LECTURE No. 15. Anemia and leukemia in children

1. Anemia

Anemia (anemia) is a polyetiological disease characterized by a decrease in hemoglobin content, often in combination with a decrease in the number of red blood cells.

Clinic. The disease is manifested by changes in external signs (pallor of the skin, mucous membranes, sclera), weakness, dizziness, shortness of breath, tachycardia, memory impairment, the appearance of disorders of the muscular system (weakness, decreased tissue turgor), deviations in the central nervous system (lethargy, apathy, mild excitability), functional disorders of the cardiovascular system (expansion of boundaries, the appearance of systolic murmur), the development of hepatomegaly and splenomegaly, a decrease in the total amount of hemoglobin in the blood, red blood cells, and their osmotic resistance.

Anemia classification. Primary (hereditary) and secondary (acquired).

Because of:

1) deficiency anemia, iron deficiency, vitamin deficiency, protein deficiency;

2) hypo- and aplastic anemia: Fanconi congenital anemia, Diamond-Blackfan anemia, acquired anemia;

3) hemolytic anemia: spherocytic, sickle cell, autoimmune.

By severity:

1) mild anemia - hemoglobin in the range of 90-110 g/l, the number of red blood cells decreases to 3 million;

2) moderate anemia - hemoglobin 70 - 80 g/l, the number of red blood cells decreases to 2,5 million;

3) severe anemia - hemoglobin is below 70 g / l, the number of red blood cells is below 2,5 million.

By color index:

1) normochromic;

2) hyperchromic;

3) hypochromic.

iron deficiency anemia characterized by a decrease in hemoglobin content due to iron deficiency, associated with a violation of the synthesis of porphyrins, thalassemia, erythrocyte content as a result of its violation upon admission, assimilation or pathological losses.

Etiology. Antenatal reasons:

1) violation of the uteroplacental circulation, placental insufficiency (toxicosis, the threat of interruption and re-carrying of pregnancy, hypoxemic syndrome, exacerbation of somatic and acute infectious diseases);

2) feto-maternal and feto-placental bleeding;

3) intrauterine melena;

4) prematurity, multiple pregnancy;

5) deep and prolonged iron deficiency in the body of a pregnant woman.

Internal causes:

1) fetoplacental transfusion;

2) premature or late ligation of the umbilical cord;

3) internal bleeding due to traumatic obstetric aids and (or) anomalies in the development of the placenta and umbilical cord vessels.

Postnatal:

1) insufficient intake of iron with food (early artificial feeding, the use of unadapted milk formulas, feeding with cow or goat milk, an unbalanced diet devoid of a sufficient content of meat products);

2) an increase in the need for iron in children with accelerated growth rates (premature, children with high birth weight, children with a lymphatic type of constitution, children of the pre- and pubertal period);

3) increased loss of iron due to bleeding of various etiologies, intestinal absorption disorders (hereditary and acquired malabsorption syndromes, chronic bowel disease, hemorrhagic uterine bleeding in girls during the formation of the menstrual cycle in puberty), impaired iron metabolism in the body due to hormonal disorders (pre- and pubertal hormonal imbalance), violations of iron transport due to a decrease in the activity or content of transferrin in the body.

Clinic. History: insufficient, unhealthy diet, lethargy, increased fatigue, dryness, roughness of the skin, brittle nails, curvature and cross-striations of nails, hair loss, perversions of taste and smell, asthenovegetative disorders, disturbances in intestinal absorption processes, palpitations, shortness of breath during physical exertion . Based on the content of hemoglobin and red blood cells, anemia is divided into mild (hemoglobin within 90-109 g/l, red blood cells less than 4-3,5 x 10¹²), anemia of moderate severity (hemoglobin in the range of 89 - 70 g / l, red blood cells less than 3,5 x 10¹²), severe anemia (hemoglobin less than 70 g/l, erythrocytes less than 2,5 x 10¹²).

