Presentation of iron deficiency anemia picture of peripheral blood. Hypo-, aplastic anemia
Anemia Criteria (WHO): for men: hemoglobin level 
Clinical and pathogenetic classification of anemia: I. Anemia due to acute blood loss II. Anemia resulting from deficient erythropoiesis III. Anemia resulting from increased destruction of red blood cells. IV.* Anemia developing as a result of combined causes;
II. Anemia resulting from deficient erythropoiesis Due to impaired maturation (microcytic): Iron deficiency; Violation of iron transport; Violation of iron utilization; Violation of iron recycling; 2) Due to impaired differentiation of erythrocytes; A / hypoplastic anemia (congenital, will acquire.) Dyserythropoietic anemia; 3) Due to impaired proliferation of erythropoiesis precursor cells (macrocytic); B12 deficiency; Folic deficiency;
III. Anemia resulting from increased destruction of red blood cells 1) Acquired hemolysis (non-erythrocyte causes): Autoimmune; Non-immune (poisons, medicines, etc.) Traumatic (artificial valves, hemodialysis); Clonal (PNG); 2) Hemolysis due to erythrocyte abnormalities: Membranopathy; Fermentopathies; Hemoglobinopathies; 3) Hypersplenism - intracellular hemolysis (first, the level of platelets decreases, anemia develops later);
Description: Any infectious and inflammatory disease of the body is accompanied by a decrease in the level of production of red blood cells in the bone marrow, and this leads to their quantitative decrease in the blood. But, anemia in chronic diseases can only develop if this disease is chronic and severe. The level of anemia directly depends on the severity of the chronic disease.
So, anemia of chronic diseases occurs in cases of: chronic infections, inflammatory chronic processes in the body, chronic renal failure, collagenoses, malignant tumors, diseases of the endocrine system, chronic liver diseases and pregnancy. Chronic diseases most often lead to anemia of a different nature in old age. And the most popular type of anemia then is iron recycling anemia, when the body's ability to absorb iron decreases, while the life span of red blood cells is shortened and microscopic blood loss occurs in the body.
Symptoms Anemia of chronic diseases, due to its slow development and mild course (accompanying), as a rule, does not have any symptoms. All manifestations usually refer to those diseases against which, or as a result of which, anemia develops. And yet, the symptoms that manifest developing anemia include increased fatigue of the body, its general weakness, a sharp decrease in efficiency, obvious irritability, frequent dizziness, drowsiness, noise sensations in the ears, "flies" before the eyes, rapid heartbeat and shortness of breath during physical exertion or at rest.
Diagnosis All methods that are used to diagnose anemia of chronic diseases depend on the chronic disease itself, against which anemia develops. But, in any case, if anemia takes place in the body, then the patient is prescribed a general and biochemical blood test and a bone marrow puncture to establish the nature and type of anemia.
Treatment Anemia that develops against or as a result of a chronic disease does not need separate treatment. All methods in this case will be aimed at eliminating the cause of anemia, that is, at treating the chronic disease itself. When diagnosing, primary anemia should be excluded, and then, for each specific case, a course of treatment and a therapeutic technique are selected. For example, renal inflammation is treated with erythropoietin replacement therapy, which leads to the correction of developing anemia. To reduce the severity of the anemic process and improve the general condition of the patient, erythropoietin can be administered subcutaneously to the patient in moderate dosages, followed by their decrease. This is done no more than three times in seven to eight days. In the treatment of anemia with erythropoietin, strict medical monitoring of the patient's intravenous and intracranial blood pressure is necessary, since this drug can cause stroke, thrombosis and hypertension. In rare exceptional cases, when the anemia of a chronic disease becomes severe, a treatment method such as a red blood cell transfusion is used. The methods of hormonal therapy and blood transfusion (hemotransfusion) can also be used.
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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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Iron-deficiency anemia
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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 iron losses 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 the syndrome of myocardial dystrophy, 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 in 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, a 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, redness 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 due to 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 - stopping 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 implementation of various laboratory tests, allows you to identify this disease in a timely manner and choose the appropriate method of treatment.
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KGBPOU "Kansk Medical College" TREATMENT OF ANEMIA: IRON-DEFICIENCY, B12-DEFICIENCY, HYPO- AND APLASTIC, HEMOLYTIC Lecturer: Ershova A.Yu.
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Criteria for anemia (WHO) lower limit of normal Population Hemoglobin (g/l) Hematocrit Children 6 months. – 59 months 110 0.33 Children 6-11 years old 115 0.34 Children 12-14 years old 120 0.36 Non-pregnant women (over 15 years old) 120 0.36 Pregnant women 110 0.33 Men (over 15 years old) 130 0.39
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Pathogenetic variants of anemia I. Anemia due to blood loss (acute and chronic) II. Anemia due to impaired blood formation: a) iron deficiency anemia b) anemia associated with impaired DNA synthesis - megaloblastic anemia (B12-deficient, folate-deficient) c) anemia associated with bone marrow failure: hypo- and aplastic anemia (from toxic effects , from radiation exposure, immune genesis) d) anemia associated with dysregulation of erythropoiesis. III. Anemia due to hemorrhage - hemolytic anemia (congenital, acquired, acute and chronic). IV. Mixed anemia (anemia of chronic diseases, etc.)
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MKB - 10 NUTRITIONAL ANEMIA (D50-D53) D50 Iron deficiency anemia D51 Vitamin B12 deficiency anemia D52 Folate deficiency anemia D53 Other nutritional anemia
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MKB - 10 HEMOLYTIC ANEMIA (D55-D59) D55 Anemia due to enzyme disorders
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MKB - 10 APLASTIC AND OTHER ANEMIA (D60-D64) D60 Acquired pure red cell aplasia [erythroblastopenia] Inclusions: red cell aplasia (adults) (acquired) (with thymoma) D61 Other aplastic anemias Excludes: agranulocytosis (D70) D62 Acute posthemorrhagic anemia D63* Anemia in chronic diseases classified elsewhere D64 Other anemias
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When determining the pathogenetic variant of anemia, the doctor should be guided by the following provisions: Do not prescribe iron preparations before determining the level of serum iron. Do not prescribe vitamin B12 before counting the number of reticulocytes and bone marrow puncture.
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If it is impossible to examine the bone marrow, for example, with a categorical refusal of the patient, and suspected B12-deficiency anemia (after determining the initial level of reticulocytes), it is permissible to make several injections of vitamin B12, followed by a re-examination of the number of reticulocytes in 3-7 days to detect reticulocyte crisis. The same is true for folic acid deficiency.
