Classification of anemias

Anemia - a large group of different diseases, characterized by a decline in the number of erythrocytes and hemoglobin or one of those indicators in unit volume of blood.

Causes of anemia can be different, According to the main mechanism of development, they are divided into three groups:

• associated with blood loss;
• with poor circulation;
• with increased blood destruction.

The nature of anemia can be judged not only when the content of hemoglobin and red blood cells in the blood decreases below the conventional norm, but even in that case, when at the time of the study these indicators are normal. So, eg, if a patient with hemolytic anemia experiences an increase in bilirubin levels during a period of normal hemoglobin levels, increase in reticulocyte content and, Consequently, signs of shortened red blood cell lifespan, you should think about the nosological form of the disease, and not about hemolytic jaundice, since the latter is only a partial symptom in a number of forms of hemolytic anemia, regardless of the degree of compensation.

Below is the classification of anemia, including all their main forms.

1.Anemia, associated with blood loss.

1.1. Acute posthemorrhagic (normohromnaja) anemia.

1.2. Chronic posthemorrhagic (hypochromic) anemia (cm. 2.1.1.1).

2.Anemia, associated with impaired blood formation.

2.1. Anemia, related to violation of the formation of hemoglobin.

2.1.1. Iron deficiency anemia.

2.1.1.1. Chronic posthemorrhagic iron deficiency anemia (cm. 1.2).

2.1.1.1.1. Caused by external blood loss.

2.1.1.1.1.1. Associated with heavy and prolonged menstruation, hemorrhages.

2.1.1.1.1.2. Associated with minor, recurring bleeding from the stomach and intestines.

2.1.1.1.1.3. Associated with persistent hematuria.

2.1.1.1.1.4. Associated with nosebleeds, bleeding gums.

2.1.1.1.1.5. Related to ongoing blood donation from donors.

2.1.1.1.2. Caused by blood loss into closed cavities with subsequent disturbances in iron reutilization.

2.1.1.1.2.1. For bleeding into the abdominal cavity.

2.1.1.1.2.2. For isolated pulmonary siderosis and Goodpasture's syndrome (pulmonary-renal hereditary syndrome).

2.1.1.1.2.3. In endometriosis, without communication with the uterine cavity.

2.1.1.1.2.4. For glomus tumors.

2.1.1.2. Iron deficiency anemia, associated with insufficient baseline iron levels.

2.1.1.2.1. In premature babies.

2.1.1.2.2. In newborns with low maternal iron reserves.

2.1.1.2.3. In newborns from multiple pregnancies.

2.1.1.2.4. In newborns due to excessive penetration of fetal blood into the bloodstream of the mother or twin.

2.1.1.3. Iron deficiency anemia, associated with increased iron requirements (no blood loss).

2.1.1.3.1. During pregnancy and lactation (often against the background of existing iron deficiency).

2 1.1.3.2. With increased growth at an early age or during puberty (early, or juvenile, chlorosis) against the background of existing deficiency and insufficient intake of iron from food.

2.1.1.4. Iron deficiency anemia, associated with impaired absorption of iron and its intake from food.

2.1.1.4.1. For chronic enteritis.

2.1.1.4.2. After extensive resection of the small intestine.

2.1.1.4.3. After gastrectomy.

2.1.1.4.4. With insufficient iron in food.

2.1.1.4.5. In case of impaired iron absorption in infants due to initially low levels in the blood and impaired activity of intestinal enzymes, containing iron.

2.1.1.5. Iron deficiency anemia, associated with impaired iron transport.

2.1.1.5.1. For hereditary atransferrinemia.

2.1.1.5.2. For infection and inflammation (cm. 2.1.2.1).

2.1.2. Anemia, associated with iron redistribution.

2.1.2.1. Anemia, caused by infection and inflammation (cm. 2.1.1.5.2 and 2.6.3.2).

2.1.3. Anemia, associated with violation of the synthesis of porphyrins or recycling.

2.1.3.1. Hereditary, caused by impaired enzyme activity, involved in the synthesis of porphyrins and heme.

2.1.3.1.1. Inherited recessively, concatenated with the floor, associated with impaired activity of erythrocyte coproporphyrine decarboxylase.

