Introduction
Blood platelets, or thrombocytes, are cells in the blood that play an important role in blood clotting, i.e. stopping bleeding. Along with red blood cells and immune cells (leukocytes), they are one of the main components of the blood. The technical term thrombocyte for blood platelets is derived from the Greek von thrombos for “clot”, which also very aptly describes their function – they form clots.
Place of platelet formation
The thrombocytes are formed in the bone marrow. Here are so-called megakaryocytes (thrombocyte-forming giant cells), from which the thrombocytes are strangulated. Up to 8000 thrombocytes can be strangulated from one megakaryocyte. This process is called thrombopoiesis. The formation of thrombocytes from megakaryocytes is promoted by the hormone thrombopoietin.
Life span and number of platelets
In the blood there are usually between 150. 000 and 380. 000 thrombocytes per μl blood. That makes them the second most common cells in the blood. The life span of platelets is about eight to twelve days.
Platelet size
Platelets are small disc-like platelets with a diameter between 1.5 and 3 μm μm and are therefore the smallest cells in the blood. Due to their small size they also have no cell nucleus. During hemostasis, the platelets change their shape and get small spurs in all directions (pseudopodia). In this way they can increase their surface area.
Blood platelets Standard values
Platelet norms vary according to age group. In adults, there should be between 150,000 and 350,000 platelets per μl blood. In newborns, only 100,000 to 250,000 platelets per μl blood are normal and in adolescents (up to 17 years) 200,000 to 400,000 platelets per μl blood.
One speaks of thrombocytopenia (lack of blood platelets) if the value is less than 150,000 thrombocytes per μl blood. One speaks of thrombocytosis if the value is 500,000 thrombocytes per μl blood. The blood platelets (thrombocytes) have the task of coagulating the blood.
If an injury occurs in a vessel, the platelets are supposed to prevent a larger bleeding by closing the vessel as quickly as possible. This works by releasing messenger substances when a vessel is injured. The thrombocytes are transported with the blood stream to the injured area and are activated by the messenger substances.
They can now bind to specific receptors (docking sites) on the tissue beneath the injured vessel. After binding, various mechanisms are activated. On the one hand, the platelets release substances that cause even more platelets to reach the injured site and bind to the existing platelets.
This activates the platelets and changes their shape. They form small projections in different directions and can thus clump together. There are also various modulators, the coagulation factors, e.g. the von Willebrand factor, which support this reaction.
The reaction is also known as thrombocyte aggregation. This is also where some drugs (known as thrombocyte aggregation inhibitors) come into play, for example aspirin (ASS). The connected blood platelets form a clot called a red thrombus.
This temporarily seals the injury. At the same time, the thrombocytes release other substances that activate the coagulation cascade. This leads to the activation of a number of substances, first thrombin and then fibrin.
After activation by thrombin, the fibrin forms threads and thus forms a clot. This is called a white thrombus. It permanently closes the vascular injury.
This part of the hemostasis reaction is called blood clotting. The coagulation of the blood can also be interfered with by various drugs (anticoagulants). These are for example heparins (Clexane syringe e.g. after operations).
Normally there are always 150,000 – 380,000 platelets in a microlitre of blood, which in a man weighing 80 kilos is several trillion cells. Nevertheless, their number seems negligible when you think of the 4-5 million red blood cells (or erythrocytes) per microlitre of blood found in an average person. Blood platelets are indispensable for the body because of their function – the closure of damaged vessels.
A lack of platelets leads to a shortened bleeding stop. The physician refers to this as thrombobyztopenia. By definition, thrombocytopenia occurs when the number of thrombocytes or blood platelets falls below 150,000 per microlitre of blood.
There is a very wide range of causes for a lack of blood platelets, which is why only the most common diseases will be discussed below. In principle, three approaches can be distinguished here: 1) A lack of production can be the result of a congenital or acquired educational disorder: An example of a congenital educational disorder is the hereditary Wiskott-Aldrich syndrome, with a frequency of 1 in 250,000. Acquired educational disorders such as bone marrow damage, which can be caused by a drug, radiation, or a toxic substance, occur much more frequently.
Leukaemia is also one of them and can lead to a platelet deficiency, as it impairs the production in the bone marrow. 2) A shortened life span can simply be caused by bleeding: In the case of severe blood loss, every single platelet is urgently needed, which logically means that less platelets are available. Prolonged therapy with the thrombosis inhibitor heparin, which may be necessary in bedridden patients, can also trigger a platelet deficiency: The body forms antibodies against the blood platelets due to the heparin administration, whereupon they agglutinate, i.e. agglomerate.
Now the thrombocyte level in the blood drops to below 50% of the normal level – an acute platelet deficiency is the result. This is known as heparin-induced thrombocytopenia of the second type, HIT2 for short. An immediate change of the anti-thrombosis therapy is indicated!
Another conceivable cause of a severe drop in blood platelets is a so-called transfusion incident, in which, for example, a patient with blood group A receives a blood bag from a donor with blood group B. The recipient’s body reacts to the foreign blood by sending all its platelets out to bind it. This results in an immediate clotting of the transfused blood and a life-threatening shock.
In order to avoid such accidents, every doctor is instructed to carry out the so-called bedside test before administering blood preserves, in which patient blood and donor blood are mixed on a small card to prevent clumping. This test is of course only the last link in a series of strict testing mechanisms! A lack of vitamin B12 or autoimmune diseases such as Werlhof’s disease (antibody formation against platelets) can also cause a platelet deficiency.
3)A distribution disorder occurs when the spleen is enlarged. The spleen sorts out damaged platelets and destroys them. If the function of the spleen is impaired, the platelets do not distribute themselves evenly throughout the body.
The above causes are only a brief outline of the wide range of diseases that can lead to a platelet deficiency. However, some diseases with less than 100 documented cases worldwide are so minor in their relevance that it would go beyond the scope of this report to mention them all here. In addition to the already mentioned platelet deficiency, there is also, as one can imagine, the excess of platelets.
This too is dangerous for the body and, by definition, occurs when the platelet count exceeds 500,000 per microlitre of blood. The technical term for this is thrombocytosis. The danger with thrombocytosis is the reduced fluidity of the blood and the resulting reduced blood flow.
It also leads to increased formation of thrombi, i.e. blood clots, which in an emergency can flow into the heart, lungs or brain and block the vessels there. This results in reduced blood flow to the tissue behind the heart, lungs or brain, which leads to a loss of function and decline of the affected organ. Known clinical pictures are the cerebral infarction, also called stroke, the heart attack, and the lung infarction.
In principle, however, any organ can be affected. Conversely, the above-mentioned clinical pictures are not exclusively due to a pathological increase in the blood platelet count. Other factors such as stress, alcohol, nicotine and lack of exercise are much more common! The cause of thrombocytosis is usually a compensatory overproduction of blood platelets after major surgery with blood loss, malignant tumours, chemotherapy, but also chronic inflammatory diseases such as Crohn’s disease. – 1: A deficient production of blood platelets
- 2: a shortened life span/prolonged degradation
- 3: Distribution disorders in the blood
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