Platelet Activation, Adhesion, And Formation Of Platelet Plug

The procedure that halts bleeding at the site of an injury is called hemostasis, and platelets, also referred to as thrombocytes, are essential to this process. The formation of blood clots and the restoration of injured blood arteries depend heavily on their adherence, activation, and activity. Below is a summary of these procedures:

Platelet Activation

After an injury, endothelin and vasoconstrictor molecules are released, which causes the smooth muscle to contract and triggers reflex vasoconstriction.

Platelet activation is the next phase in the platelet phase, which is accomplished through the arachidonic acid pathway, which converts arachidonic acid in the endothelial vascular endothelium into prostaglandins, specifically thromboxane and prostacyclin. The first step in the platelet phase is platelet adhesion, which is facilitated by glycoprotein 2B3A and glycoprotein 1B/V/9. Glycoprotein 2B3A directly adheres platelets to the basement membrane, while glycoprotein 1B/V/9 plays an indirect role.

Prostacyclin is a vasodilator that causes vasodilation, whereas thromboxane is a vasoconstrictor and stimulant that helps to reduce blood loss. These two agents have opposite effects on the body.

Thrombine-induced release of ADP from platelets triggers platelet activation and aggregation through its interaction with platelet receptors P2Y1 and P2Y12.  P2Y1 starts the process of activating platelets, and P2Y12 finishes it. This causes platelets to aggregate and form clots.
The coagulation pathway has distinct roles during tissue injury and operates in parallel with the platelet phase.

Thromboxane:  Vasoconstrictor & stimulator (Reduces blood loss).    

• Prostacyclin:  Vasodilator (Causes vasodilation)
• Release of ADP (Platelet Activation):  Thromboxane effect
• ADP Acts on Platelet Receptors:  P2Y1 (Initiates platelet activation)
• And  P2Y12 (Completes activation, leads to aggregation)
• Platelet Aggregation (Forming a clot)
• Coagulation Pathway (Parallel to Platelet Phase)
• Different functions during tissue injury
• Formation of Blood Clot

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Platelet Function

By acting as GP2B3 receptor antagonists, several medications block platelets' ability to adhere to the basement membrane underneath them, hence inhibiting platelet activity.  By acting as GP2B3A inhibitors, drugs such as tirofiban, eptifibatide, and abciximab stop platelet adhesion and aggregation.

Platelet Adhesion And Aggregation

A deficit of glycoprotein 1B/V/9 in Bernard-Soulier syndrome can result in a congenital platelet adhesion deficiency, known as Glanzmann thrombasthenia.  The adhesion process cannot be started by a single factor, such as von Willebrand factor deficit; von Willebrand factor release upon endothelial injury is crucial for starting glycoprotein 2B3 attachment and glycoprotein 1B/V/9 activation, which in turn causes platelet adherence.

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Formation Of Platelet Plug

 Targeting ADP, which is in charge of activating receptors P2Y1 and P2Y12, crucial for platelet aggregation, clopidogrel prevents the formation of a platelet plug.

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Mechanism Of Action Of Anti Platelet Drugs

Several classes of antiplatelet medications, such as: ADP receptor antagonists (such as clopidogrel) ,Thromboxane and cyclooxygenase inhibitors (such as aspirin)
o Inhibitors of glycoprotein 2B3A, such as abciximab
o Inhibitors of plaque aggregation, such as dipyridamole

When a blood artery bursts, clot formation happens in 15–20 seconds for severe trauma and 1–2 minutes for minor injuries. The degree of trauma affects how long it takes for a clot to form; it typically takes three to six minutes for a clot to fill the whole length of a ruptured vessel.
The clot retracts after 20 to 60 minutes, shutting the blood vessels and tightening the vessel wall even more.

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