Blood platelets (thrombocytes)


Thrombocytes are blood platelets, of which each person carries approximately 150,000 to 350,000 per μl of blood. The thrombocytes perform an important function in blood clotting. Platelets therefore ensure that when a patient cuts himself or herself, the wound is closed again as quickly as possible and with as little blood loss as possible without losing too much blood beforehand.

An imbalance in platelets (too many or too few platelets) can therefore lead to various diseases. Since the thrombocytes originate from the so-called megakaryocytes, which are formed in the bone marrow, a malfunction in the bone marrow can be responsible for the reduced or increased thrombocyte count. A normal number of platelets is also important, as platelets can be partly responsible for heart disease and calcification of the blood vessels (arteriosclerosis).


Thrombocytes, also known as blood platelets, are constrictions of their progenitor cells, the so-called megakaryocytes located in the bone marrow. In the non-activated state, they correspond to a biconvex disc, i.e. they are bulging in both directions. This particular form of platelets is stabilized by a kind of fibrous supporting framework, the microtubules.

In addition, they also have a fibrous system which, when activated, gives them the ability to change their shape and form a large number of offshoots, so-called pseudopodia, which then serve as contact points for attachment and mutual networking. Due to the fact that platelets are only strangulations, they are not considered to be full cells and also do not have a cell nucleus, so further cell division is impossible. So-called mitochondria, the cell’s energy-producing organs, are still contained in the thrombocyte, however, which provides the necessary energy for the activation process. In addition, the blood platelets also contain various types of globules, so-called granules. These can receive coagulation-promoting messenger substances or enzymes and are released during the activation process.


The platelets fulfill a crucial function in blood clotting. If a patient cuts his or her finger, it starts bleeding briefly, but after a few seconds the bleeding stops and does not last for minutes. They have the function of forming a small thrombocyte clot (white platelet thrombus) locally in case a blood vessel is injured, and to increase the coagulation of the coagulation factors.

Without the platelets, a person would bleed to death in case of minor injuries or spontaneous bleeding, e.g. from the nose. As soon as there is damage to blood vessels, the platelets come into contact with the so-called von Willebrandt-factor, which normally has no contact with the thrombocytes due to the intact tissue. The von Willebrandt-Faktor together with the thrombocytes lead to thrombocyte aggregation, which means that the thrombocytes stick together by the von Willebrandt-Faktor.

This leads to the formation of a plug which closes the defective area in the blood vessel. This leads very quickly to hemostasis, triggered by the thrombocytes. This process is described as primary hemostasis or cellular hemostasis (synonym for hemostasis: hemostasis).

In addition, the coagulation factors of the blood are activated during secondary hemostasis. This leads to an activation of the protein fibrinogen, which, after its activation as fibrin, accumulates together and also forms connections with the existing thrombocyte network. This creates a much denser clot in which red blood cells can also become entangled, creating a piece of solid tissue that reliably seals the injury site of the vessel and thus stops the bleeding.

It is therefore also clear that thrombocytes should always be present in sufficient quantities in the blood, otherwise adequate hemostasis is not possible. At the same time, there should not be too many thrombocytes in the blood to avoid an increased formation of blood clots (thrombus). These thrombi can be carried over and then lead to a pulmonary embolism.

In addition, deep leg vein thrombosis and other diseases, sometimes also heart problems, can occur. This is particularly the case when patients carry many risk factors. Women are more frequently affected by leg vein thrombosis than men.Other risk factors include obesity, smoking, taking oral contraceptives, little exercise and drinking little, and eating foods that are too fatty.

All these risk factors favour the aggregation of the thrombocytes. The general rule is: The slower the blood flows, the more time is left for the platelets in the blood to settle together. If a person drinks little, the blood flow slows down as the blood becomes more viscous.

If a patient does not move enough, the blood accumulates in the legs and there is an increase in platelet aggregation in the leg veins (deep vein thrombosis). These examples show that it is not the thrombocytes themselves that “fail” in thrombosis because they congregate and form a thrombus. Rather, it is the circumstances in which they find themselves, i.e. the blood and the vessels through which they flow. Of course there is also a family history of thrombosis, which plays an important role in the formation of thrombi, i.e. the aggregation of thrombocytes. In general, however, platelets perform their function very well as long as they are not exposed to too many risk factors.