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BASIC PRINCIPLES OF DIAGNOSIS OF ANEMIA ANEMIA is a clinical and laboratory syndrome characterized by a decrease in the level of hemoglobin, red blood cells and hematocrit per unit volume of blood. Criteria for anemia (WHO): for men: hemoglobin level<130 г/л гематокрит менее 39%; для женщин: уровень гемоглобина <120 г/л гематокрит менее 36%; для беременных женщин: уровень гемоглобина <110 г/л Клинико-патогенетическая классификация анемий: классификация D.Natan; F.Oski, 2003 г. I. Анемии, обусловленные острой кровопотерей II. Анемии, возникающие в результате дефицитного эритропоэза III. Анемии, возникающие в следствие повышенной деструкции эритроцитов. IV.* Анемии, развивающиеся в результате сочетанных причин; II. Анемии, возникающие в результате дефицитного эритропоэза 1) За счёт нарушенного созревания (микроцитарные): Железодефицитные; Нарушение транспорта железа; Нарушение утилизации железа; Нарушение реутилизации железа; 2) За счет нарушения дифференцировки эритроцитов; А/гипопластическая анемия (врожденная, приобрет.) Дизэритропоэтические анемии; 3) За счет нарушения пролиферации клеток- предшественниц эритропоэза (макроцитарные); В12-дефицитнве; Фолиево-дефицитные; III. Анемии, возникающие в следствие повышенной деструкции эритроцитов 1)Приобретенный гемолиз (неэритроцитарные причины): Аутоиммунный; Неиммунный (яды, медикаменты, и др.) Травматический (искусственные клапаны, гемодиализ); Клональный (ПНГ); 2) Гемолиз, обусловленный аномалиями эритроцитов: Мембранопатии; Ферментопатии; Гемоглобинопатии; 3) Гиперспленизм – внутриклеточный гемолиз (сначала снижается уровень тромбоцитов, анемия развивается позже); Clinical picture anemia: 1. Anemic syndrome 2. Hemolysis syndrome; 3. Ineffective erythropoiesis syndrome; 4. Dyserythropoiesis syndrome; 5. Sideropenia syndrome; 6. Hypersplenism syndrome; 7. Iron overload syndrome; Anemic syndrome Manifestations depend on the depth of anemia and the speed of its development; This indicator is characterized by RDW; Microcytes are red blood cells whose diameter, when counted in a smear, is less than 6.5 microns; Schizocytes are red blood cells with a diameter of less than 3 microns, as well as fragments of red blood cells; Macrocytes - large red blood cells with a diameter of more than 8 microns, with preserved clearing in the center; Megalocytes are giant red blood cells with a diameter of more than 12 microns without clearing in the center.< 70 г/л Морфологические варианты анемии Микроцитарная Нормоцитарная Макроцитарная MCV < 75 фл MCV 75-95 фл MCV >95 fl Hypochromic Normochromic Hyperchromic MCH< 24 пг MCH 24-34 фл МCH >34 pg MCHC< 30 г/л MCHC 30-38 г/л MCHC >38 g/l Differential diagnosis of anemia Differential diagnosis of anemia depending on the number of reticulocytes Increased number of reticulocytes Regenerative anemia Rt = 1.5-5% Hyperregenerative anemia Rt > 5% Membranopathy of erythrocytes;< 0,5% Ретикулоцитоз не соответствует тяжести анемии В12/фолиево-дефицитная анемия; Апластическая анемия; ЖДА 3 степени; ВДА; Большая форма талассемии; СБА; ПНГ Анемия, обусловленные острой кровопотерей - острая постгеморрагическая анемия СТАДИИ: 1)рефлекторно-сосудистая компенсация Первые сутки – лейкоцитоз (20 тыс/мл) с нейтрофильным сдвигом; гипертромбоцитоз (до 1 млн/мл). 2) гидремическая компенсация – снижение НЬ, Ht и эритроцитов, возможен гемолиз, азотемия; 3) костномозговая компенсация: повышение Эпо, гиперплазия эритроидного ростка в костном мозге, ретикулоцитоз, пойкилоцитоз, полихромазия, нормобластоз Железодефицитная анемия (ЖДА) Полиэтиологичное заболевание, развивающееся в результате снижения Enzymopathies of erythrocytes; Hemoglobinopathies;< 75 фл Гипохромная MCH < 24 пг MCHC < 30 г/л Нормо- или гипорегенераторная Rt 0,5 – 1 % Возможен тромбоцитоз на ранних этапах Микроскопическая картина крови при ЖДА Синдром сидеропении и состояние латентного дефицита железа Дистофия кожи и её придатков; Извращение вкуса и обоняния; Мышечная гипотония (недержание мочи); Мышечные боли, Снижение внимания; Ухудшение памяти и т.д. Внешний вид при сидеропении Изменения кожи при сидеропении ГЛОССИТ Изменения ногтей при сидеропении КОЙЛОНИХИИ Наиболее частые причины ЖДА Алиментарный дефицит железа (диеты, вегетарианство, недоедание); Повышение потребности в железе (частые роды, многоплодная беременность; лактация; быстрый рост; интенсивные занятия спортом; недоношенность); Кровопотеря (носовые кровотечения, диафрагмальная грыжа; дивертикул, полип или опухоль ЖКТ; метроррагии; синдром Гудпасчера); Снижение абсорбции (мальабсорбция; воспалительные процессы в кишечнике; ахлоргидрия; гастрэктомия) Показатели обмена железа при ЖДА Сывороточное железо СЖ 12,5-30 нг/мл; ↓↓ Общая железосвязывающая способность сыворотки ОЖСС 45-62,2 мкмоль/л >60 µmol/l 30 – 300 ng/ml ↓↓↓ ↓↓ Serum ferritin Transferrin saturation with iron Soluble transferrin receptors NTG rTGF 25 – 45% Principles of treatment of IDA Elimination of the cause of iron deficiency, if possible; Iron preparations, the dose of which is calculated based on the content of atomic iron: 200-300 mg of iron per day for 3 doses on an empty stomach;) or folic acid Microscopic picture of blood in pernicious anemia Morphological characteristics of erythrocytes in MBA Macrocytic MCV > 100 fL Hyperchromic MCH > 100 pg MCHC > 36 g/l Hyporegenerative Rt< 0,5 % ВОЗМОЖНО: Лейкопения, сдвиг «вправо», гиперсегментация ядер нейтрофилов, умеренная тромбоцитопения. Основные причины развития МБА Дефицит витамина В12 Неадекватное поступление Увеличенная потребность Нарушения абсорбции Дефицит фолиевой кислоты Недостаточное питание Быстрый рост Гемодиализ Недоношенность Вскармливание козьим молоком Острые инфекции Беременность Ранний возраст Лактация Хрон. гемолиз Беременность Лактация Целиакия Врожд.дефицит Заболевания тощей кишки внутр.ф.Кастла амилоидоз Гастрэктомия Алкоголизм С.Золлингера-Эллисона Лимфома, целиакия Панкреатит Дефицит Б.Крона дигидрофолатредуктазы Резекция кишечника Др.нарушения метаболизма фолатов Глисты и др. Строгая вегетарианская диета (редко) Лекарственные препараты, приём которых приводит к развитию МБА Ингибиторы дегидрофолатредуктазы (метотрексат; сульфасалазин; аминоптерин; прогуанил; триметоприм; триамтерен); Антиметаболиты (6-меркаптопурин; 6-тиогуанин; азатиоприн; ацикловир; 5-фторурацил; зидовудин); Ингибиторы редуктазы РНК (цитозар; гидрокссимочевина); Антиконвульсанты (дифенил; фенобарбитал); КОК ДРУГИЕ (метформин; неомицин; колхицин) Клиническая картина: 1. Анемический синдром; 2.Желудочно-кишечные нарушения (анорексия, глоссит, снижение секреции в желудке); 3. Neurological symptoms(B12) (paresthesia, hyporeflexia, gait disturbances, etc.) 4. Syndrome of ineffective erythropoiesis;

5. Dyserythropoiesis syndrome; Principles of treatment for MBA: Adequate nutrition; deworming;

Vitamin B12 (cyanocobalamin) 200-400 mcg 1 time per day IM for 4-5 weeks; Dynamics of laboratory parameters: reticulocyte crisis on days 5-8; Lifelong maintenance doses of vitamin B12 (200-400 mcg per month); Er.mass according to vital indications; Folic acid: 5-10 mg/day for 3-4 months. Taking maintenance doses. Microscopic picture of blood in sickle cell anemia