Diagnostics - based on clinical and laboratory data. in a blood test - a decrease in red blood cells, hemoglobin, serum iron concentration, a decrease in blood elements, anisocytosis, poikilocytosis. The color index is usually low (sometimes below 0,5); pronounced hypochromia of erythrocytes, their anisocytes, poikilocytosis; ESR is usually slightly increased. The most important indicator of the disease is a decrease in serum iron levels (normal is 13-28 mmol/l for men; 11-26 mmol/l for women). Low levels of serum iron and ferritin, as well as an increase in the level of total iron-binding capacity of serum.

Treatment aimed at eliminating iron deficiency and restoring the necessary supply of iron in the body. Therapy must begin with the elimination of the causes of its cause and the organization of a proper, balanced diet (foods rich in vitamins and iron, especially meat, should be included in the diet). Treatment with parenteral iron preparations is less effective than taking it in the form of oral tablets.

For intramuscular administration, Jectofer, Ferbitol, Ferrum Lek, etc. are used. The latter drug is also produced for intravenous administration. Indications for parenteral administration of iron for iron deficiency anemia are severe enteritis, conditions after extensive resections of the small intestine (but not gastric resections). Doses are prescribed at the rate of 1,5 mg of iron per 1 kg of body weight per day. Jectofer is administered intramuscularly at 2 ml per day to a patient weighing 60 kg. Blood transfusion when the hemoglobin level is below 60 g/l. Taking iron supplements increases bone marrow production of red blood cells and is accompanied by an increase in the level of reticulocytes in the blood 8-12 days after the start of therapy (a fact that has differential diagnostic significance).

Forecast favorable. Dispensary observation for 12 months.

Anemia associated with vitamin B deficiency₁₂ regardless of the reasons for this deficiency, they are characterized by the appearance of megaloblasts in the bone marrow, intramedullary destruction of erythrocytes, thrombocytopenia and neutropenia, atrophic changes in the mucous membrane of the gastrointestinal tract and changes in the nervous system.

Etiology. Vitamin deficiency is rarely of an exogenous (usually endogenous) nature, associated with increased consumption (with helminosis) and impaired absorption of various natures (with stomach diseases, malabsorption syndrome).

Pathogenesis. Vitamin B deficiency₁₂ more often associated with a violation of the production of a glycoprotein that combines with dietary vitamin B₁₂ and providing its absorption (intrinsic factor). Often the first signs of the disease appear after suffering enteritis, hepatitis. In the first case, this is due to malabsorption of vitamin B₁₂ in the small intestine, in the second - with the expenditure of its reserves in the liver, which is the main depot of vitamin B₁₂. Development B₁₂- deficiency anemia after total gastrectomy (when the secretion of the intrinsic factor is completely eliminated) occurs 5-8 years or more after the operation. During this period, patients live with vitamin reserves in the liver with minimal replenishment due to insignificant absorption in the small intestine, not connected with the internal factor of the vitamin. Rare form B₁₂-deficiency anemia is a violation of the assimilation of the vitamin during invasion with a wide tapeworm, when the parasite absorbs a large amount of vitamin B₁₂. Causes of impaired absorption of vitamin B₁₂ with intestinal damage, there may be severe chronic enteritis, diverticulosis of the small intestine, terminal ileitis, the occurrence of a blind loop of the small intestine after surgery on it.

Clinic vitamin B deficiency₁₂ characterized by damage to the hematopoietic tissue, digestive and nervous systems. There are weakness, fatigue, palpitations during physical exertion. Gastric secretion is depressed, persistent achlorhydria is possible. Often there are signs of glossitis - a polished tongue, a burning sensation in it. The skin is slightly icteric, the level of indirect bilirubin in the blood serum is increased (due to the increased death of hemoglobin-containing megaloblasts in the bone marrow). A slight increase in the spleen is determined, less often the liver.

