Thrombosis also occurs when blood is allowed to pool, which causes clotting factors and platelets to form a blood clot even in the absence of an injury. Platelets are membrane-bound cell fragments derived from megakaryocytes, which are produced during thrombopoiesis.
Platelets are small, clear, irregularly-shaped cell fragments produced by larger precursor cells called megakaryocytes. Platelets are also called thrombocytes because they are involved in the blood clotting process, which is necessary for wound healing.
Platelets are continuously produced as a component product of hematopoiesis blood cell formation. Platelets are produced during hematopoiesis in a sub-process called thromopoiesis, or production of thrombocytes.
Thrombopoiesis occurs from common myeloid progenitor cells in the bone marrow, which differentiate into promegakaryocytes and then into megakaryocytes. Megakaryocytes stay in the bone marrow and are thought to produce protoplatelets within their cytoplasm, which are released in cytoplasmic extensions upon cytokine stimulus.
The protoplatelets then break up into hundreds of platelets that circulate throughout the bloodstream, while the remaining nucleus of the ruptured megakaryocyte is consumed by macrophages. Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced by the liver and kidneys.
Thrombopoietin stimulates differentiation of myeloid progenitor cells into megakaryocytes and causes the release of platelets.
Thrombopoietin is regulated by a negative feedback mechanism based on platelet levels in the body so that high levels of platelets result in lower levels of thrombopoietin, while low levels of platelets result in higher levels of thrombopoietin.
Each megakaryocyte produces between 5, and 10, platelets before its cellular components are fully depleted. The average lifespan of a platelet is just 5 to 10 days. Old platelets are destroyed by macrophage phagocytosis in the spleen and by Kupffer cells in the liver.
Hematopoiesis : Myeloid progenitor cells differentiate into promegakaryocytes, and megakaryocytes, which release platelets. Balanced thrombopoiesis is important because it directly influences the amount of platelets in the body and their associated complications. If the number of platelets is too low, excessive bleeding can occur, even from minor or superficial injuries.
If the number of platelets is too high, blood clots can form thrombosis and travel through the bloodstream, which may obstruct blood vessels and result in ischemic events. These include stroke, myocardial infarction, pulmonary embolism, or infarction of other tissues.
An abnormality or disease of the platelets is called a thrombocytopathy, which could be either a low number of platelets thrombocytopenia , a decrease in function of platelets thrombasthenia , or an increase in the number of platelets thrombocytosis. In any case, issues with the number of circulating platelets is often due to issues in thrombopoietin feedback regulation, but may also be associated with genetic characteristics and certain medications and diseases.
For example, thrombocytopenia often occurs in leukemia patents. Cancerous myeloid cells crowd out healthy ones in the bone marrow, causing impaired thrombopoiesis. As megakaryocytes develop into giant cells, they undergo a process of fragmentation that results in the release of over 1, platelets per megakaryocyte. The dominant hormone controlling megakaryocyte development is thrombopoietin often abbreviated as TPO.
Platelet Structure. Platelets are actually not true cells but merely circulating fragments of cells. But even though platelets are merely cell fragments, they contain many structures that are critical to stop bleeding.
They contain proteins on their surface that allow them to stick to breaks in the blood vessel wall and also to stick to each other. They contain granules that can secrete other proteins required for creating a firm plug to seal blood vessel breaks. Also platelets contain proteins similar to muscle proteins that allow them to change shape when they become sticky. The pictures above show normal platelets on the left.
They are shaped like a plate, therefore their name. When platelets are stimulated by a break in the blood vessel wall they change shape as shown in the other three pictures. They become round and extend long filaments. They may even look like an octopus, with long tentacles reaching out to make contact with the broken blood vessel wall or with other platelets.
With these long filaments, platelets then form a plug to seal the broken blood vessel. In addition to being the smallest blood cell, platelets are also the lightest.
Therefore they are pushed out from the center of flowing blood to the wall of the blood vessel. There they roll along the surface of the vessel wall, which is lined by cells called endothelium. The endothelium is a very special surface, like Teflon, that prevents anything from sticking to it. However when there is an injury or cut, and the endothelial layer is broken, the tough fibers that surround a blood vessel are exposed to the liquid flowing blood.
It is the platelets that react first to injury. The tough fibers surrounding the vessel wall, like an envelop, attract platelets like a magnet, stimulate the shape change that is shown in the pictures above, and platelets then clump onto these fibers, providing the initial seal to prevent bleeding, the leak of red blood cells and plasma through the vessel injury. The color photograph is a microscopic picture of a drop of blood spread out onto a glass slide.
The magnification is not as high as the pictures above, so the platelets seem very small. It can be seen that as the platelets touch the glass, they begin to stick together forming a long string. This illustrates the basic function of platelets, to stick to any foreign surface and then to stick together. The red blood cells in this picture are normal, with their round shape and their thin center. Disorders of Platelet Function. The most common disorder of platelet function is caused by aspirin.
Aspirin blocks one of the steps required for platelets to stick together. This effect of aspirin is what makes it an effective treatment for patients who have disorders of blood clotting or thrombosis. For example, a person coming to an emergency room with severe chest pain and a suspected heart attack is immediately given aspirin.
This prevents some of the platelet clumping which can obstruct the blood flow to the heart. Aspirin is an effective medicine to prevent these clots, but it does not totally paralyze the platelet. Therefore many people take daily aspirin and have no problems with bleeding. However aspirin can be potentially dangerous in patients who already have a risk for bleeding, such as boys with hemophilia or patients who have too few platelets and depend on each platelet having full function.
Rare conditions result in the bone marrow producing too many platelets, sometimes as many as one million or two million per microliter. In some of these patients, there are increased risks for blood clots, but many patients with these disorders have no problems. Thrombocytopenia is the principal focus of this website. Thrombocytopenia can be caused by failure of the bone marrow to produce normal numbers of platelets.
Bone marrow failure has multiple causes. These are not discussed on this website. Essential thrombocythemia. In this condition, your bone marrow makes too many platelets. People with this condition may have platelet counts of more than 1 million, which can lead to bleeding. Other symptoms can include blood clots that form and block blood supply to the brain or the heart. Doctors don't fully know what causes this type of thrombocythemia, but changes in bone marrow cells called mutations can lead to some cases.
Secondary thrombocytosis. This is another condition caused by too many platelets. Secondary thrombocytosis is more common. It's not caused by a bone marrow problem. Instead, another disease or condition stimulates the bone marrow to make more platelets. Causes include infection, inflammation, some types of cancer, and reactions to medicines. Symptoms are usually not serious. The platelet count goes back to normal when the other condition gets better. Platelet dysfunction.
Many rare diseases are linked to poor platelet function. This means the number of platelets is normal, but the platelets don't work as they should.
Medicines such as aspirin can cause this.
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