Anemia is a condition characterized by a decrease in hemoglobin (Hb) per unit volume of blood due to a decrease in its total amount in the body. IDA is a clinical and hematological symptom complex characterized by impaired formation of Hb due to iron deficiency in the blood serum and bone marrow and the development of trophic disorders in organs and fabrics The main protein containing iron is hemoglobin. Proteins containing iron reserves are ferritin and hemosiderin. A protein that binds iron in serum and transports it to the bone marrow and other tissues is transferrin (a blood plasma protein related to β-globulins), which is synthesized mainly liver. Intake of iron into the body Iron in food is found in two forms: - Fe 3+ not included in the heme composition (fruits, vegetables, cereals) - 1-7% is absorbed - Fe 2+ in the heme composition (meat,

Domestic bird , fish) – 17-22% is absorbed (Moore C.V., 1974) With a balanced diet, mg of iron is supplied, but only 10-12% is absorbed, i.e. 1-2 mg Absorption of iron from human milk reaches 38-49% (McMillan I.A. et al., 1976; Saarin I.M., 1997; WHO. 1980) Risk groups for the development of anemia in children Children of the first 2 years of life: - premature and low birth weight - with high birth weight, fast growing - those on artificial feeding, especially unadapted formulas, products based on whole milk - children of mothers who had anemia during pregnancy Teenage girls: - hormonal imbalance, juvenile

IDA is an acquired disease from the group of deficiency anemias, occurs with iron deficiency, accompanied by microcytic, hypochromic, normoregenerative anemia, the clinical manifestations of which are a combination of sideropenic and anemic syndromes

Clinical classification: I degree (mild) – Hb level g/l; II degree (medium) – Hb level g/l; III degree (severe) – Hb level less than 70 g/l.

Sideropenic syndrome is characterized by following symptoms: skin changes: dryness, appearance of small pigment spots of “café au lait” color; changes in the mucous membranes: “jams” in the corner of the mouth, glossitis, atrophic gastritis and esophagitis; dyspeptic symptoms from the gastrointestinal tract; hair changes - bifurcation of the tip, fragility and loss up to alopecia areata; changes in nails - transverse striation of the nails of the thumbs (in severe cases and toenails), fragility, delamination into plates; change in sense of smell – the patient’s addiction to the strong smells of varnish, acetone paint, car exhaust, concentrated perfume; changes in taste - the patient’s addiction to clay, chalk, raw meat, dough, dumplings, etc.; pain in the calf muscles.

The following symptoms are characteristic of anemic syndrome: loss of appetite; noise in ears; flickering of flies before the eyes; poor tolerance to physical activity; weakness, lethargy, dizziness, irritability; fainting; dyspnea; decreased performance; decreased cognitive function; decreased quality of life; pallor of the skin and visible mucous membranes; changes in muscle tone in the form of a tendency to hypotension, hypotension of the bladder muscles with the development of urinary incontinence; expansion of the boundaries of the heart; muffled heart sounds; tachycardia; systolic murmur at the apex of the heart.

Criteria for laboratory diagnosis of the disease OAC, performed by the “manual” method - a decrease in Hb concentration (less than 110 g/l), a slight decrease in the number of red blood cells (less than 3.8 x 1012/l), a decrease in CP (less than 0.85), an increase in ESR ( more than mm/hour), normal reticulocyte content (10-20). Additionally, the laboratory doctor describes anisocytosis and poikilocytosis of erythrocytes. IDA is a microcytic, hypochromic, normoregenerative anemia. Biochemical blood test - decreased serum iron concentration (less than 12.5 µmol/l), increased total iron-binding capacity of serum (more than 69 µmol/l), decreased transferrin saturation coefficient with iron (less than 17%), decreased serum ferritin (less than 30 ng/l). ml). In recent years, it has become possible to determine soluble transferrin receptors (sTFR), the number of which increases under conditions of iron deficiency (more than 2.9 μg/ml).

Non-drug treatment Elimination of etiological factors; Rational therapeutic nutrition (for newborns - natural breastfeeding, and in the absence of mother's milk - adapted milk formulas fortified with iron. Timely introduction of complementary foods, meat, offal, buckwheat and oatmeal, fruit and vegetable purees, hard cheeses; reduction in phosphate intake , tannin, calcium, which impair iron absorption).

Drug treatment Age-specific therapeutic doses of oral iron preparations for the treatment of IDA in children (WHO, 1989) Age of the child Daily dose elemental iron Iron salt preparations Children under 3 years of age Children over 3 years of age Adolescents 3 mg/kg mg to 120 mg Iron preparations based on HPA ferric iron Any age 5 mg/kg

Principles of rational therapy for IDA in children Treatment with iron supplements is recommended under the supervision of a physician. It is recommended to prescribe iron supplements to children after consulting a pediatrician. Iron supplements should not be prescribed to children against the background inflammatory processes(ARVI, sore throat, pneumonia, etc.), since in this case iron accumulates at the site of infection and is not used for its intended purpose. Iron deficiency anemia should be treated mainly with drugs for internal use. Iron must be divalent, since it is divalent iron that is absorbed. The use of iron supplements should be combined with optimization of the diet, with the mandatory introduction of meat dishes into the menu. For maximum absorption of iron, the drug should be taken 0.5-1 hour before meals with water. If they appear side effects, you can take the medicine with food. Iron is absorbed worst of all if the drug is taken after meals.

Oral iron supplements should be taken at least 4 hours apart. Do not chew tablets and pills containing iron! The inclusion of ascorbic acid in complex iron preparations improves the absorption of iron (as an antioxidant, ascorbic acid prevents the conversion of Fe-II ions into Fe-III, which are not absorbed in the gastrointestinal tract) and allows you to reduce the prescribed dose. Iron absorption also increases in the presence of fructose, succinic acid. You cannot combine iron supplementation with substances that inhibit its absorption: milk (calcium salts), tea (tannin), herbal products (quotes and chelates), a number of medications (tetracycline, antacids, blockers , H2 receptors, proton pump inhibitors). Taking combination drugs that, along with iron, contain copper, cobalt, folic acid, vitamin B12 or liver extract, makes it extremely difficult to control the effectiveness of iron therapy (due to the hematopoietic activity of these substances).

The average duration of treatment for IDA is from 4 to 8 weeks. Treatment with an iron supplement should be continued after relief of IDA to restore tissue and stored iron. The duration of the maintenance course is determined by the degree and duration of iron deficiency (ID) and the level of SF. Vitamin B12 should not be used in the treatment of IDA. folic acid, vitamin B6, pathogenetic in no way related to iron deficiency. The ineffectiveness of IDA therapy with oral iron supplements requires a revision of the diagnosis (often the diagnosis of IDA is established in patients with anemia of a chronic disease in which treatment with iron supplements is ineffective), checking the patient’s compliance with the doctor’s prescriptions in dosage and timing of treatment. Iron malabsorption is very rare. Parenteral administration of iron supplements is indicated only: for the syndrome of impaired intestinal absorption and the condition after extensive resection of the small intestine, nonspecific ulcerative colitis, severe chronic enterocolitis and dysbiosis, intolerance to oral iron supplements. Limitation of parenteral administration is associated with high risk development of local and systemic adverse reactions. In addition, parenteral use of iron supplements is much more expensive than oral therapy due to the labor costs of medical personnel and the higher cost of the dosage form. Parenteral administration of iron supplements should only be done in a hospital!

The simultaneous administration of iron preparations orally and parenterally (intramuscularly and/or intravenously) should be completely excluded! Red blood cell transfusions should not be used in the treatment of IDA. Donor iron is not reutilized by the recipient's body and remains in the hemosiderin of macrophages. It is possible to transmit dangerous infections through donor blood. Exceptions that allow transfusion of donor red blood cells are: 1) severe hemodynamic disturbances; 2) upcoming additional blood loss (childbirth, surgery) with severe anemia (hemoglobin less than 70 g/l);

Complications of treatment The use of iron salt preparations may be accompanied by complications in the form of gastrointestinal toxicity with the development of symptoms such as pain in the epigastric region, constipation, diarrhea, nausea, and vomiting. This leads to low compliance with treatment of IDA with iron salt preparations - 30-35% of patients who started treatment refuse to continue it. Overdose and even poisoning with iron salt preparations are possible due to passive uncontrolled absorption.

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Iron-deficiency anemia. Plan. Definition of the concept ICD-10 Clinical classification of IDA Formulation of the diagnosis. Clinical picture of IDA Diagnosis of IDA Treatment of IDA Examination of the ability to work of patients with IDA Medical examination for IDA. Prevention Conclusions.

