thrombus, must form to make a longer lasting seal on larger injured blood vessels. The thrombus must be able to maintain a seal on the damaged blood vessel wall, especially that of an artery where the blood pressure is higher than in a vein, even after the blood vessel walls are no longer constricted.

Fortunately, the clotting process is self-limiting. Substances called antithrombins prevent the clot from continuing to enlarge, otherwise the established clot would block the flow of blood within the vessel.

Activation of prothrombin in the platelet aggregation phase sets off a series of additional events, starting with activation of factor X, that leads to formation of the thrombus.

Activated factor X known as Stuart-Prower leads to activation of prothrombin. Prothrombin in it’s active form is referred to as thrombin. Several substances, including thromboplastin, calcium, and vitamin k, play a role in activation of prothrombin to thrombin.

Thrombin helps to convert fibrinogen to fibrin. Fibrin is an insoluble protein, when it reacts with many other substances it polymerizes to form strands that web together to form the basis of the thrombus.

thrombus formation

The web of fibrin is referred to as fibrin mesh. Fibrinase is activated to serve as additional stabilization of the fibrin mesh. When viewing the fibrin mesh that has been stabilized with fibrinase under microscope, it is said to have the appearance of cross stitching on loosely woven fabric.

Within a few hours of the injury, as part of the inflammatory process that normally occurs following damage to tissue, white blood cells gather at the site of the injury to help reduce the risk of infection.

Local inflammation is identified by the presence of pain, redness, heat, swelling, and loss of function.

Systemic inflammation is identified by the presence of fever. The thrombus may contain red blood cells, therefore it is sometimes referred to as the red thrombus.

Dissolution of the clot

Dissolution of the clot, known as fibrinolysis occurs when a negative feedback system signals that sufficient healing of the blood vessel wall has occurred, and a substance called plasminogen is activated.

Plasminogen in its active form is called plasmin. Plasmin signals the clotting mechanism to inactivate the clotting process and begins the anticoagulant process, with the use of naturally occurring heparin. This is achieved by digesting the fibrin, which is the main component of the thrombus. The body then returns to it’s state of balance called homeostasis.

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