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Donetsk National Medical University Department of Hospital Therapy Anemia

Donetsk National Medical University Department of Hospital Therapy Anemia. Kalinkina N.V. Anemia - decrease in level of hemoglobin and red blood cell (RBC) mass.

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Donetsk National Medical University Department of Hospital Therapy Anemia

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  1. Donetsk National Medical UniversityDepartment of Hospital TherapyAnemia Kalinkina N.V.

  2. Anemia- decrease in level of hemoglobin and red blood cell (RBC) mass. • Anemic syndrome - is combination of laboratory signs of an anemia and its clinical manifestations caused by a hypoxia and a hypoxemia

  3. Anemic syndrome Complaints • General: weaknesses, fatigue, dizziness, syncopal and orthostatic condition, decrease of memory. • From the cardiovascular system: a dyspnoe, palpitation; in case of presence coronary artery disease - worsening of its symtoms.

  4. Anemic syndrome Physical examination • at external medical examination - pallor; • from the cardiovascular system: a tachycardia, systolic murmur above an apex cordis

  5. Laboratory methods The World Health Organization's criterion for anemia in adults is Hb values less than 12.5 g/dL. Usually, US values are slightly higher. Anemia is suggested in males with Hb levels less than 13.5 g/dL and in females with Hb levels less than 12.5 g/dL.

  6. Classification of anemia І. Pathogenetic: 1. As a result of loss of erythrocytes during the bleeding (acute and chronic posthemorrhagic anemia); 2. As a result of increase destruction of erythrocytes (hemolytic anemia); 3. As a result of the broken synthesis of hemoglobin (iron-deficiency) and maturing of erythrocytes (megaloblastic and aplastic anemia).

  7. Classification of anemia II. By a degree of severity: 1. Easy - decrease Hb on 5-19,9 % from initial 2. Average - on 20 -39,9 % 3. Heavy - more than on 40 % The decrease Hb up to 5 % is considered as norm

  8. III. On ability to regeneration:1.Normoregenerative - reticulocytes 0,2-1,2 %2.Hyporegenerative - reticulocytes < 0,2 %3.Hyperregenerative - reticulocytes > 0,2 %

  9. IV. Under the contents of a hemoglobin in erythrocytes:1. Hypochromic (mean corpuscular hemoglobin concentration (MCHC) < 32 g/dL) - at iron-deficiency

  10. 2.Hyperchromic (MCHC > 36 g/dL) - В12-deficiency anemia

  11. 3. Normochromic (MCHC 32-36 g/dL) - majority of other anemia

  12. V. On a diameter of erythrocytes:1. Normocytic (mean corpuscular volume (MCV) -84-96 fL)

  13. 2. Microcytic (MCV < 84 fL) - iron-deficiency, hemolytic anaemia

  14. 3. Macrocytic ( MCV > 96 fL) - В12-deficiency

  15. Sideropenic syndromes • From the skin covers, appendages of a skin and mucous membranes: • dryness of a skin, • fragility of a hair fragility and banding nails, they become flat, sometimes accept the concave form (koilonychias);

  16. Sideropenic syndromes 2. From the gastrointestinal tract: • decrease and distortion of appetite, • dysphagy, • constipations or diarrhea, • glossitis, burning of tongue, • esophagitis;

  17. Sideropenic syndromes • unusual predilections for some smells - acetone, petrol; • angular stomatitis; • the distortion of taste as desire is a chalk, tooth paste, ashes, paint; • abnormality of a swallowing with sensation of an alien body in a throat.

  18. Causes of development of iron-deficiency states: • Blood loss • Vegetarians • Prolonged achlorhydria • Extensive surgical removal of the proximal small bowel or chronic diseases, such as pancreatitis, enteritis. • Increased iron requirement: From birth to age 2 and during adolescence During pregnancyand lactation

  19. Lab StudiesI. In chronic iron deficiency anemia, the cellular indices shows a microcytic and hypochromic erythropoiesis

  20. Lab Studies • Decrease of iron concentration. Normal serum iron is 13 to 27 μmol/L for men and 11 to 25 μmol/L for women. • Increase of iron-binding capacity. Total iron-binding capacity is 45 to 81 μmol/L. • Decrease of serum ferritin. The range of normal in most laboratories is 30 to 300 ng/m.