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Iron-deficiency anemia

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Definition of the concept ICD-10 Clinical classification of IDA Formulation of diagnosis. Clinical picture of IDA Diagnosis of IDA Treatment of IDA Examination of the ability to work of patients with IDA Medical examination for IDA. Prevention Conclusions

The most common form of anemia, which occurs due to 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 anemias, IDA is the most common and accounts for about 80%. Iron deficiency affects almost half of the world's population (mostly women), and 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 anemias that develop due to repeated small blood losses - metrorrhagia, epistaxis, hematuria, etc. 2. IDA during pregnancy. The causes of anemia in this group are different: nutritional imbalance in pregnant women and the associated deterioration in iron utilization, transfer of a significant amount of it to the developing fetus by the mother’s body, loss of iron during lactation, etc. 3. IDA associated with gastrointestinal pathology. These include anemia that occurs after gastrectomy, extensive resections small intestine, for various enteropathies. At its core, it is IDA, caused by a gross, severe dysfunction of iron absorption in the proximal region duodenum. 4. IDA secondary, arising from infectious, inflammatory or tumor diseases. Anemia in these cases develops due to large losses of iron due to the death of tumor cells, tissue breakdown, micro- and even macrohemorrhages, and an increased need for iron in areas of inflammation.

IDA, in which the most thorough anamnestic and laboratory search does not reveal the generally known causes of iron deficiency. Most patients have a special form of iron malabsorption.

Stage I – loss of iron exceeds its intake, gradual depletion of reserves, absorption in the intestine increases compensatoryly;

Stage II – depletion of iron stores (serum iron level is below 50 mcg/l, transferrin saturation is below 16%) interferes with normal erythropoiesis, erythropoiesis begins to fall;

Stage III – 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;

Pallor of the skin and visible mucous membranes is detected, and often there is some pastiness in the area of ​​​​the legs, feet, and face. Morning swelling is characteristic - “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, dullness of heart sounds, and soft systolic murmur at all auscultatory points. With severe and prolonged anemia, myocardial dystrophy can lead to severe circulatory failure. IDA develops gradually, so the patient’s body adapts to low level 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: perversion of taste (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 quite often observed in adult women; addiction to hot, salty, sour, spicy foods; perversion of smell - addiction to odors that are perceived by most others as unpleasant (smells of gasoline, acetone, varnishes, paints, shoe polish, etc.); severe muscle weakness and fatigue, muscle atrophy and decreased muscle strength due to a deficiency of myoglobin and tissue respiration enzymes; dystrophic changes in the skin and its appendages (dryness, peeling, tendency to rapid formation of cracks in the skin; dullness, fragility, hair loss, early graying of hair; thinning, fragility, transverse striations, dullness of nails; symptom of koilonychia - spoon-shaped concavity of nails);

Cracks, “jams” in the corners of the mouth (occur in 10–15% of patients); glossitis (in 10% of patients) – characterized by a feeling of pain and distension in the tongue, redness of its tip, and later – atrophy of the papillae (“lacquered” tongue); there is often a tendency to periodontal disease and caries; atrophic changes 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 food (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, the synthesis of collagen in the sclera is disrupted, it becomes thinner and shines through it choroid eyes; imperative urge to urinate, inability to hold urine when laughing, coughing, sneezing, possibly even bedwetting, which is caused by weakness of the bladder sphincters; “sideropenic subfebrile condition” – characterized by a prolonged increase in temperature to subfebrile levels; a pronounced predisposition to acute respiratory viral and other infectious and inflammatory processes, chronic infection, which is caused by a violation of the phagocytic function of leukocytes and a weakening of the immune system;

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

In practice, the criteria for IDA are: – low color index; – hypochromia of erythrocytes, microcytosis; – decrease in serum iron levels; – increase in life expectancy; – decrease in serum ferritin levels. A biochemical blood test, in addition to a decrease in serum iron and ferritin levels, also reveals changes caused by the underlying cancer or other disease.

Currently, there are the following stages of treatment for IDA: Stage 1 – relief therapy aimed at increasing hemoglobin levels and replenishing peripheral iron stores;

Stage 2 – therapy that restores tissue iron reserves;

Stage 3 – anti-relapse treatment. Includes: elimination of etiological factors (treatment of the underlying disease); therapeutic nutrition;

For oral administration are the following: – administration of pancreas with sufficient content of ferric iron; – inappropriateness of simultaneous administration of B vitamins (including B12), folic acid without special indications; – avoidance of oral administration of pancreatic acid if there are 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 normalization of hemoglobin levels in appropriate situations.

For an adequate increase in hemoglobin levels 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 iron absorption does not increase. Individual fluctuations in the amount of required iron are determined by the degree of its deficiency in the body, depletion of reserves, the rate of erythropoiesis, absorption, tolerance and some other factors. Taking this into account, when choosing a medicinal pancreas, you should focus not only on the total amount contained in it, but also, mainly, on the amount of ferric iron, which is only absorbed in the intestine.

Pancreas for oral administration: – absence of iron deficiency (incorrect interpretation of the nature of hypochromic anemia and erroneous prescription of pancreas); – insufficient dosage of pancreas (underestimation of the amount of ferric iron in the drug);– insufficient duration of treatment for pancreas; – impaired absorption of pancreas prescribed orally to patients with the corresponding pathology;– simultaneous use of drugs that interfere with iron absorption;

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

Persons with latent iron deficiency are not subject to medical examination. If IDA is a consequence of some pathological process, then special dispensary observation is not required, because patients have already been registered according to their underlying 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 for: pregnant and breastfeeding women; teenage girls and women, especially those with heavy menstruation; donaram. Secondary prevention is carried out for 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 particularly vulnerable populations - young children, pregnant women, the elderly and people with serious chronic diseases. However, this abnormal condition can and must be fought. Correct diagnosis, including various laboratory tests, allows you to promptly identify this disease and choose the appropriate treatment method.

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. Anemic syndrome can be clinically leading or moderately severe. In addition to the circulatory-hypoxic syndrome common to all anemias, each anemia has its own specific symptoms.

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

Cells of pathological regeneration of erythrocytes, arising from impaired erythropoiesis 1. Megalocyte, megaloblast; red blood cells with Jolly bodies and Cabot rings; erythrocytes with basophilic granularity. 2. Anisocytosis - pathology of the size of erythrocytes: 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. 3. Poikilocytosis - change in the shape of erythrocytes (sickle cell, target-shaped, ovalocytes, acanthocytes, stomatocytes, etc.) 4. Anisochromia - different colors of erythrocytes (hypo-, hyper-, normochromic, polychromasia) 5. Sideroblasts are erythrokaryocytes of the bone marrow containing iron (normal 20-40%)

According to WHO recommendations: 1. The lower limit of HB content in men is 130 g/l, in women – 120 g/l, in pregnant women – 110 g/l. 2. The lower limit of erythrocyte content in men is 4.0 * 10 12 / l, in women - 3.9 * 10 12 / l. 3. Hematocrit - the ratio of blood cells and plasma volume. Normally, in men it is 0.4-0.48%, in women it is 0.36-0.42%. 4. Hb content in the erythrocyte: Hb (g/l) : Er (l) = pg. 5.Color index: Hb(g/l)*0.03: Er(l) = 0.85-1.0. 6. Serum iron in men – µmol/l, in women – 11.5-25 µmol/l.

7.Total iron-binding capacity of blood serum (TIBC) - the amount of iron that can bind one liter of blood serum. Normal – µmol/l, 8.OZHSSK – syv. iron = latent FSSCC. Normal is µmol/l. 9. Syv. iron: TISS = transferrin saturation with iron. Normal is 16-50%. 10.Assessment of iron reserves in the body: determination of ferritin in blood serum (radioimmune and enzymoimmune methods), normal - μg/l, in men 94 μg/l, in women 34 μg/l; determination of protoporphyrin content in erythrocytes – µmol/l; desferal test (desferal binds only iron reserves). 500 mg of desferal is administered intramuscularly; normally, 0.6-1.3 mg of iron is excreted in the urine. According to WHO recommendations:

Etiopathogenetic classification of anemia 1. Acute posthemorrhagic (APHA) 2. Iron deficiency (IDA) 3. Associated with impaired synthesis or utilization of porphyrins (sideroachrestic) (SAA) 4. Associated with impaired DNA and RNA synthesis (B12 and folate deficiency, megaloblastic) (MGBA) 5. Hemolytic (HA) 6. Aplastic, hypoplastic - with inhibition of bone marrow cells (AA) 7. Other types of anemia: in infectious diseases, kidney diseases, liver diseases, endocrine pathology etc. Classification of anemia by pathogenesis 1. Anemia due to blood loss (OPHA, IDA) 2. Anemia due to impaired blood formation (IDA, SAA, MGBA, AA) 3. Anemia due to increased blood destruction (HA)

