Deficiency (alimentary) anemia Decrease in hemoglobin is associated with insufficient intake of erythropoietic factors in the body The most common form of anemia, especially among children and pregnant women About 80% of deficiency anemias are due to predominant iron deficiency

Definition, epidemiology of IDA is a decrease in Hb per unit of blood volume, due to a lack of such an erythropoietic factor as iron. The most common iron deficiency occurs in children under 3 years of age, especially in the second half of the first year of life. – 1st place The greatest risk of developing IDA is in children of early and puberty and women of childbearing age

Epidemiology of iron deficiency Iron deficiency according to WHO, % of infants 43% under 4 years old 37% from 5 to 12 years old Russia - iron deficiency In young children up to 85% In schoolchildren - more than 30% IDA according to WHO, 1% (dev.) - 39% (development) up to 4 years 5.9% (development) - 48.1% (development) from 5 to 14 years Russia - explicit IDA Per 1 g.zh. 1/2 children

The role of iron in the body Participation in the life of each cell An indispensable component of various proteins and enzymatic systems Provides the necessary level of systemic and cellular aerobic metabolism Participates in redox reactions Destruction of peroxidation products Plays an important role in maintaining a high level of immune resistance of the body Provides growth of the body and nerves, myelination of nerve fibers, the normal functioning of the brain As part of hemoglobin, it is involved in the transfer of oxygen

Consequences of ID (due to a decrease in Fe in the brain tissue) Deceleration of motor development and impaired coordination Delayed speech development and scholastic achievements Psychological and behavioral disorders Mental retardation 80% of the iron found in the adult brain is stored in the first decade of life

Iron pools Hemic (erythrocyte) - 60% (in young children - 80%) Hemoglobin (heme = protoporphyrin + iron) Tissue Myoglobin (oxygen transport in muscles) Enzyme iron (cytochromes, catalase, peroxidase, succinate dehydrogenase, xanthine oxidase) Non-enzymatic biocatalysts Transport Transferrin Reserve Ferritin (liver, muscles) Hemosiderin (macrophages of the brain, spleen, liver) heme iron non-heme iron

Iron absorption About 10% of dietary iron is absorbed in the duodenum and the initial part of the small intestine With ID, the absorption zone expands distally +2 Fe +3 is reduced to Fe +2 under the action of HCl From breast milk - 49%, from cow's - 10%

Regulation of iron absorption by enterocytes Endothelial cells of the intestinal mucosa contain transferrin and ferritin Transferrin transports iron to the membrane Iron + apoferritin oxidation of enterocyte ferritin (3-val) Through the cell membrane into plasma - only 2-val with the help of the DCT1 carrier protein (divalent cation transporter) No ID - excessive synthesis of apoferritin, iron is retained in the cell in combination with ferritin and is lost due to desquamation of the epithelium after 2-3 days. With ID, the synthesis of DCT1 is increased, the synthesis of apoferritin is reduced.

Transport of iron in the blood Fe in the bloodstream combines with transferrin Transferrin is synthesized in the liver, binds 2 molecules of Fe +3 Can bind chromium, copper, magnesium, zinc, cobalt, but the affinity of these metals is lower than that of iron Transferrin transfers iron to the bone marrow, tissues , depot In an adult, 90% of the iron circulation occurs in a closed cycle In children, in addition, endogenous iron is accumulated to ensure growth and increase in blood volume. Iron from degraded erythrocytes also enters the plasma after the breakdown of myoglobin, tissue enzymes

Intracellular metabolism of iron For iron to enter the cell on the membrane, transferrin receptors (TR) The Fe +3-transferrin receptor complex enters the cell by endocytosis, where it dissociates Iron is used in the life of the cell or is deposited in it in the form of ferritin Transferrin is released into the bloodstream The receptor returns to the cell surface, some of the receptors are dumped by the cell into the blood, forming soluble receptors (RTR) capable of binding transferrin.

Deposition of iron Ferritin - apoferritin protein + nitrous oxide Fe +3 (FeOOH) On average, 1 ferritin molecule contains about 2000 Fe +3 atoms of deposited iron Hemosiderin - crystallization of ferritin in siderosomes + other components In a macrophage in an amorphous state Insoluble in water, iron is hardly mobilized and is practically not used

Ante- and intranatal causes of the development of ID (endogenous ID) Transplacental transport of iron occurs only in one direction - from mother to fetus, against the concentration gradient of M.b. impaired in diseases and toxicosis of the 2nd half of pregnancy, when the function of the placenta is impaired In premature babies, children from multiple pregnancies, iron stores per kg of weight do not differ from those of healthy newborns Children with low body weight quickly gain it, then iron deficiency in general affects Feto -fetal, fetomaternal transfusion Early and late cord ligation Bleeding during childbirth

Postnatal causes of ID development Insufficient iron intake Artificial feeding Low consumption of meat (heme), fish, vegetables, fruits Iron bioavailability decreases with an increase in the content of phosphates, phytates, oxalates, tannin, calcium in food Increased needs Rapid growth in infancy, puberty Small and large birth weight

Postnatal causes of GI development Excessive losses Intensive desquamation of the epithelium (exudative diathesis, skin diseases, diarrhea, malabsorption syndrome) bleeding from the gastrointestinal tract, nasal, uterine helminthic invasions (absorption of iron by hookworm) Violation of iron transport violation of the protein-synthetic function of the liver, malabsorption syndrome)

Pathogenesis of GI The reserve fund of iron is consumed first - prelatent iron deficiency In adults - an increase in absorption in the intestine This does not occur in children (a decrease in the activity of ferroabsorption enzymes) Then the transport and tissue funds are consumed - LJ Decrease in the activity of iron-containing enzymes Sideropenic symptoms

IDA pathogenesis IDA - affects the heme fund Iron incorporation into heme is impaired The number of young, non-hemoglobinized cells increases Normoblasts mature more slowly Premature cell division occurs, the formation of microcytes Hypochromia of red blood cells is due to a low content of hemoglobin at a relatively normal level of erythrocytes A decrease in Hb leads to the development of hemic hypoxia

IDA clinic (general symptoms) The severity of the clinic does not depend on the severity of anemia, but on the duration of the disease, adaptation to hypoxia M.b. absence of symptoms with a decrease in Hb M.b. a distinct clinic in LJ Brain hypoxia and tissue iron deficiency Psychomotor development retardation (early age) Asthenia, fatigue, shortness of breath during physical activity, fainting, deterioration in academic performance (schoolchildren) Pallor - usually with a significant decrease level Hb, but m.b. and with LVH (with the phenomenon of shunting - the discharge of blood into larger vessels of the skin) Tachycardia, changes in the sonority of heart sounds, systolic murmur, a tendency to decrease in blood pressure In severe anemia, the boundaries of relative dullness of the heart are expanded, the size of the liver, spleen are enlarged

Clinic of IDA (sideropenic symptoms) Dystrophic changes in the skin and its derivatives Skin is dry, rough Hair is thin and brittle, split ends Nails lose their shine, exfoliate, flatten, transverse and longitudinal striation occurs Koilonychia (practically does not occur before 3 years) Atrophic glossitis, angular stomatitis, atrophic gastritis Decreased appetite, perversion of taste (pica chlorotica), smell Muscle weakness urinary incontinence when coughing, enuresis Decreased immunity

By severity Hemoglobin level 120 (110) - 90 g/l - mild g/l - moderate less than 70 g/l - severe Erythrocyte level 3.5-3.0 x /l 3.0-2.5 x / l less than 2.5 x / l

Erythrocyte indices Color index CP=Nvx3/er=120x3/400=0.9 (N=0.8-1.0) SSGE (MCH) SSGE=Nv/er=120/4=30 pg (N=24-33 pg) 1 pg= g SCGE (MCHC) SCGE=Hvx0.1/Ht=120x0.1/0.4=30% (N=30-38%) Mean erythrocyte volume (MCV) MCV=Htx1000/er=0, 4x1000/4=100 fl (µm 3) (N=75-95 fl) can be measured

Clinical blood test for IDA Hemoglobin level is reduced The level of erythrocytes is slightly reduced or the norm of CP, SSGE, SGE, MCV are reduced Diameter of erythrocytes - anisocytosis with a tendency to microcytosis Form of erythrocytes - poikilocytosis Erythrocytes are hypochromic, anulocytes (radius of enlightenment-darkening is normal 1:1) Hematocrit reduced, ESR increased (decrease in blood viscosity) Reticulocytosis - with bleeding or a reaction to iron therapy

Indicators of iron metabolism SF - μmol / l Serum iron associated with transferrin TIBC - up to 1 year - 53 - 72 μmol / l, after 1 year - μmol / l Total transferrin, siderophilin - how much iron can bind all plasma transferrin (never fully saturated does not occur) LVVR is 2/3 of the TIBC The amount of iron that the plasma can additionally bind LVVR = FIBC-FV CNT - 25-40% CNT = FV / FVBC x 100%

Indicators of iron metabolism DSU - not less than 0.4 mg / day SF more than 12 μg / l Samples with radioactive iron (study of labeled iron absorption) in children are not carried out Number of sideroblasts (Prussian blue stain) 22-30% of erythroid cells of the bone marrow, siderocytes – fractions of a percent (iron is gradually utilized as it matures) Soluble transferrin receptors

Biochemical parameters in IDA and LVH Not detected during treatment with iron preparations The level of SF is reduced less than 14 µmol/l TIH is compensatory increased more than 63 µmol/l LVVR is increased more than 47 µmol/l CST is reduced less than 17% (15%) DSU is reduced less than 0, 4 mg/day SF level is reduced below 12 µg/l The number of sideroblasts is reduced The concentration of soluble transferrin receptors is increased

Differential diagnosis FormClinicAdditionally Megaloblast Subicteria, neurological disorders Complete blood count: hyperchromic anemia, macrocytosis, megaloblasts may enter the peripheral blood; sternal punctate: megaloblastic type of hematopoiesis Hemolytic Hemolytic crises, splenomegaly; acquired anemia - acute onset, congenital - dysembryogenesis stigmas complete blood count: normochromic anemia, reticulocytosis, impaired ORE; congenital anemia - abnormal forms of red blood cells; blood biochemistry: increase in the level of bilirubin due to indirect, increase in the level of SF; sternal punctate: irritation of the erythroid germ

Differential diagnosis Hypoplastic hemorrhagic syndrome, enlarged liver and spleen; congenital anemia Fanconi - multiple malformations; acquired - acute onset complete blood count: normochromic regenerator anemia, thrombocytopenia, leukopenia, a significant increase in ESR; sternal punctate: inhibition of all blood sprouts O. post-hemorrhagic possible syncope, anemic coma complete blood count: first, the number of all cells is normal (a decrease in proportion to the decrease in plasma volume), then normochromic anemia and a decrease in hematocrit, a shift in the formula to the left