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Severity of anemia (according to A.A. Miterev) - mild Hb 120-90g/l - moderate Hb 90-70g/l - severe Hb less than 70g/l
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Iron metabolism: benefits of intravenous iron therapy Stages of development of iron deficiency anemia5 5 Crichton RR, 2006 WHO Definition Stage 1 Stage 2 Normal Iron deficiency Iron deficiency anemia<30 < 15 Насыщениетрансферрина(%) 20-45 <20 <20 Гемоглобин(г/дл) норма(12-13) норма(12-13) пониженный (< 12-13)
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Total body iron: 2.5-4 g Each ml of blood contains approximately 0.5 mg of iron 1 Huch R, 2006 8 Hentze WM, 2004 Found mainly in the cardiovascular system, liver and muscles1: Erythrocytes 1.8g Macrophages RES 0.6g Liver 1.0g Bone brain 0.3g Muscles (myoglobin) 0.3g Other tissues8 0.1g Due to transport protein Transferrin 0.003g
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Iron is stored in the form of ferritin Ferritin is a protein containing up to 4,500 iron ions5 Ferritin is found in all cells of the body The liver and spleen are ferritin storage organs Serum ferritin contains a very low concentration of iron1 Ferritin The ferritin protein consists of 24 subunits The "assembly" subunit of ferritin U.S. National Library of Medicine 1 Huch R, 2006 5 Crichton RR, 2006 Women 25-180mcg/l Men 30-300mcg/l
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Serum ferritin correlates with storage iron levels1 Serum iron levels are a reliable indicator of the amount of iron stored in the body A drop below 15 mg/l indicates an absolute iron deficiency 1 µg/l serum ferritin = 10 mg of stored iron in a healthy individual 1 Huch R, 2006 5 Crichton RR 21 Brownlie T, 2004
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Iron metabolism in inflammation5 Plasma ferritin is an acute phase protein and may be normal or elevated during infection, inflammation, or malignancy, regardless of iron deficiency. Plasma ferritin can also increase in acute or chronic liver damage. Soluble transferrin receptors marker of iron status regardless of inflammation 5 Crichton RR, 2006
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Transferrin is the transport form of iron Transferrin saturation is a measure of the amount of iron in circulating transferrin When saturated< 20% недостаточно железа поступает в костный мозг и эритропоэз становится «железонедостаточным» Трансферрин 200-400 мг/л Насыщениетрансферрина 20-45%
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Iron absorption: 1 to 3 mg/day Normal iron absorption is 1 to 2 mg/day in the duodenum8 Absorption may increase up to 2-3 mg/day when demand is increased9 Absorbed iron is transported to the liver and other tissues Transport protein: transferrin (Tf)8 Henzte MW, 2004 9 Huch R, 2006 Transport
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Iron deficiency anemia The goal of treatment: recovery (complete clinical and hematological remission within 5 years). Tasks: restoration of normal indicators of red blood and serum iron; maintaining normal performance at the proper level. 1. Organization of treatment. Most patients are treated on an outpatient basis, except in cases of severe or etiologically unclear iron deficiency anemia. In such cases, patients are hospitalized, based on the principle of the most probable nature of anemia, in the gynecological, gastroenterological or other departments. 2. Monitoring of treatment. During the period of the first detection or exacerbation of the disease, the blood is monitored once every 10-14 days, the frequency of medical examinations should be the same. You should not count on an increase in the numbers of erythrocytes and hemoglobin after 3-5 days. During the period of partial remission, when the patient is able to work, but the hematological norm is not reached, blood control and medical examination are carried out monthly. During the period of complete remission with a normal composition of red blood, observation is carried out during the first year quarterly, then once every 6 months. Recovery is considered to be the absence of exacerbations within 5 years. Consultation of a hematologist during an exacerbation - 1 time in 2 months, then 1 time in 4-6 months.
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3. Planned therapy A. Information for the patient and his family: 1. The reason for the development of anemia in this patient. 2. Fundamental curability of the disease. 3. Terms of drug therapy (initial course of iron therapy - 2-3 months, full course - up to 1 year). 4. Possibility of self-control (norms of red blood and serum iron). 5. Explanation of the harm for this category of patients of unqualified treatment, vegetarianism, fasting, "recipes" for self-treatment.
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B. Tips for the patient and his family: Start treatment with iron preparations from the moment the disease is detected, with the exception of the very initial stages, when erythrocytes > 3.5x10 | 2 / l, and Hb > N0 g / l. In these cases, you can use diet and herbal medicine as an independent method, but if it is ineffective for 1 month. it is necessary to convince the patient of the need for drug therapy. If possible, eliminate etiological factors: apply hemostatic herbal medicine in case of menorrhagia; to treat chronic diseases of the gastrointestinal tract, kidneys; to convince the patient (tka) of the need for surgical treatment of hemorrhoids or uterine fibroids with persistent bleeding. Organize a healthy diet with a predominance of meat products (meat, liver, blood sausages contain heme 2-valent iron, which is well absorbed, and is better absorbed with the non-heme form of iron - 3-valent, contained in plant products such as cereals - bran bread, wheat, beans, buckwheat, millet, oatmeal, apples, pomegranates, apricots, cherry plums, pears, peaches, nuts, carrots, beets, tomatoes, parsley, milk) and natural sources of vitamins, especially vitamin C, which improves digestibility iron from products and preparations (blackcurrant, lemons, sea buckthorn). Women with heavy periods - pomegranates and nuts. Exclude chronic household, professional and, if possible, drug intoxication for the period of treatment (gasoline, dyes, non-steroidal anti-inflammatory drugs, biseptol).
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Treatment of IDA It is not realistic to cure IDA with diet alone. Therapy of choice is oral iron preparations (to avoid overdose and severe allergic reactions). It is desirable that the daily dose of iron be about 200-300 mg. The duration of treatment is until the normalization of hemoglobin levels at the full therapeutic dose and then for another 2-3 months at a half therapeutic dose to normalize iron stores in the depot. With continued blood loss - regular preventive courses of treatment with iron preparations.
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Iron preparations for parenteral administration - according to strict indications: in violation of iron absorption, enteritis, extensive bowel resections, intolerance to oral administration of drugs or contraindications to it (peptic ulcer, ulcerative colitis in the acute stage, etc.). Blood transfusions are carried out only for health reasons - with severe hemodynamic disorders (“focus not on the hemometer, but on the tonometer”), the threat of anemic coma or the need for urgent surgery
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IRON PREPARATIONS Based on iron salts (sulfate, fumarate, gluconate, chloride) Containing Fe +++ as part of the polymaltose complex Maltofer, Maltofer Fol Ferrum Lek Fe +++ Fe ++ : Aktiferrin, Sorbifer Durules, Fenyuls, Tardiferon, Hemofer, Ferroplex, Totema
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IRON ABSORPTION Substances that enhance Fe++ absorption Substances that reduce Fe++ absorption Ascorbic acid Amber acid Fructose Cysteine Sorbitol Nicotinamide Tannin Phosphates Calcium salts Antacids Tetracyclines
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Maltofer Iron (III) hydroxide polymaltose 100 mg, chewable tablets N30 20 mg / 1 ml, syrup, vial, 75 ml or 150 ml 50 mg / 1 ml, drops for oral administration, vial, 30 ml 20 mg / 1 ml, solution for oral administration, bottle 5 ml N 10 50 mg / 1 ml, solution for injection, ampoules 2 ml N 5
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Advantages of Maltofer Maltofer has a high degree of effectiveness in the treatment of IDA and LJ Maltofer is well tolerated and causes significantly fewer side effects, compared to other iron preparations Maltofer does not interact with food or other drugs Maltofer has a wide range of dosage forms and a pleasant taste - ease of use and high adherence to therapy
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Interaction with drugs In preclinical studies, the interaction of Maltofer with various drugs was studied. The absorption of radioisotope-labeled PGCs in the presence of other drugs was compared. None of the administered drugs affected the absorption of PCOLs There were no interactions with any of the most commonly used drugs Food components do not affect absorption - Maltofer is taken with food
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Maltofer Fol Iron (III) hydroxide polymaltose Composition: 100 mg of iron and 0.35 mg of folic acid
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Iron preparations for parenteral administration Iron (III) hydroxide sucrose complex (Venofer) - solution for intravenous administration 100 mg, 5 ml (50 mg on the first day, then 100 mg 1-3 times a week, preferably intravenously drip) Iron (III) hydroxide polymaltose (Ferrum lek) - solution for intramuscular injection 100 mg, 2 ml. (Federal Guidelines for the Use of Medicines, 2009)
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Standard dosage Adults and elderly patients: 5-10 ml of Venofer® (100-200 mg of iron) 1-3 times a week, depending on the level of hemoglobin. Children: There are only limited data on the use of the drug in children. if necessary, it is recommended to administer no more than 0.15 ml of Venofer® (3 mg of iron) per kg of body weight 1-3 times a week, depending on the level of hemoglobin
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The maximum tolerated single dose Adults and elderly patients: for jet administration: 10 ml of Venofer® (200 mg of iron), the duration of administration is at least 10 minutes; for drip administration: depending on the indications, a single dose can reach 500 mg of iron. The maximum allowable single dose is 7 mg / kg and is administered once a week, but it should not exceed 500 mg of iron. The time of administration of the drug and the method of dilution, see above.
