Premature destruction of platelets or excessive consumption of platelets leads to thrombocytopenia in the surrounding blood. Platelet life is shortened, and the number of megakaryocytes in bone marrow is normal or compensatory hyperplasia. Because of the complex symptoms of thrombocytopenia, the etiology of thrombocytopenia is also very complicated. What are the causes of thrombocytopenia?
Immunodestruction: a drug related antibody that produces a corresponding antibody. Immune thrombocytopenia can be caused by some abnormal immune response diseases. Infection associated thrombocytopenia is common in virus and bacterial infections. Immunological thrombocytopenia, after transfusion of purpura and neonate purpura, is the cause of thrombocytopenia.
Non immune destruction: the vascular intima is rough, and the intravascular foreign bodies cause mechanical destruction of the platelets. The causes of thrombocytopenia include vasculitis, artificial heart valves, arterial cannulation, cardiopulmonary bypass, hemodialysis, etc. Disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are all associated with thrombocytopenia, which is associated with excessive platelet consumption.
Causes of thrombocytopenia in vivo platelet production, such as bone marrow problems, patients suffering from aplastic anemia, Yao lead to bone marrow damage, cancer (leukemia) or other cancers. Thrombocytopenia is the cause of thrombocytopenia, such as immune thrombocytopenia, which is generally the most common thrombocytopenic purpura.
The platelet content of normal people is 150x109 per liter of blood. If it falls to 50x10 (9 power), the body will suffer from some collisions and it will easily become black. If it falls to 10x109, it will easily bleed, and the situation is very serious. The common symptoms of low platelet are subcutaneous and mucosal parts, such as nasal and oral teeth, which are easy to bleed, while intra articular bleeding can lead to joint swelling and thrombocytopenia.
Acute type ITP occurs mostly in the recovery period of virus infection or upper respiratory tract infection, such as rash, measles, chickenpox, parotid cancer and so on. Patients had higher antiviral antibodies in the serum. Thrombocytopenia, including increased platelet surface associated antibodies, was thought to be caused by viral antigens. The pathogenesis may be antigen antibody complexes including viral antigens, which react with platelet Fc receptors or autoantibodies produced by virus antigens, react with platelet membrane, damage platelets and be cleared away by phagocytes.
There is no history of prodrome infection before the onset of chronic ITP, which is caused by autoantibodies caused by changes in platelet structural antigen. The 80% to 90% medical records had platelet surface related antibodies, of which 95% were PalgG, 2/3 was PalgG and PalgM, and a few were PalgA and PAC. The antibody acts directly on the glycoprotein of platelet membrane. A small number of interactions with Gbib complex make platelet life shortened and function change are the causes of thrombocytopenia.