Principles of treatment of IDA It is impossible to eliminate iron deficiency only by diet without the use of iron preparations Iron deficiency is eliminated by iron preparations (not vitamins B12, B6, copper preparations in the absence of their deficiency) Preparations for the treatment of iron deficiency anemia are prescribed mainly per os Therapy should not be stopped after normalization of iron levels, because the heminal fund is restored first, only then the tissue and reserve blood transfusions are carried out according to vital indications, guided not by the level of hemoglobin, but by the condition of the child

Treatment Hospitalization - with a significant decrease in Hb Correction factors (apple, yolk), complementary foods are introduced weeks earlier Heme iron is absorbed better than liver iron and vegetable products meat - 25-30% other animal products (fish, eggs) - 10-15 % vegetable products - 3-5%, rice 1% The consumption of products containing oxalates, phosphates, tannin decreases 20 times higher)

The content of iron in a number of products Prunes 15.0 Beans 12.4 Beef tongue 5.0 Beef 2.8 Apples 2.5 Carrots 0.8 Strawberries 0.7 Beef liver 9.0 Yolk 5.8 Chicken 1.5 Rice 1, 3 Potatoes 1.2 Oranges 0.4 Cow's milk 0.1 Rich in iron (more than 5 mg per 100 g of product) Moderately rich in iron (1-5 mg per 100 g of product) Poor in iron (less than 1 mg per 100 g of product)

Iron preparations Before meals (for dyspeptic symptoms after eating) Initial dose 1/3 age After normalization of the blood picture 1/2 treatment 1 month Do not drink tea, milk, do not use with calcium, tetracycline, chloramphenicol, antacids Do not use for infections At 7 -10 day - reticulocyte crisis

Long-acting iron preparations: ferrogradumet, feospan, tardiferon, fenyuls Small and medium doses of iron (ferroplex, ferramid) Liquid dosage forms in drops or in the form of syrup (hemofer, maltofer, aktiferrin) Do not use reduced iron preparations (dyspepsia), phytoferrolactol (phytin ), aloe syrup with iron (low dose, dyspepsia)

Iron preparations Ferrous sulfate (20% active iron): ferroplex, tardiferon, ferrogradumet, aktiferrin, haemofer prolongatum, sorbifer Ferrous gluconate (12% active iron): ascofer, ferronal, apoferrogluconate Ferrous fumarate (33% active iron): heferol, khefenol, ferretab, ferronat, maltofer, ferlatum Complex preparations: gynotardiferon, fefol, fenyuls, irovit, irradian, maltofer-fol Fe 2 salts Fe 3 complexes kg 3-7 years mg Older than 7 years - up to 200 mg Heading dose (for parenteral drugs) D = mx (78 - 0.35 x Hb)

Parenteral administration For parenteral administration, ferrum-lek, ferbitol, ferlecit, venofer, ectofer, as well as preparations containing a course dose for a single intravenous injection - dextrafer, imferon are used. days faster The phenomena of dyspepsia are usually not indications for parenteral administration (they disappear when the drug is changed)

Complications When taken per os Anorexia Metallic taste in the mouth Nausea, vomiting Constipation, diarrhea Possibility of activation of gram-negative opportunistic siderophilic flora of the intestine When administered parenterally Phlebitis Post-injection abscesses Darkening of the skin at the injection site Allergic reactions (urticaria, arthralgia, fever, anaphylactic shock ) In case of overdose - the development of hemosiderosis of internal organs

Blood transfusion More often erythrocyte mass or fresh washed erythrocytes Hb level g/l in combination with signs of central hemodynamic disorders, hemorrhagic shock, anemic coma, hypoxic syndrome If Hb and Ht values ​​are higher than critical, transfusion is performed if massive acute blood loss occurs Short-term effect Calculated ml /kg, older children ml

Causes of treatment failure Misdiagnosis of IDA Insufficient dosage of the drug Unspecified ongoing blood loss Blood iron loss exceeds the intake with the drug Taking oral drugs for malabsorption syndrome Taking drugs that interfere with iron absorption Bivalent anemia (B 12)

Prevention Nutrition Natural feeding with the timely introduction of complementary foods and correction Mixtures enriched with iron Up to 3-4 months endogenous iron is utilized and unabsorbed iron can cause activation of siderophilic gram-negative UPF Regular consumption of meat products Iron preparations Pregnant women in the 3rd trimester (with repeated pregnancy in the 2nd and 3rd trimester) Children at risk: premature, from multiple pregnancy, with toxicosis of the 2nd half of pregnancy, children with ECD, fed with unadapted mixtures, with rapid growth With blood loss, surgical interventions

Dispensary observation For patients receiving iron preparations - 1 time in 2 weeks (+ clinical blood test) After normalization of the hemogram - 1 r / month, later - quarterly Before deregistration, indicators of iron metabolism are determined Deregistration is removed after 6-12 months after normalization of clinical and laboratory parameters

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Presentation on the topic: ANEMIA

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ANEMIA is a clinical and hematological syndrome characterized by a decrease in the total amount of hemoglobin per unit volume of blood (often, with a parallel decrease in the number of red blood cells). ANEMIA is a clinical and hematological syndrome characterized by a decrease in the total amount of hemoglobin per unit volume of blood (often, with a parallel decrease in the number of red blood cells). All anemias are considered secondary. The anemic syndrome can be leading in the clinic or moderately pronounced. In addition to the circulatory-hypoxic syndrome common to all anemias, each anemia has its own specific signs.

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Immune, endocrine and nervous mechanisms are involved in the regulation of erythropoiesis. Immune, endocrine and nervous mechanisms are involved in the regulation of erythropoiesis. Erythropoiesis is influenced by heredity and environmental factors. Normal erythropoiesis is possible if the body has enough amino acids, iron, vitamins B1, B2, B6, B12, C, folic acid, trace elements Co, Cu, and other substances. Erythropoiesis is activated - erythropoietinogen synthesized in the liver, erythrogenin of the juxtaglomerular apparatus of the kidneys, local erythropoiesis hormone - erythropoietin. Stimulate the production of erythropoietin - ACTH, corticosteroids, growth hormone, androgens, prolactin, vasopressin, thyroxine, insulin. Inhibit erythropoiesis - estrogen, glucagon.

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Cells of pathological regeneration of erythrocytes, arising in violation of erythropoiesis Cells of pathological regeneration of erythrocytes, arising in violation of erythropoiesis Megalocyt, megaloblast; erythrocytes with Jolly bodies and Cabot rings; erythrocytes with basophilic granularity. Anisocytosis - pathology of erythrocyte size: Normally, the diameter of an erythrocyte is 7.2-7.5 microns; Microcytes - less than 6.7 microns; Macrocytes - more than 7.7 microns; Megalocytes (megaloblasts) - more than 9.5 microns; Microspherocytes are intensely stained - less than 6.0 µm. Poikilocytosis is a change in the shape of erythrocytes (sickle-cell, target-shaped, ovalocytes, acanthocytes, stomatocytes, etc.) Anisochromia is a different color of erythrocytes (hypo-, hyper-, normochromic, polychromasia) Sideroblasts are bone marrow erythrocytes containing iron (normally 20-40 %)

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According to WHO recommendations: The lower limit of Hb content in men is 130 g/l, in women – 120 g/l, in pregnant women – 110 g/l. The lower limit of the content of erythrocytes in men is 4.0 * 1012 / l, in women - 3.9 * 1012 / l. Hematocrit is the ratio of blood cells to plasma volume. Normal in men - 0.4-0.48%, in women - 0.36-0.42%. The content of Hb in the erythrocyte: Hb (g / l): Er (l) \u003d 27-33 pg. Color index: Hv (g / l) * 0.03: Er (l) \u003d 0.85-1.0. Serum iron in men is 13-30 µmol/l, in women it is 11.5-25 µmol/l.

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According to the WHO recommendation: The total iron-binding capacity of blood serum (TIBCB) is the amount of iron that one liter of blood serum can bind. Normal - 50-84 µmol / l, OZHSSSK - syv. iron = latent YSSCC. Normal - 46-54 µmol / l. Siv. iron: FIHSS = transferrin saturation with iron. Normally - 16-50%. Assessment of iron stores in the body: determination of ferritin in blood serum (radioimmune and enzyme-immune methods), normal - 12-150 μg / l, for men ≈ 94 μg / l, for women ≈ 34 μg / l; determination of the content of protoporphyrin in erythrocytes - 18-90 μmol / l; desferal test (desferal binds only iron reserves). 500 mg of Desferal are injected intramuscularly, 0.6-1.3 mg of iron is normally excreted in the urine.

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Etiopathogenetic classification of anemias Etiopathogenetic classification of anemias Acute posthemorrhagic (APHA) Iron deficiency (IDA) Associated with impaired synthesis or utilization of porphyrins (sideroahrestic) (CAA) Associated with impaired DNA and RNA synthesis (B12 and folate-deficient, megaloblastic) (MGBA) Hemolytic (HA) Aplastic , hypoplastic - with oppression of bone marrow cells (AA) Other variants of anemia: in infectious diseases, diseases of the kidneys, liver, endocrine pathology, etc. Classification of anemia by pathogenesis Anemia due to blood loss (OPHA, IDA) Anemia due to impaired blood formation MGBA, AA) Anemia due to increased blood destruction (HA)

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Classification of anemia by color index Classification of anemia by color index AA) Reticulocyte - the youngest cell of the erythroid series, which goes to the periphery - this is an indicator of germ regeneration (norm 1.2 - 2%) l) Heavy (Hb 70-50 g/l)

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Stages of diagnosis in anemia syndrome Anamnesis, to identify the possible cause of anemia (heredity, provoking factors). Examination, determination of the variant of anemia. Mandatory research methods: KLA (Er, Hb, CP or Hb content in Er) Ht (hematocrit) reticulocytes (N = 1.2-2%) leukocytes and platelets serum iron sternal puncture with bone marrow examination (cellular composition, ratio of cells in bone marrow)

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Stages of diagnosis in anemia syndrome Additional research methods: trephine biopsy of the ilium (tissue relationship in the bone marrow: cells / fat = 1/1) Coombs test urine for hemosiderin osmotic resistance of erythrocytes hemoglobin electrophoresis study for life expectancy Er c Cr51. Determination of the underlying disease that led to anemia: feces for occult blood (Gregersen or Weber methods). Calculation of stool radioactivity within 7 days after the intravenous injection of own washed erythrocytes labeled with Cr51. The study of radioactive iron given orally, followed by the determination of the radioactivity of feces for several days (normally 20% of iron is absorbed); EGDFS; RRS, irrigo-, colonoscopy; consultation of women with a gynecologist; study of the blood coagulation system, etc.