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The total amount of the drug Venofer® for treatment In the case when the total therapeutic dose exceeds the maximum allowable single dose, it is recommended to administer the drug fractionally. If after 1-2 weeks after the start of treatment with Venofer® there is no improvement in hematological parameters, it is necessary to reconsider the initial diagnosis.
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Classification of polynuclear iron (III)-hydroxide carbohydrate complexes Stable/labile - Weak/strong type 1 type 2 example of a dextran iron complex iron saccharate name of the drug Cosmofer, Ferrum Lek Venofer characteristic stable and strong medium stable and moderately strong molecular weight, kDa >100 30-100 reactivity with transferrin (iron μg%) 52.7 140.7
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Type 1 - iron dextran High molecular weight parenteral preparations cause more allergic reactions than low molecular weight ones1 All iron complexes based on dextran can cause dextran-induced anaphylactic reactions1,2 % of cases in dialysis patients at first dose3 30 iron dextran-related deaths reported in the USA4 Gastroenterology/Inflammatory Bowel Disease
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Type 2 - iron sucrose Lower molecular weight in terms of development of side effects - an advantage over type 1 complexes 1 Does not contain biological polymers, leading to fewer serious adverse reactions compared to iron dextran 1 Regular post-marketing safety reports confirmed that sucrose ironase is considered to be the safest of all existing parenteral iron preparations 5 Gastroenterology/Inflammatory Bowel Disease
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Iron carboxymaltose (Ferinject®) is a new, effective drug with favorable safety profile in patients with anemia associated with IBD More effective, faster response of hemoglobin levels, more increase in iron stores, better tolerated and improves the quality of life of patients to a greater extent than oral iron preparations All information regarding the optimal management of anemia in IBD is summarized in the Guidelines for the Diagnosis and Management of Iron Deficiency and Anemia in Inflammatory Bowel Disease, published by Gachet et al. (Gasche C et al. Guidelines on the diagnosis and management of iron deficiency and anemia in inflammatory bowel diseases) Inflamm Bowel Dis 2007:13;1545–53 The preferred route of iron administration in IBD patients is intravenous. This route of administration has been shown to be more efficient, promote faster hemoglobin response, and provide better iron replenishment than oral iron. In addition, intravenous iron improves quality of life to a greater extent than oral iron and appears to be the best choice for the treatment of anemia in patients with IBD. anemia in IBD. For complete application information, see the Ferinject® Product Profile. All information regarding the optimal management of anemia in IBD is summarized in Guidelines for the Diagnosis and Management of Iron Deficiency and Anemia in Inflammatory Bowel Disease, published by Gachet et al. (Gasche C et al. Guidelines on the diagnosis and management of iron deficiency and anemia in inflammatory bowel diseases)
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Calculation of the course dose of iron in mg A = M * (Hb1-Hb2) x 0.24 + D where: A - the amount of iron in mg; M is body weight in kg; Hb1 - standard value of hemoglobin for body weight less than 35 kg 130 g/l, more than 35 kg - 150 g/l; Hb2 - patient's hemoglobin level in g/l; D - the calculated value of iron depot for body weight less than 35 kg - 15 mg / kg, for body weight more than 35 kg - 500 mg.
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Indications for prophylactic administration of Fe preparations in pregnant women (Recommendations of the All-Russian Society of General Practitioners) Hb level below 110 g / l at the beginning of pregnancy The patient's tendency to anemia The patient's last childbirth within 2 years to date Young age (less than 20 years) The patient adheres to a special diet that excludes meat.
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Indications for prophylactic administration of Fe preparations in pregnant women Use of an intrauterine device before pregnancy Heavy menstrual bleeding before pregnancy Multiple pregnancy
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Decreased ferritin levels<30 мкг/л указывает на снижение запасов железа; <15 мкг/л – на истощение запасов железа <12 мкг/л – развитие ЖДА Снижение насыщения трансферрина <15% свидетельствует на неадекватное обеспечение эритрона и тканей железом
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In the USA, universal prevention of IDA in pregnant women is recommended from the time of the first visit to the clinic until the time of delivery in the form of oral iron supplements 30 mg/day. In Denmark - 50-70 mg of iron per day from the 20th week until delivery.
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According to Nils Milman (2008): Women with a serum ferritin level >70 mcg/l - do not need iron supplementation With a ferritin level of 30-70 mcg/l - iron should be given 30-40 mg/day With a ferritin level<30 мкг/сут следует назначить железо 80-100 мг/сут
47 slide
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Hemoconcentration Hemoconcentration (Hb > 135 g/l) in the 2nd and 3rd trimester of pregnancy is associated with daily intake of Fe preparations, especially when doses are high or started early, at the beginning of pregnancy. High Hb (>135 g/l) in the second half of pregnancy is associated with the risk of having a premature baby or a baby with low body weight, and the risk of preterm birth is also increased by 2 times.
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Main documents Draft national standard "Protocol for the management of patients with iron deficiency anemia", 2011 1 TREATMENT OF MANIFEST IRON DEFICIENCY IN PREGNANT WOMEN AND PURPOSE WOMEN (medical technology) Moscow, 2010 Serov V.N., Burlev V.A., Konovodova E.N., etc. .
49 slide
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Modern view of iron preparations The effectiveness and safety of the prophylactic use of oral Fe or Fe + folic acid in women during pregnancy was: 49 studies in 23,200 pregnant women The Cochrane Collaboration techniques through randomized controlled trials. Research results in the form of systematic reviews, meta-analyses are published in the Collaboration database - Cochrane Library (English) Russian. Cochrane Collaboration Centers are also involved in the creation of evidence-based clinical guidelines. The collaboration brings together more than 28,000 volunteer scientists from 100 countries. The name of the organization is associated with the name of the epidemiologist Archibald Cochran. The Cochrane Collaboration interacts with the World Health Organization at the board level and implements common projects. One of the most important is the WHO Reproductive Health Library. A branch of the Cochrane Collaboration, which is part of The Nordic Cochrane Centre, has been established in Russia.
50 slide
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Prevention of prelatent and latent iron deficiencies PREVENTION OF MANIFEST IRON DEFICIENCY IN PREGNANT WOMEN AND PARTNERSHIPS (medical technology) Moscow, 2010 Serov V.N., Burlev V.A., Konovodova E.N., and others. I and II trimesters, it is advisable to prevent the development of PJ by prescribing multivitamin preparations for pregnant women containing at least 20 mg of elemental iron in a daily dose ... With standard values of iron metabolism in the III trimester, as well as pregnant women and puerperas with PJ, for the prevention of LJ, a reception is indicated 50mg of elemental iron per day for 4 weeks…
51 slide
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FeSO4, Fe(II) - 45mg compensates for the deficiency of Fe in the body Vitamin C - 50mg improves iron absorption Vitamins B1, B2, B5, B6, PP have an antihypoxic effect, restore the disturbed metabolism of carbohydrates, proteins and fats that arose due to iron deficiency PP - strengthens the cell wall of blood vessels The original composition of Iron sulfate + vitamins Fenuls FENYULS contains 6 out of 9 essential water-soluble vitamins necessary for the effective prevention of congenital malformations. The remaining 3 are B9 (folic acid), B8 and B12.
52 slide
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Safety Stable concentration of Fe in the blood Low risk of overdose Innovative formulation: capsules with microdialysis granules Absence of pathological deposition
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Good tolerance Fe2+ ions do not irritate the gastric mucosa Min side effects on the part of the gastrointestinal tract Microdialysis granules In Fenyuls enteric capsules No irritating effect on the gastric mucosa is completely excluded.