2.1.3.1.1.1. Treatable with pyridoxal phosphate.

2.1.3.1.1.2. Refractory to treatment with pyridoxal phosphate.

2.1.3.1.1.3. Compensated, manifests itself only during treatment with anti-tuberculosis drugs.

2.1.3.1.2. Inherited autosomal recessively, associated with impaired synthesis of δ-aminolevulinic acid.

2.1.3.2. Hereditary, associated with impaired activity of enzymes involved in the synthesis of pyridoxal phosphate from pyridoxine (pyridoxal kinase) erythrocyte.

2.1.3.3. Acquired forms.

2.1.3.3.1. Anemia, lead poisoning (cm. 3.2.4.1).

2.1.3.3.2. Anemia, associated with pyridoxine deficiency (Vitamin B₆).

2.1.4. Anemia, related to violation of the synthesis of globin (cm. 3.1.3).

2.1.4.1. Anemia, associated with impaired synthesis of globin chains.

2.1.4.1.1. β-Thalassemia.

2.1.4.1.1.1. Homozygous.

2.1.4.1.1.2. Heterozygous.

2.1.4.1.2. bd-Талассемия.

2.1.4.1.3. a-Талассемия.

2.1.4.1.3.1. Homozygous for four genes.

2.1.4.1.3.2. Hemoglobinopathy-H.

2.1.4.1.3.3. Homozygous for two main genes.

2.1.4.1.3.4. Homozygous for two accessory genes.

2.1.4.1.3.5. Heterozygous for the main and auxiliary genes.

2.1.4.1.3.6. Heterozygous for the main gene.

2.1.4.1.3.7. Heterozygous for the accessory gene.

2.1.4.1.4. Heroge group hemoglobinopathy.

2.1.4.2. Anemia, associated with disruption of the structure of globin chains (The name of abnormal hemoglobin is given, the location of the amino acid substitution is indicated, chain, serial number from N-end, helix or non-helical region, number in this spiral, nature of amino acid substitution, shape (homo- or heterozygous),a combination of two or more types of hemoglobin, combination with thalassemia.).

2.1.4.2.1. Caused by hemoglobin carriage (S), modifying structure in hypoxia.

2.1.4.2.2. Caused by the carriage of stable abnormal hemoglobins (C, D, IS, O and others.).

2.1.4.2.3. Caused by the carriage of unstable abnormal hemoglobins.

2.2. Anemia, associated with impaired DNA and RNA synthesis (interregional).

2.2.1. Anemia, associated with deficiency of cyanocobalamin - vitamin B₁₂ (derivatives) (cm. 3.2.5.2).

2.2.1.1. B₁₂-deficiency anemias, caused by impaired secretion of intrinsic factor.

2.2.1.1.1. With atrophy of the gastric mucosa due to exposure to damaging factors.

2.2.1.1.2. Autoimmune form with the production of antibodies to the gastric mucosa or intrinsic factor.

2.2.1.1.3. With an autosomal recessive inherited disorder of intrinsic factor production.

2.2.1.1.4. After gastrectomy.

2.2.1.2. B₁₂-deficiency anemias, caused by impaired intestinal absorption of cobalamins.

2.2.1.2.1. For chronic enteritis and malabsorption syndrome.

2.2.1.2.2. After extensive resection of the small intestine.

2.2.1.2.3. For hereditary intestinal epitheliopathy (Immerslund-Gresbeck syndrome).

2.2.1.2.4. In the hereditary absence of receptors for attaching intrinsic factor to the intestine.

2.2.1.3. B₁₂-deficiency anemias, caused by competitive consumption of cobalamins in the intestines.

2.2.1.3.1. When infested with broad tapeworm.

2.2.1.3.2. In the presence of blind loop syndrome and intestinal anastomosis after side-to-side or end-to-side resection.

2.2.1.3.3. In the presence of multiple small intestinal diverticula.

2.2.1.4. B₁₂-defitsitnaya anemia, caused by impaired cleavage of R-protein by proteolytic enzymes (in patients with pancreatitis).

2.2.1.5. B₁₂-defitsitnaya anemia, caused by impaired transport of cobalamins due to hereditary deficiency of transcobalamin II.

2.2.2. Anemia, associated with folic acid deficiency (cm. 3.5.2.3).

2.2.2.1. Anemia, caused by insufficient folic acid in food.

2.2.2.2. Anemia, caused by folic acid malabsorption.

2.2.2.2.1. For enteritis and malabsorption syndrome.

2.2.2.2.2. For alcoholism.

2.2.2.2.3. When using proti- seizure medicines.

2.2.2.2.4. For blind loop syndrome.

2.2.2.2.5. With hereditary isolated malabsorption of folic acid.

2.2.2.3. Anemia, caused by an increased need for folic acid.

2.2.2.3.1. During pregnancy against the background of an initial folic acid deficiency or increased erythrocytopoiesis.

2.2.2.3.2. With a sharp activation of erythrocytopoiesis.

2.2.3. Anemia, associated with the use of antimetabolite and alkating cytostatic drugs (cm. 2.4.2.3.2).

2.2.4. Anemia, associated with a hereditary disorder of enzyme activity, involved in the synthesis of purine and pyrimidine bases.

