Platelets / Thrombocytes

Introduction:
Platelets are also called as thrombocytes.
Size: they are very small discs with diameter varying from 1 to 4 micrometers.
The normal concentration of platelets in the blood is between 150,000 and 450,000 per microliter.

Formation:
They are formed in the bone marrow from megakaryocytes. The latter are extremely large cells in the marrow and they fragment into the minute platelets either in the bone marrow or soon after entering the blood.

Destruction:
The platelet has a half-life in the blood of 8 to 12 days. Then it is eliminated from the circulation mainly by the tissue macrophage system. More than one half of the platelets are removed by macrophages in the spleen, where the blood passes through a latticework of tight trabeculae.

Platelets do not have nuclei and cannot reproduce. Yet, they have many functional characteristics of whole cells.
1) Actin and myosin molecules are present in their cytoplasm. They are contractile proteins similar to those found in muscle cells and still another contractile protein, thrombosthenin that can cause the platelets to contract.
2) There are also residuals of both the endoplasmic reticulum and the Golgi apparatus that synthesize various enzymes and especially store large quantities of calcium ions.
3) Mitochondria and enzyme systems can produce ATP and ADP.
4) There are also enzyme systems that synthesize prostaglandins. These cause many vascular and other local tissue reactions.

The cell membrane of the platelets is also important. On its surface is a coat of glycoproteins that repulses adherence to normal endothelium and yet causes adherence to injured areas of the vessel wall, especially to injured endothelial cells and even more so to any exposed collagen from deep within the vessel wall. In addition, the platelet membrane contains large amounts of phospholipids that activate multiple stages in the blood-clotting process.

Mechanism of the Platelet Plug:
1) When platelets come in contact with a damaged vascular surface, especially with collagen fibers in the vascular wall, the platelets immediately change their own characteristics drastically. They begin to swell and assume irregular forms with numerous irradiating pseudopods protruding from their surfaces.
2) Their contractile proteins contract forcefully and cause the release of granules that contain multiple active factors.
3) They also become sticky so that they adhere to collagen in the tissues and to a protein called von Willebrand factor that leaks into the traumatized tissue from the plasma.
4) They secrete large quantities of ADP and their enzymes form thromboxane A2. The ADP and thromboxane in turn act on nearby platelets, activate them and increase their stickiness. This causes more platelets to adhere to the original activated platelets.
The above steps form a platelet plug which is usually loose and can only successfully block blood loss from small vascular openings.

The platelet-plugging mechanism is extremely important for closing minute ruptures in very small blood vessels that occur many thousands of times daily. Indeed, multiple small holes through the endothelial cells themselves are often closed by platelets actually fusing with the endothelial cells to form additional endothelial cell membrane. A person who has few blood platelets develops each day literally thousands of small hemorrhagic areas under the skin and throughout the internal tissues, but this does not occur in the normal person.

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