54 slide
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Erythropoietin: mechanism of action Erythropoietin Erythroblasts Reticulocytes BOE-E COE-E Apoptosis (in the absence of erythropoietin) BOE-E, burst-forming erythroid unit; CFU-E, Colony-forming erythroid unit Fisher erythrocytes. Exp Biol Med 2003; 228: 1–14 Endogenous erythropoietin acts (together with various cytokines) by stimulating the formation of erythrocytes from progenitor cells.1 Erythropoietin also affects the later stages of erythropoiesis, in particular colony-forming erythroid (CFE) cells. As a result, these cells proliferate and differentiate through normoblasts into reticulocytes and mature erythrocytes. In the absence of erythropoietin, COE cells undergo apoptosis; erythropoietin inhibits cell apoptosis in the bone marrow, which allows erythroid progenitor cells to transform into mature erythrocytes.
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ERYTROPOETIN ACTION Erythropoietin stimulates the proliferation, differentiation and maturation of determined erythroid progenitor cells with the formation of morphologically identifiable normoblasts
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Subcutaneous administration of Recormon (epoetin beta) Recommended for patients with chronic renal failure by European and American standards of treatment Safer, with less frequency of side effects (rarely increased blood pressure) Allows to reduce the therapeutic dose by 20-30%
57 slide
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Recormon (epoetin beta) - a variety of dosage forms Syringe tubes of 1000, 2000, 10,000 IU - ready-to-use solution Cartridges for the "Reco-Pen" pen of 10,000, 20,000 IU - powder for solution preparation
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GOAL OF TREATMENT WITH RECORMONE Relieve symptoms of anemia Target hemoglobin level of 11-12 g/dL Eliminate the need for blood transfusions
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Treatment of anemia with Recormon in patients with chronic renal failure Correction phase Maintenance therapy phase
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Correction phase Correction of hemoglobin level to 11g/dl (10-12g/dl) S/C - 20 IU/kg x 3 times/week or IV - 40 IU/kg x 3 times/week Four weeks later - control of hematocrit, hemoglobin If hematocrit increases by 0.5 vol.% (Hb 1.5 g / dl) per week or more, continue treatment at the same dose dl) per week, then the dose is increased by 20 IU / kg x 3 times a week s / c or by 40 x 3 times a week Regardless of the route of administration, the dose per week should not exceed 720 IU / kg (i.e. 240 IU /kg once)
62 slide
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Maintenance therapy Maintenance of hematocrit 30-35 vol%, hemoglobin level 10-12 g / dl The dose from the previous administration should be reduced by half In the future, the dose is adjusted individually under the control of Hb, Hst
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ERYTROPOETIN (Russia) - solution for intravenous and s / c administration (ampoules) 0.5 and 2 thousand IU / ml 1 ml
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4. Drug therapy Iron preparations should be prescribed in sufficient doses and for a long time. Due to low efficiency and pronounced side effects, the following should not be prescribed: reduced iron, aloe syrup with iron, hemostimulin, ferramid. Food supplements containing iron are unsuitable for therapeutic purposes, since the iron content in them does not exceed 18 mg, with a need of at least 250 mg / day. Their use is possible only during the period of complete remission for the prevention of relapses. The drugs of choice should be considered retard forms, which contain a sufficient dose of iron and additives that stimulate its absorption. Tardiferon (gipotardiferon for pregnant women). Assigned to 1-2 tables. per day (1 tab - 80 mg of iron +2), strictly after meals. Contains mucoprotease, which protects the gastric mucosa, has a high bioavailability. Gipotardiferon contains folic acid necessary for pregnant women. Sorbifer. Assigned to 1 table. 2 times a day (1 tab - 100 mg of iron + 2), after meals. Well tolerated, contains ascorbic acid, which facilitates the absorption of the drug.
66 slide
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Sorbifer. Assigned to 1 table. 2 times a day (1 tab - 100 mg of iron + 2), after meals. Well tolerated, contains ascorbic acid, which facilitates the absorption of the drug. Aktiferrin. It is prescribed depending on the severity of anemia from 1 to 3 caps (1 caps - 34.8 mg of iron + 2), per day. There are forms for children: syrup and drops. The drug is highly effective, but individual intolerance is possible. Ferroplex. Assigned to 2 tables. 4 times a day (1 tab - 10 mg of iron + 2). In comparison with the above-described retard forms, it is ineffective, but it is well tolerated, almost no side effects. May be prescribed for anemia in pregnancy. NB! Warn the patient that the color of the feces turns black and that all iron preparations, without exception, are taken strictly after meals, regardless of the manufacturer's instructions. Parenteral use of iron (Ferrumlek) is limited to two situations: complete intolerance to oral drugs; the need to quickly and briefly stabilize red blood numbers, for example, in preparation for an emergency operation. May cause anaphylactic reactions, hypercoagulability. On an outpatient basis, it is prescribed only intramuscularly, injections (the contents of one ampoule) are carried out every other day, the course is 10-15 injections.
67 slide
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*The duration of the course of treatment is 6-10 weeks, depending on the severity of IDA. *Early discontinuation of iron therapy leads to relapses of IDA. * The duration of the prophylactic course of pr-mi iron in order to create a depot-iron: with a mild degree - 1.5-2 months, medium - 2 months, severe - 2.5-3 months. * The first "+" clinical sign in the treatment of iron preparations is the disappearance or decrease in muscle weakness (because iron is part of the enzymes involved in the contraction of myofibrils). * Criteria for the effectiveness of treatment with iron preparations: 1. The appearance of a reticulocyte crisis on the 7-10th day of treatment; 2. Significant increase in Hb after 3-4 weeks; 3. Complete normalization of clinical and laboratory parameters by the end of the course of treatment.
68 slide
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5. Auxiliary drugs A. To improve iron absorption and stimulate erythropoiesis - multivitamin preparations with the addition of trace elements: Complivit 1 table. per day, during meals. B. For the correction of protein metabolism - potassium orotate, 1 table. (0.5 g) 3 times a day for 20 days. The appointment of B vitamins in injectable form is not justified. B. Phytotherapy. Rosehip decoction. Grind the berries and pour boiling water at the rate of 1 cup of boiling water per 1 tbsp. l. berries, insist 20-30 minutes. Drink during the day. Antianemic collection. Mix nettle, string, currant leaf, strawberry leaf equally, pour cold water (1 glass of water per 1 tbsp mixture) for 2-3 hours, then put on fire, boil for 5-7 minutes, cool, strain. Drink during the day. Approximate scheme for the treatment of iron deficiency anemia in pregnant women: hypotardiferon 1 tab. morning and evening after meals; pregnavit 1 caps. 2 times a day, orotatkalia 1 tab. (0.5 g) 3 times a day for 20 days; phytotherapy; diet therapy. An approximate treatment regimen for iron deficiency anemia in the elderly: sorbifer 1 tab. morning and evening after meals; undevit 1 tablet 2 times a day, potassium orotate 1 tab. (0.5 g) 3 times a day for 20 days; herbal medicine, diet therapy.
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Rehabilitation therapy and prevention Primary: Persons at risk of iron deficiency (premature babies, children from multiple pregnancies, girls in puberty with rapid growth, women with mennorrhagia, pregnant women, women who are breastfeeding, women with gastric obstruction, liver, small intestine, patients with chronic blood loss): they are recommended a diet rich in iron and periodic blood tests. Secondary: During the period of partial remission, when the patient is able to work, until the normalization of hemoglobin numbers, daily medication should be continued. When the amount of hemoglobin reaches 120 g / l, one of the iron preparations is prescribed for 7 days after menstruation or 7 days of each month, up to a year. In the period of complete remission, when hemoglobin numbers are normal without treatment, one-month anti-relapse courses of ferroplex or tardiferon in spring and autumn. Criteria for the effectiveness of rehabilitation therapy: maintaining normal numbers of red blood and serum iron for three years when conducting one-month anti-relapse courses of treatment in spring and autumn.