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Vitamin B12 and folic acid are involved in the main stages of the exchange of purine and pyrimidine bases in the process of DNA and RNA synthesis. Vitamin B12 and folic acid are involved in the main stages of the exchange of purine and pyrimidine bases in the process of DNA and RNA synthesis. The body contains 4 mg of vitamin B12, which lasts for 4 years.

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Causes of Vitamin B12 Deficiency Lack of B12 in food. Malabsorption: violation of the synthesis of gastromucoprotein: atrophic gastritis of the fundus of the stomach; autoimmune reactions with the production of antibodies to the parietal cells of the stomach and gastromucoprotein; gastrectomy (after resection of the stomach, the half-life of B12 is 1 year; after gastrectomy, signs of B12 deficiency occur after 5-7 years); stomach cancer; congenital deficiency of gastromucoproteins; malabsorption of B12 in the small intestine; diseases of the small intestine, accompanied by malabsorption syndrome (chronic enteritis, celiac disease, sprue, Crohn's disease) resection of the ileum; small intestine cancer; congenital absence of receptors for the vitamin B12 complex + gastromucoprotein in the small intestine; competitive uptake of vitamin B12; invasion with a wide tapeworm; pronounced intestinal dysbacteriosis. Decreased production of transcobalamin-2 in the liver and impaired transport of vitamin B12 to the bone marrow (with cirrhosis of the liver).

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The main differential criteria for B12 deficiency anemia Circulatory-hypoxic syndrome No sideropenic syndrome Gastroenterological syndrome: loss of appetite, body weight, glossitis (smooth red tongue), heaviness in the epigastrium, unstable stool, achlorhydria, m.b. hepatosplenomegaly Neurological syndrome (funicular myelosis): dystrophic processes in the posterior-lateral columns of the spinal cord associated with the accumulation of toxic methylmalonic acid, manifested by: impaired sensitivity of the limbs, changes in gait and coordination of movements, stiffness of the lower limbs, impaired movements of the fingers, ataxia, impaired vibration sensitivity.

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Hematological syndrome: Hematological syndrome: hyperchromic anemia (CP above 1.1-1.3); anisocytosis (megalocytosis), poikilocytosis, basophilic granularity, Cabot rings, Jolly bodies; three-pronged cytopenia; hypersegmental neutrophilia; megaloblastic type of hematopoiesis (according to sternal puncture); a decrease in B12 in the blood is less than 200 pg / ml;

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Occurs less frequently than B12-deficient Occurs less frequently than B12-deficient FA reserve in the body is designed for 2-3 months FA is present in all products, when heated it is destroyed Absorbed in the entire jejunum, m.b. diarrhea FA absorption does not require transport proteins Congenital FA defects are associated with mental retardation and are not corrected by FA administration

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The main differential criteria for folate deficiency anemia History data: pregnancy, neonatal period, chronic alcoholism, chronic hemolysis, myeloproliferative diseases, medication (folic acid antagonists, anti-tuberculosis, anticonvulsants). Erythropoiesis suffers. There is no funicular myelosis, lesions of the stomach. No reticulocyte crisis on B12. In the bone marrow, megaloblasts stain only with B12-deficiency anemia, but not with folate deficiency anemia. The decrease in folic acid in the blood is less than 3 mg / ml (N - 3-25 mg / ml).

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Treatment of megaloblastic anemia (MGBA) Vitamin B12 (cyanocobalamin) - IM 400-500 mcg (4-6 weeks). For neurological disorders: B12 (1000 mcg) + cobalamide (500 mcg) until the disappearance of neurological symptoms. If necessary, lifelong administration of B12 (500 mcg) 1 time in 2 weeks or prophylactic treatment - B12 (400 mcg) for 10-15 days 1-2 times a year. Erythromass transfusion only for health reasons (for all anemias!): Nv< 50 г/л, Нв < 70 г/л с нарушением гемодинамики, развитие прекомы и комы, срочная подготовка к операции и т.д. Дегельминтизация – выведение лентеца широкого (феносал, мужской папоротник). Фолиевая кислота 5-15 мг/сут (до 30 мг/сут); профилактическая доза – 1-5 мг/сут. Критерии эффективности лечения субъективные улучшения в первые дни лечения; ретикулоцитарный криз на 5-7 день лечения; улучшение показателей крови ко второй неделе лечения, с нормализацией через 3-4 недели.

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Aplastic anemia (AA) AA is a hematological syndrome caused by a large number of endogenous and exogenous factors, qualitative and quantitative changes in the stem cell and its microenvironment, the cardinal morphological feature of which is pancytopenia in the peripheral blood and fatty degeneration of the bone marrow. P. Ehrlich (1888) first described AA. The term "aplastic anemia" was introduced in 1904 by Chauffard. Incidence 4-5 people per 1 million population per year (in Europe) Age peaks of incidence 20 and 65 years

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Causes of AA Causes of AA drugs, chemicals, viruses, autoimmune processes; in 50% of cases, the etiology is unknown (idiopathic AA). Pathogenesis AA Functional insufficiency of the bone marrow with inhibition of 1, 2 or 3 germs (pancytopenia). Defeat of a pluripotent blood stem cell Suppression of hematopoiesis Effect of immune (cellular, humoral) mechanisms Deficiency of factors stimulating hematopoiesis Iron, B12, protoporphyrin cannot be used by hematopoietic tissue.

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Aplastic anemia can be Aplastic anemia can be Congenital (with or without a syndrome of congenital anomalies) Acquired AA is isolated with the flow Acute Subacute Chronic Forms of AA Immune Non-immune Clinical syndromes of AA Circulatory-hypoxic Septic-necrotic Hemorrhagic

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Data of laboratory and instrumental studies Data of laboratory and instrumental studies of CP and iron content in erythrocytes are normal (normochromic A), reticulocytes are reduced (regenerator A), increased serum iron, saturation of transferrin with iron by 100%, erythrocytes ↓, HB ↓ (up to 20- 30 g / l), thrombocytopenia (may be up to 0), leukopenia (may be up to 200 per µl), liver, spleen and lymph nodes are usually not enlarged, bone marrow (trepanobiopsy of the ilium): aplasia of all sprouts, replacement bone marrow fat. In 80% of AA - pancytopenia, 8-10% - anemia, 7-8% - anemia and leukopenia, 3-5% - thrombocytopenia.

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Severe AA Severe AA In the peripheral blood (2 out of 3 germs are depressed) Granulocytes 0.5-0.2 * 109 / l Platelets less than 20 * 109 / l Reticulocytes less than 1% Myelogram Myelokaryocytes less than 25% of the norm Myelokaryocytes 25-50%, and myeloid cells less than 30% Trepanobiopsy In mild form - 40% of adipose tissue In moderate - 80% In severe form - the absolute predominance of adipose tissue (panmyelophthisis) Differential diagnosis of AA The debut of acute leukemia Chronic lymphocytic leukemia (bone marrow form) Metastases of cancer in the bone marrow Pancytopenia in the elderly, as a manifestation of B12 deficiency anemia

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AA treatment Bone marrow reconstitution: cyclosplrin A (sandimmune), antilymphocyte Ig (ALG), antiplatelet Ig (ATG), corticosteroids, donor bone marrow transplantation (performed in severe cases at age<40 лет, в ранние сроки). Заместительная терапия компонентами крови. Асептические условия; купирование и профилактика инфекции (АБТ). Если АТ, то плазмоферез. Андрогенные стероиды (нерабол, ретаболил). Спленэктомия. Колониестимулирующие факторы (агранулоцитарный колониестимулирующий фактор – лейкомакс; гранулоцитарный колониестимулирующий фактор - лейкоген). Эритропоэтин, тромбопоэтин. При необходимости выведение избытков железа.

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Evaluation of AA therapy Complete remission: Hb > 100 g/l; granulocytes > 1.5*109/l; platelets > 100*109/l; no need for blood transfusions. Partial remission: Hb > 80 g/l; granulocytes > 0.5*109/l; platelets > 20*109/l; no need for blood transfusions. Clinical and hematological improvements: improvement of hematological parameters; reduction in the need for replacement blood transfusion for more than two months. No effect: no hematological improvement; the need for blood transfusion is preserved.

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Systems whose violation causes hemolysis Glutathione system: protects important cell components from denaturation by oxidizing agents, peroxides, heavy metal ions. Phospholipids: determine the permeability of the membrane for ions, determine the structure of the membrane, affect the enzymatic activity of proteins. Erythrocyte membrane protein: 20% spectrin - a heterogeneous mixture of polypeptide chains; 30% - actomyosin. Glycolysis is a method of anaerobic conversion of glucose into lactic acid, during which ATP is formed - an accumulator of the chemical energy of cells. Other substrates of glycolysis: fructose, mannose, galactose, glycogen. The pentose phosphate cycle is an anaerobic oxidative pathway for the conversion of glucose. Adenyl system: adenylate kinase and ATPase.