2.2.4.1. Anemia, caused by impaired enzyme activity, participating in the formation of coenzyme forms of folic acid.

2.2.4.2. Anemia, caused by impaired enzyme activity, involved in the metabolism of orotic acid.

2.2.4.3. Hereditary megaloblastic anemia with hyperuricemia (Lesch-Nyhan syndrome).

2.2.4.4. Hereditary megaloblastic anemia in Rogers syndrome (deafness, diabetes mellitus and megaloblastic anemia), treatable with thiamine (Vitamin B₁).

2.3. Anemia, related to the violation of the fission process erythrokaryocytes.

2.3.1. Hereditary anemia dizeritropoeticheskie.

2.3.1.1. Type I anemia with myonucleation of erythrokaryocytes without signs of disruption of the antigenic structure of the erythrocyte membrane.

2.3.1.2. Anemia type II with multinucleation, double membrane and a change in the antigenic structure of the erythrocyte membrane and with a positive serum acid test.

2.3.1.3. Type III anemia with multinucleated giant erythrokaryos- tsytamy.

2.3.1.4. Anemia type IV with multinucleation, double membrane, without changing the antigenic structure of the membrane with a negative acid-serum test.

2.3.2. Acquired dizeritropoeticheskie anemia.

2.3.2.1. Anemia, associated with somatic mutation (refractory sideroblastic anemia).

2.3.2.2. Anemia, associated with the presence of antibodies to erythrokaryocytes (cm. 3.2.1.5).

2.4. Anemia, associated with inhibition of bone marrow cell proliferation.

2.4.1. Congenital forms.

2.4.1.1. Familial aplastic anemia with chromosomal abnormalities and skeletal abnormalities (Fanconi anemia) .

2.4.1.2. Congenital partial red cell aplasia of Diamond-Blackfan type (cm. 3.2.1.5.0.2).

2.4.2. Acquired forms.

2.4.2.1. Idiopathic (associated with depletion of stem cells, dysfunction of the microenvironment).

2.4.2.2. Associated with exposure to autoantibodies and immune lymphocytes against the common progenitor antigen of erythrokaryocytes and other bone marrow cells (autoimmune pancytopenia) (cm. 3.2.1.4).

2.4.2.3. Symptomatic forms.

2.4.2.3.1. Associated with individual intolerance to certain drugs (levomicetina, ʙutadiona, sulfonamide drugs, etc.).

2.4.2.3.2. Associated with the use of cytotoxic drugs.

2.4.2.3.3. Related to the use of toxic chemicals.

2.4.2.3.4. Related to exposure to ionizing radiation.

2.4.2.3.5. Associated with suppression of stem cell differentiation by pathological pluripotent cells (with the development of acute leukemia and paroxysmal nocturnal hemoglobinuria).

2.4.2.3.6. Related to vitamin deficiencies (partial red cell aplasia with riboflavin deficiency and its coenzyme- Comrade).