Classification of anemia by color index 1. Hypochromic (IDA, SAA, thalassemia) 2. Hyperchromic (MGBA) 3. Normochromic (OPHA, AA, GA) According to the state of bone marrow hematopoiesis 1. Regenerative (IDA, MGBA, SAA, OPHA) 2. Hyperregenerative (GA) 3. Regenerative (AA) Reticulocyte - the youngest cell of the erythroid series, which goes to the periphery - this is an indicator of germ regeneration (normal 1.2 - 2%) By severity 1. Mild (Nv g/l) 2. Moderate severity (Hv g/l) 3.Heavy (Hv g/l)

Stages of diagnosis for anemia syndrome 1. History, to identify the possible cause of anemia (heredity, provoking factors). 2. Examination, determination of anemia variant. Required Methods studies: CBC (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 the bone marrow )

Additional research methods: trephine biopsy ilium(tissue relationship in the bone marrow: cells/fat = 1/1) Coombs test urine for hemosiderin osmotic resistance of erythrocytes electropharesis of hemoglobin life expectancy study Er c Cr Determination of the underlying disease that led to anemia: feces for occult blood (Gregersen or Weber methods) . Calculation of fecal radioactivity within 7 days after intravenous administration of one’s own washed red blood cells labeled with Cr 51. Study of radioactive iron given orally, followed by determination of fecal radioactivity over 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. Stages of diagnosis for anemia syndrome

Vitamin B 12 and folic acid take part 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 is enough for 4 years. Anemia associated with impaired DNA and RNA synthesis

Metabolism of vitamin B 12 (cyanocobalamin) Normal hematopoiesis Metabolism fatty acids Methylcobalamin Intake B 12 with food (daily requirement 1 mcg) + Intrinsic Castle factor in the stomach (gastromucoprotein) Absorbed in the ileum Folic acid 5-deoxyadenosylcobalamin Tetrahydrofolic acid Methylmalonic acid (toxic) + propionic acid DNA synthesis Succinic acid In blood B 12 + transcobalamin-2 Portal vein Liver (depot B 12)

Causes of vitamin B 12 deficiency 1. Insufficient B 12 content in food. 2. Malabsorption: a) violation of gastromucoprotein synthesis: atrophic gastritis of the fundus of the stomach; autoimmune reactions with the production of antibodies to gastric parietal cells and gastromucoprotein; gastrectomy (after gastrectomy, the half-life of B 12 is 1 year; after gastrectomy, signs of B 12 deficiency appear after 5-7 years); stomach cancer; congenital deficiency of gastromucoproteins; b) malabsorption of 12 V 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 B 12 + gastromucoprotein complex in the small intestine; c)competitive uptake of vitamin B12; broad tapeworm infestation; pronounced intestinal dysbiosis. 3. Reduced production of transcobalamin-2 in the liver and impaired transport of vitamin B 12 to the bone marrow (with cirrhosis of the liver).

The main pathogenetic links in the development of B 12 deficiency anemia Disturbance of DNA synthesis in hematopoietic cells, mainly erythroblasts Disturbance cell division Embryonic type of hematopoiesis (megaloblastic) Megaloblasts rarely mature into megalocytes due to their hemolysis in the bone marrow and do not provide hematopoietic function (increased content of unconjugated bilirubin, urobilin, stercobilin, possibly increased serum iron with hemosiderosis of internal organs) The cell nucleus slowly matures , in the protoplasm there is an increased content of Hb - hyperchromia (Jolly bodies, Cabot rings), hypersermonuclearity of neutrophils

Main differential criteria for B 12-deficiency anemia 1. Circulatory-hypoxic syndrome 2. No sideropenic syndrome 3. Gastroenterological syndrome: decreased appetite, body weight, glossitis (smooth red tongue), heaviness in the epigastrium, unstable stool, achlorhydria, m.b. hepatosplenomegaly 4. Neurological syndrome (funicular myelosis): dystrophic processes in the posterolateral columns 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 lower limbs, impaired finger movements, ataxia, impaired vibration sensitivity.

5. Hematological syndrome: hyperchromic anemia (CP above 1.1-1.3); anisocytosis (megalocytosis), poikilocytosis, basophilic granularity, Cabot rings, Jolly bodies; trilinear cytopenia; hypersegmental neutrophilosis; megaloblastic type of hematopoiesis (according to sternal puncture); decrease in B12 in the blood is less than 200 pg/ml; Main differential criteria for B 12 deficiency anemia

Occurs less frequently than B12 deficiency. The reserve of FA in the body is designed for 2-3 months. FA is present in all products; when heated, it is destroyed Absorbed throughout jejunum, m.b. diarrhea FC absorption does not require transport proteins Birth defects FC are combined with mental retardation and are not corrected by introducing FC Folate-deficiency anemia

Main differential criteria for folate deficiency anemia 1. Medical history: pregnancy, neonatal period, chronic alcoholism, chronic hemolysis, myeloproliferative diseases, medication (folic acid antagonists, antituberculosis, anticonvulsants). Erythropoiesis suffers. 2. There is no funicular myelosis, gastric damage. 3. There is no reticulocyte crisis on reception B. In the bone marrow, megaloblasts are stained with a dye only in B 12-deficiency anemia, but not in folate-deficiency anemia. 5. Decrease in folic acid in the blood is less than 3 mg/ml (N – 3-25 mg/ml).

Treatment of megaloblastic anemia (MGBA) 1. Vitamin B 12 (cyanocobalamin) – intramuscular mcg (4-6 weeks). 2. For neurological disorders: B12 (1000 mcg) + cobalamide (500 mcg) until neurological symptoms disappear. 3.If necessary, lifelong administration of B12 (500 mcg) once every 2 weeks or preventive treatment– B12 (400 mcg) for days 1-2 times a year. 4. Transfusion of erythromass only for health reasons (for all anemias!): HB

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 sign of which is pancytopenia in the peripheral blood and fatty degeneration bone marrow. P. Ehrlich (1888) first described AA. The term “aplastic anemia” was introduced in 1904 by Shoffar. Incidence 4-5 people per 1 million population per year (in Europe) Age peaks of incidence 20 and 65 years

Etiological factors AA drugs, chemical substances, viruses, autoimmune processes; in 50% of cases the etiology is unknown (idiopathic AA). Pathogenesis of AA Functional bone marrow failure with inhibition of 1, 2 or 3 germs (pancytopenia). Damage to a pluripotent blood stem cell Suppression of hematopoiesis a) Action of immune (cellular, humoral) mechanisms b) Deficiency of factors stimulating hematopoiesis c) Iron, B12, protoporphyrin cannot be used by hematopoietic tissue.

Aplastic anemia can be 1. Congenital (with syndrome congenital anomalies or without it) 2. Acquired Along the course, AA is distinguished 1. Acute 2. Subacute 3. Chronic Forms of AA 1. Immune 2. Non-immune Clinical syndromes of AA 1. Circulatory-hypoxic 2. Septic-necrotic 3. Hemorrhagic

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

Severe AA 1. In peripheral blood (2 out of 3 germs are suppressed) Granulocytes 0.5-0.2 * 10 9 / l Platelets less than 20 * 10 9 / l Reticulocytes less than 1% 2. Myelogram Myelokaryocytes less than 25% of the norm Myelokaryocytes % , and myeloid cells less than 30% 3. Trepanobiopsy In mild form - 40% adipose tissue In moderate form - 80% In severe form - absolute predominance of adipose tissue (panmyelophthisis) Differential diagnosis AA Debut acute leukemia Chronic lymphocytic leukemia (bone marrow form) Cancer metastases to the bone marrow Pancytopenia in the elderly as a manifestation of B12-deficiency anemia

100 g/l; granulocytes > 1.5*10 9 /l; platelets > 100*10 9 /l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l; no consumption" title=" Assessment of AA therapy 1. Complete remission: HB > 100 g/l; granulocytes > 1.5 * 10 9 / l; platelets > 100 * 10 9 / l; no need for blood transfusions. 2. Partial remission: Hb > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l;" class="link_thumb"> 31 !} Assessment of AA therapy 1. Complete remission: HB > 100 g/l; granulocytes > 1.5*10 9 /l; platelets > 100*10 9 /l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l; no need for blood transfusions. 3. Clinical and hematological improvements: improvement of hematological parameters; reduced need for blood replacement transfusion for more than two months. 4. Lack of effect: no hematological improvements; the need for blood transfusion remains. 100 g/l; granulocytes > 1.5*10 9 /l; platelets > 100*10 9 /l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l; no consumption "> 100 g/l; granulocytes > 1.5 * 10 9 / l; platelets > 100 * 10 9 / l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0, 5*10 9 /l; platelets > 20*10 9 /l; no need for blood transfusions. 3. Clinical and hematological improvements: improvement in hematological parameters; reduction in the need for replacement blood transfusions for more than two months. improvements; the need for blood transfusion is preserved."> 100 g/l; granulocytes > 1.5*10 9 /l; platelets > 100*10 9 /l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l; no consumption" title=" Assessment of AA therapy 1. Complete remission: HB > 100 g/l; granulocytes > 1.5 * 10 9 / l; platelets > 100 * 10 9 / l; no need for blood transfusions. 2. Partial remission: Hb > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l;"> title="Assessment of AA therapy 1. Complete remission: HB > 100 g/l; granulocytes > 1.5*10 9 /l; platelets > 100*10 9 /l; no need for blood transfusions. 2. Partial remission: HB > 80 g/l; granulocytes > 0.5*10 9 /l; platelets > 20*10 9 /l; lack of consumption"> !}

Systems whose disruption causes hemolysis Glutathione system: protects important cell components from denaturation by oxidizing agents, peroxides, ions heavy metals. Phospholipids: determine the permeability of the membrane for ions, determine the structure of the membrane, influence the enzymatic activity of proteins. Red blood cell 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 - the accumulator of 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.