70 slide
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Medical examination Examination of temporary disability. The terms of labor loss are determined by the medical (clinic, numbers of erythrocytes and hemoglobin) and social factors - the nature of the patient's work. With heavy physical labor and hazardous industries, men's ability to work is restored with hemoglobin numbers of 130 g / l, for women - 120 g / l. With light physical labor, hemoglobin numbers are allowed by 10 g / l, for mental workers - by 20 g / l below those given. Medical and social expertise. Patients with severe, difficult to correct anemia are referred to MSEC. In the diagnostic formulation, anemia takes the place of a symptom or complication of the underlying disease.
71 slide
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Megaloblastic anemia B12 deficiency anemia 1849 - Addison described pernicious or malignant anemia 1872 Biermer called "progressive pernicious anemia"
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B12 duodenum Ileum R+B12 WF WF+B12 R+B12 Blood TrK II+B12 WF+B12 Lumen Epithelium Stomach TrK II+B12 TrK II B12 VF+B12 TrK II WF Tissue cells Scheme of vitamin B12 metabolism R – R-protein WF – internal factor Castle TrK - transcobalamin trypsin
73 slide
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Source of vitamin B12 Meat, liver, kidneys, eggs, dairy products B12 reserves in the body are 2-5 mg (reserve for 3-6 years) The daily requirement for food vitamin B12 is 3-7 mcg
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Causes of vitamin B12 deficiency (most common) Lack of HF secretion Atrophic gastritis (including autoimmune) Gastrectomy Hereditary defects in HF production Advanced forms of gastric cancer Malabsorption syndrome Various diseases with malabsorption syndrome: Celiac disease Chr. enteritis Resection of the small intestine Tumors of the small intestine, granulomatous lesions Competitive uptake of vitamin B12 Tapeworm invasion Blind loop syndrome Multiple diverticulosis of the small intestine
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Causes of Vitamin B12 Deficiency (Rare) Ting R. et al., Arch Intern Med. 2006;166:1975-1979. ↓ Dietary intake of B12 Strict vegetarian diet Medications PAS Colchicine Neomycin Metformin (?) Extremely rare causes Deficiency of TrK II Congenital enzyme defects Immerslund-Gresbeck syndrome (absence of receptors for WF)
76 slide
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Peripheral blood picture in B12 (folate deficiency) anemia Jolly bodies Cabot rings Pancytopenia CP>1 Reticulocytes ↓ Anisocytosis with a tendency to macrocytosis Hyperchromia of erythrocytes Jolly bodies, Cabot rings, basophilic puncture of erythrocytes Hypersegmentation of granulocytes Hypersegmented granulocytes Macrocytes overloaded with Hb
77 slide
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Macrocytosis is not specific to B12 or folate deficiency anemia! Most common causes of macrocytosis other than B12 deficiency and folic acid deficiency Drugs Alcoholism Liver disease Hypothyroidism Multiple myeloma Myelodysplastic syndrome Aplastic anemia Acute leukemia Cited in Aslinia F., et al.; 2006
78 slide
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In the bone marrow - megaloblastic type of hematopoiesis, irritation of the red sprout of Megaloblasts
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In the biochemical analysis of blood, moderate hyperbilirubinemia (up to 47 μmol / l) is characteristic due to free bilirubin
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VITAMIN-B12 AND FOLIO-DEFICIENCY ANEMIA The goal of treatment is to achieve and maintain stable clinical and hematological remission. Tasks: transfer of hematopoiesis from megaloblastic to normoblastic; lifelong maintenance of the normoblastic type of hematopoiesis by permanent administration of vitamin B12 and (or) folic acid. 1. Organization of treatment. Megaloblastic anemias are treated on an outpatient basis. However, in cases requiring transfusion therapy for health reasons, hospitalization in a therapeutic or hematological department is necessary. Consultation with a hematologist is advisable at the first detection of the disease, upon the onset of remission, and then once a year.
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2. Planned therapy A. Information for the patient and his family: Brief information about the nature of the disease. It is fundamentally possible to create a stable clinical and hematological remission with adequate maintenance therapy. It is necessary to control the blood test once every 3 months, the introduction of vitamin B12 monthly, even during the period of stable remission. B. Tips for the patient and his family: Nutrition, complete in protein and vitamin composition (meat, liver, kidneys, eggs, dairy products). The daily requirement for the diet B12 is 3-7mcg. B12 reserves in the body are 2-5 mg (reserve for 3-6 years). If necessary, it is necessary to undergo a course of treatment for chronic diseases of the gastrointestinal tract.
82 slide
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Treatment of B12-deficiency anemia Cyanocobalamin 500 mcg 1 time per day / m or s / c for 4-6 weeks (in severe cases, 2 times a day). With funicular myelosis - the dose is increased to 1000 mcg per administration (folic acid can increase neurological symptoms). An indicator of the effectiveness of treatment is the onset of a reticulocyte crisis on days 5-8 and the gradual achievement of complete clinical and hematological remission. In the case of anemic coma, severe hemodynamic disorders - transfusion of a single-group compatible erythromass.
83 slide
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In order to prevent the development of vitamin B12 deficiency, it is necessary to administer maintenance doses of cyanocobalamin (500 mcg 2 times a month). The lack of effect of vitamin B12 therapy indicates an incorrect diagnosis.
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An approximate scheme for the treatment of pregnant women: vitamin B12 500 mcg intramuscularly daily for 10 days, then 10 injections every other day, then 200 mcg 1 time in 10 days; folic acid 15 mg / day from the 1st to the 30th day from the start of treatment with vitamin B12; hypotardiferon 1 tab. per day from the 30th day for 1-2 months. Iron preparations are necessary, because. in pregnant women, anemia, as a rule, is of mixed origin. An approximate treatment regimen for the elderly: vitamin B12 500 mcg intramuscularly daily for 10 days, then 10 injections every other day, then 500 mcg 1 time per week, 2-3 months, then 1 time in 2 weeks - 2 months, then 1 time per month. for life; folic acid 10 mg/day; multivitamin preparation (undevit) 1 tab. 2 times a day from the 30th day from the start of treatment with vitamin B12, for 1-2 months, with breaks for 2-3 months.
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Rehabilitation therapy and prevention 1. Primary prevention does not exist. 2. Dispensary registration of patients: during the period of complete remission, 500 mcg of vitamin B12 is administered once a month. If necessary (if there are signs of megaloblastic hematopoiesis), vitamin B12 is administered in the amount of 200 mcg once every 10 days in spring and autumn. B12- and folic deficiency anemia during the period of clinical and hematological remission is not a contraindication to spa treatment, does not entail restrictions in taking physiotherapy. 3. Persons who have undergone a total resection of the stomach: VitB12 - 100 mcg once a month for life + iron preparations in courses 2 times a year for 1-1.5 months. Criteria for the effectiveness of rehabilitation therapy: Preservation of normoblastic hematopoiesis (normal numbers of erythrocytes, Hb, color index not higher than 1.1; absence of macrocytosis) in the presence of only maintenance therapy. Absence of neurological disorders: taste perversions, numbness of the feet and hands, paresthesia, etc. Medical examination The patient is temporarily unable to work until the signs of megaloblastic hematopoiesis completely disappear and red blood numbers are restored to normal.
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Features of folate deficiency anemia Hematological syndrome - similar to that of B12 deficiency anemia No neurological disorders Internal reserves of folic acid can be depleted after 4 months.
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↓ intake of folic acid from food Unbalanced diet (eg, with chronic alcoholism) Malabsorption Increased consumption of folic acid Pregnancy Increased body growth Chr. hemolytic anemia Causes of folic acid deficiency anemia Daily requirement 100-200 mcg Folic acid is found in meat, liver, yeast, spinach Drugs: MT Anticonvulsants Trimethoprim Triamteren
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Treatment of folic acid deficiency anemia Folic acid orally 5-15 mg/day 4-6 weeks until complete remission For prophylactic purposes (with chronic hemolysis, pregnancy, lactation) 1 mg/day of folic acid.
