MORPHOLOGY OF PATHOLOGICAL FORMS OF PLATELETS

Аннотация

Platelets are small (2-3 microns) nuclear-free, flat, colorless shaped blood cells. They are formed by fragmentation of their megakaryocyte precursors in the bone marrow, with a platelet lifespan of 5-9 days. For a long time, researchers have proposed various classifications of platelet morphological forms based on variations in one parameter or another. They play an important role in the body, performing a number of complex functions, participating in various processes. It is on platelets that the preservation of blood in a liquid state, the dissolution of formed blood clots and the protection of the walls of blood vessels from damage depend. Key words: platelets, megakaryocytes, granulomer, hyalomer, thrombocytopathies. МОРФОЛОГИЯ ПАТОЛОГИЧЕСКИХ ФОРМ ТРОМБОЦИТОВ Аннотация. Тромбоциты — это небольшие (2–3 мкм) безъядерные, плоские, бесцветные клетки крови. Образуются путем фрагментации своих предшественников мегакариоцитов в костном мозге, продолжительность жизни тромбоцитов составляет 5–9 дней. Исследователи давно предлагают различные классификации морфологических форм тромбоцитов, основанные на вариациях тех или иных параметров. Они играют важную роль в организме, выполняя ряд сложных функций, участвуя в различных процессах. Именно от тромбоцитов зависит сохранение крови в жидком состоянии, растворение образовавшихся тромбов и защита стенок сосудов от повреждений. Ключевые слова: тромбоциты, мегакариоциты, грануломер, гиаломер, тромбоцитопатии. Platelets are an important component of the hemostatic system: platelet adhesion to the site of vascular injury, aggregation, secretion of coagulation factors, subsequent clot retraction, spasm of small vessels and the formation of a white platelet thrombus stop bleeding in microcirculatory vessels with a diameter of up to 100 nm. Activation of the coagulation system induces the formation of fibrin on the surface of activated platelets and the formation of a full-fledged thrombus. When platelets are activated by natural stimulants such as thrombin or collagen, which are exposed when the vascular wall is damaged, they are able to eject the contents of their granules containing clotting factors, peroxidase, serotonin, calcium ions – Ca2+, ADP, Willebrand factor, platelet fibrinogen, platelet growth factor, etc. At the highest degree of activation, the platelet surface becomes procoagulant due to the exposure of phosphatidyl serine and stimulates the 749 ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 2 formation of a blood clot. Platelets also play an essential role in the healing and regeneration of damaged tissues by releasing growth factors that stimulate cell division and proliferation in the damaged area. Hereditary platelet dysfunction encompasses a diverse group of hemorrhagic diseases caused by congenital defects in platelet morphology and/or function in normal numbers. Various structures can be damaged and various processes in platelets can be disrupted: membrane receptors, intra-platelet signaling, granules, etc. This leads to various clinical manifestations of bleeding [2-4]. Thrombocytopathies are characterized primarily by the development of spontaneous and post-traumatic mucosal bleeding. The recognition and differentiation of thrombocytopathies is based on the detection of microcirculatory bleeding with impaired functional properties, morphology and biochemical characteristics of platelets. Based on these manifestations, the modern classification of thrombocytopathies is based, which is divided into 2 large groups – hereditary and acquired. Clinical manifestations depend on the characteristics of qualitative and quantitative platelet defects – the severity of hemorrhagic syndrome can vary significantly and does not depend directly on the degree of defect. With mild bleeding, there may be a tendency to bruising with minor and minor injuries, at the site of compression with an elastic band; periodic excessive nosebleeds, familial prolonged menstruation in women, etc. In the case of massive hemorrhagic syndrome, life-threatening blood loss may develop. Let's look at some thrombocytopathies in more detail. Glanzmann's thrombasthenia is a hereditary disease characterized by hemorrhagic manifestations, in which there is an elongation of bleeding time, as well as a complete absence or a sharp decrease in the intensity of blood clot retraction against the background of a normal platelet count per unit volume of blood [5, 6]. This is the result of a decrease in platelet aggregation capacity. The disease was first described in 1918. Dr. Edward Glanzman. Glanzmann's thrombasthenia gravis is a rare disease and occurs with a frequency of approximately 1 case per 1 million [7]. The manifestation of the disease occurs in early childhood. The main clinical manifestations are cutaneous hemorrhagic syndrome, bleeding from mucous membranes, including gastrointestinal, up to life-threatening. The formation of soft tissue hematomas of various localization is possi