Hemolytic anemia (HA) HA combines a number of hereditary and acquired diseases, the main symptom of which is increased decay of Er and a shortening of their life expectancy from up to days. Hereditary HA are associated with defects in the Er structure, which become functionally defective. Acquired HAs are caused by various factors that contribute to the destruction of Er (hemolytic poisons, mechanical effects, autoimmune processes, etc.). Pathological hemolysis can be 1. By localization a) intracellular (RES cells, mainly the spleen) b) intravascular 2. By course a) acute b) chronic

Main criteria for GA 1. Increased bilirubin due to unconjugated bilirubin: bile pigments in the urine are negative; urobilin in urine and stercobilin in feces; “lemon” jaundice without itching. 2. Splenomegaly with intracellular hemolysis. 3.Anemia: normochromic, hyperregenerative, hyperplasia of the erythroid lineage in the bone marrow. 4. Hemolytic crises. 5.M.b. gallstones (pigment stones). Intravascular hemolysis is characterized by: hemoglobinemia (free HB in the blood plasma); hemoglobinuria and hemosiderinuria (red or black urine); hemosiderosis of internal organs; tendency to microthrombosis of various localizations.

HA with intravascular hemolysis 1. Hereditary HA: A. Enzymopathies (G-6-PD deficiency). B. Hemoglobinopathies (sickle cell anemia). 2. Acquired HAs: A. Immune - AIHA with thermal and biphasic hemolysins. B. Non-immune – PNH, mechanical for prosthetics of valves, blood vessels, marching.

Classification of hereditary hemolytic anemias A. Membranopathy due to disruption of the protein structure of the erythrocyte membrane 1. Microspherocytosis, elliptocytosis, stomatocytosis, piropoikilocytosis. 2. Disturbance of erythrocyte membrane lipids: acanthocytosis, deficiency of lecithin-cholesterol-aryltransferase activity, increased lecithin content in the erythrocyte membrane, infantile pycnocytosis.

B. Enzymopathies 1. Deficiency of enzymes of the pentose phosphate cycle. 2. Deficit of activity of glycolysis enzymes 3. Deficit of activity of glutathione metabolism enzymes. 4.Deficit activity of enzymes involved in using ATP. 5. Deficiency of ribophosphate pyrophosphate kinase activity. 6.Impaired activity of enzymes involved in the synthesis of porphyrins. B. Hemoglobinopathies 1. Caused by an anomaly in the primary structure of Hb. 2. Caused by a decrease in the synthesis of polypeptide chains that make up normal HB. 3. Caused by a double heterozygous state. 4.Anomalies of HB not accompanied by the development of the disease.

Hereditary enzymopathies Insufficiency of glucose-6-phosphate dehydrogenase (G-6-FDG) in Er It is more common in the countries of Africa, Latin America, the Mediterranean, in our country - Azerbaijan, Armenia, Dagestan; Suffer mainly from men (recessive sex-linked gene); Acute infections provoke a crisis, medications(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 a crisis in Er, Heinz bodies (denatured Hb) can be detected. Diagnosis in the group of hereditary fermentopathy is based on the detection in Er of a deficiency of various enzymes of the hexose or pentose cycles.

Membranopathies The most common among them is hereditary microspherocytosis (Minkowski-Choffard disease), in which a defect in the Er membrane is accompanied by an increase in the passage of Na and H 2 O 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

Hemoglobinopathies Hereditary HA 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 Mediterranean countries, Africa, India and the Transcaucasian republics. Homozygous patients have severe, sometimes fatal manifestations of the disease from childhood, while heterozygotes have mild forms with a survival rate of > years. Er's lifespan has been shortened. The site of hemolysis is examined using Er labeled with Cr 51. Anomalies of Hb (S, F, A2, etc.) are detected by Hb electrophoresis (immunophoresis). Maybe quantitation abnormal Hb. 20-30 years. Er's lifespan has been shortened. The site of hemolysis is examined using Er labeled with Cr 51. Anomalies of Hb (S, F, A2, etc.) are detected by Hb electrophoresis (immunophoresis). Quantitative determination of abnormal HB is possible.">

Sickle cell HA Intravascular hemolysis. Pathological HB S leads to a change in the shape of Er in the form of a sickle. Homozygotes - Hb S in % of cases are found in Er, constantly in the blood of Er in the form of a sickle with hemolysis. Heterozygotes are periodic hemolytic crises with the appearance of sickle-shaped Er, which are provoked by hypoxic conditions (infections, airplane flights, climbing mountains, etc.). Diagnostic test- taking blood from a finger tied with a tourniquet (in heterozygotes).

Thalassemia Intracellular hemolysis. Increase in fetal Hb Fe in Er up to 20% (in N – 4%) and Hb A2. Increased osmotic resistance of Er. Hypochromic anemia with high serum Fe (sideroachresia with hemosiderosis of internal organs). Target-like shape of Er and basophilic granularity in them.

Classification of acquired hemolytic anemias A. Immune hemolytic anemias 1. HA associated with exposure to antibodies (immune HA): – isoimmune (alloimmune): Rh conflict, transfusion of incompatible blood; –heteroimmune, caused by diseases, viruses; – transimmune - antibodies are transmitted through the placenta from mother to fetus; 2. Autoimmune HAs with antibodies to their own unchanged Er: – with incomplete warm agglutinins (detected in % of autoimmune HAs using a direct Coombs test), – with warm hemolysins, – with complete cold agglutinins, – associated with biphasic cold hemolysins. 3. Autoimmune HA with antibodies against bone marrow normocyte antigen.

Agglutinins often produce intracellular hemolysis, while hemolysins produce intravascular hemolysis. Incomplete heat agglutinins do not cause autoagglutination, but cold ones do and are often combined with Raynaud's syndrome. HA can develop in diseases associated with ineffective erythropoiesis: –B 12 deficiency anemia; – erythropoietic porphyrias; – primary “shunt” hyperbilirubinemia.

Acquired HA Paroxysmal nocturnal hemoglobinuria (Marchiafava-Micheli disease) A clone of defective Er is formed due to somatic mutation type benign tumor blood systems with 2 populations of Er: with normal and defective membrane; simultaneously leukocytes and platelets mutate 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.

Autoimmune GAs are more common than others; Divided into: a) idiopathic - unknown etiology (18.8-70%), b) symptomatic - due to malignant neoplasms, systemic blood diseases, CTD, CAH, UC, malaria, toxoplasmosis, sepsis, etc. The presence of antibodies is determined by direct Coombs test, PCR, ELISA, radioimmunoassay.

Treatment of autoimmune GA 1. Glucocorticoid hormones in the acute phase with thermal agglutinins; prednisolone mg/day, distributed into 3 doses at the rate of 3: 2: 1. 2. For chronic HA with incomplete thermal agglutinins, prednisolone mg/day. 3. For HA with complete cold agglutinins, with severe exacerbation, prednisolone mg/day. 4. Splenectomy – in case of ineffectiveness of hormones, rapid relapses after hormone withdrawal, complications of hormone therapy. 5. Cytostatics: azathioprine mg/day; cyclophosphamide 400 mg every other day; vincristine 2 mg once a week intravenously; chlorobutine 2.5-5 mg/day for 2-3 months – in the absence of effect from hormones. 6.Transfusion of washed red blood cells selected using the indirect Coombs test for severe anemia. 7.Plasmapheresis for severe HA, complications DIC syndrome. 8. Immunoglobulin C 0.5-1 g/kg body weight.

Principles of treatment of HA with intravascular hemolysis 1. Infusion therapy - prevention of acute renal failure: soda, glucose solution with inulin, aminophylline 10-20 ml, furosemide 40-60 mg, mannitol 1 g/kg body weight. 2. Prevention of DIC - small doses of heparin. 3. Fighting infection - antibiotics (sickle cell anemia). 4. Increasing acute renal failure – peritoneal dialysis, hemodialysis.

