A. Thrombocytes (= platelets)


Thrombocytes (also called platelets):

  • do have a plasma membrane
  • do NOT have a nucleus
  • are small disks
  • contain many chemicals (serotonin, calcium, ADP, prostaglandin's)
  • live for a short period (10 days)









B. Origin of the Platelets:

The platelets are fragments (=pieces) from large cells in the bone marrow: the Megakaryoblast.

The megakaryocyt develops extensions that rupture, releasing pieces of cytoplasm into the blood of a local capillary. In each fragment, the plasma membrane quickly seals (=closes) the fragment thereby creating a small cell (without a nucleus).

There are about 250,000 - 500,000 platelets in mm3 (cubic millimeter) blood.




C. Hemostasis



Hemostasis is the mechanism that stops a bleeding. In the diagram, a wound is present thereby creating a "hole" in a blood vessel. Note that the vessel is surrounded by muscles. The inner layer of the vessel is, as usual, formed by endothelial cells (= the endothelium).

When a wound occurs, the following three steps are taken to stop the bleeding:

  1. Vascular spasms: the muscle layers in the vessel wall will contract. This is initiated by many factors such as release of local chemicals (potassium ions) from (damaged) endothelial cells, platelets) but also by local (pain) reflexes. This response is very fast and last for 20-30 minutes. This contraction can reduce and sometimes even stop the bleeding thereby giving time for the next step.
  2. Plug Formation: Platelets in the neighborhood of injured endothelial cells start to swell and become sticky. This will make them accumulate in the neighborhood of the hole. There they start releasing chemicals such as serotonin (which prolongs the vascular spasm), ADP (which attracts additional platelets) and Thromboxane A2 (which promotes both events). All this will start to close the hole and reduce or stop even more the blood flow. However, this "plug" is very delicate and can easily be rubbed off if the next step does not occur.
  3. Coagulation: this is the name for the final blood clotting. This is a complicated process (which will be discussed in the Hematology & Immunology module next year) in which, as the last step, fibrinogen is converted into fibrin. The fibrinogen is already present and available in plasma and is soluble. Because of this coagulation step, the fibrinogen start to stick together into a mesh, a network, called fibrin. This fibrin is insoluble. The fibrin mesh traps the platelets and other blood cells in the plug, and makes this plug very hard. This is now called a (blood) clot.


D. Thrombocytopenia



If a person suffers from a reduced number of thrombocytes (=thrombocytopenia), he will have difficulty with hemostasis. In the case of a wound, the first step (spasms) and the third step (clotting) are still functioning, but there will be less or no plug formation.

These patients typically show small purple bleedings in their skin, called petechiae.

This disease illustrates an important point. In daily life, because of wear and tear, we suffer constantly from (small) bleeding. The vast majority of these bleedings are not noticed because they are very small and are resolved before becoming visible.

If a person however does not have enough platelets then plug formation is impaired. So, in that case, the spasms still occur (reducing the blood flow) and the third step (clotting) will also occur (because there is enough damage in that neighbourhood) but there will be a small amount of blood lost in the tissue. This becomes visible as small clots (purple or dark red). These petechiae most often occur where the tissue works most (wear and tear at joints, hand and feet) but can also occur in tissues inside the body, which are not visible.

The point this disease illustrates is that the hemostasis machine is working all the time to stop the bleeding in those (small) vessels that ruptured spontaneously all the time.