Thrombocytopenia generally refers to thrombocytopenic purpura, but there may also be other causes, as described below: There are two causes of thrombocytopenia:
1. It is produced in the body Insufficient platelets, such as bone marrow problems, patients suffering from aplastic anemia, bone marrow damage caused by drugs, blood cancer (leukemia) or other cancers, etc.;
2. Platelets are consumed too quickly, such as immune platelets Hypoxia, generally the most common is thrombocytopenic purpura.
Normal people's platelet content is 150x109 per liter of blood. If it drops to 50x109, the body will easily become black when encountering some collisions; if it drops to 10x109, subcutaneous bleeding will occur easily, and the situation is very serious.
The general symptom of low platelets is that subcutaneous and mucosal parts such as the nose, mouth and teeth tend to bleed easily, and bleeding in the joints can lead to joint swelling. Low platelets can be detected through blood tests. If the patient's condition worsens and dies within a short period of time, it may be caused by blood cancer. If detected in time, appropriate treatment can be provided and the condition may not worsen.
Clinical symptoms of thrombocytopenic purpura: Severe thrombocytopenia, regardless of the cause, can cause typical bleeding, multiple ecchymoses, and purpura, most commonly in the lower legs; or in the lower legs; Small scattered ecchymoses appear at sites of minor trauma; mucosal bleeding (epistaxis, gastrointestinal and genitourinary tract and vaginal bleeding) and massive bleeding after surgery. Massive gastrointestinal bleeding and bleeding within the central nervous system can be life-threatening.
Thrombocytopenic purpura is divided into two categories: primary and secondary. Idiopathic thrombocytopenic purpura is an immune syndrome and a common bleeding disorder. It is characterized by the presence of anti-platelet antibodies in the blood circulation, which causes excessive platelet destruction and causes purpura; while the megakaryocytes in the bone marrow are normal or increased, and become immature. Clinically, it can be divided into two types: acute and chronic. The pathogenesis and manifestations of the two are significantly different.
Idiopathic Thrombocytopenic Purpura (ITP) is an acquired bleeding disorder caused by excessive platelet destruction and megakaryocyte maturation disorders. It is also called idiopathic thrombocytopenic purpura. Purpura. Because more than 85% of cases have IgG antibodies in the serum or platelet surface, and because the pathogenesis of essential thrombocytopenia is related to autoimmunity, it is also called autoimmune Thrombocytopenic Purpura (ATP). Essential thrombocytopenia can sometimes be combined with autoimmune hemolytic anemia, which becomes Evans syndrome.
Secondary thrombocytopenia, also known as acquired thrombocytopenia, is a thrombocytopenia secondary to other diseases and involves many diseases. Such as drug-induced immune thrombocytopenia, other immune thrombocytopenia such as Evans syndrome, chronic lymphocytic leukemia, various acute leukemias, lymphoma, systemic lupus erythematosus, rheumatoid arthritis, hyperthyroidism, etc.
Causes and pathogenesis of thrombocytopenia:
Idiopathic Thrombocytopenic Purpura (ITP) is a common disease caused by excessive destruction of peripheral platelets. bleeding disorders. The etiology and pathogenesis of idiopathic thrombocytopenic purpura have not been elucidated so far, and it is mostly believed to be an immune-related disease.
It is currently believed that the disease is due to the production of anti-platelet antibodies in the body, which causes excessive destruction of platelets and shortens the life of platelets. However, the megakaryocytes in the bone marrow are normal or increased, and the megakaryocytes degenerate and become immature. Because of its pathogenesis and It is related to autoimmunity, also known as Autoimmune Thrombocytopenic Purpura (ATP).
This disease is an acquired bleeding disorder. Research on the etiology shows that the causes of acute ITP include rubella, measles, chickenpox, mumps, infectious mononucleosis, and live virus injection. In recent years, experiments have confirmed that certain viruses, such as chickenpox virus, can be the cause of acute ITP. The cause of chronic ITP remains unknown.
Research on the pathogenesis has gradually made progress. It is now believed that acute ITP is caused by the production of antibodies related to the virus (antigen) in the body after viral infection, which cross-react with the platelet membrane, causing non-specific damage to the platelets and being absorbed by the mononuclear cells. It is cleared by the macrophage system; or it is caused by anti-viral antibodies combining with corresponding antigens to form immune complexes and attaching to the surface of platelets.
The pathogenesis of chronic ITP is that the anti-platelet antibody IgG (PAIgG) mainly produced by the spleen first specifically binds to the relevant antigens on the platelet membrane through its Fab fragment, exposing the Fc fragment, and combines with the macrophilia The Fc receptor of the cell binds, causing the platelets to be phagocytized and destroyed; in addition, the immune complex (CIC) binds to the Fc receptor on the platelet through the Fc fragment on the IgG molecule, and activates complement C3, fixing C3 on the platelet, and is eventually Macrophage recognition and phagocytosis. The role of cellular immunity in this disease is unclear. It is known that the ratio of helper and suppressor T cells is imbalanced and TA cell function is defective. The main sites of platelet destruction are the spleen, liver and bone marrow.