Principles of treatment of HA with intracellular hemolysis 1. Infusion therapy. 2. Transfusions of washed red blood cells, desferal, folic acid (thalassemia). 3.AIHA – prednisolone mg/day. 4. Blood transfusions for health reasons. 5. Splenectomy.

Treatment of hemolytic crisis 1. Replacement of circulating blood volume: rheopolyglucin ml; reoglumal ml; isotonic solution sodium chloride 1000 ml; albumin 10% ml under control of central venous pressure. 2. Neutralization of toxic products and stimulation of diuresis. Hemodez (low molecular weight polyvinylpyrrolidone, colloidal solution) ml, 2-8 infusions per course. Polidez Jr. Stimulation of diuresis: furosemide mg intravenously, if necessary, again after 4 hours. Eufillin solution 2.4% ml per 10 ml of isotonic sodium chloride solution (in the absence of arterial hypotension).

3. Elimination of acidosis: 4% ml of sodium bicarbonate intravenously. 4. Extracorporeal therapy - in the absence of effect from the above measures - plasmapheresis, hemodialysis. 5. Glucocorticoid hormones: for autoimmune HA, shock, collapse - prednisolone intravenously 1-1.5 mg/kg of the patient’s body weight, again after 3-4 hours (if necessary). 6. Relief of anemia: when HB decreases to 40 g/l and below - transfusion of individually selected erythrocytes per ml; red blood cells should be washed 4-5 times, fresh frozen, selected using the indirect Coombs test. In case of crisis against the background of NPH, red blood cells are 7-9 days old from the moment of preparation (fresh ones increase the risk of hemolysis).

1N Reticulocytes N or N or Syv. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/b N Liver N Often N Bone marrow Moderate erythrocyte hyperplasia" title=" Differential diagnosis of anemia Signs JDASAAGAMBAAA CP 1N Reticulocytes N or N or Dry. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/b N Liver NN Often N Bone marrow Moderate erythrocyte hyperplasia" class="link_thumb"> 60 !} Differential diagnosis of anemia Signs ZhDASAAGAMBAAA CP 1N Reticulocytes N or N or Syv. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/b N Liver N Often N Bone marrow Moderate hyperplasia of the erythrocyte lineage, sideroblasts. Moderate hyperplasia of the erythrocyte lineage, sideroblasts. Severe hyperplasia of the erythrocyte lineage. Megaloblastic type of hematopoiesis Suppression 1N Reticulocytes N or N or Syv. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/w N Liver N Often N Bone marrow Moderate erythrocyte hyperplasia "> 1N Reticulocytes N or N or Dry. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/w N Liver N Often N Bone marrow Moderate hyperplasia of the erythrocyte lineage, sideroblasts. Moderate hyperplasia of the erythrocyte lineage, sideroblasts. Severe hyperplasia of the erythrocyte lineage. Megaloblastic type of hematopoiesis. Depression "> 1N Reticulocytes N or N or Syv. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/b N Liver N Often N Bone marrow Moderate erythrocyte hyperplasia" title=" Differential diagnosis of anemia Signs JDASAAGAMBAAA CP 1N Reticulocytes N or N or Dry. Fe N or Platelets NNN or Leukocytes NNN Spleen NN Often M/w N Liver NN Often N Bone marrow Moderate erythrocyte hyperplasia"> title="Differential diagnosis of anemia Signs ZhDASAAGAMBAAA CP 1N Reticulocytes N or N or Syv. Fe N or Platelets NNN or Leukocytes NNN Spleen NNN Often M/b N Liver N Often N Bone marrow Moderate erythrocyte hyperplasia"> !}

Treatment of HA caused by deficiency of the G-6-FDG enzyme. Vitamin E. Xylitol 0.25-0.5 3 times a day + riboflavin 0.02-0.05 3 times a day (in case of impaired glutathione synthesis). Prevention of acute renal failure: infusion of ml of 5% glucose, insulin, sodium bicarbonate, 2.4% ml of aminophylline, 10% mannitol (1 g/kg) + ml of Lasix: prevention of disseminated intravascular coagulation - small doses of heparin. hemodialysis. infusion of washed red blood cells selected using the indirect Coombs test, sometimes splenectomy.

Treatment of microspherocytosis Splenectomy Indications: severe anemia with hemolytic crises; complications of GA: cholelithiasis, biliary colic; complications of GA: trophic ulcers shins; persistent hemolytic jaundice. Relative indications for splenectomy: crisis course with remissions; splenomegaly, hypersplenism; less pronounced absolute readings. For health reasons, red blood cell transfusion

Treatment of sickle cell anemia 1. Prevention of dehydration 2. Prevention infectious complications(from 3 months to 5 years - penicillin mg orally daily; after 3 years - polyvalent vaccination pneumococcal vaccine). 3. Transfusion of washed or thawed red blood cells is the main method of treatment in adults and children. Indications for red blood cell transfusion: severe anemia, decreased reticulocytes; stroke prevention; blood transfusions reduce the content of Hb 6 in red blood cells and reduce the risk of stroke; preparation for abdominal operations; trophic ulcers of the leg; taking folic acid 1 mg/day daily in the presence of anemia.

Treatment of thalassemia Treatment of the homozygous form: transfusion of washed or thawed red blood cells to maintain the HB level within g/l; if frequent blood transfusions are complicated by hemosiderosis - desferal (complexone that removes iron from the body) at a dose of 10 mg/kg body weight with mg of ascorbic acid taken orally; in the presence of splenomegaly, hypersplenism - splenectomy Treatment of the heterozygous form: folic acid 0.005 2 times a day; Iron supplements are contraindicated.

Treatment of paroxysmal nocturnal hemoglobinuria 1. Transfusion of washed or freshly frozen red blood cells with a shelf life of at least 7 days in case of severe anemia; in the presence of anti-erythrocyte or anti-leukocyte antibodies - transfusion of red blood cells selected according to the indirect Coombs test. 2. Anabolic hormones: Nerobol 0.005 * 4 times a day for at least 2-3 months under the control of cholestasis indicators. 3. Antioxidants: vitamin E – erevit intramuscularly 3-4 ml/day (0.15-0.2 g tocopherol acetate); in capsules of 0.2 ml of 5% vitamin E solution, 2 capsules per day after meals; course 1-3 months. 4. For severe iron deficiency - iron supplements in small doses (Ferroplex 1 tablet 3 times a day) under the control of bilirubin levels. 5. Treatment of thrombosis: heparin 2.5 thousand 2 times a day under the skin of the abdomen.

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

Anemia is called a clinical hematological syndrome,
characterized by a decrease
number of red blood cells and hemoglobin
in blood.
A wide variety of pathological
processes can serve as the basis
development of anemic conditions, in
What is the connection with anemia?
considered as one of the symptoms
underlying disease.
Prevalence of anemia
varies significantly in the range from
0.7 to 6.9%.
The cause of anemia may be one of
three factors or a combination of them:
blood loss, insufficient
formation of red blood cells or
their increased destruction (hemolysis).

Among the various anemic conditions, iron deficiency anemia
are the most common and make up 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 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 (post-hemorrhagic):
1. spicy
2. chronic
II. Anemia due to impaired blood formation:
1. Deficiency anemias:
iron deficiency
protein deficient
vitamin deficient
2. Anemia associated with impaired synthesis and utilization of porphyrins:
hereditary
acquired
aplastic anemia
metaplastic anemia
dysregulatory

III. Anemia due to increased blood destruction
(hemolytic):
1. Hereditary:
membranopathy
fermentopathy
hemoglobinopathies
2. Purchased

Etiology

The main etiopathogenetic factor in the development of IDA is iron deficiency.
Most common reasons occurrence of iron deficiency conditions
are:
1. Iron loss due to chronic bleeding (the most common
reason reaching 80%):
– bleeding from gastrointestinal tract: peptic ulcer,
erosive gastritis, varicose veins esophageal veins,
colon diverticula, hookworm infestations, tumors, UC,
haemorrhoids;
– long and heavy menstruation, endometriosis, fibroids;
– macro- and microhematuria: chronic glomerulus and pyelonephritis, urolithiasis, polycystic kidney disease, kidney tumors
and bladder;
– nosebleeds, 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;
breastfeeding period;
playing sports;
4. Insufficient intake of iron from food:
–
–
newborns;
Small children;
–
vegetarianism.