2.4.3. Anemia, associated with bone marrow redistribution due to weightlessness (anemia of astronauts).

2.5. Anemia, associated with the replacement of hematopoietic bone marrow by a tumor process.

2.6. Anemia, associated with impaired erythropoietin production or the appearance of erythropoietin inhibitors.

2.6.1. Anemia, associated with decreased oxygen demand.

2.6.1.1. Anemia due to hypothyroidism.

2.6.1.2. Anemia during fasting.

2.6.1.3. Anemia with insufficient pituitary function and after hypophysectomy.

2.6.2. Anemia, associated with increased oxygen supply to tissues.

2.6.2.1. Anemia, associated with exposure to hyperoxia.

2.6.2.2. Anemia, associated with hemoglobinopathies with reduced oxygen affinity (cm. 2.1.4.2.3).

2.6.3. Anemia, associated with impaired erythropoietin production.

2.6.3.1. In case of kidney failure (cm. 3.2.4.6).

2.6.3.2. For infection and inflammation (cm. 2.1.2.1).

2.6.4. Anemia, associated with increased destruction of erythropoietin.

2.6.4.1. Partsialynaya krasnokletochnaya aplasia, associated with the production of antibodies to erythropoietin.

3. Anemia, associated with increased blood destruction.

3.1. Hereditary hemolytic anemia.

3.1.1. Hereditary hemolytic anemia, associated with disruption of the red blood cell membrane.

3.1.1.1. Anemia, caused by disruption of the membrane protein structure.

3.1.1.1.1. Hereditary microspherocytosis.

3.1.1.1.2. Hereditary elliptoditosis.

3.1.1.1.3. Hereditary stomatotsitoz.

3.1.1.1.4. Gemoliticheskaya anemia, associated with hereditary absence of RH antigens (RH disease_null).

3.1.1.2. Anemia, caused by a violation of the structure of membrane lipids.

3.1.1.2.1. Hereditary acanthocytosis.

3.1.1.2.2. Nasledstvennaya gemoliticheskaya anemia, associated with impaired phosphatidylcholine renewal.

3.1.1.2.3. Hereditary anemia with intravascular hemolysis, associated with a decrease in the amount of membrane polyunsaturated fatty acids.

3.1.2. Hereditary hemolytic anemia, related to the violation of enzyme activity of erythrocytes.

3.1.2.1. Hemolytic anemia, caused by impaired activity of enzymes of the pentose phosphate cycle.

3.1.2.1.1. Anemia, associated with deficiency of glucose-6-phosphate dehydrogenase activity (G-6-FD).

3.1.2.1.1.1. Acute hemolytic anemia, caused by taking medications.

3.1.2.1.1.2. Chronic hemolytic anemia, caused by a deficiency of G-6-PD activity.

3.1.2.1.1.3. Favism.

3.1.2.1.1.4. Hemolytic anemia of newborns, caused by enzyme deficiency.

3.1.2.1.2. Anemia, associated with deficiency of 6-phosphogluconate dehydrogenase activity (6-FGD).

3.1.2.2. Hemolytic anemia, caused by impaired activity of glycolytic enzymes.

3.1.2.2.1. Anemia, associated with deficiency of pyruvate kinase activity.

3.1.2.2.2. Anemia, associated with deficiency of triosephosphate isomerase activity.

3.1.2.2.3. Anemia, associated with deficiency of glucose phosphate isomerase activity.

3.1.2.2.4. Anemia, associated with deficiency of 2,3-diphosphoglycerate mutase activity.

3.1.2.2.5. Anemia, associated with deficiency of glyceraldehyde phosphate dehydrogenase activity.

3.1.2.2.6. Anemia, associated with deficiency of hexokinase activity.

3.1.2.2.7. Anemia, associated with deficiency of phosphoglycerokinase activity.

3.1.2.2.8. Anemia, associated with deficiency of phosphofructokinase activity.

3.1.2.3. Hemolytic anemia, caused by disorders of glutathione metabolism.

3.1.2.3.1. Anemia, associated with deficiency of glutathione synthetase activity.

3.1.2.3.2. Anemia, associated with deficiency of glutathione reductase activity.

3.1.2.3.3. Anemia, associated with deficiency of glutathione peroxidase activity.

3.1.2.4. Hemolytic anemia, caused by impaired enzyme activity, involved in the use of ATF.

3.1.2.4.1. Anemia, associated with deficiency of ATPase activity.

3.1.2.4.2. Anemia, associated with deficiency of adenylate kinase activity.

3.1.2.5. Hemolytic anemia, caused by impaired activity of enzymes of the nucleotide metabolism system.

3.1.2.5.1. Anemia, associated with deficiency of pyrimidine-5-nucleotide nucleosidase activity.

3.1.2.6. Hemolytic anemia, caused by excessive synthesis of porphyrins.

3.1.2.6.1. Èritropoètičeskaâ uroporfiriâ.

3.1.2.6.2. Erythropoietic protoporphyria.

3.1.3. Hereditary hemolytic anemia, associated with a violation of the structure or synthesis of hemoglobin (cm. 2.1.4).

3.2. Acquired hemolytic anemia.

3.2.1. Hemolytic anemia, associated with exposure to the antibodies.

3.2.1.1. Alloimmune hemolytic anemias.

3.2.1.1.1. Hemolytic disease of newborn.

3.2.1.1.2. Post-transfusion hemolytic anemia.

3.2.1.2. Transimmune hemolytic anemias.

3.2.1.2.1. Anemia of newborns, associated with penetration of maternal autoantibodies through the placenta, suffering from autoimmune hemolytic anemia.

