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Download presentation on anemia. Presentation "Anemia" in biology - project, report

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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 there may be errors in the determination (not clean tubes), so normal level 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. In the early 20th century, this anemia was one of the most frequent illnesses blood that is not amenable 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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Defeat 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, a feeling of crawling "goosebumps" in lower limbs; then stiffness of legs and unsteadiness of gait appear. In rare cases, they are involved upper limbs, impaired sense of smell, hearing, there are mental disorders, delusions, hallucinations. 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 - has crucial in diagnostics. 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 a cytogram bone marrow megaloblasts are found (large atypical cells with a peculiar morphology of the nucleus and cytoplasm) varying degrees maturity, which allows morphological confirmation of the diagnosis. 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 carried by an immune mechanism: The most common variant are 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.

BASIC PRINCIPLES OF DIAGNOSTICS OF ANEMIA ANEMIA is a clinical and laboratory syndrome characterized by a decrease in the level of hemoglobin, erythrocytes and hematocrit in a unit of blood volume 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 (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); Clinical picture of anemia: 1. Anemia syndrome 2. Hemolysis syndrome; 3. Syndrome of ineffective erythropoiesis; 4. Syndrome of dyserythropoiesis; 5. Syndrome of sideropenia; 6. Syndrome of hypersplenism; 7. Iron overload syndrome; Anemic syndrome Manifestations depend on the depth of anemia and the speed of its development; Weakness; fatigue; Decrease, perversion of appetite; Dyspnea; heartbeat; Dizziness; Noise in the ears, flashing "flies"; fainting; Aggravation of angina attacks; hemolysis syndrome; REASONS: defects in the erythrocyte membrane; destruction by antibodies; intracellular destruction; non-immune damage ... CLINIC: icteric staining of the sclera, skin, dark urine, enlarged liver and spleen; LABORATORY: possible decrease in Hb and erythrocytes, increase in ESR; reticulocytosis, increased indirect bilirubin and LDH (4-5), urobilinogen in urine, stercobilin in feces; Myelogram: irritation of the erythroid germ Syndrome of ineffective erythropoiesis, a condition in which the activity of the bone marrow is increased, but the output of mature erythrocytes into the blood is reduced due to increased destruction of erythroblasts in the bone marrow. CLINICAL SITUATIONS: severe anemia, regardless of cause; anemia in chronic diseases; some forms of hereditary anemia; Clonal anemia (PNH, MDS) SYMPTOMS: possible development of bone deformities with prolonged existence due to the expansion of the hematopoietic foothold Dyserythropoiesis syndrome Morphological signs of impaired maturation of erythrocytes in the bone marrow, an indirect indication of the existing ineffective erythropoiesis (multinuclear erythroblasts, lobular nuclei, chromatin bridges, karyorhexis). CLINICAL SITUATIONS: MDS, severe forms of any anemia, megaloblastic anemia, thalassemia, sideroblastic anemia; CLINIC: non-severe hemolysis accompanying other signs of anemia Sideropenia syndrome and a state of latent iron deficiency Dystophia of the skin and its appendages; Perversion of taste and smell; Muscular hypotension(urinary incontinence); Muscle pain , Decreased attention; Memory impairment, etc. Hypersplenism syndrome Combination of enlarged spleen with increased bone marrow cellularity and cytopenic state of peripheral blood. CLINICAL SITUATIONS: Venous stasis, extrahepatic portal hypertension; Cellular infiltration of the spleen in tumor processes and lymphoproliferative conditions; Sarcoidosis; Amyloidosis; Extramedullary hematopoiesis; Gaucher disease; Infections (CMV, toxoplasmosis), etc. Iron overload syndrome; REASONS: Increased absorption; Additional introduction; er.mass transfusions; The formation of iron with increased cell death; CONSEQUENCES: hemosiderosis of the internal organs BASIC LABORATORY DIAGNOSIS OF ANEMIA Basic red blood parameters and erythrocyte indices RBC Red Blood Cells Red blood cell count Hb Hemoglobin Hemoglobin Ht Hematocrit Hematocrit MCV Mean Cell Volume Mean concentration of hemoglobin in erythrocytes CHCH* Mean Cellular Hemoglobin Concentration Mean cellular concentration of hemoglobin RDW Red Distribution