Recommended daily norm iron intake 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.
Dysfunction of molecules
hemoglobin in the blood causes anemia.
These blood cells, enlarged in
900 times, taken from a person who has
sickle cell abnormality
red blood cells

Prelatent iron deficiency in the body

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

Latent iron deficiency in the body

If iron deficiency is not adequately replaced
at the first stage, the second stage of iron deficiency begins
condition - latent iron deficiency. At this stage in
as a result of disruption of the supply of the necessary metal to
tissue there is a decrease in the activity of tissue enzymes
(cytochromes, catalase, succinate dehydrogenase, etc.), which
manifested by the development of sideropenic syndrome.
TO clinical manifestations sideropenic syndrome refers
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, the
changes in laboratory parameters. Not only are they registered
depletion of iron stores in the depot - decreased ferritin concentration
serum, but also a decrease in iron content in serum and transport 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). Phenomena of tissue iron deficiency
absent only in some iron deficiency anemias,
caused by impaired iron utilization when the depot
full of iron.
Thus, iron deficiency anemia in its course
There are two periods: the period of hidden iron deficiency and the period
obvious anemia caused by iron deficiency.
During the period of hidden 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 there can be observed
perversion of taste, dryness and tingling of the tongue, impaired
swallowing with a sensation of a foreign body in the throat (syndrome
Plummer-Vinson), palpitations, shortness of breath.
An objective examination of patients reveals
“minor symptoms of iron deficiency”: atrophy of the tongue papillae,
cheilitis (“jams”), dry skin and hair, brittle nails, burning sensation
and itching of the vulva. All these signs of trophic disturbances
epithelial tissues are associated with tissue sideropenia and
hypoxia.

Hidden iron deficiency may be the only sign
iron deficiency.
Such cases include mild sideropenia,
developing over a long period of time in women of mature age
age due to repeated pregnancies, childbirth and abortions, in women -
donors, in persons of both sexes during periods of increased growth.
In most patients with ongoing iron deficiency after
when its tissue reserves are exhausted, 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
anemia is not so much a consequence of anemia as a consequence of tissue
iron deficiency. Proof 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 hidden iron deficiency.

Deathly pale hand of a patient suffering
iron deficiency anemia (left) and normal hand
healthy woman.

Patients with iron deficiency anemia report general weakness, rapid
fatigue, difficulty concentrating, sometimes drowsiness.
Headache after overwork and dizziness appear. At
severe anemia may cause fainting.
These complaints, as a rule, depend not on the degree of anemia, but on
duration of the disease and 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 tint (chlorosis) and
easily occurring blush of the cheeks, it becomes dry, flabby,
peels off and cracks easily form.
Hair loses its shine, turns gray, becomes thinner, breaks easily, thins and
are turning grey.
Changes in nails are specific: they become thin, matte,
flatten, easily delaminate and break, and striations appear. At
With pronounced changes, the nails acquire a concave, spoon-shaped shape
(koilonychia).

Patients with iron deficiency anemia experience muscle weakness,
which is not observed in other types of anemia. She is classified as
manifestations of tissue sideropenia.
Atrophic changes occur in the mucous membranes
digestive canal, respiratory organs, genital organs. Defeat
mucous membrane of the digestive canal - a typical sign
iron deficiency conditions.
There is a decrease in appetite. There is a need for sour,
spicy, salty foods. In more severe cases there are
perversions of smell, taste (pica chlorotica): eating chalk,
lime, raw cereals, pogophagia (craving to eat ice).
Signs of tissue sideropenia quickly disappear after administration
iron preparations.

Patients with iron deficiency anemia constantly experience shortness of breath,
palpitations, chest pain, swelling.
Expansion of the borders 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 reveals changes indicating a repolarization phase.
Iron deficiency anemia in severe cases in elderly patients
may cause cardiovascular failure.
A manifestation of iron deficiency is sometimes fever, temperature
usually does not exceed 37.5 °C and disappears after treatment with iron.
Iron deficiency anemia has chronic course with periodic
exacerbations and remissions. In the absence of the correct pathogenetic
remission therapy is incomplete and is accompanied by permanent tissue
iron deficiency.

Distribution of IDA symptoms in different age groups
Frequency (%)
Symptoms of IDA
Adults
Children
Teenagers
Muscle weakness
++
++
-
Headache
+
-
+
Memory loss
++
-
±
Dizziness
+
-
+
Brief fainting
+
-
±
Arterial hypotension
++
±
-
Tachycardia
++
-
-
Shortness of breath on exertion
++
+
++
Pain in the heart area
++
-
-
Symptoms of gastritis
++
-
±
Perversion of taste
+
++
-
Perversion of smell
±
+
-
++ - often occurs, + - occurs rarely, - - does not occur, ± - may
meet

Diagnostics

General blood analysis
IN general analysis blood levels with IDA will decrease
hemoglobin and red blood cell levels.
Morphological characteristics of red blood cells:
Red blood cell size – normal, enlarged (macrocytosis) or
decreased (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 different shapes.
In IDA, there may be pronounced poikilocytosis.
Anisochromia of erythrocytes - different colors of individual erythrocytes
in a blood smear.

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

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

Regardless of the pharmacological treatment of patients with iron deficiency anemia, it is recommended
a varied diet including meat products: veal, liver and plant 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.
Treatment goals: replenishing iron deficiency, ensuring regression of anemia symptoms.
Non-pharmacological treatment: regardless of pharmacological treatment is recommended
varied diet, inclusion of meat in any form.
Drug treatment
Treatment of underlying IDA conditions should prevent further iron loss, but
all patients should be prescribed iron therapy, both to correct anemia and to
replenishment of body reserves.
Ferrous sulfate** 200 mg 2-3 times a day, iron gluconate and fumarate are also effective.
Ascorbic acid improves iron absorption (recommendation level B) and should be considered
with a bad answer.
Parenteral administration should only be used if 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 - natural breast

Basic principles of treatment
Elimination of etiological factors
rational therapeutic nutrition (for newborns - natural breast
feeding, and in the absence of milk from the mother - adapted milk
mixtures enriched with iron. Timely introduction of complementary foods, meat, especially
veal, offal, buckwheat and oatmeal, fruit and vegetable purees,
hard varieties of cheese; reduction in intake of phytates, phosphates, tannin, calcium,
which impair iron absorption.
pathogenetic treatment with iron preparations, mainly in the form of drops,
syrups, tablets.
Parenteral administration of iron supplements is indicated only: for the syndrome
impaired intestinal absorption and conditions after extensive resection
small intestine, nonspecific ulcerative colitis, severe chronic
enterocolitis and dysbacteriosis, intolerance to oral medications
glandular diseases, severe anemia.

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

Preventive measures to prevent relapse of anemia
Correction of iron deficiency in mild anemia is carried out
mainly due to rational nutrition, sufficient stay
child in the fresh air. Prescribing iron supplements for levels
hemoglobin 100 g/l and above – not shown.
Daily therapeutic doses of oral iron supplements 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
over 7 years – up to 100 mg/day of elemental iron
The effectiveness of the prescribed dose is monitored by determining
an increase in the level of reticulocytes on the 10-14th day of treatment. Iron therapy
carried out until the hemoglobin level normalizes with further
reducing the dose by ½. Duration of treatment is 6 months, and for children
premature babies – for 2 years to replenish iron reserves in the body.
In older children, a maintenance dose lasts 3–6 months, in girls
puberty - intermittently throughout the year - every week after
menstruation.

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

It is advisable to prescribe ferric iron preparations due to their
optimal absorption and absence of 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 prescription 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 800-1600 g, (in
time of decrease in blood hemoglobin concentration below 110 g/l, 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 subcutaneously, 250 units/kg/day three times a day for 2-4
weeks, with vitamin E (10-20 mg/kg/day) and folic acid (1 mg/kg/day).
Longer use of erythropoietin - 5 times a week, followed by
its reduction up to 3 times, prescribed to children with severe intrauterine or
postnatal infection, as well as children with low reticulocyte response
for therapy.

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

Parenteral iron supplements 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
over 3 years of age - 40-50 mg/day
The course dose of elemental iron is calculated using the formula:
MTґ (78-0.35ґ Hb), where
MT - body weight (kg)
Hb – child’s hemoglobin (g/l)
The course dose of an iron-containing drug is KJ: SZhP, where
KID – course dose of iron (mg);
SIP – iron content (mg) in 1 ml of the drug
Course number of injections – KDP: SDP, where
KDP - course dose of the drug (ml);
DDP – daily dose of the drug (ml)
Blood transfusions are carried out only for health reasons, when there is
place of acute massive blood loss. Advantage provided
red blood cells or washed red blood cells.

Contraindications for ferrotherapy: aplastic and hemolytic anemia, hemochromatosis, hemosiderosis, sideroachrestic anemia, thalassemia, etc.

