HEMORRHAGIC DIATHESES CAUSED BY PATHOLOGY OF THROMBOCYTIC LINK OF HEMOSTASIS

Аннотация

Hemorrhagic diathesis caused by pathology of platelet link of hemostasis is a group of diseases characterized by increased tendency to bleeding due to quantitative or qualitative disorders of platelets.These pathologies include thrombocytopenias (decreased platelet count) and thrombocytopathies (functional defects of platelets), which may be inherited or acquired. The article discusses the main mechanisms of pathogenesis, clinical manifestations, diagnostic methods and modern approaches to the treatment of these conditions. Special attention is paid to the distinguishing features of platelet hemorrhagic diatheses, their differential diagnosis with coagulopathies, as well as relevant methods of laboratory research.Therapeutic strategies including the use of hemostatic drugs, immunomodulatory therapy, platelet transfusions and innovative treatment methods such as target therapy and genetic engineering are considered. The relevance of the topic is due to the high prevalence of platelet disorders and their potential danger to the life of patients. Modern research in the field of hematology is aimed at developing newdiagnosticmethods and personalized approaches tothe treatment ofthese pathologies. Keywords: Hemorrhagic diathesis, Thrombocytopenia, Thrombocytopathy, Thrombocytic link of hemostasis, Primary hemostasis, Immune thrombocytopenia, Idiopathic thrombocytopenic purpura, Glanzmann's disease, Bleeding disorders, Coagulopathy, Hemostasiology, Platelet receptors, Hypersplenism, Aplastic anemia, Myelodysplastic syndrome, Platelet sequestration, DIC. Hemorrhagic diathesis (HD) is a group of pathological conditions characterized by an increased propensity to bleeding due to disorders of the hemostasis system. A special role in the pathogenesis of these conditions plays a platelet link, which provides primary hemostasis. Violations may be associated with a decrease in the number of platelets (thrombocytopenia) or withtheir functional defect (thrombocytopathies). Plateletsare bloodcell elements involved in stoppingbleeding. Their functions include: -adhesion to damaged endothelium (viaGPIb-V-IX and vonWillebrand factorreceptors), -aggregation with each other(mediated byGPIIb/IIIa andfibrinogen), page1276 INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE ISSN:2692-5206,ImpactFactor:12,23 AmericanAcademicpublishers,volume05,issue02,2025 Journal: https://www.academicpublishers.org/journals/index.php/ijai -secretion ofcoagulation factors and biologically activesubstances. Violationof any ofthese functions leads topathologic bleeding. The main cause of bleeding in this type of hemorrhagic diathesis is thrombocytopenia. The cause of increased platelet destruction in this disease is the formation of antiplatelet antibodies related to Ig G. Contribute to the development of the disease viral infections, taking medications such as sulfonamides, butadione, quinine, dopegit, etc. The life span of platelets is shortened to a few hours instead of7-10 days. The clinical picture of the disease is manifested at a platelet level of less than 150-109 /L. The course of the disease is chronic, recurrent, but can be acute. The first manifestations, as a rule, are not associated with any previous disease. Appear spotty-petechial bruise hemorrhages, bleeding from mucous membranes. In some patients, an enlarged spleen is detected.Heteroimmune thrombocytopenia is distinguished. In this form of the disease, a viral infection or certain drugs play the role of a hapten associated with the platelet. The AT formed causes platelet destruction and increased bleeding. The type and severity of bleeding, established during theexamination, greatly facilitates the diagnosticsearch. I. Hematomicwith painful tensehemorrhages both in the soft tissuesand joints -typical ofhemophiliaA and B; II. petechial-staining (bruising) - characteristicofthrombocytopenia, hemophiliaA and B. thrombocytopenia, thrombocytopathies and somedisorders of blood coagulation blood- hypo- and dysfibrinogenemia, hereditary deficiency offactors Xand II, sometimes VII; III. mixed bruising-hematoma -characterized bya combinationof petechial-stained bleeding with theappearance ofindividual large hematomas (retroperitoneal, in thewall oftheintestine, etc.) in theabsenceof lesion jointsand bones (unlike thehematoma type) or with isolated hemorrhages inthejoints and bones (unlikethehematomatype). hemorrhages into joints: bruises may be extensive and painful. This type of bleeding is observed in severe deficiency of prothrombin complex factors and factor XIII, Willebrand's disease, DIC, overdose of anticoagulants and thrombolytics, with the appearance of immune inhibitors of factors VIII orIX inthe blood; IV. vasculitic-purpurictype ischaracterized byhemorrhages in theform of symmetrical small-pointed rash, possible accession of inflammation of the kidney and intestinal bleeding; observed in infectious andimmune vasculitis. page1277 INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE ISSN:2