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HEMOLYTIC ANEMIA The goal of treatment is to create a stable clinical and hematological remission in the absence of hemolysis phenomena. Objectives: 1. stopping the process of hemolysis with the help of medications. If necessary, splenectomy; 2. restoration of normal hematopoiesis, normal indicators of red blood; 3. development and application of a maintenance therapy regimen to prevent the occurrence of hemolytic crises.
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Hemolytic anemia General signs of hemolysis: ↓ Hb Reticulocytosis Possible splenomegaly of the level of free bilirubin with intracellular hemolysis of the level of free hemoglobin, hemoglobinuria, hemosiderinuria with intravascular hemolysis In the bone marrow - irritation of the red germ
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Hereditary hemolytic anemia Due to a violation of the structure of the membrane protein: - hereditary (micro) spherocytosis, elliptocytosis, stomatocytosis Due to a violation of the lipids of the erythrocyte membrane: - hereditary acanthocytosis Due to a violation of the synthesis of globin chains: --thalassemia, β-thalassemia, hemoglobinopathy H
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Hereditary hemolytic anemia Associated with a violation of the structure of globin chains - hemoglobinopathies: - sickle cell anemia Associated with a violation of the activity of erythrocyte enzymes - enzymopathies: - deficiency of the activity of G-6-PDG, pyruvate kinase, etc.
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Hereditary spherocytosis (Minkowski-Choffard disease) Intracellular hemolysis - chronic or in the form of a crisis (anemia, jaundice, splenomegaly) Skeletal deformities (tower skull, Gothic palate, wide bridge of the nose, shortening of the little finger, etc.) Early development of cholelithiasis Hereditary history
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Hereditary enzymopathies (= hereditary non-spherocytic hemolytic anemias) Most common deficiency of glucose-6-phosphate dehydrogenase However, persistent hemolytic anemia (with intracellular hemolysis) is rare After taking drugs (sulfonamides, nitrofurans, 5-NOCs, nevigramon, antimalarials), beans – hemolytic crisis with intravascular hemolysis
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Emergency conditions and their relief at the prehospital stage A hemolytic crisis with severe jaundice and a sharp decrease in red blood numbers is an indication for emergency hospitalization in a hematological hospital, you should not try to stop it on an outpatient basis! 1. Organization of treatment. At the first detection of a condition that causes suspicion of hemolytic anemia, the patient is subject to planned (in mild cases) or emergency (in severe) hospitalization in a hematological hospital. The volume before the inpatient examination: a clinical blood test, a general urinalysis, a urine test for bile pigments, an examination by an infectious disease specialist, for women - an examination by a gynecologist, if possible - an ultrasound of the abdominal organs. During the period of exacerbation in a patient with an established diagnosis of hemolytic anemia in severe cases - hospitalization in a hematological hospital, in non-severe cases - a mandatory consultation of a hematologist for the appointment of corticosteroid therapy and management of the patient together with a hematologist until remission is achieved.
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2. Planned therapy A. Information for the patient and his family: 1. Possible etiology of the disease in this patient. 2. Fundamental possibility of achieving clinical and hematological remission. 3. Rationale for the need for corticosteroid therapy. 4. If necessary, justification of indications for splenectomy. 5. Explanation of the features of the regimen, employment, hypoallergenic diet, drug restrictions, contraindications to physiotherapy. In case of congenital hemolytic anemia, information on genetic risk. B. Tips for the patient and his family: 1. Work and rest regimen: if the patient works in a hazardous industry, resolve the issue of employment without occupational hazard; to exclude rest in the summer in the southern resorts, insolation. 2. Exclude uncontrolled intake of medications, especially analgesics and non-steroidal anti-inflammatory drugs. .Follow a hypoallergenic diet with the exception of coffee, citrus fruits, chocolate, raspberries, strawberries, hot spices. Limit your intake of eggs. 4. Exclude extreme temperature effects: visiting a steam bath, sauna, winter hunting and fishing. 5. In the case of congenital autosomal and dominantly inherited hemolytic anemia (spherocytic, ovalocytic), childbearing is strongly discouraged due to the high genetic risk.
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C. Drug therapy 1. At the first detection or exacerbation of the disease, bed rest is necessary, a diet with the exception of products that can cause allergies (chocolate, eggs, strawberries, raspberries). 2. Treatment depends on the severity of anemia: with minimal severity of anemia: GCS in small doses. Observation; with moderate: prednisolone at an initial dose of 60 mg / day for 2-3 weeks. If there is no effect, then a splenectomy is performed. If there is no effect again, the following are prescribed: Cyclophosphamide 100 mg/day, Azathioprine 150 mg/day, Rituximab 375 mg/m2 per week. If there is an effect on prednisolone, then a rapid dose reduction to 20 mg / day. in severe: prednisolone 60 mg / day and >, intravenous immunoglobulin, splenectomy. During the period of partial remission, when the number of reticulocytes is normalized (which indicates the cessation of hemolysis) - treatment, as in iron deficiency anemia, hepatoprotectors are prescribed.
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Rehabilitation therapy and prevention In spring and autumn, iron preparations are used in prophylactic doses, the appointment of hepatoprotectors (karsil, etc.) is mandatory. Sanatorium treatment is contraindicated! During the period of exacerbation, blood control and medical examination - 1 time in 3-5 days, during the period of partial remission - 1 time in 14 days, during the period of complete remission - 1 time in 2-3 months. Rehabilitation therapy is effective if: the patient maintains a normal number of reticulocytes (hemolysis is absent); red blood numbers are normal; no increase in jaundice of the skin. Medical examination Examination of temporary disability. The patient is unable to work until the normalization of reticulocyte counts. For criteria for working capacity, depending on the numbers of hemoglobin, see "Iron deficiency anemia". Medical and social expertise. Indications for referral to MSEC: severe hemolytic anemia with frequent crises, persistently impairing the patient's ability to work. Condition after splenectomy. Persistent uncorrectable pancytopenia as a consequence of immune hemolysis.
104 slideAnemia in bone marrow failure Normochromic (less often hyperchromic) Hyporegenerative (↓reticulocyte) Leukopenia due to a decrease in the content of neutrophilic granulocytes (granulocytopenia) Thrombocytopenia Fever, infectious complications, ulcerative necrotic lesions of the mucous membranes Hemorrhagic syndrome Changes in the picture of bone marrow hematopoiesis in accordance with the nature of the underlying pathological process (replacement with adipose tissue, infiltration by blast cells, etc.).
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HYPOPLASTIC ANEMIA Treatment goal: maintaining the state of clinical and hematological compensation, lengthening the patient's life. Tasks: stimulation of bone marrow hematopoiesis; correction of immunological disorders. Emergency conditions and their relief at the prehospital stage Severe hemorrhagic and purulent-necrotic manifestations are possible. Even in their absence, the suspicion of hypoplastic anemia is an indication for emergency hospitalization in a hematological hospital. Attempts to stop bleeding and treat purulent complications on an outpatient basis will not give an effect!