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Hemolytic anemias (HA) HA unite a number of hereditary and acquired diseases, the main feature of which is an increased breakdown of Er and a shortening of their life expectancy from 90-120 to 12-14 days. Hereditary GA are associated with defects in the structure of Er, which become functionally inferior. Acquired GA are caused by various factors contributing to the destruction of Er (hemolytic poisons, mechanical effects, autoimmune processes, etc.). Pathological hemolysis can be 1. Localized intracellular (RES cells, mainly spleen) intravascular 2. Acute chronic

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Basic criteria for GA Increased bilirubin due to unconjugated: bile pigments in the urine are negative; urobilin in urine and stercobilin in feces; "Lemon" jaundice without itching. Splenomegaly with intracellular hemolysis. Anemia: normochromic, hyperregenerative, erythroid hyperplasia in the bone marrow. hemolytic crises. M.b. gallstones (pigmented) stones - cholelithiasis. Intravascular hemolysis is characterized by: hemoglobinemia (free Hb in blood plasma); hemoglobinuria and hemosiderinuria (red or black urine); hemosiderosis of internal organs; tendency to microthromboses of various localizations.

slide number 36

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GA with intravascular hemolysis Hereditary GA: A. Enzymopathies (deficiency of G-6-PD). B. Hemoglobinopathies (sickle cell anemia). 2. Acquired HA: A. Immune - AIHA with thermal and biphasic hemolysins. B. Non-immune - PNH, mechanical when prosthetic valves, blood vessels, marching.

slide number 37

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slide number 38

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slide number 39

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Classification of hereditary hemolytic anemias A. Membranopathy due to violation of the protein structure of the erythrocyte membrane Microspherocytosis, elliptocytosis, stomatocytosis, pyropoykylocytosis. Violation of erythrocyte membrane lipids: acanthocytosis, deficiency of lecithin-cholesterol-aryltransferase activity, an increase in the content of lecithin in the erythrocyte membrane, infantile infantile pycnocytosis.

slide number 40

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B. Fermentopathies B. Enzymopathies Deficiency of enzymes of the pentose phosphate cycle. Deficiency of activity of glycolysis enzymes Deficiency of activity of glutathione metabolism enzymes. Deficiency in the activity of enzymes involved in the use of ATP. Deficiency of ribophosphate pyrophosphate kinase activity. Violation of the activity of enzymes involved in the synthesis of porphyrins. B. Hemoglobinopathies Caused by an anomaly in the primary structure of Hb. Caused by a decrease in the synthesis of polypeptide chains that make up normal Hb. Due to the double heterozygous state. Hb anomalies that are not accompanied by the development of the disease.

slide number 41

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slide number 42

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Hereditary fermentopathy Insufficiency of glucose-6-phosphate dehydrogenase (G-6-PDH) in Er More common in Africa, Latin America, the Mediterranean, we have Azerbaijan, Armenia, Dagestan; Men are predominantly affected (recessive sex-linked gene); Provoke a crisis of acute infections, drugs (paracetamol, nitrofurans, sulfonamides, tuberculostatics, etc.) and some legumes, acidosis in diabetes and chronic renal failure. intravascular hemolysis. The morphology of Er is not changed. Osmotic resistance Er in N or slightly . After the crisis in Ayr, Heinz bodies (denatured Hb) can be found. Diagnosis in the group of hereditary fermentopathy is based on the detection in Er of insufficiency of various enzymes of the hexose or pentose cycles.

slide number 43

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Membranopathy The most common among them is hereditary microspherocytosis (Minkowski-Choffard disease), in which the Er membrane defect is accompanied by an increase in the permeability of Na and H2O ions into the cell with the formation of a spherocyte. The spherocyte, passing through the sinuses of the spleen, decreases in diameter from 7.2-7.5 microns to< 6 (при этом кривая Прайс-Джонса сдвигается влево). Внутриклеточный гемолиз. Гемолитические кризы провоцируются инфекциями, переохлаждением, беременностью и др. Характерно снижение осмотической резистентности Эр: min до 0,6-0,7, max до 0,4% (в N – min – 0,46-0,48, max – 0,32-0,34%). Прибавление к Эр глюкозы значительно уменьшает гемолиз.

slide number 44

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slide number 45

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Hemoglobinopathies Hereditary GA with impaired synthesis of the protein part of Hb. The Hb molecule consists of 4 heme molecules and 4 polypeptide chains (2 α and 2 β). Substitution of amino acids in polypeptide chains leads to the formation of pathological Hb (S, F, A2, etc.). The disease occurs more often in homozygotes in the countries of the Mediterranean, Africa, India and the republics of Transcaucasia. Homozygous patients have severe, sometimes fatal manifestations of the disease since childhood, while heterozygotes have mild forms with a survival > 20-30 years. Er's lifetime has been shortened. The hemolysis site is examined with Cr51-labeled Er. Hb anomalies (S, F, A2, etc.) are detected by Hb electrophoresis (immunophoresis). It is possible to quantify abnormal Hb.

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slide number 50

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Classification of acquired hemolytic anemias A. Immune hemolytic anemias of HA associated with exposure to antibodies (immune HA): isoimmune (alloimmune): Rhesus conflict, transfusion of incompatible blood; heteroimmune, caused by diseases, viruses; transimmune - antibodies are transmitted through the placenta from mother to fetus; Autoimmune HA with antibodies to its own unchanged Er: with incomplete thermal agglutinins (detected in 70-80% of autoimmune HA using a direct Coombs test), with thermal hemolysins, with complete cold agglutinins associated with two-phase cold hemolysins. Autoimmune GA with antibodies against the antigen of bone marrow normocytes.

slide number 53

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Acquired GA Paroxysmal nocturnal hemoglobinuria (Marchiafava-Micheli disease) A clone of defective ER is formed due to a somatic mutation of the type of a benign tumor of the blood system with 2 populations of ER: with a normal and defective membrane; leukocytes and platelets mutate simultaneously with the development of pancytopenia; intravascular hemolysis; a change in blood pH towards acidosis in the presence of complement leads to hemolysis (Hem, Crosby, sucrose tests); direct Coombs test is negative.

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Treatment of autoimmune GA Glucocorticoid hormones in the acute phase with thermal agglutinins; prednisolone 60-80 mg / day, with a distribution of 3 doses at the rate of 3: 2: 1. In chronic HA with incomplete thermal agglutinins, prednisolone 20-40 mg / day. With GA with complete cold agglutinins with a pronounced exacerbation, prednisolone 20-25 mg / day. Splenectomy - with the ineffectiveness of hormones, rapid relapses after hormone withdrawal, complications of hormone therapy. Cytostatics: azathioprine 100-150 mg/day; cyclophosphamide 400 mg every other day; vincristine 2 mg once a week intravenously; chlorbutin 2.5-5 mg/day 2-3 months - in the absence of the effect of hormones. Transfusion of washed erythrocytes selected according to the indirect Coombs test for severe anemia. Plasmapheresis in severe HA, with complications of DIC. Immunoglobulin C 0.5-1 g/kg of body weight.

slide number 56

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Principles of treatment of HA with intravascular hemolysis Infusion therapy - prevention of acute renal failure: soda, glucose solution with inulin, eufillin 10-20ml, furosemide 40-60mg, mannitol 1g/kg of body weight. Prevention of DIC - low doses of heparin. Fight infection - antibiotics (sickle cell anemia). Increasing acute renal failure - peritoneal dialysis, hemodialysis.

slide number 57

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slide number 58

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Treatment of hemolytic crisis Compensation of circulating blood volume: reopoliglyukin 400-800 ml; reoglumal 400-800 ml; isotonic sodium chloride solution 1000 ml; albumin 10% 150-200 ml under the control of central venous pressure. Neutralization of toxic products and stimulation of diuresis. Hemodez (low molecular weight polyvinylpyrrolidone, colloidal solution) 300-500 ml, 2-8 infusions per course. Polidez 250-1000 ml. Stimulation of diuresis: furosemide 40-80 mg intravenously, if necessary, after 4 hours again. Eufillin solution 2.4% 10-20 ml per 10 ml isotonic sodium chloride solution (in the absence of arterial hypotension).

slide number 59

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Elimination of acidosis: 4% 200-400 ml of sodium bicarbonate in/venously. Elimination of acidosis: 4% 200-400 ml of sodium bicarbonate in/venously. Extracorporeal therapy - in the absence of the effect of the above measures - plasmapheresis, hemodialysis. Glucocorticoid hormones: in autoimmune GA, shock, collapse - intravenous prednisolone 1-1.5 mg / kg of the patient's body weight, again after 3-4 hours (if necessary). Relief of anemia: with a decrease in Hb to 40 g / l and below - transfusion of individually selected erythrocytes in 150-300 ml; erythrocytes should be washed 4-5 times, fresh frozen, selected according to the indirect Coombs test. In a crisis against the background of NPG, erythrocytes are 7-9 days old from the moment of preparation (fresher ones increase the risk of hemolysis).

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Treatment of sickle cell anemia Prevention of dehydration Prevention of infectious complications (from 3 months to 5 years - penicillin daily orally at 125-250 mg; after 3 years - vaccination with a polyvalent pneumococcal vaccine). The transfusion of washed or thawed red blood cells is the main method of treatment in adults and children. Indications for erythromass transfusion: severe degree of anemia, decrease in reticulocytes; stroke prevention; blood transfusions reduce the content of Hb6 in erythrocytes and reduce the risk of stroke; preparation for abdominal operations; trophic ulcers of the lower leg; taking folic acid 1 mg/day daily in the presence of anemia.

slide number 64

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Treatment of thalassemia Treatment of the homozygous form: transfusion of washed or thawed erythrocytes to maintain the level of Hb within 90-100 g/l; with the complication of frequent blood transfusions with hemosiderosis - desferal (a complexon that removes iron from the body) at a dose of 10 mg / kg of body weight with ingestion of ascorbic acid 200-500 mg; in the presence of splenomegaly, hypersplenism - splenectomy Treatment of the heterozygous form: folic acid 0.005 2 times a day; iron preparations are contraindicated.

slide number 65

Description of the slide:

Treatment of paroxysmal nocturnal hemoglobinuria Transfusion of washed or freshly frozen erythrocytes with a shelf life of at least 7 days in severe anemia; in the presence of anti-erythrocyte or antileukocyte antibodies - transfusion of erythrocyte mass, selected according to the indirect Coombs test. Anabolic hormones: nerobol 0.005 * 4 times a day for at least 2-3 months under the control of cholestasis. Antioxidants: vitamin E - erevitis intramuscularly 3-4 ml / day (0.15-0.2 g of tocopherol acetate); in capsules of 0.2 ml of a 5% solution of vitamin E, 2 capsules a day after meals; course 1-3 months. With severe iron deficiency - iron preparations in small doses (ferroplex 1 tablet 3 times a day) under the control of bilirubin. Treatment of thrombosis: heparin 2.5 thousand 2 times a day under the skin of the abdomen.

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Iron-deficiency anemia. Plan. Definition of the ICD-10 concept. Clinical classification of IDA. Formulation of the diagnosis. Clinical picture of IDA Diagnosis of IDA Treatment of IDA Examination of working capacity of patients with IDA Clinical examination with IDA. Prevention Conclusions.

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Definition of the concept of ICD-10 Clinical classification of IDA Formulation of the diagnosis. Clinical picture of IDA Diagnosis of IDA Treatment of IDA Examination of the working capacity of patients with IDA Clinical examination with IDA. Prevention Conclusions

The most common form of anemia that occurs when there is a lack of iron in the body and is characterized by a decrease in the level of hemoglobin per unit volume of blood in combination with clinical signs of anemia. Among all hanemias, IDA occurs most frequently and accounts for about 80%. Iron deficiency affects almost half of the world's population (mostly women), the disease affects almost all age groups.

