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HEMOLITIC ANEMIA.

Congenital (familial) spherocytic hemolytic anemia (synonyms for Minkowski-Shoffar disease; hereditary spherocytosis). Anemia is associated with membranopathy. This is normochromic anemia. Microspherocytosis (erythrocyte diameter below 7.55 μm), reticulocytosis, decreased osmotic resistance of red blood cells (below 0.5%). With an exacerbation of the disease, the presence of clinical symptoms: splenomegaly, jaundice, increased levels of indirect bilirubin, urobilinemia, urobilinuria.

Hemolytic anemia associated with deficiency in red blood cells, glucose-6-phosphate dehydrogenase (G-6-PD).
This anemia is associated with enzymopathy. This anemia is most often triggered by the use of drugs with an oxidizing effect (analgesics, antipyretics, sulfonamides, primaquin) or the intake of certain plant products (Vicia fava beans). Normochrome anemia. Clinically massive hemolysis of red blood cells is accompanied by sharp chills, fever (hemolytic fever), jaundice, hemoglobinuria (the appearance of black urine). The level of indirect bilirubin rises (the norm is up to 16.5 μmol / l).
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HEMOLITIC ANEMIA.

  1. ACUTE HEMOLITIC ANEMIA CONDITIONED BY EXOGENOUS HEMOLYTIC FACTORS
    Acute hemolytic processes accompanied by severe anemia and jaundice occur when poisoning with hemolytic poisons of organic and inorganic origin (snake venom, fungal poison, saponins, arsenic hydrogen, phosphorus, phenylhydrazine), with severe burns or in connection with septic, streptococcal or anaerobic infections . To hemolytic anemia of an infectious nature
  2. ACQUIRED HEMOLITIC ANEMIA
    Acquired hemolytic anemia includes: • immune hemolytic anemia; • medicinal hemolytic anemia; • traumatic and microangiopathic hemolytic anemia; • anemia due to the influence of hemolytic poisons, chemicals, bacterial toxins; • paroxysmal night
  3. Acquired hemolytic anemia
    This is a heterogeneous group of hemolytic anemia that occurs under the influence of a number of factors that have the ability to damage red blood cells and cause their premature destruction. Classification of acquired hemolytic anemia [Idelsson L. I., 1975] I. Hemolytic anemia associated with exposure to antibodies. 1. Isoimmune hemolytic anemia 1) hemolytic disease of the newborn
  4. HEMOLITIC ANEMIA IN CHILDREN
    Hemolytic anemia - a group of anemia characterized by hemolysis syndrome - increased destruction of red blood cells. Red blood cells live for about 120 days, then they are destroyed - they are phagocytosed by macrophages, mainly the spleen. With hemolytic anemia, the erythrocyte life span is significantly shortened, and with its reduction below 30 days, a hemolytic clinic appears.
  5. HEREDITARY HEMOLITIC ANEMIA
    The following groups of hereditary hemolytic anemia are distinguished: 1. Due to a violation of the structure of the erythrocyte membrane. 2. Associated with impaired activity of red blood cell enzymes. 3. Associated with a violation of the structure or synthesis of hemoglobin. Hereditary hemolytic anemia due to a violation of the erythrocyte membrane Hereditary hemolytic anemia associated with
  6. Hemolytic anemia
    Hemolytic anemia constitutes an extensive group of anemic conditions of various etiologies, a common sign of which is the pathologically increased destruction of red blood cells. It is known that the average lifespan of red blood cells does not exceed 100-120 days. Hemolytic anemia is characterized by a shortened life span of red blood cells. Hemolysis can occur intracellularly or
  7. HEMOLITIC ANEMIA
    Hemolytic anemia includes an extensive group of anemic conditions that occur when blood destruction processes prevail over hematopoiesis. The clinical picture of hemolytic anemia is very variable and depends both on the nature of the hemolytic agent and the duration of its effect on the body, and on the degree of compensation of the hemolytic process. Classification.
  8. HEMOLITIC ANEMIA
    A common sign of hemolytic anemia is increased destruction of red blood cells, causing anemia on the one hand and increased formation of decay products, and reactive erythropoiesis on the other. An increase in red blood cell breakdown products is clinically manifested by jaundice of a lemon hue, an increased content of unbound (unconjugated) bilirubin in the blood, with its
  9. Acquired hemolytic anemia
    1. Immunogemolytic anemia a) autoimmune b) isoimmune 2. Acquired membranopathy a) paroxysmal nocturnal hemoglobinuria b) sporoccellular anemia 3. Associated with mechanical damage to red blood cells a) marching hemoglobinuria b) Moshkovich disease (microangiopathic thrombocytopenia)
  10. IMMUNE HEMOLITIC ANEMIA
    L. I. Idelson (1979) identifies the following variants of immune hemolytic anemia: • isoimmune hemolytic anemia - associated with isoantibodies against group factors of red blood cells. This variant of anemia develops when antibodies to red blood cells enter the fetus from the mother’s blood (hemolytic disease of the fetus or newborn), as well as during transfusion of red blood cells that are incompatible
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