3.2.1.3. Heteroimmune hemolytic anemias.

3.2.1.3.1. Hapten anemia, associated with taking drugs (penicillina, cephalosporins, quinine, etc.).

3.2.1.3.2. Anemia, associated with fixation of the virus on the surface of the erythrocyte or its effect on erythrocyte antigens.

3.2.1.4. Autoimmune hemolytic anemia with antibodies against peripheral blood erythrocyte antigens.

3.2.1.4.1. Anemia, associated with incomplete thermal agglutinins.

3.2.1.4.1.1. Idiopathic.

3.2.1.4.1.2. Symptomatic in patients with chronic lymphocytic leukemia, acute leukemia, chronic myeloid leukemia, myelofibrosis, Hodgkin's disease, multiple myeloma, systemic lupus erythematosus, hypogammaglobulinemia, nonspecific ulcerative colitis, and also related to the use of the drug (α-methyldopa).

3.2.1.4.2. Anemia, associated with thermal hemolysins.

3.2.1.4.2.1. Idiopathic.

3.2.1.4.2.2. Symptomatic in patients with myelofibrosis, chronic lymphocytic leukemia.

3.2.1.4.3. Anemia, associated with complete cold agglutinins.

3.2.1.4.3.1. Idiopathic (cold- hemagglutinin disease).

3.2.1.4.3.2. Symptomatic in patients with viral pneumonia, infectious mononucleosis, hematosarcoma chronic hepatitis.

3.2.1.4.4. Anemia, associated with biphasic cold hemolysins of the Donath-Landsteiner type (paroksizmalynaya holodovaya gemoglobinuriya).

3.2.1.4.4.1. Idiopathic.

3.2.1.4.4.2. Symptomatic in patients with syphilis.

3.2.1.5. Autoimmune hemolytic anemia with antibodies against bone marrow erythrokaryocyte antigen (collective krasnokletočnaâ Aplasia) (cm. 2.4.2.1).

3.2.1.5.0.1. Idiopathic.

3.2.1.5.0.2. Congenital Diamond-Blackfan type.

3.2.1.5.0.3. Symptomatic in patients with thymoma, chronic myeloid leukemia, Hodgkin's disease, systemic lupus erythematosus.

3.2.2. Hemolytic anemia, associated with changes in membrane structure, caused by somatic mutation.

3.2.2.1. Disease Markiafavy-Micheli (paroxysmal nocturnal hemoglobinuria).

3.2.3. Hemolytic anemia, associated with mechanical damage to the erythrocyte membrane.

3.2.3.1. Anemia, caused by the destruction of red blood cells when they come into contact with a prosthetic heart or septum.

3.2.3.2. March hemoglobinuria.

3.2.3.3. Microangiopathic hemolytic anemias.

3.2.3.3.1. Thrombotic thrombocytopenic purpura.

3.2.3.3.2. Hemolytic uremic syndrome.

3.2.3.3.3. Anemia, caused by malignant hypertension.

3.2.3.3.4. Anemia, caused by vascular tumor.

3.2.3.3.5. Hemolytic anemia with splenomegaly.

3.2.4. Hemolytic anemia, caused by chemical damage to red blood cells.

3.2.4.1. When exposed to lead (cm. 2.1.3.3.1).

3.2.4.2. When exposed to heavy metals.

3.2.4.3. In case of acid poisoning.

3.2.4.4. When exposed to organic hemolytic poisons.

3.2.4.5.Excessive alcohol intake and liver damage (21eue syndrome).

3.2.4.6. In case of kidney failure as a result of exposure of erythrocytes to nitrogen metabolism products (cm. 2.6.3.1).

3.2.5. Hemolytic anemia, caused by a lack of vitamins.

3.2.5.1. Anemia, associated with tocopherol deficiency (Vitamin E).

3.2.5.2. Anemia, associated with deficiency of cyanocobalamin - vitamin B₁₂ (and its derivatives - cobalamin) (cm. 2.2.1).

3.2.5.3. Anemia, associated with folic acid deficiency (cm. 2.2.2).

3.2.6. Hemolytic anemia, caused by the destruction of red blood cells by parasites.

3.2.6.1. When exposed to Plasmodium malaria.

3.2.7. Gemoliticheskaya anemia, due to the effects of weightlessness (anemia in astronauts) (cm. 2.4.3).