The classification of diseases of the 10th revision (ICD-10) takes into account the following forms of anemia associated with absolute and relative iron deficiency: D50. Iron deficiency anemia (asiderotic, sideropenic, hypochromic). D50.0. Iron deficiency anemia associated with chronic blood loss (chronic posthemorrhagic anemia). D50.1. Sideropenic dysphagia (Kelly-Patterson or Plummer-Vinson syndromes). D50.8. Other iron deficiency anemias. D50.9. Iron deficiency anemia, unspecified.

1. IDA posthemorrhagic. This group consists of anemia that develops on the basis of repeated small blood loss - metrorrhagia, epistaxis, hematuria, etc. 2. IDA in pregnant women. The causes of anemia in this group are different: imbalance in the nutrition of pregnant women and the associated deterioration in iron utilization, the transfer of a significant amount of it by the mother's body to the developing fetus, iron loss during lactation, etc. 3. IDA associated with gastrointestinal pathology. These include anemia that occurs after gastrectomy, extensive resections of the small intestine, with various enteropathies. At its core, these are IDA, caused by a gross, severe violation of the function of iron absorption in the proximal duodenum. 4. IDA secondary, arising from infectious, inflammatory or neoplastic diseases. Anemia in these cases develops as a result of large losses of iron during the death of tumor cells, tissue breakdown, micro- and even macrohemorrhages, and an increase in the need for iron in inflammation foci.

IDA, in which the most thorough anamnestic and laboratory search does not reveal the well-known causes of iron deficiency. Most patients have a special form of iron malabsorption. 6. Juvenile IDA - anemia that develops in young girls (and extremely rarely in boys). This form of iron deficiency anemia is associated with genetic or phenotypic dyshormonal phenomena. 7. IDA of complex origin. This group includes alimentary anemia.

Stage I - the loss of iron exceeds its intake, the gradual depletion of reserves, absorption in the intestine compensatory increases; Stage II - depletion of iron stores (serum iron level - below 50 μg / l, transferrin saturation - below 16%) prevents normal erythropoiesis, erythropoiesis begins to fall; Stage III - the development of mild anemia (100–120 g / l hemoglobin, compensated), with a slight decrease in the color index and other indices of saturation of erythrocytes with hemoglobin; Stage IV - severe (less than 100 g / l hemoglobin, subcompensated) anemia with a clear decrease in the saturation of erythrocytes with hemoglobin; Stage V - severe anemia (60-80 g / l hemoglobin) with circulatory disorders and tissue hypoxia. By severity: mild (Hb content - 90–120 g/l); medium (70–90 g/l); heavy (less than 70 g/l).

The diagnosis indicates the severity of anemia, the etiological factor. Diagnosis example. Iron deficiency anemia of moderate severity due to chronic blood loss. Chronic hemorrhoids. Iron deficiency anemia of severe nutritional origin. Mild iron deficiency anemia due to increased iron consumption (pregnancy, childbirth and lactation).

Clinical manifestations of IDA are two major syndromes - anemic and sideropenic. Anemia syndrome is caused by a decrease in hemoglobin content and a decrease in the number of red blood cells, insufficient oxygen supply to tissues and is represented by nonspecific symptoms. Patients complain of general weakness, increased fatigue, decreased performance, dizziness, tinnitus, flies before the eyes, palpitations, shortness of breath during exercise, the appearance of fainting. There may be a decrease in mental performance, memory impairment, drowsiness. Subjective manifestations of anemic syndrome first disturb patients during exercise, and then at rest (as anemia develops).

Pallor of the skin and visible mucous membranes is found, often - some pastosity in the area of ​​\u200b\u200bthe legs, feet, face. Typical morning swelling - "bags" around the eyes. Anemia causes the development of myocardial dystrophy syndrome, which is manifested by shortness of breath, tachycardia, often arrhythmia, moderate expansion of the borders of the heart to the left, deafness of heart sounds, low systolic murmur at all auscultatory points. In severe and prolonged anemia, myocardial dystrophy can lead to severe circulatory failure. IDA develops gradually, so the patient's body adapts to a low level of hemoglobin, and subjective manifestations of anemic syndrome are not always pronounced.

(hyposiderosis syndrome) is caused by tissue iron deficiency, which leads to a decrease in the activity of many enzymes (cytochrome oxidase, peroxidase, succinate dehydrogenase, etc.). Sideropenic syndrome is manifested by numerous symptoms, such as: taste perversion (pica chlorotica) - an irresistible desire to eat something unusual and inedible (chalk, tooth powder, coal, clay, sand, ice), as well as raw dough, minced meat, cereals ; this symptom is more common in children and adolescents, but is often observed in adult women; addiction to spicy, salty, sour, spicy foods; perversion of the sense of smell - an addiction to smells that most people around perceive as unpleasant (smells of gasoline, acetone, varnishes, paints, shoe polish, etc.); severe muscle weakness and fatigue, muscle atrophy and a decrease in muscle strength due to a deficiency of myoglobin and tissue respiration enzymes; dystrophic changes in the skin and its appendages (dryness, peeling, tendency to quickly form cracks on the skin; dullness, brittleness, loss, early graying of hair; thinning, brittleness, transverse striation, dullness of nails; symptom of koilonychia - spoon-shaped concavity of nails);

Cracks, "jamming" in the corners of the mouth (occur in 10-15% of patients); glossitis (in 10% of patients) - characterized by a feeling of pain and fullness in the region of the tongue, reddening of its tip, and later - atrophy of the papillae ("varnished" tongue); often there is a tendency to periodontal disease and caries; atrophic changes in the mucous membrane of the gastrointestinal tract - this is manifested by dryness of the mucous membrane of the esophagus and difficulty, and sometimes pain when swallowing food, especially dry (sideropenic dysphagia); development of atrophic gastritis and enteritis; symptom of "blue sclera" - characterized by a bluish color or pronounced blueness of the sclera. This is explained by the fact that with iron deficiency, collagen synthesis in the sclera is disrupted, it becomes thinner and the choroid of the eye shines through it; imperative urge to urinate, the inability to hold urine when laughing, coughing, sneezing, perhaps even bedwetting, which is due to the weakness of the sphincters of the bladder; "Sideropenic subfebrile condition" - characterized by a prolonged increase in temperature to subfebrile values; a pronounced predisposition to acute respiratory viral and other infectious and inflammatory processes, chronic infections, which is due to a violation of the phagocytic function of leukocytes and a weakening of the immune system;

With a decrease in the content of hemoglobin iron, changes in the general blood test characteristic of IDA appear: a decrease in the level of hemoglobin and erythrocytes in the blood; decrease in the average content of hemoglobin in erythrocytes; decrease in color index (IDA is hypochromic); hypochromia of erythrocytes, characterized by their pale staining, and the appearance of enlightenment in the center; predominance in the smear of peripheral blood among erythrocytes of microcytes - erythrocytes of reduced diameter; anisocytosis - unequal size and poikilocytosis - a different form of red blood cells; normal content of reticulocytes in the peripheral blood, however, after treatment with iron preparations, an increase in the number of reticulocytes is possible; tendency to leukopenia; the platelet count is usually normal; with severe anemia, a moderate increase in ESR (up to 20-25 mm / h) is possible.

In practice, the criteria for IDA are: - low color index; – erythrocyte hypochromia, microcytosis; – decrease in the level of serum iron; - increase in OLSS; - Decreased serum ferritin content. In a biochemical blood test, in addition to a decrease in the level of serum iron and ferritin, changes are also detected due to the underlying oncological or other disease.

Currently, there are the following stages of treatment of IDA: 1st stage - cupping therapy aimed at increasing the level of hemoglobin and replenishing peripheral iron stores; 2nd stage - therapy that restores tissue iron reserves; 3rd stage - anti-relapse treatment.

Includes: elimination of etiological factors (treatment of the underlying disease); medical nutrition; treatment with iron-containing drugs; elimination of iron deficiency and anemia; replenishment of iron stores (satiation therapy). anti-relapse therapy.

IDA, the main treatment should be aimed at its elimination (surgical treatment of a tumor of the stomach, intestines, treatment of enteritis, correction of alimentary insufficiency, etc.). In a number of cases, radical elimination of the cause of IDA is not possible, for example, with ongoing menorrhagia, hereditary hemorrhagic diathesis, manifested by nosebleeds, in pregnant women and in some other situations. In such cases, pathogenetic therapy with iron-containing drugs is of primary importance. The route of administration of the drug to a patient with IDA is determined by the specific clinical situation. When carrying out cupping therapy, oral and parenteral administration of iron preparations (PJ) to the patient is used. The first route - oral - is the most common, although it gives more delayed results.

For oral administration are the following: - the appointment of the pancreas with a sufficient content of ferric iron; - inadvisability of the simultaneous appointment of B vitamins (including B12), folic acid without special indications; - avoiding the appointment of pancreas inside in the presence of signs of malabsorption in the intestine; - sufficient duration of the saturating course of therapy (at least 3-5 months); - the need for maintenance therapy of the pancreas after the normalization of hemoglobin in appropriate situations. For an adequate increase in hemoglobin parameters in patients, it is necessary to prescribe from 100 to 300 mg of ferric iron per day. The use of higher doses does not make sense, since the absorption of iron does not increase. Individual fluctuations in the amount of iron needed are due to the degree of its deficiency in the body, depletion of reserves, the rate of erythropoiesis, absorbability, tolerance, and some other factors. With this in mind, when choosing a medicinal pancreas, one should focus not only on the content of the total amount in it, but also, mainly, on the amount of ferric iron, which is only absorbed in the intestine.

PG for oral administration: - lack of iron deficiency (misinterpretation of the nature of hypochromic anemia and erroneous appointment of PG); - insufficient dosage of the pancreas (underestimation of the amount of ferric iron in the preparation); - insufficient duration of treatment of the pancreas; - violation of the absorption of the pancreas, administered orally to patients with the corresponding pathology; - concomitant use of drugs that violate the absorption of iron; - the presence of chronic (occult) blood loss, most often from the digestive tract; - combination of IDA with other anemic syndromes (B12 deficiency, folic acid deficiency).

Parenteral administration, which can be intramuscular and intravenous. Indications for the use of pancreas parenterally may be the following clinical situations: - malabsorption in intestinal pathology (enteritis, malabsorption syndrome, resection of the small intestine, resection of the stomach according to the Billroth II method with the exclusion of the duodenum); - exacerbation of peptic ulcer of the stomach or duodenum; - intolerance to the pancreas for oral administration, not allowing further continuation of treatment; - the need for faster saturation of the body with iron, for example, in patients with IDA who are to undergo surgery (uterine fibroids, hemorrhoids, etc.).