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1. Organization of treatment. In cases of first detection and exacerbations - hospitalization in a hematological hospital. During the compensation period, the patient is observed weekly, hematologist consultation - monthly. In case of clinical and hematological remission (very rarely observed) - a general practitioner or a local therapist examines the patient monthly, a hematologist - once every 3 months. 2. Planned therapy In the hospital - massive transfusion and hormonal therapy (glucocorticosteroids up to 60-100 mg / day), according to indications - splenectomy. If there are indications and conditions - bone marrow transplantation. Rehabilitation therapy and prevention A. Outpatient - prednisolone in individually selected doses (15-45 mg / day), anabolic steroids. B. Phytotherapy, homeopathic treatment are ineffective! C. It is required, if possible, to completely exclude drugs that can cause hematopoietic hypoplasia (chloramphenicol, sulfonamides, chlorpromazine, bucarban, butadione), eliminate contact with household chemicals, prohibit insolation and physiotherapy. Pregnancy and childbirth are not recommended. In case of detection of hypoplastic anemia in a pregnant woman - termination of pregnancy! Sanatorium treatment is strictly contraindicated! Medical examination Medical and social examination. All patients with hypoplastic anemia are disabled during the first detection, as well as exacerbation of the disease, and after inpatient examination and treatment, they are subject to referral to MSEC. As a rule, these are invalids of the II group for life, only in rare cases, with stable blood counts, the III group of disability is established and light work is allowed.
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clinical picture. The initial manifestations are due to the rapid development of hypovolemia (decrease in BCC): dizziness, fainting, pallor, cold sweat. Pulse is thready, frequent. Blood pressure is low. After 12-18 hours, the symptoms of anemia proper join: weakness, tinnitus, visual disturbances; tachycardia and arterial hypotension are noted. Immediately after blood loss, the numbers of hemoglobin and erythrocytes are close to normal. After 1-2 days, there is a progressive uniform decrease in red blood indices without a decrease in the color index - anemia is normochromic in nature. 4-5 days after blood loss, a reticulocyte crisis occurs - a sharp increase in the number of reticulocytes as a result of increased bone marrow activity (the norm is 0.5-1.2%). Young forms of the granulocytic series may appear in the blood: metamyelocytes, less often myelocytes. With sufficient reserves of iron in the plasma after this phase, recovery quickly occurs, with sideropenia (decrease in iron stores in the body), a picture of hypochromic iron deficiency anemia develops. Diagnosis of acute posthemorrhagic anemia with external bleeding is not difficult. With massive internal bleeding, the Gregersen test for occult blood in the feces, a blood test for residual nitrogen in case of bleeding from the gastrointestinal tract, and puncture of the cavities help diagnose.
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Treatment: 1. Hospitalization (surgical, trauma, gynecological department). 2. Stop bleeding: - mechanical methods: application of a tourniquet, pressure bandages, hemostatic sponge; - stop uterine bleeding; - in / in, in / m - 12.5% solution 2-4ml dicynone, 1% solution 3-5ml vikasol; - in / in-drip - 100-200 ml of 5% solution of aminocaproic acid; 3. In case of shock: - lower the head end of the bed; -in\in-drop - crystalloid solutions (saline): 0.9% NaCl solution, Ringer solution, 5% glucose solution, disol, acesol, lactosalt (their volume should significantly exceed the volume of blood loss); Following their introduction - in / in-drop - 100 ml or more of 5% albumin solution Or colloidal blood substitutes: polyglucin (400-800 ml or more), reopoliglyukin (400-800 ml or more), gelatinol (1000 ml or more). The ratio of crystalloid solutions to colloidal ones is 2:1 or 3:1 (colloidal solutions are administered only after abundant administration of crystalloid ones, since colloidal ones cause dehydration of tissues, metabolic complications, deepen acute renal failure, contribute to the development of DIC). 4. To resort to blood transfusions should be resorted to with large blood loss - more than 1-1.5 liters. in adults. 5. Planned and rehabilitation therapy for IDA is carried out.
Description of the slide:
Everything that the doctor does, let him do it correctly and beautifully. Hippocrates.
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ANEMIA Anemia is a decrease in the level of hemoglobin and (or) erythrocytes per unit volume of blood. The determining criterion is hemoglobin, since with some anemia, a decrease in red blood cells is not always observed (IDA, thalassemia). Prezentacii.com
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IRON DEFICIENCY ANEMIA IDA - a disorder in which the iron content in the blood serum, bone marrow and depot decreases, which leads to a violation of the formation of Hb, erythrocytes, the occurrence of anemia and trophic disorders in tissues.
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REASONS FOR IDA. 1. Chronic blood loss 2. Increased iron intake 3. Alimentary iron deficiency 4. Violation of iron absorption 5. Redistributive iron deficiency 6. Violation of iron transport in hypo-, atransferrinemia
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DIAGNOSIS OF KLA: Hemoglobin, color index, erythrocytes decrease (to a lesser extent). The shape and size of erythrocytes change: poikilocytosis (different form of erythrocytes), microcytosis, anisocytosis (unequal size). Bone marrow: generally normal; moderate hyperplasia of the red germ. With special staining, a decrease in sideroblasts (erythrocaryocytes containing iron) is detected. Biochemistry. Determination of serum iron (reduced). Normally 11.5-30.4 µmol/l in women and 13.0-31.4 in men. This analysis is very important, but errors in the determination are possible (not clean test tubes), so the normal level of syv. iron does not yet rule out IDA. Total serum iron-binding capacity (TIBC) – i.e. the amount of iron that can be bound by transferrin. The norm is 44.8-70 µmol / l. With IDA, this indicator increases.
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TREATMENT Rational treatment of IDA provides for a number of principles: 1. You cannot stop IDA only with a diet 2. Compliance with the stages and duration of treatment - stopping anemia - restoring iron depot in the body The first stage lasts from the start of therapy to the normalization of hemoglobin (4-6 weeks), the second stage - "saturation" therapy - 2-3 months. 3. Correct calculation of the therapeutic dose of iron
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VITAMIN B12 DEFICIENCY ANEMIA This anemia was first described by Addison and subsequently Birmer more than 150 years ago (1849), and is accordingly known by the name of these two researchers. At the beginning of the 20th century, this anemia was one of the most common blood diseases that did not respond to any therapy - hence another name - pernicious or pernicious anemia.
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CAUSES OF VITAMIN B12 DEFICIENCY IN THE BODY 1. Malabsorption 2. Competitive consumption of B12 3. Decrease in vitamin B12 stores 4. Lack of food 5. Absence of transcobalamin-2 or production of antibodies to it (rarely).
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Damage to the gastrointestinal tract. Glossite is typical, first of all, according to the author's description - Gunther's: red lacquered, raspberry tongue. It is not detected in everyone - in the presence of a significant and prolonged deficiency of vitamin B12 (10-25%). Some patients may have less pronounced manifestations of glossitis - pain in the tongue, burning, tingling, in some cases, inflammation, erosion. Objectively, the tongue has a crimson color, the papillae are smoothed, there are areas of inflammation at the tip and edges. Other lesions of the gastrointestinal tract include atrophic gastritis, which may also be the result of vitamin B12 deficiency.
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Damage to the nervous system The peripheral nerves are most often affected, followed by the posterior and lateral columns of the spinal cord. Symptoms appear gradually, starting with peripheral paresthesia - tingling, numbness of the legs, crawling sensation in the lower extremities; then stiffness of legs and unsteadiness of gait appear. In rare cases, the upper limbs are involved, the sense of smell, hearing are disturbed, mental disorders, delirium, hallucinations occur. Objectively revealed loss of proprioceptive and vibrational sensitivity, loss of reflexes. Later, these disturbances increase, the Babinski reflex appears, and ataxia sets in.
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DIAGNOSIS OF UAC. Increase in color index (greater than 1.1) and MCV. The size of erythrocytes is increased, there may be megaloblasts, i.e. anemia hyperchromic and macrocytic. Anisocytosis and poikilocytosis are characteristic. In erythrocytes, basophilic puncture is found, the presence of nuclear residues in the form of Joly bodies and Cabot rings. Changes in leukocytes, platelets and reticulocytes. Leukocytes - the number decreases (usually 1.5-3.0 10), the segmentation of neutrophils increases (up to 5-6 or more). Platelets - moderate thrombocytopenia; hemorrhagic syndrome usually does not happen. Reticulocytes - the level is sharply reduced (from 0.5% to 0).