Width Distribution width of erythrocytes by volume HDW* Hemoglobin Distribution Width Width of distribution of erythrocytes by hemoglobin concentration This indicator is characterized by RDW; Microcytes - erythrocytes, whose diameter, when counted in a smear, is less than 6.5 microns; Schizocytes - erythrocytes with a diameter of less than 3 microns, as well as fragments of erythrocytes; Macrocytes - large erythrocytes with a diameter of more than 8 microns, with preserved enlightenment in the center; Megalocytes - giant erythrocytes with a diameter of more than 12 microns without enlightenment in the center. Poikilocytosis - an increase in the number of red blood cells of various shapes in a blood smear. They have a differential diagnostic value: Spherocytes, ovalocytes, stomatocytes, sickle-shaped cells They are determined in a wide range of pathologies: Target-shaped erythrocytes, acanthocytes, dacryocytes, schizocytes, echinocytes Normal hemogram parameters Hemoglobin index g/l Men 130-160 Women 120-140 Erythrocytes mln/mkl 4.0 - 5.1 3.7 - 4.7 40 - 48 36 - 42 0.86 - 1.05 0.86 - 1.05 MCV, fl 80 - 95 80 - 95 MCH, pg 25 - 33 25 - 33 MCHC, g / l 30 - 38 30 - 38 11.5 - 14.5 11.5 - 14.5 2 - 15 2 - 15 Hematocrit % Color index, units. RDW, % Reticulocytes, */oo CALCULATION OF ERYTHROCYTE INDEXES Ht (l/l; %) = RBC x MCV 12 MCV (fl) = Ht (l/l) x 1000/RBC x 10 12 MCH ((pg) = Hb ( g/l) / RBC x 10 MCHC (g/l) = Hb (g/l) / Ht (l/l) RDW (%) = SD / MCV x 100 Where SD is the standard deviation of the CPU = 3xHb/RBC* * 3 leading digits of RBC score Possible causes of falsely low results Ht Microcytosis, in vitro hemolysis; autoagglutinins RBC Cold agglutinins; thrombosis; MCV hemolysis in vitro; erythrocyte fragmentation MCH MCHC WBC > 50 thousand/mL WBC WBC > 70 thousand/mL Plt Presence of platelet agglutinins , heparin use Possible causes of falsely high results Ht Cryoproteins, giant platelets, WBC > 50 thousand/ml; hyperglycemia RBC WBC > 50 thousand/ml hyperlipidemia MCV WBC > 50 thousand/ml, autoagglutinins, reticulocytosis, diabetic ketoacidosis; hyperlipidemia, methanol poisoning MCH WBC > 50 thousand/ml, cold agglutinins, hemolysis in vivo, monoclonal proteins in the blood, lipidemia, hyperglycemia; high concentration heparin MCHC cold agglutinins; hemolysis in vivo; autoagglutinins; high lipidemia; high heparin concentration, incorrect calibration of the WBC device Presence of cryoglobulins, platelet aggregation, presence of nucleated red cells Plt Presence of microcytic forms of erythrocytes Assessment of the severity of anemia Mild Hb 110 - 90 g/l Moderate Hb 90 - 70 g/l Severe anemia Hb< 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% RBC membranopathies; erythrocyte fermentopathy; Hemoglobinopathies; Intermediate form of thalassemia; TMAGA; AIHA Decreased reticulocyte count Hypo/regenerator anemia Rt< 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 Iron-deficiency anemia(IDA) A polyetiological disease that develops as a result of a decrease in the total amount of iron in the body and is characterized by progressive microcytosis and hypochromia of erythrocytes. Morphological characteristics of erythrocytes in IDA Microcytic MCV< 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 common causes IDA Alimentary iron deficiency (diet, vegetarianism, malnutrition); Increased need for iron (frequent births, multiple pregnancies; lactation; rapid growth; intensive classes sports; prematurity); Blood loss (nosebleeds, diaphragmatic hernia; diverticulum, polyp or tumor of the gastrointestinal tract; metrorrhagia; Goodpasture's syndrome); Decreased absorption (malabsorption; inflammatory processes in the intestine; achlorhydria; gastrectomy) Indicators of iron metabolism in IDA Serum iron SF 12.5-30 ng/ml; ↓↓ Total serum iron-binding capacity TIBC 45-62.2 µmol/l > 60 µmol/l 30-300 ng/ml ↓↓↓ ↓↓ Serum ferritin Saturation of transferrin with iron Soluble transferrin receptors NVT rTGF 25-45% Treatment principles for IDA Elimination of the cause 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; The first 3 days - 50% of the dose; Control laboratory indicators every 7-10 days (Rt) and every month (SG, FS); Reception of a maintenance dose after the normalization of indicators; The total duration of treatment is 4-6 months. Some drugs for the treatment of IDA Hemofer Ferrous sulfate dragee 105 mg Actiferrin Ferrous sulfate + serine capsules 34.5 mg MaltoferFol Iron hydroxide + folic acid tablets 100 mg Ferrous gluconate and Drinking microelements solution Iron hydroxide tablets 50 mg Totem Ferrum-Lek 100 mg Ferroplex Ferrous sulfate + ascorbin. acid Dragee 10 mg Tardiferon Sulfan of iron + ascorbic acid tablets 51 mg Overdose of iron preparations CLINIC: epigastric