Patients with IDA Temporary ability to work is due to both anemia itself and the disease that caused it. With a mild form of anemia (Hb below 90 g / l), the ability to work is determined by the course of the underlying disease. Patients are usually able to work. With anemia of moderate severity (Hb 70-90g / l), patients are able to work. In case of severe anemia, persons of physical labor can be recognized as disabled of the lll group in the absence of its possible elimination.

Persons with a latent iron deficiency are not subject to clinical examination. If IDA is a consequence of some pathological process, then special dispensary observation is not required, because. Patients are already registered according to the main disease. Patients with IDA are monitored by a local doctor. The frequency of observations in the acute period is 1-2 times a year.

Primary prevention is carried out: pregnant and breastfeeding; adolescent girls and women, especially those with heavy periods; donars. Secondary prevention is carried out in persons with previously cured IDA, in the presence of conditions that threaten the development of relapse of anemia (heavy menstruation, uterine fibroids, etc.)

Anemia has become a pressing problem for a large number of people around the world. It affects especially vulnerable segments of the population - young children, pregnant women, the elderly and those suffering from serious chronic diseases. However, this anomalous state can and should be combated. Proper diagnosis, including the performance of various laboratory tests, allows you to timely identify this disease and choose the appropriate method of treatment.

Primary prevention - is carried out by a group of people who do not currently have anemia, but there are predisposing circumstances: pregnant and lactating. All pregnant women with a gestational age of 8 weeks are divided into groups: 0 (zero) - a normal pregnancy. Prescribe prophylactic Fe (30-40 mg) from 31 weeks of pregnancy for 8 weeks. Group 1 - pregnant women with a normal blood test, but with risk factors (pathology of the gastrointestinal tract, heavy and prolonged menstruation before pregnancy, multiple births, insufficient intake of Fe with food, the presence of infection, early toxicosis with frequent vomiting). Preventive therapy begins from the 12-13th week to the 15th, then from the 21st from the 31st to the 37th week. Group 2 - women who have anemia during pregnancy. Apply therapeutic doses of drugs. Group 3 - women with pregnancy that occurred against the background of already existing IDA. Treatment is carried out with the appointment of therapeutic doses of drugs, then saturation therapy and courses of preventive therapy (2 courses of 8 weeks) in combination with the intake of antioxidants (vit E, aevita, vit C, multivitamins, calcium preparations) Adolescent girls and women with abundant and prolonged monthly (prescribe 2 courses of preventive therapy for 6 weeks or after menstruation for 7-10 days during the year.

Topic: Iron deficiency anemia
Completed by: Shadimetova M.A.7
04 group.
Checked by: Latyeva M.Sh. .

Anemia is called clinical hematological syndrome,
characterized by a decrease
erythrocyte and hemoglobin counts
in blood.
A variety of pathological
processes can serve as the basis
development of anemic conditions, in
connection with which anemia should
regarded as one of the symptoms
underlying disease.
Prevalence of anemia
varies considerably from
0.7 to 6.9%.
One of the causes of anemia can be
three factors or a combination of them:
bleeding, not enough
the formation of red blood cells or
their increased destruction (hemolysis).

Among the various anemic conditions, iron deficiency anemia
are the most common and account for about 80% of all
anemia.
According to the World Health Organization, every 3rd
woman and every 6th man in the world (200 million people)
suffer from iron deficiency anemia
Iron deficiency anemia (IDA) is a hematological syndrome,
characterized by impaired hemoglobin synthesis due to
iron deficiency and manifested by anemia and sideropenia.
The main causes of IDA are blood loss and lack of
heme-rich foods - meat and fish.

classification
I. Anemia due to blood loss (posthemorrhagic):
1. sharp
2. chronic
II. Anemia due to impaired blood formation:
1. Deficiency anemia:
iron deficiency
protein-deficient
vitamin deficiency
2. Anemia associated with impaired synthesis and utilization of porphyrins:
hereditary
acquired
aplastic anemia
metaplastic anemias
dysregulatory

III. Anemia due to increased hemorrhage
(hemolytic):
1. Hereditary:
membranopathies
fermentopathy
hemoglobinopathies
2. Acquired

Etiology

The main etiopathogenetic factor in the development of IDA is iron deficiency.
The most common causes of iron deficiency conditions
are:
1. Loss of iron in chronic bleeding (the most common
reason reaching 80%):
- bleeding from the gastrointestinal tract: peptic ulcer,
erosive gastritis, esophageal varicose veins,
colonic diverticula, hookworm invasions, tumors, UC,
haemorrhoids;
- prolonged and heavy menstruation, endometriosis, fibromyoma;
– macro- and microhematuria: chronic glomerulo and pyelonephritis, urolithiasis, polycystic kidney disease, kidney tumors
and bladder;
- nasal, pulmonary bleeding;
- blood loss during hemodialysis;
– uncontrolled donation;

2. Insufficient absorption of iron:
–
–
–
–
resection of the small intestine;
chronic enteritis;
malabsorption syndrome;
intestinal amyloidosis;
3. Increased need for iron:
–
–
–
–
intensive growth;
pregnancy;
the period of breastfeeding;
sports;
4. Insufficient intake of iron from food:
–
–
newborns;
Small children;
–
vegetarianism.

The recommended daily intake of iron from food: for
men - 12 mg,
for women - 15 mg,
for pregnant women - 30 mg.

Pathogenesis

Depending on the severity of iron deficiency in the body, there are three
stages:
prelatent iron deficiency in the body;
latent iron deficiency in the body;
Iron-deficiency anemia.
Violation of the functions of molecules
hemoglobin in the blood causes anemia.
These blood cells, enlarged
900 times taken from a person with
sickle cell anomaly
erythrocytes.

Prelatent iron deficiency in the body

At this stage, depot depletion occurs in the body.
Ferritin is the main form of iron storage.
water soluble glycoprotein complex
found in macrophages of the liver, spleen, bone marrow,
erythrocytes and blood serum
Laboratory sign of iron depletion in the body
is a decrease in serum ferritin levels.
At the same time, the level of serum iron remains within
normal values. Clinical signs at this stage
absent, the diagnosis can only be made on the basis of
determination of the level of serum ferritin.

Latent iron deficiency in the body

If there is no adequate replenishment of iron deficiency
in the first stage, the second stage of iron deficiency occurs
states - latent iron deficiency. At this stage in
as a result of a violation of the supply of the necessary metal in
tissue, there is a decrease in the activity of tissue enzymes
(cytochromes, catalase, succinate dehydrogenase, etc.), which
manifested by the development of sideropenic syndrome.
The clinical manifestations of sideropenic syndrome include
perversion of taste, addiction to spicy, salty, spicy foods,
muscle weakness, dystrophic changes in the skin and appendages, etc.
At the stage of latent iron deficiency in the body are more pronounced
changes in laboratory parameters. Register not only
depletion of iron stores in the depot - a decrease in the concentration of ferritin
serum, but also a decrease in the content of iron in serum and carrier proteins.

Iron-deficiency anemia

Iron deficiency depends on the degree of iron deficiency
and the rate of its development and includes signs of anemia and tissue
iron deficiency (sideropenia). The phenomena of tissue iron deficiency
absent only in some iron deficiency anemias,
caused by a violation of the utilization of iron, when the depot
full of iron.
Thus, iron deficiency anemia in its course
two periods pass: the period of latent iron deficiency and the period
apparent anemia due to iron deficiency.
During the period of latent iron deficiency, many
subjective complaints and clinical signs characteristic of
iron deficiency anemia, only less pronounced.

Clinical picture

Patients report general weakness, malaise, decreased
performance. Already during this period can be observed
taste perversion, dryness and tingling of the tongue, impaired
swallowing with sensation of a foreign body in the throat (syndrome
Plummer-Vinson), palpitations, shortness of breath.
An objective examination of patients reveals
"small symptoms of iron deficiency": atrophy of the papillae of the tongue,
cheilitis ("jam"), dry skin and hair, brittle nails, burning
and itching of the vulva. All these signs of trophic disturbance
epithelial tissues are associated with tissue sideropenia and
hypoxia.

Hidden iron deficiency may be the only sign
iron deficiency.
These cases include mild sideropenia,
developing over a long period of time in mature women
age due to repeated pregnancies, childbirth and abortions, in women -
donors, in persons of both sexes in a period of increased growth.
In most patients with ongoing iron deficiency after
exhaustion of its tissue reserves, iron deficiency anemia develops,
which is a sign of severe iron deficiency in the body.
Changes in the function of various organs and systems in iron deficiency
Anemias are not so much the result of anemia, but of tissue
iron deficiency. Evidence of this is the discrepancy between the severity
clinical manifestations of the disease and the degree of anemia and their appearance already in
stages of latent iron deficiency.

The deathly pale hand of a patient suffering from
iron deficiency anemia (left) and a normal arm
healthy woman.

Patients with iron deficiency anemia note general weakness, rapid
fatigue, difficulty concentrating, sometimes drowsiness.
There is a headache after overwork, dizziness. At
severe anemia may cause fainting.
These complaints, as a rule, do not depend on the degree of anemia, but on
the duration of the disease and the age of the patients.
Iron deficiency anemia is characterized by changes in the skin, nails, and
hair.
The skin is usually pale, sometimes with a slight greenish tinge (chlorosis) and with
easily occurring blush of the cheeks, it becomes dry, flabby,
peeling off, cracks are easily formed.
Hair loses its luster, becomes grey, thinner, breaks easily, thins and early
turn gray.
Nail changes are specific: they become thin, dull,
flatten, easily delaminate and break, striation appears. At
pronounced changes, the nails acquire a concave, spoon-shaped shape
(koilonychia).

Patients with iron deficiency anemia develop muscle weakness,
which is not observed in other types of anemia. She is attributed to
manifestations of tissue sideropenia.
Atrophic changes occur in the mucous membranes
alimentary canal, respiratory organs, reproductive organs. Defeat
mucous membrane of the alimentary canal - a typical symptom
iron deficiency states.
There is a decrease in appetite. There is a need for acidic
spicy, salty foods. In more severe cases, there are
perversions of smell, taste (pica chlorotica): eating chalk,
lime, raw cereals, pogophagia (an attraction to the use of ice).
Signs of tissue sideropenia quickly disappear after taking
iron preparations.

