Chapter 22: Blood

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22.20:

Formation of the Platelet Plug

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Anatomy and Physiology

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Formation of the Platelet Plug

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22.9: Factors Affecting Erythropoiesis

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22.21: Coagulation

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In an injured blood vessel, the platelet phase – which overlaps with the vascular phase – begins about 15-20 seconds after the onset of vascular spasm. As the blood vessel constricts, the damaged endothelial cells contract on the basement membrane. As a result, the collagen fibers in the underlying connective tissue are used for adhesion of the circulating platelets. The von Willebrand factor, a large plasma protein, stabilizes the platelet-collagen association. Once adhered, the platelets activate and develop cytoplasmic processes that extend toward nearby platelets. The activated platelets become stickier and release chemical messengers like adenosine diphosphate or ADP, calcium, serotonin, and thromboxane. ADP aggregates more platelets to stick to the damaged endothelium, while serotonin and thromboxane promote further vascular spasm. As more platelets arrive, they release more chemical messengers, stimulating further aggregation. The platelets aggregate to form a plug within a minute of injury, which, along with vascular spasm, controls blood loss. Later, this plug is converted into a more permanent clot.

22.20:

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.

As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets circulating in the blood adhere to these exposed collagen fibers at the injury site.

A crucial plasma protein called the von Willebrand factor plays a pivotal role in stabilizing the bond between platelets and collagen fibers, ensuring steadfast attachment of platelets to the injury site.

Once adhered, platelets activate and become more adhesive. They release substances, such as Adenosine Diphosphate (ADP), serotonin, and thromboxane A2, which attract more platelets to the site and further promote vascular spasm. This platelet aggregation process culminates in forming a platelet plug within a minute of the injury. This plug collaborates with the vascular spasm to effectively control blood loss.

The platelet phase of hemostasis plays a vital role in averting excessive bleeding following an injury. This phase temporarily seals off the wound by forming a platelet plug, allowing the subsequent coagulation phase to create a more permanent clot. In addition, the substances released by activated platelets promote wound healing.

Several key factors limit the growth of the platelet plug. Prostacyclin, a prostaglandin released by endothelial cells, inhibitory compounds by white blood cells, and circulating plasma enzymes break down ADP near the plug to check on the platelet aggregation. Certain compounds can also inhibit plug formation when present in abundance. For instance, serotonin, at high concentrations, blocks the action of ADP. Lastly, developing a blood clot reinforces the platelet plug but isolates it from the general circulation.