Diagnostics - based on clinical and laboratory data. In the blood test - hyperchromic anemia, leukopenia, thrombocytopenia, pronounced anisocytosis of erythrocytes along with very large (more than 12 microns in diameter) cells - megapocytes, the sharpest poikilocytosis, increased saturation of erythrocytes with hemoglobin - hyperchromia, the appearance of polysegmented neutrophils, hyperchromic, less often normochromic nature of anemia , thrombocytopenia, leukopenia. A study of the bone marrow reveals a sharp increase in the number of elements of the erythroid series in it with a predominance of megaloblasts. Red cells, very reminiscent of megaloblasts, may occur in acute erythromyelosis, which, like B₁₂- deficiency anemia, accompanied by a slight icterus, often combined with leuko- and thrombocytopenia. However, with this leukemia, there is no such pronounced aniso- and poikilocytosis as with B₁₂-deficiency anemia, and most importantly - in the bone marrow, along with megaloblast-like cells, there are a large number of myeloblasts or undifferentiated blasts. In doubtful cases, vitamin B therapy should be started after bone marrow puncture.₁₂, which at B₁₂-deficiency anemia in 8-10 days will lead to a sharp increase in the percentage of reticulocytes in the blood (recyclic cell crisis), an increase in hemoglobin levels, the disappearance of pronounced anisocytosis in the blood, and in the bone marrow - megaloblasts.

Treatment. Cyanocobalamin (vitamin B₁₂) is administered daily subcutaneously at a dose of 200-500 mg once a day for 1-4 weeks. After normalization of hematopoiesis and blood composition, which occurs after 6-1,5 months, the vitamin is administered once a week for 2-1 months, then 2 times a month for six months (in the same doses as at the beginning of the course). In the future, patients should be registered at the dispensary; they are given prophylactic vitamin B₁₂ 1-2 times a year in short courses of 5-6 injections. This recommendation may be changed depending on the dynamics of blood counts, intestinal condition, and liver function.

folate deficiency anemia - megaloblastic anemia similar to B₁₂- deficiency anemia; develops with folic acid deficiency. Violation of the absorption of folic acid is observed in pregnant women suffering from hemolytic anemia, in premature babies, when feeding them with goat's milk, in persons who have undergone resection of the small intestine, with celiac disease, as well as with long-term use of anticonvulsants such as phenobarbital, diphenin.

Clinic similar to vitamin B deficiency₁₂.

Diagnostics - based on clinical and laboratory data. In the blood test - a decrease in the level of folic acid in erythrocytes and blood serum.

Prevention. Prescription of folic acid to persons who have suffered from its deficiency, pregnant women, and those suffering from hemolytic anemia.

Hypo- and aplastic anemias. The basis of this disease is a decrease in the production of bone marrow cells.

Hemolytic anemia develop as a result of the destruction of erythrocytes, are characterized by an increase in the blood content of erythrocyte decay products - bilirubin or free hemoglobin, or the appearance of hemosiderin in the urine. An important sign is a significant increase in reticulocytes in the blood due to an increase in the production of red blood cells. The bone marrow in hemolytic anemia is characterized by a significant increase in the number of red cells.

Anemia posthemorrhagic acute - anemia due to acute blood loss for a short period of time.

Etiology. The cause of blood loss can be trauma, surgery, bleeding from a stomach or duodenal ulcer, from dilated veins of the esophagus, from impaired hemostasis, ectopic pregnancy, lung diseases, etc.

Pathogenesis consists of the phenomena of acute vascular insufficiency caused by acute devastation of the vascular bed, loss of plasma; with massive blood loss, hypoxia also occurs due to the loss of erythrocytes, when this loss can no longer be compensated by the acceleration of circulation due to increased heart rate.

Clinic. Vascular disorders (palpitations, shortness of breath, drop in arterial and venous pressure, pallor of the skin and mucous membranes).