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Sternal puncture - is crucial in the diagnosis. It must be carried out before the start of the introduction of vitamin B12, because. normalization of bone marrow hematopoiesis occurs within 48-72 hours after the introduction of adequate doses of vitamin B12. In the cytogram of the bone marrow, megaloblasts (large atypical cells with a peculiar morphology of the nucleus and cytoplasm) of varying degrees of maturity are found, which makes it possible to confirm the diagnosis morphologically. The ratio L:Er= 1:2, 1:3 (N= 3:1, 4:1) due to the sharp pathological hyperplasia of the red germ. There is a pronounced violation of maturation and death of megaloblasts in the bone marrow, there are no oxyphilic forms, so the bone marrow looks basophilic - “blue bone marrow”.
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TREATMENT OF B12-DEFICIENCY ANEMIA The course of treatment consists of daily intramuscular injections of vitamin B12, 500 mcg, 30-40 injections per course. Subsequently, maintenance therapy is recommended at 500 mcg once a week for 2-3 months, then 2 times a month for the same period. According to the recommendations of American hematologists, maintenance therapy should be carried out for life - 250 mcg once a month (or course treatment 1-2 times a year, 400 mcg / day for 10-15 days).
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Hemolytic anemia is a group of diseases in which there is a shortening of the life span of erythrocytes, i.e. hemorrhage predominates over hemorrhage.
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ACQUIRED HEMOLYTIC ANEMIA Most often caused by an immune mechanism: The most common variant is autoimmune hemolytic anemia. In this case, antibodies are produced to their own unchanged erythrocyte antigen. The reason is the disruption of natural immunological tolerance, in connection with which one's own antigen is perceived as a foreign one. Autoimmune G.A. may be symptomatic or idiopathic.
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Laboratory characteristic. KLA: anemia in most cases is not severe (Hb decreases to 60-70 g / l), but in acute crises there may be lower numbers. Anemia is often normochromic (or moderately hyperchromic). Reticulocytosis is noted - initially insignificant (3-4%), upon exiting the hemolytic crisis - up to 20-30% or more. Changes in the size of erythrocytes are observed: macrocytosis, microcytosis, the latter being more characteristic. The number of leukocytes is moderately increased (up to 20+10 9/l), with a shift to the left (leukemoid reaction to hemolysis). Biochemistry of blood. Slight hyperbilirubinemia (25-50 µmol/l). There may be an increase in globulins in the proteinogram.
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. tissues
The main protein containing iron is hemoglobin Proteins containing iron reserves are ferritin and hemosiderin The protein that binds iron in serum and transports it to the bone marrow and other tissues is transferrin (blood plasma protein related to β-globulins), which is synthesized mainly liver.
Intake of iron in the body Iron in food is in two forms: - not part of the heme Fe 3+ (fruits, vegetables, cereals) - absorbed 1-7% - as part of the heme Fe 2+ (meat, poultry, 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 Iron absorption 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 underweight - with high birth weight, fast-growing - artificially fed, especially with unadapted mixtures, products based on whole milk - children of mothers who had anemia during during pregnancy Teenage girls: -hormonal imbalance, juvenile uterine bleeding -malnutrition
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) - the level of Hb g / l; II degree (medium) - the level of Hb g / l; III degree (severe) - the level of Hb is less than 70 g / l.
The following symptoms are characteristic of sideropenic syndrome: skin changes: dryness, the appearance of small pigment spots of the color "coffee with milk"; changes in the mucous membranes: "jamming" in the corner of the mouth, glossitis, atrophic gastritis and esophagitis; dyspeptic phenomena from the gastrointestinal tract; hair changes - bifurcation of the tip, brittleness and loss up to alopecia areata; nail changes - transverse striation of the nails of the thumbs (in severe cases and legs), brittleness, delamination into plates; change in smell - the patient's addiction to pungent odors of varnish, acetone paint, car exhaust gases, concentrated perfumes; taste changes - the patient's addiction to clay, chalk, raw meat, dough, dumplings, etc .; pain in the calf muscles.
The anemic syndrome is characterized by the following symptoms: loss of appetite; noise in ears; flashing flies before the eyes; poor exercise tolerance; weakness, lethargy, dizziness, irritability; fainting; dyspnea; decrease in working capacity; cognitive decline; reduced quality of life; pallor of the skin and visible mucous membranes; change in muscle tone in the form of a tendency to hypotension, hypotension of the muscles of the bladder with the development of urinary incontinence; expanding the boundaries of the heart; muffled heart tones; tachycardia; systolic murmur at the apex of the heart.
Criteria for laboratory diagnosis of UAC disease, performed by the "manual" method - a decrease in the concentration of Hb (less than 110 g / l), a slight decrease in the number of erythrocytes (less than 3.8 x 1012 / l), a decrease in CP (less than 0.85), an increase in ESR ( more than mm/hour), normal content of reticulocytes (10-20). Additionally, the laboratory assistant describes anisocytosis and poikilocytosis of erythrocytes. IDA is microcytic, hypochromic, normoregenerative anemia. Biochemical analysis of blood - a decrease in the concentration of serum iron (less than 12.5 μmol / l), an increase in the total iron-binding capacity of serum (more than 69 μmol / l), a decrease in the saturation coefficient of transferrin with iron (less than 17%), a decrease in 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 clinical nutrition (for newborns - breastfeeding, and in the absence of milk from the mother - adapted milk formulas enriched with iron. Timely introduction of complementary foods, meat, offal, buckwheat and oatmeal, fruit and vegetable purees, hard cheeses; reducing the intake of phosphates , 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 of 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 ferric HPA Any age 5 mg/kg
Principles of rational therapy for IDA in children Treatment with iron preparations is recommended under medical supervision. Iron preparations are recommended for children after consulting a pediatrician. You should not prescribe iron preparations to children against the background of inflammatory processes (ARVI, tonsillitis, pneumonia, etc.), since in this case iron accumulates in the focus 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 ferrous, since it is ferrous iron that is absorbed. The use of iron preparations should be combined with the 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 side effects occur, you can take the medicine with meals. Worst of all, iron is absorbed if the drug is taken after meals.
Oral iron preparations should be taken at least 4 hours apart. Tablets and dragees containing iron should not be chewed! The inclusion of ascorbic acid in complex preparations of iron 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 reduces the prescribed dose. Iron absorption also increases in the presence of fructose, succinic acid. It is impossible to combine taking an iron preparation with substances that inhibit its absorption: milk (calcium salts), tea (tannin), herbal products (citations and chelates), a number of drugs (tetracycline, antacids, blockers , H2 receptors, proton pump inhibitors). Taking combined preparations 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 4 to 8 weeks. Treatment with an iron preparation should be continued even after stopping IDA to restore tissue and deposited iron. The duration of the maintenance course is determined by the degree and duration of iron deficiency (ID), the level of SF. In the treatment of IDA, vitamin B12, folic acid, vitamin B6 should not be used, pathogenetic in no way associated with iron deficiency. The ineffectiveness of IDA therapy with oral iron preparations 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 preparations is ineffective), checking the patient's compliance with the doctor's prescriptions in the dosage and timing of treatment. Iron malabsorption is very rare. Parenteral administration of iron preparations is indicated only: in the syndrome of impaired intestinal absorption and the condition after extensive resection of the small intestine, ulcerative colitis, severe chronic enterocolitis and dysbacteriosis, intolerance to oral iron preparations. Restriction of parenteral administration is associated with a high risk of developing local and systemic adverse reactions. In addition, parenteral iron preparations are 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 preparations should be done only 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 carry dangerous infections through donated blood. Exceptions that allow transfusion of donor erythrocytes are: 1) severe hemodynamic disorders; 2) forthcoming additional blood loss (delivery, 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 toxicity to the gastrointestinal tract with the development of symptoms such as pain in the epigastric region, constipation, diarrhea, nausea, and vomiting. This leads to low compliance of IDA treatment 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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