pain, nausea, hematemesis, diarrhea, workload, pallor, cyanosis, convulsions, coma, anuria, death is possible after 3-5 days; LABORATORY INDICATORS: metabolic acidosis, leukocytosis; AUTOPSY: kidney and liver necrosis after 2 days TREATMENT: induce vomiting, gastric lavage, give milk or sorbent to drink, hospitalization: intravenous infusion of desferal (deferoxamine). Anemia in chronic diseases Secondary conditions that develop with long-term infectious, inflammatory, systemic and oncological diseases and are accompanied by reduced production of red blood cells and impaired iron recycling. Nosological forms accompanied by the development of ACD 1. Infections (tuberculosis, bronchiectasis, endocarditis, brucellosis); 2. Malignant tumors; 3. Systemic connective tissue diseases (RA, SLE); 4. Chronic diseases of the liver, intestines; 5. Kidney diseases accompanied by CKD Pathogenesis of ACD 1) 2) 3) 4) Violation of iron metabolism; Suppression of erythropoiesis; Inadequate Epo production; Hemolytic process; Principles of correction of ACD Treatment of the underlying disease; Appointment of erythropoietin (150-500 IU / kg 2-3 times a week); RBC transfusions; Appointment of vitamins of group B; Megaloblastic anemia A group of diseases characterized by specific changes in blood cells and bone marrow as a result of a violation of DNA synthesis caused by a lack of vitamin B12 (Addison-Birmer's disease, pernicious anemia) 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 disorders, etc.) 4. Syndrome of ineffective erythropoiesis; 5. Syndrome of dyserythropoiesis; Principles of MBA treatment Complete nutrition; deworming; Vitamin B12 (cyanocobalamin) 200-400 mcg once a day IM for 4-5 weeks; Dynamics of laboratory parameters: reticulocyte crisis on the 5-8th day; Lifetime maintenance doses of vitamin B12 (200-400 micrograms per month); Er.mass according to vital indications; Folic acid: 5-10mg/day for 3-4 months. Maintenance doses. Microscopic picture of blood in sickle cell 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 organism are 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, chronic inflammatory processes in the body, chronic renal failure, collagenoses, malignant tumors, in diseases endocrine system, chronic liver disease 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 analysis blood and 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 general condition the patient can be administered subcutaneously to the patient erythropoietin in moderate dosages, with their subsequent decrease. This is done no more than three times in seven to eight days. In the treatment of anemia with erythropoietin, strict medical control of intravenous and intracranial blood pressure patient, because 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 small intestine, with various enteropathies. At its core, these are IDA, caused by a gross, severe violation of the function of iron absorption in 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. The majority of patients have special shape iron absorption disorders. 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 anemia mild degree(100–120 g/l hemoglobin, compensated), with a slight decrease in the color index and other hemoglobin saturation indices of erythrocytes; 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 medium degree 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 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 translucent through it. choroid eyes; imperative urge to urinate, the inability to hold urine when laughing, coughing, sneezing, possibly even bedwetting, which is due to weakness of the sphincters 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 characteristic of IDA appear general analysis blood: 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 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 eliminating it ( surgical treatment tumors 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. Application more high 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; - simultaneous reception 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 small intestine, resection of the stomach according to the method of Billroth II with the exclusion of the duodenum); - exacerbation peptic ulcer 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 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 especially vulnerable populations - 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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Anemia (Greek αναιμία, anemia) is a group of clinical and hematological syndromes, the common point for which is a decrease in the concentration of hemoglobin in the blood, more often with a simultaneous decrease in the number of erythrocytes (or the total volume of erythrocytes).