Patients with iron deficiency anemia often experience shortness of breath,
palpitations, chest pain, swelling.
The expansion of the boundaries of cardiac dullness to the left, anemic
systolic murmur at the apex and pulmonary artery, "top murmur" at the jugular
vein, tachycardia and hypotension.
The ECG shows changes that indicate the phase of repolarization.
Iron deficiency anemia in severe course in elderly patients
may cause cardiovascular failure.
Iron deficiency is sometimes associated with fever,
usually does not exceed 37.5 ° C and disappears after iron treatment.
Iron deficiency anemia has a chronic course with periodic
exacerbations and remissions. In the absence of the correct pathogenetic
remission therapies are incomplete and are accompanied by permanent tissue
iron deficiency.

Distribution of IDA symptoms in different age groups
Frequency (%)
IDA symptoms
adults
Children
Teenagers
muscle weakness
++
++
-
Headache
+
-
+
Decreased memory
++
-
±
dizziness
+
-
+
Brief syncope
+
-
±
Arterial hypotension
++
±
-
Tachycardia
++
-
-
Shortness of breath on exertion
++
+
++
Pain in the region of the heart
++
-
-
Symptoms of gastritis
++
-
±
perversion of taste
+
++
-
Perversion of smell
±
+
-
++ - often occurs, + - rarely occurs, - - does not occur, ± - may
meet

Diagnostics

General blood analysis
In the general blood test with IDA, a decrease in
hemoglobin and erythrocyte levels.
Morphological characteristics of erythrocytes:
RBC size - normal, enlarged (macrocytosis) or
reduced (microcytosis).
IDA is characterized by the presence of microcytosis.
Anisocytosis - differences in the size of red blood cells in the same
person.
IDA is characterized by pronounced anisocytosis.
Poikilocytosis - the presence in the blood of the same person
erythrocytes of various shapes.
With IDA, there may be pronounced poikilocytosis.
Anisochromia of erythrocytes - different coloring of individual erythrocytes
in a blood smear.

hyperchromic erythrocytes (CP>1.15) - hemoglobin content in
erythrocytes increased. In a blood smear, these erythrocytes have more
intense coloration, the clearance in the center is significantly reduced or
missing. Hyperchromia is associated with an increase in the thickness of red blood cells and often
combined with macrocytosis;
polychromatophiles - erythrocytes stained in a blood smear in light violet, lilac color. With special supravital staining, this is -
reticulocytes. Normally, they can be single in a smear.
Blood chemistry
With the development of IDA in a biochemical blood test, there will be
register:
decrease in serum ferritin concentration;
decrease in serum iron concentration;
increase in OZhSS;
decrease in transferrin saturation with iron.

The color index of erythrocyte cells (CR) depends on
their hemoglobin content.
The following options for staining erythrocytes are possible:
normochromic erythrocytes (CP = 0.85-1.15) - normal content
hemoglobin in erythrocytes. Erythrocytes in a blood smear have a uniform
pink color of moderate intensity with a slight enlightenment in
center;
hypochromic erythrocytes (CP<0,85) – содержание гемоглобина в
erythrocyte is reduced. In a blood smear, such erythrocytes have a pale pink color.
coloring with a sharp enlightenment in the center. For IDA, erythrocyte hypochromia
is characteristic and often associated with microcytosis;

Regardless of the pharmacological treatment of patients with iron deficiency anemia, it is recommended
varied diet including meat products: veal, liver and vegetable products
origin: beans, soybeans, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins,
rice, buckwheat, bread. Treatment tactics: in all cases, it is necessary to establish the cause
anemia, treat diseases that caused anemia.
Goals of treatment: replenishment of iron deficiency, ensuring regression of symptoms of anemia.
Non-pharmacological treatment: regardless of pharmacological treatment, it is recommended
a varied diet, the inclusion of meat in any form.
Medical treatment
Treatment of underlying IDA disorders should prevent further iron loss, but
All patients should be treated with iron supplements, both to correct anemia and to
replenishment of body reserves.
Ferrous sulfate ** 200 mg 2-3 times a day, ferrous gluconate and ferrous fumarate are also effective.
Ascorbic acid improves iron absorption (recommendation grade B) and should be considered
with a bad answer.
Parenteral administration should only be used in cases of intolerance to at least two
oral medications or in the absence of compliance.

Basic principles of treatment Elimination of etiological factors rational therapeutic nutrition (for newborns - breast natural in

Basic principles of treatment
Elimination of etiological factors
rational medical nutrition (for newborns - breast natural
feeding, and in the absence of milk in the mother - adapted dairy
mixtures enriched with iron. Timely introduction of complementary foods, meat, especially
veal, offal, buckwheat and oatmeal, fruit and vegetable purees,
hard cheeses; reduced intake of phytates, phosphates, tannins, calcium,
that impair iron absorption.
pathogenetic treatment with iron preparations, mainly in the form of drops,
syrups, tablets.
Parenteral administration of iron preparations is indicated only: in the syndrome
malabsorption and conditions after extensive resection
small intestine, nonspecific ulcerative colitis, severe chronic
enterocolitis and dysbacteriosis, intolerance to oral drugs
glandular disease, severe anemia.

Preventive measures to prevent the recurrence of anemia Correction of iron deficiency in mild anemia is carried out

Preventive measures to prevent the recurrence of anemia
Correction of iron deficiency in mild anemia is carried out
mainly due to a balanced diet, sufficient stay
child outdoors. The appointment of iron supplements at the level
hemoglobin 100 g/l and above - not shown.
Daily therapeutic doses of oral iron preparations for IDA
moderate and severe:
up to 3 years - 3-5 mg / kg / day of elemental iron
from 3 to 7 years - 50-70 mg / day of elemental iron
older than 7 years - up to 100 mg / day of elemental iron
Monitoring the effectiveness of the prescribed dose is carried out by determining
rise in the level of reticulocytes on the 10-14th day of treatment. iron therapy
is carried out until the hemoglobin level normalizes with further
dose reduction by ½. The duration of treatment is 6 months, and for children
preterm - within 2 years to replenish iron stores in the body.
In older children, a maintenance dose in a course of 3 to 6 months, in girls
puberty - during the year intermittently - every week after
monthly.

It is advisable to prescribe ferric iron preparations due to their optimal absorption and the absence of side effects. In children ml

It is advisable to prescribe ferric iron preparations due to their
optimal absorption and no side effects.
In young children, IDA is predominantly of alimentary origin and
most often represents a combination of deficiency not only of iron, but
and protein, vitamins, which determines the appointment of vitamins C, B1, B6,
folic acid, correction of protein content in the diet.
Since 50-100% of premature babies develop late anemia, from 20-25
days of life at a gestational age of 27-32 weeks, body weight of 800-1600 g, (in
the time of decrease in the concentration of hemoglobin in the blood below 110 g/l, the amount
erythrocytes below 3.0 ґ 10 12/l, reticulocytes less than 10%), except for drugs
iron (3-5 mg / kg / day) and sufficient protein supply (3-3.5 g / kg / day),
erythropoietin is prescribed s / c, 250 units / kg / day three times a day for 2-4
weeks, with vitamin E (10-20mg/kg/day) and folic acid (1mg/kg/day).
Longer use of erythropoietin - 5 times a week, followed by
its decrease to 3 times, is prescribed for children with severe intrauterine or
postnatal infection, as well as children with a low reticulocyte response
for therapy.

Parenteral iron preparations should be used strictly only for special indications, due to the high risk of developing local

Parenteral iron preparations should be used strictly only for
special indications, due to the high risk of developing local and
systemic adverse reactions.
The daily dose of elemental iron for parenteral administration is:
for children 1-12 months - up to 25 mg / day
1-3 rocks - 25-40 mg / day
older than 3 years - 40-50 mg / day
The course dose of elemental iron is calculated by the formula:
МТґ (78-0.35ґ Hb), where
BW - body weight (kg)
Hb - child's hemoglobin (g / l)
Heading dose of an iron-containing drug - KJ: SZhP, where
KJ - course dose of iron (mg);
FFP - iron content (mg) in 1 ml of the drug
Course number of injections - KDP: ADP, where
KDP - course dose of the drug (ml);
ADP - daily dose of the drug (ml)
Blood transfusions are carried out only for health reasons, when
site of acute massive blood loss. Advantage granted
erythrocyte mass or washed erythrocytes.

Ferrotherapy contraindications: aplastic and hemolytic anemia hemochromatosis, hemosiderosis sideroachrestic anemia thalassemia others

Ferrotherapy contraindications:
aplastic and hemolytic anemia
hemochromatosis, hemosiderosis
sideroahrestic anemia
thalassemia
other types of anemia not associated with iron deficiency in the body
Prevention
Antenatal: women from the 2nd half of pregnancy are prescribed drugs
iron or multivitamins fortified with iron.
In case of repeated or multiple pregnancy, it is necessary to take drugs
iron during the 2nd and 3rd trimester.

Some oral iron preparations

A drug
Compound
Medicinal
i form and
general
contained
iron
Content
elementary
foot
gland
(on the
reception)
Manufacturer
b
Monocomponent preparations of iron II
Ferronal
Gland
gluconate
Tablets 300
mg
12%
CTS
ferronat
Gland
fumarate
Suspension 30
mg/ml
10 mg/ml
Galena
Hemopher
prolongate
m
Gland
sulfate
Dragee 325 mg
105 mg
Glaxo Wellcome
Poznan
Ferronal
Gland
gluconate
Tablets 300
mg
12%
Technologist
Heferol
Gland
fumarate
Capsules 350 mg
100 mg
alkaloid
Hemopher
Ferric chloride
Drops 157
mg/ml
45 mg/ml
Terpol

Sorbifer
durules
iron sulfate,
acid
ascorbic
Tablets 320 mg
100 mg
Egis
Tardyferon
iron sulfate,
mucoproteosis,
acid
ascorbic
Depot tablets
256.3 mg
80 mg
Robapharm Pierre
fabre
Ginotardiferon
iron sulfate,
acid
folic
mucoproteosis,
acid
ascorbic
Dragee 256.3 mg
80 mg
Robapharm Pierre
fabre
Ferroplex
iron sulfate,
acid
ascorbic
Tablets 50 mg
20%
Biogal
Totem
iron gluconate,
manganese
gluconate, copper
gluconate
Solution for vnutr.
applications
Ampoules 5
mg/ml
50 mg
Innotech
International
Fenyuls
iron sulfate,
acid
ascorbic,
nicotinamide,
vitamins
group B
Capsules 150 mg
45 mg
Ranbaxy

Prevention

Periodic monitoring of the blood picture;
eating foods high in iron (meat, liver and
others);
preventive intake of iron preparations in risk groups.
prompt elimination of sources of blood loss.
Dispensary observation
Patients with iron deficiency anemia should be
dispensary registration.
The purpose of dispensary observation is the diagnosis and treatment
diseases leading to iron deficiency, including surgery
elimination of sources of blood loss, periodic (at least 2-4 times per
year) monitoring of the blood picture and the level of serum iron,
repeated (1-2 times a year) courses of treatment with iron preparations for
maintenance of its reserves in the body.