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

Some oral iron supplements

A drug
Compound
Medicinal
I am the form and
general
contained
no iron
Content
elementary
nogo
gland
(on
reception)
Manufacturer
b
Monocomponent iron II preparations
Ferronal
Gland
gluconate
Tablets 300
mg
12%
CTS
Ferronate
Gland
fumarate
Suspension 30
mg/ml
10 mg/ml
Galena
Hemofer
prolongata
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
Hemofer
Ferric chloride
Drops 157
mg/ml
45 mg/ml
Terpol

Sorbifer
Durules
Ferrous sulfate,
acid
ascorbic acid
Tablets 320 mg
100 mg
Egis
Tardiferon
Ferrous sulfate,
mucoproteosis,
acid
ascorbic acid
Depot tablets
256.3 mg
80 mg
Robapharm Pierre
Fabre
Gynotardiferon
Ferrous sulfate,
acid
folic
mucoproteosis,
acid
ascorbic acid
Dragee 256.3 mg
80 mg
Robapharm Pierre
Fabre
Ferroplex
Ferrous sulfate,
acid
ascorbic acid
Tablets 50 mg
20%
Biogal
Totema
Iron gluconate,
manganese
gluconate, copper
gluconate
Solution for internal
applications
Ampoules 5
mg/ml
50 mg
Innotech
International
Fenyuls
Ferrous sulfate,
acid
ascorbic acid,
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
etc.);
preventive administration of iron supplements in risk groups.
prompt elimination of sources of blood loss.
Dispensary observation
Patients with iron deficiency anemia should be on
dispensary registration.
The purpose of clinical observation is diagnosis and treatment
diseases leading to iron deficiency, including surgical
elimination of sources of blood loss, periodic (at least 2 - 4 times per
year) monitoring the blood picture and serum iron level,
repeated (1 - 2 times a year) courses of treatment with iron preparations for
maintaining its reserves in the body.

Course and prognosis

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 the Latin perniciosus - disastrous, dangerous) or B12-deficiency anemia or megaloblastic anemia or Addison-Biermer disease

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

Cyanocobalamin deficiency can be caused by the following reasons: - low content in the diet; - vegetarianism; - low absorption; - shortage

Cyanocobalamin deficiency can be caused by the following reasons:
- low content in the diet;
- vegetarianism;
- low absorption;
- deficiency of internal factor;
- pernicious anemia;
- gastrectomy;
- damage to the gastric epithelium by 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 gastrointestinal anastomosis;
- diverticula of the jejunum;
- intestinal stasis or obstruction due to strictures;
- helminthic infestation;
- broad 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 caused by the use of neomycin, colchicine.

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

Causes of folate deficiency may include:
1. Insufficient intake
- poor 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
- intestinal lymphoma
- reduction of the reabsorbing surface after resection of the jejunum
- taking anticonvulsants
3. Increased need
- 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 have few symptoms. Clinical signs a

Symptoms of B12 deficiency anemia:
B12 deficiency anemia develops relatively slowly and may be
asymptomatic. 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
atrophy of the papillae, varnished tongue, there may be an enlargement of the spleen and
liver. Gastric secretion sharply decreases. With fibrogastroscopy
atrophy of the gastric mucosa is detected, which is confirmed
histologically. Symptoms of damage to the nervous system are also observed
(funicular myelosis), which do not always correlate with severity
anemia. The main neurological manifestations are demyelination of nerves.
fibers There is distal paresthesia, peripheral polyneuropathy,
sensitivity disorders, increased tendon reflexes.
Thus, B12 deficiency anemia is characterized by a triad:
- blood damage;
- damage to the gastrointestinal tract;
- damage to the nervous system.

Diagnosis of B12-deficiency anemia: 1. Clinical blood test - decreased number of red blood cells - decreased hemoglobin - increased 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 punctation of erythrocytes, the presence of Joll bodies and Cabot rings in them
- appearance of orthochromic megaloblasts
- decrease in reticulocytes
- leukopenia
- thrombocytopenia
- decrease in monocytes
- aneosinphilia
2. In stained smears there is a typical picture: along with characteristic oval macrocytes
there are erythrocytes of normal size, microcytes and schizocytes - poikilo- and anisocytosis.
3. Serum bilirubin level is increased due to the indirect fraction
4. Bone marrow puncture is mandatory, since such a picture in the periphery may be due to leukemia,
hemolytic anemia, aplastic and hypoplastic conditions (however, it should be noted
that hyperchromia is characteristic of B12-deficiency anemia). Bone marrow cell, number
nucleated erythroid elements are increased 2-3 times against the norm, but erythropoiesis
ineffective, as evidenced by a decrease in the number of reticulocytes and erythrocytes in the periphery and
shortening their life expectancy (normally, a red blood cell lives 120-140 days). Find typical
Megaloblasts are the main criterion for diagnosing B12 deficiency anemia. These are cells with “nuclear cytoplasmic dissociation” (with mature hemoglobinized cytoplasm, tender, mesh
structure of the nucleus with nucleoli); Large granulocytic cells are also found and
giant megakaryocytes.

Treatment of B12-deficiency anemia Impact on the cause of B12-deficiency anemia - getting rid of worms (that have entered the body flat or

Treatment of B12 deficiency anemia
Impact on the cause of B12-deficiency anemia - getting rid of
worms (flatworms or roundworms that have entered the body),
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. If the nervous system is damaged, a dose of vitamin
B12 is increased to 1000 mcg per day for 3 days, then the usual
scheme.
Rapid replenishment of red blood cells
blood) - transfusion of red blood cells (red blood cells isolated
from donor blood) for health reasons (that is, if there is a threat to
patient's life). Life-threatening for a patient with B12 deficiency
There are two conditions of anemia:
anemic coma (loss of consciousness with lack of response to external
irritants due to insufficient oxygen supply to
brain as a result of significant or rapidly developing
decrease in the number of red blood cells);
severe anemia (blood hemoglobin level below 70 g/l, that is
grams of hemoglobin per 1 liter of blood).

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

A set 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 be guided by the following points:
- an indispensable condition for the treatment of B12 - deficiency anemia due to helminthic infestation is
deworming (to expel the tapeworm, fenasal is prescribed according to a certain
scheme or male fern extract).
- for organic intestinal diseases and diarrhea, enzyme enzymes should be used
drugs (panzinorm, festal, pancreatin), as well as fixing agents (carbonate
calcium in combination with dermatol).
- normalization of intestinal flora is achieved by taking enzyme preparations
(panzinorm, festal, pancreatin), as well as the selection of a diet that helps eliminate
syndromes of putrefactive or fermentative dyspepsia.
- balanced diet with sufficient vitamins, protein, unconditional
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 normalization of altered indicators
central hemodynamics and neutralization of antibodies to gastromucoprotein ("internal
factor") or the complex of gastromucoprotein + vitamin B12 (corticosteroid therapy).
Blood transfusions are carried out only when there is a significant decrease in hemoglobin and manifestations
symptoms of coma. It is recommended to administer 250-300 ml of red blood cells (5-6 transfusions).
Prednisolone (20 - 30 mg/day) is recommended for the autoimmune nature of the disease.

Principles of therapy: - saturate the body with vitamins - maintenance therapy - prevention of the possible development of anemia Most often used

Principles of therapy:
- saturate the body with vitamins
- maintenance therapy
- prevention of the possible development of anemia
Cyanocobalamin is most often used in doses of 200-300 micrograms (gmm).
This dose is used if there are no complications (funicular myelosis,
coma). Now they use 500 micrograms daily. Enter 1-2 times per
day. If there are complications, 1000 micrograms. After 10 days dose
decreases. The injections continue for 10 days. Then, within 3
months, 300 micrograms are administered weekly. After this, within 6
months, 1 injection is given every 2 weeks.
Criteria for assessing the effectiveness of therapy:
- sharp reticulocytosis after 5-6 injections, if it is not there, then it is present
diagnostic error;
- complete restoration of blood counts occurs within 1.5 - 2
months, and the elimination of neurological disorders within six months.

Literature:

Belous A.M., Konnik K.T. Physiological role of iron. - K.:
Sci. Dumka, 1991.
Idelson L.I. Hypochromic anemia. - M.: Medicine, 1981.
Pharmaceutical care: Course of lectures for pharmacists and family
doctors / A. A. Zupanets, V. P. Chernykh, S. B. Popov, etc.; edited by IN.
P. Chernykha, I. A. Zupanca, V. A. Usenko. - Kh.: Megapolis, 2003
Korovina N. A., Zaplatnikov A. L., Zakharova I. N.
Iron deficiency anemia in children. Guide for doctors. 2nd
ed. - Moscow, 1999
Vorobiev A.I. Guide to Hematology. Moscow., "Medicine".
1985.
Dvoretsky L.I. Iron deficiency anemia. Moscow.,
"Newdiamed", 1998.
Baidurin S.A. Diseases of the blood system, Astana, 2007
Ado A.D., Novitsky V.V. Pathological physiology, Tomsk, 1994