slide 3: anemia

Decrease in the number of erythrocytes and the level of hemoglobin per unit volume of blood due to blood loss, impaired production of erythropoiesis cells, increased destruction of erythrocytes, or a combination of both.

Slide 4: Hemogram of healthy people

parameters Men Women Leukocytes, x 10 9/l 4.0-9.0 Erythrocytes, x 10 12/l 4.0-5.1 3.7-4.7 Hemoglobin, g/l 130-160 120-140 Platelets , х 10 9/l 180.0-320.0 Hematocrit, % 42-50 36-45 Stab, х % 1-6 Segmented, х % 45-70 Eosinophils, % 0-5 Basophils, % 0-1 Lymphocytes, % 18-40 Monocytes, % 2-9 ESR, mm/h 1-10 2-15

Slide 5: Normal blood smear

Slide 6: I. Anemia associated with increased destruction or loss of red blood cells

Posthemorrhagic · Acute or chronic blood loss Hemolytic · Damage to erythrocytes due to external factors: d hypersplenism; and immune disorders; mechanical damage; t oxins and infection Damage to erythrocytes due to internal factors: erythrocyte membranopathies, erythrocyte enzyme deficiencies, hemoglobinopathies, heme defects (porphyrias)

Slide 7: II. Anemia associated with impaired division and differentiation of normoblasts (deficient)

Iron deficiency: blood loss (uterine, menstrual, gastrointestinal, etc.), nutritional deficiency, malabsorption, increased consumption (growth, pregnancy, lactation) Megaloblastic: vitamin B12 deficiency (pernicious, agastric, with helminthic invasion), folate deficiency acids (pregnancy, alcoholism, cytostatics) Sideroachrestic: vitamin B6 deficiency, lead poisoning m Hypoproliferative: kidney failure(erythropoietin deficiency), protein-energy deficiency

Slide 8: III. Aplastic anemia

Idiopathic (autoimmune) Acquired (radiation, benzene, cytostatics, insecticides) Hereditary.

Slide 9: By severity of development

Acute: proceed in the form of crises with a pronounced clinical picture: hypoxia, symptoms of dehydration, shortness of breath, nausea; require resuscitation Chronic: develop gradually, the symptoms strictly correspond to a deficiency of red blood cells and hemoglobin.

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Signs Mild disorders Moderate disorders Severe disorders Erythrocytes (x 10 12 /l) Above 3.5 3.5 - 2.5 Below 2.5 Hemoglobin (g / l) 110 - 90 90 - 60 Below 60 Hematocrit (% ) Above 30 30 - 15 Below 15 Defeat cardiovascular and nervous system No Moderate (I degree) Severe (II degree) Tolerance to physical activity(watts) High (more than 100) Reduced (100 – 75) Low (less than 50) Severe

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Anemic precoma (Hb 60-30g/l); Anemic coma (Hb< 30г/л).

slide 12: by color index

Normochromic - CP- 0.85-1.05 Hypochromic - CP-< 0,85 Гиперхромные – ЦП > 1,1

Slide 13: iron deficiency anemia

Chronic blood loss (> 5 ml / day) : menstrual, gastrointestinal tract, donation, etc. Increased consumption: active growth, pregnancy, lactation Low dietary intake: starvation Malabsorption: resection of the small intestine, malabsorption, consumption of malabsorption products - tea Violation transport: atransferrinemia, antibodies to transferrin, increased proteinuria IDA is based on uncompensated iron losses (normal or excessive) Causes of deficiency

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Slide 15: CAUSES OF IRON DEFICIENCY

Deficiency of Fe reserves Fe - deficient erythropoiesis Fe - deficient anemia rapid growth of the child and adolescents menstrual blood loss dietary deficiency donation blood loss (menstrual, uterine, gastrointestinal tract) pregnancy malabsorption syndrome hemodialysis, plasma-, cytopheresis, bloodletting (polycythemia) operations, helminthic invasion) severe malabsorption syndrome (PEN II-III, sprue, gastrectomy, UC)

Slide 16: Foods that affect iron absorption

Ascorbic acid Organic acids (citric, malic, tartaric) Animal proteins (meat and fish) The absorption of iron from bread and vegetables is enhanced by the addition of citrus fruits (it is useful to drink orange juice with meals) Sorbitol Alcohol Phytates of plant products that form insoluble complexes with Fe ( 5-10 g of phytates reduce the absorption of Fe by 2 times) Vegetable fibers, bran Tannins: strong tea should not be consumed; complexing of tannins with Fe ions reduces their absorption by 50% Fats (limit to 70-80 g/day) Oxalates and phosphates Ca salts, milk Increase absorption: Inhibit absorption:

Slide 17: The pathogenesis of IDA

Slide 18: STAGES OF DEVELOPMENT

I. Prelatent iron deficiency Absence of anemia, reduced iron stores in the body ( ferritin) II. Latent iron deficiency Preservation of the hemoglobin fund (no anemia) Appearance clinical signs sideropenic syndrome ( tissue fund)  serum iron level III. Iron-deficiency anemia