Treatment start by stopping the bleeding.

hereditary anemiaassociated with a violation of the synthesis of porphyrins (sideroahrestic anemia), are characterized by hypochromia of erythrocytes, an increase in the level of serum iron, iron deposition with a picture of hemosiderosis of organs.

Pathogenesis associated with a violation of the synthesis of protoporphyrin, which leads to a violation of the binding of iron and its accumulation in the body with a sharply disturbed formation of hemoglobin.

Clinic. There are no complaints or slight weakness and fatigue. Men are more often affected. The disease is inherited in a recessive manner, inheritance linked to the X chromosome. At the beginning of the disease, a slight enlargement of the spleen is noted, later, due to increased iron deposition in the organs, hemosiderosis of the liver (the liver enlarges and becomes dense) and the pancreas (a picture of diabetes mellitus appears) develops. The accumulation of iron in the heart muscle leads to severe circulatory failure, testicular hemosiderosis is accompanied by the development of eunuchoidism. Sometimes the skin takes on a gray tint.

Diagnostics - based on clinical and laboratory data. In the blood test - pronounced hypochromia of erythrocytes (color index 0,4 - 0,6), the level of hemoglobin is reduced, the number of erythrocytes is changed to a lesser extent, the level of serum iron is increased. Morphologically, anisocytosis, poikilocytosis, and sometimes a small number of target-shaped forms are noted. The content of reticulocytes is usually normal.

Treatment. Prescribe pyridoxine (vitamin B₆) 1 ml of a 5% solution i/m 2 times a day. With effective therapy, after 1,5 weeks, the content of reticulocytes sharply increases, and then the level of hemoglobin also increases.

Megaloblastic anemias - a group of anemias, a common feature of which is the detection in the bone marrow of peculiar erythrokaryocytes with structural nuclei that retain these features in the later stages of differentiation (the result of impaired DNA and RNA synthesis in cells called megaloblasts), in most cases megaloblastic anemia is characterized by a color index above one. Since the synthesis of nucleic acids concerns all bone marrow cells, frequent signs of the disease are a decrease in the number of platelets, leukocytes, and an increase in the number of segments in granulocytes.

2. Leukemia

Leukemia is the general name for malignant tumors arising from hematopoietic cells and affecting the bone marrow. The incidence ranges from 1 to 5 per 1 child population, with a peak between the ages of 000 and 000 years. Chronic myeloid leukemia is a tumor that arises from differentiating cells - the precursors of myelopoiesis.

Etiology. Not established, but the most common theory is viral-genetic. The role of factors that weaken the body’s reactivity: immunodeficiency states, chromosomal abnormalities, congenital and hypoplastic Fanconi anemia, ionizing radiation, acceleration with lymphatism.

Pathogenesis. Leukemia cells are the offspring of one mutated bone marrow hematopoietic cell that has lost the ability to mature, but retains the ability to reproduce.

Tumor progression in leukemia: inhibition of normal hematopoietic growths, changes in the morphology of the affected hematopoietic cell and the clone of tumor cells emanating from it, metastasizing and growing outside the hematopoietic organs; release by leukemia cells of substances that inhibit normal hematopoiesis; self-maintenance of the leukemic clone and the dynamism of its properties during treatment with the acquisition of high aggressiveness and resistance to the action of cytostatics.

Classification: acute leukemias (may be lymphoblastic and myeloblastic) and chronic leukemias.

Clinic. The main syndromes are anemic, intoxication, hemorrhagic, proliferative, osteoarticular, damage to internal organs, the nervous system, and infectious complications.

Diagnostics - based on clinical and laboratory data, analysis of peripheral blood, myelogram, cytochemical study of blood and bone marrow blasts.

Differential diagnosis carried out with infectious mononucleosis, infectious lymphocytosis, leukemoid reactions in infectious diseases, drug disease and poisoning.

Treatment drugs with immunosuppressive and cytostatic effects on periods of induction, consolidation, reinduction. Symptomatic therapy, treatment of infectious complications.

Author: Gavrilova N.V.

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