Anemia is usually caused by these three major causes:

I. Blood loss anemia

Acute post-blood loss anemia: It is anemia caused by rapid and massive bleeding, such as post-surgical anemia.

Chronic post-blood loss anemia:

It is a small-cell anemia due to prolonged moderate bleeding, such as intestinal ulcers, women's blood loss during menstruation, hemorrhoids, and anemia of urinary disorders.

Two, aplastic anemia

Iron deficiency anemia: also known as hemoglobin binding disorder anemia, due to insufficient iron intake, relative increase in iron needs (eg: pregnancy, growth and development period), iron absorption disorders (eg: chronic gastrointestinal diseases, after gastric resection of the stomach). At this time, a large amount of iron supplementation is needed to enhance the body's function.

Pernicious anemia: folic acid (vitamin B9) and or biotin (vitamin B12) deficiency caused by hematopoietic cell nuclear maturation disorders of anemia, need to supplement folic acid and biotin can be.

Acute aplastic anemia: the anemia is often not obvious at the beginning of the disease, but with the development of the disease, it is progressive. Almost all have bleeding tendency, more than 60% have internal bleeding, mainly manifested as gastrointestinal bleeding, hematuria, fundus hemorrhage (often accompanied by visual impairment) and intracranial hemorrhage.

Chronic aplastic anemia: slow onset, with anemia as the first and main manifestation; bleeding is mostly confined to the skin and mucous membranes and is not serious; infections can be complicated, but are often respiratory in nature and can be easily controlled. Persistence can be cured.

Three, hemolytic anemia

Hereditary: anemia that occurs when the rate of red blood cell destruction increases (life expectancy is shortened) and exceeds the compensatory capacity of the bone marrow for hematopoiesis. The bone marrow has 6 to 8 times the compensatory potential for red lineage hematopoiesis. It is due to heterozygous changes in hematopoietic stem cell genes, resulting in erythrocyte membrane defects, erythrocyte enzyme defects, and abnormal bead proteins.

Immune: Drugs (quinine, quinidine, finasteride, p-aminosalicylic acid, etc.) act as semi-antigens and bind to serum proteins to form antigens, causing an immune response that stimulates the production of antibodies (IgM, and possibly IgG). The drug and antibody firmly form an immune complex and are adsorbed on the surface of the erythrocyte membrane, which activates the complement and causes hemolysis.