Slide 19: IDA Clinic

Anemic syndrome: weakness, lethargy, dizziness, "flies" before the eyes, ringing in the ears, pallor, increased heart rate, extrasystoles, I-th tone varies, systolic murmur. Sideropenic syndrome: damage to the gastrointestinal tract (glossitis, atrophic gastritis, angular stomatitis), damage to the skin and its derivatives, Pica chlorotica (taste perversion), muscle weakness and weakness of the sphincters, decreased immunity (increased susceptibility to viral infection)

Slide 20: 3. Hematological syndrome

Hypochromia, microcytosis, Reticulocytes (normal or elevated with blood loss) Decrease in the number of sideroblasts in the myelogram (N= 25-30%) Decrease in serum iron (N= 12.5-30.4 mmol) Decrease in transferrin (N= 19.3-45 .4 µmol) Decrease in serum ferritin (N > 20 µgl) Increase in TIBC (N= 30.6-84.6 µmol) Decrease in saturation coefficient (N= 15-55%) Decrease in urinary iron excretion after desferal Increase in erythrocyte protoporphyrin content ( N= 15-50 µg%)

Slide 21: DIAGNOSTICS OF IRON A DEFICIENCY

Indicators Norm Deficiency of Fe reserves Fe - deficient erythropoiesis Fe - deficient anemia Fe reserves -ki transferrin (µmol/l) 15-25 45-50 +/-  60  10  60  10  60 % saturation of transferrin Fe 30-50  20  15  10 5 DIAGNOSTICS OF IRON DEFICIENCY A

Slide 22: Blood smear for IDA

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IDA: bone marrow punctate AG: polychromatophilic and oxyphilic normoblasts with uneven contours and poor vacuolated cytoplasm.

Slide 25: Treatment of IDA

Iron preparations (per os): For moderate and severe daily dose in adults 150-200 mg, in children 3 mg/kg of body weight With mild anemia, a daily dose of 60 mg After the elimination of anemia, a dose of 40-60 mg / day for at least 4 months. For the treatment of iron deficiency erythropoiesis and iron deficiency 40 mg / day. In order to prevent iron deficiency 10-20 mg / day. Diet

Slide 26: Iron absorption efficiency

Temp of hemoglobin growth. Treatment is effective about, if for 3 weeks. continuous use of the drug, the hemoglobin level will increase by 20 g / l or more (the average daily increase in hemoglobin is about 1.0 g / l). (Most significant performance criteria)

Slide 27: Reasons for ineffective treatment

ongoing bleeding concomitant infections malignant oncological diseases poor tolerance of the iron preparation from the gastrointestinal tract. Treatment is ineffective in 10-20% of patients

Slide 28: Indications for prescribing parenteral iron preparations

Severe iron deficiency anemia + No treatment effect with repeated modification of oral iron supplementation. Therapy per os is not able to compensate for the loss of iron with permanent blood loss, the magnitude of which cannot be reduced. Iron absorption disorder (malabsorption).

Slide 29: General

1. Developed iron deficiency is not eliminated by improving nutrition. 2. For the treatment of iron deficiency, it is not recommended to use blood transfusions. 3. Diagnosis of iron deficiency is based on special studies (iron, transferrin, ferritin and serum transferrin receptors). 4. Oral iron preparations are the basis for the treatment and prevention of iron deficiency. 5. Parenteral iron preparations have no advantages over oral ones, they are used for special indications and carefully. 6. The effectiveness of the treatment of iron deficiency anemia is evidenced by the rate of increase in hemoglobin, and the restoration of iron stores is indicated by the normalization of ferritin or serum transferrin receptors.

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IDA, atrophic glossitis - due to the flattening and disappearance of the papillae, smooth areas appear on the tongue.

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ZHDA: zaedy. Cracks and ulcerations formed in the corners of the mouth.

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Slide 33: Megaloblastic anemia

Anemia associated with a violation of the synthesis of DNA and RNA, hereditary or acquired, due to a deficiency of vit. B12, folic acid, a violation of the activity of some enzymes involved in the formation of the coenzyme form of folic acid or in the utilization of arotic acid.

Slide 34: Megaloblastic anemia - anemia associated with an absolute or relative deficiency of vit. B 12 and folic acid requirements: B 12 ~ 2 mcg / day folic acid ~ 200 mcg / day Epidemiology: ~ 0.5-1% M: F = 1: 1

Slide 35: Causes of megaloblastic anemia (1)

Vitamin B12 A deficiency. Insufficient supply with food (DIET, VEGETERIANS, ALCOHOLISM) B. Malabsorption: 1/deficiency of intrinsic factor; 2/anomalies of the terminal ileum 3/competitive uptake of vit. B12 4/ reception medicines(colchicine, neomycin) B. Transport disorder (DEFICIENCY OF TRANSCOBALAMIN II, AT TO TRANSCOBALAMIN)