Course and forecast

The course and prognosis of iron deficiency anemia are favorable
with timely diagnosis and adequate therapy, elimination
etiological factor, normalization of iron absorption,
regular prevention of iron deficiency.

Pernicious anemia (from Latin perniciosus - fatal, dangerous) or B12-deficiency anemia or megaloblastic anemia or Addison-Birmer disease

Pernicious anemia (from lat. perniciosus - fatal,
dangerous) or B12-deficient
anemia or megaloblastic anemia or disease
Addison-Birmer or (obsolete name)
malignant anemia is a disease caused by
impaired hematopoiesis due to a deficiency in the body
vitamin B12. Particularly sensitive to the deficiency of this
vitamin bone marrow and tissues of the nervous system.

Deficiency of cyanocobalamin can be caused by the following reasons: - low content in the diet; - vegetarianism; - low absorption; - deficiency

Cyanocobalamin deficiency can be caused by the following reasons:
- low content in the diet;
- vegetarianism;
- low absorption;
- deficiency of the internal factor;
- pernicious anemia;
- gastrectomy;
- damage to the epithelium of the stomach with chemicals;
- infiltrative changes in the stomach; (lymphoma or carcinoma);
- Crohn's disease;
- celiac disease;
- resection of the ileum;
- atrophic processes in the stomach and intestines;
- increased utilization of vitamin B12 by bacteria during their excessive growth;
- condition after the application of the gastrointestinal anastomosis;
- diverticula of the jejunum;
- intestinal stasis or obstruction due to strictures;
- helminthic invasion;
- wide tapeworm (Diphyllobotrium latum);
- pathology of the absorbent area;
- tuberculosis of the ileum;
- lymphoma of the small intestine;
- sprue;
- regional enteritis;
- other reasons.
- congenital absence of transcobalamin 2 (rare)
- abuse of nitrous oxide (inactivates vitamin B12 by oxidizing cobalt);
- malabsorption due to the use of neomycin, colchicine.

The causes of folate deficiency can be: 1. Insufficient intake - poor diet; - alcoholism; - neuropsychic anorexia; - pa

The causes of folate deficiency can be:
1. Insufficient supply
- meager diet;
- alcoholism;
- neuropsychic anorexia;
- parenteral nutrition;
- unbalanced diet in the elderly.
2. Malabsorption
- malabsorption
- changes in the intestinal mucosa
- celiac disease and sprue
- Crohn's disease
- regional ileitis
- bowel lymphoma
- reduction of the reabsorbing surface after resection of the jejunum
- taking anticonvulsants
3. Increasing demand
- pregnancy
- hemolytic anemia
- exfoliative dermatitis and psoriasis
4. Violation of disposal
- alcoholism;
- folate antagonists: trimethoprim and methotrexate;
- congenital disorders of folate metabolism.

Symptoms of B12 deficiency anemia: B12 deficiency anemia develops relatively slowly and may be asymptomatic. Clinical signs a

Symptoms of B12 deficiency anemia:
B12 deficiency anemia develops relatively slowly and can be
oligosymptomatic. Clinical signs of anemia are nonspecific: weakness,
fatigue, shortness of breath, dizziness, palpitations. Sick
pale, subicteric. There are signs of glossitis - with areas of inflammation and
papillary atrophy, varnished tongue, there may be an enlargement of the spleen and
liver. Gastric secretion is sharply reduced. With fibrogastroscopy
atrophy of the gastric mucosa is detected, which is confirmed and
histologically. There are also symptoms of damage to the nervous system
(funicular myelosis), which do not always correlate with the severity
anemia. Neurological manifestations are based on demyelination of nerve
fibers. There are distal paresthesias, peripheral polyneuropathy,
sensitivity disorders, increased tendon reflexes.
Thus, a triad is characteristic of B12-deficiency anemia:
- blood damage;
- damage to the gastrointestinal tract;
- damage to the nervous system.

Diagnosis of B12 deficiency anemia: 1. Clinical blood test - decrease in the number of red blood cells - decrease in hemoglobin - increase in color

Diagnosis of B12 deficiency anemia:
1. Clinical blood test
- decrease in the number of red blood cells
- decrease in hemoglobin
- increase in color index (above 1.05)
- macrocytosis (belongs to the group of macrocytic anemias)
- basophilic puncture of erythrocytes, the presence of Joll bodies and Cabot rings in them
- the appearance of orthochromic megaloblasts
- decrease in reticulocytes
- leukopenia
- thrombocytopenia
- decrease in monocytes
- aneosinphilia
2. In stained smears - a typical picture: along with characteristic oval macrocytes
there are erythrocytes of normal size, microcytes and schizocytes - poikilo- and anisocytosis.
3. Serum bilirubin level increased due to indirect fraction
4. Mandatory puncture of the bone marrow, since such a picture on the periphery can be with leukemia,
hemolytic anemia, aplastic and hypoplastic conditions (however, it should be noted that
that hyperchromia is characteristic of B12 deficiency anemia). Bone marrow cellular, number
nucleated erythroid elements increased by 2-3 times against the norm, however, erythropoiesis
ineffective, as evidenced by a decrease in the number of reticulocytes and erythrocytes in the periphery and
shortening of their life expectancy (normally, an erythrocyte lives 120-140 days). Find typical
megaloblasts are the main criterion for the diagnosis of B12 deficiency anemia. These are cells with "nucleocytoplasmic dissociation" (with a mature hemoglobinized cytoplasm, a tender, reticulated
structure of the nucleus with nucleoli); cells of the granulocytic series of large size are also found and
giant megakaryocytes.

Treatment of B12-deficiency anemia Impact on the cause of B12-deficiency anemia - getting rid of worms (introduced into the body flat or

Treatment of B12 deficiency anemia
Impact on the cause of B12-deficiency anemia - getting rid of
worms (introduced into the body of flat or round worms),
removal of the tumor, normalization of nutrition.
Replenishment of vitamin B12 deficiency. Vitamin administration
B12 intramuscularly at a dose of 200-500 mcg per day. Upon reaching
stable improvement should be administered (in the form of intramuscular
injections) maintenance doses - 100-200 mcg once a month for
several years. In case of damage to the nervous system, a dose of vitamin
B12 is increased to 1000 mcg per day for 3 days, then the usual
scheme.
Rapid replenishment of the number of red blood cells (red cells
blood) - transfusion of erythrocyte mass (erythrocytes isolated
from donated blood) for health reasons (that is, in case of a threat to
patient's life). Life threatening for a patient with B12 deficiency
Anemia is two conditions:
anemic coma (loss of consciousness with no response to external
irritants due to insufficient supply of oxygen to
brain as a result of a significant or rapidly developing
decrease in the number of red blood cells);
severe anemia (blood hemoglobin level below 70 g/l, i.e.
grams of hemoglobin per liter of blood).

A complex of therapeutic measures for B12 - deficiency anemia should be carried out taking into account the etiology, severity of anemia and the presence of neurological

A complex of therapeutic measures for B12 - deficiency anemia should be carried out with
taking into account the etiology, severity of anemia and the presence of neurological disorders. At
treatment should focus on the following points:
- an indispensable condition for the treatment of B12 - deficiency anemia with helminthic invasion is
deworming (to expel a wide tapeworm, fenasal is prescribed for a certain
scheme or male fern extract).
- in case of organic bowel diseases and diarrhea enzymes should be used
preparations (panzinorm, festal, pancreatin), as well as fixing agents (carbonate
calcium in combination with dermatol).
- normalization of the intestinal flora is achieved by taking enzyme preparations
(panzinorm, festal, pancreatin), as well as the selection of a diet that promotes the elimination
syndromes of putrefactive or fermentative dyspepsia.
- a balanced diet with a sufficient content of vitamins, protein, unconditional
the prohibition of alcohol is an indispensable condition for the treatment of B12 and folate deficiency anemia.
- pathogenetic therapy is carried out using parenteral administration
vitamin B12 (cyanocobalamin), as well as the normalization of altered indicators
central hemodynamics and neutralization of antibodies to gastromucoprotein ("internal
factor") or gastromucoprotein + vitamin B12 complex (corticosteroid therapy).
Blood transfusions are carried out only with a significant decrease in hemoglobin and the manifestation
comatose symptoms. It is recommended to inject erythrocyte mass of 250-300 ml (5-6 transfusions).
Prednisolone (20-30 mg/day) is recommended for the autoimmune nature of the disease.

Principles of therapy: - saturate the body with a vitamin - maintenance therapy - prevention of the possible development of anemia

Principles of therapy:
- saturate the body with vitamins
- maintenance therapy
- prevention of possible development of anemia
More often, cyanocobalamin is used in doses of 200-300 micrograms (gamma).
This dose is used if there are no complications (funicular myelosis,
coma). Now they use 500 micrograms daily. Administer 1-2 times per
day. In the presence of complications 1000 micrograms. Dose after 10 days
decreases. Injections continue for 10 days. Then, within 3
months, 300 micrograms are administered weekly. After that, within 6
months, 1 injection is done every 2 weeks.
Criteria for evaluating the effectiveness of therapy:
- sharp reticulocytosis after 5-6 injections, if not, then there is
diagnostic error;
- complete recovery of blood parameters occurs after 1.5 - 2
months, and the elimination of neurological disorders within six months.

Literature:

Belous A. M., Konnik K. T. The physiological role of iron.- K .:
Sciences. thought, 1991.
Idelson L. I. Hypochromic anemia.- M.: Medicine, 1981.
Pharmaceutical care: a course of lectures for pharmacists and family
doctors / A. A. Zupanets, V. P. Chernykh, S. B. Popov and others; ed. V.
P. Chernykha, I. A. Zupantsa, V. A. Usenko.- Kh.: Megapolis, 2003
Korovina N. A., Zaplatnikov A. L., Zakharova I. N.
Iron deficiency anemia in children. Guide for doctors. 2nd
publishing house - Moscow, 1999
Vorobyov A.I. Guide to hematology. Moscow., "Medicine".
1985.
Dvoretsky L.I. iron deficiency anemia. Moscow.,
"Newdiamed", 1998.
Baydurin S.A. Diseases of the blood system, Astana, 2007
Ado A.D., Novitsky V.V. Pathological physiology, Tomsk, 1994