  21. Lab Studies Decrease of sideroblasts in the bone marrow aspirate. Normally, ther are 20 to 40% sideroblasts.

  22. Medical care 1. Diet • Iron uptake is in the proximal small bowel. • Dietary iron contains both heme and nonheme iron. • Meat provides a source of heme iron. • Purified heme is absorbed poorly.

  23. Medical care 2. Medicines Ferrous sulfate 100-300 mg daily. Parenteral iron: - unable to absorb oral iron, - increasing anaemia despite adequate doses of oral iron.

  24. Megaloblastic anemia • The molecular basis for megaloblastosis is a failure in the synthesis and assembly of DNA. • The most common causes of megaloblastosis are cobalamin and folate deficiencies. • Prevalence of megaloblastosis is enlarged with the years and makes up at young persons about 0,1 %, at elderly up to 1 %. Women are sick more often.

  25. Pathophysiology • Dietary intake (meat, liver, kidneys, eggs, milk, cheese, beans) is the source of cobalamin and folate because humans cannot synthesize these substances. • Cobalamin must be bound to intrinsic factor, and this complex is taken up in the terminal ileum.

  26. Pathophysiology • Cobalamin enzymes - metabolism of nucleic acids, and at its deficiency mitotic processes in fast-growing tissues (a bone marrow, an epithelium of a GI tract) are broken, - exchange of fat acids, synthesis and neogeneses of a myelin, and at its disadvantage these processes are broken. Also a defect in adenosyl-cobalamin-dependent conversion of methylmalonyl coenzyme A to succinyl coenzyme A exists.

  27. Causes ofcobalamin deficiency • Nutritional deficiency • Food-cobalamin malabsorption (gastric anacidity) • Absence of functional intrinsic factor • Severe abnormalities in the terminal ileum due to ileal resection, regional ileitis, or lymphoma • Helminthic invasion • Blind loop syndrome • Drugs • Cytostatics • Anticonvulsants • Oral contraceptives • Nonsteroid antiinflamatory drugs • Some antidiabetic drugs • Colchicine

  28. Clinical features • Anemic syndrome • Jaundice • Gastrointestinal manifestations: anorexia; diarrhea;

  29. Clinical features sore tongue, which on inspection will be smooth and beefy red

  30. Clinical features 4.Neurologic manifestations: numbness and paresthesia in the extremities; weakness; ataxia; sphincter disturbances; diminished or increasedof reflexes; positive the Romberg and Babinski’s signs; diminish position and vibration senses; disturbances of mentation

  31. Lab Studies • macrocytosis • fully hemoglobinized erythrocytes • neutrophils show hypersegmentation of the nucleus • leukocyte and platelet count may be decreased

  32. Lab Studies Nucleated RBC

  33. Lab Studies • Decrease serum cobalamin level. The normal range is 300 to 900 pg/ml. • Bone marrow aspirate is hypercellular with a decreased myeloid/erythroid ratio. Megaloblastic RBC precursors are abnormally large and have nuclei that appear much less mature than would be expected from the development of the cytoplasm (nuclear-cytoplasmic asynchrony). The nuclear chromatin is more dispersed than expected, and it condenses in a peculiar fenestrated pattern. Abnormal mitoses may be seen.

  34. Lab Studies

  35. Lab Studies • Increase in unconjugated bilirubin and lactic acid dehydrogenase in plasma • Abdominal x-ray films, upper and lower GI series, and CT scans

  36. Medical care • Cobalamin - 1000 mcg - parenterally daily for 2 weeks, then weekly until the hematocrit value is normal, and then monthly for life.

  37. Hemolytic Anemias • group of the diseases are characterized by raised intracorpuscular (in cells of cytophagous system) or extracorpuscular (in a vascular channel) destruction (hemolysis) of erythrocytes and decrease of duration their life (less than 120 days).

  38. Classification

  39. Clinical and laboratory signs of hemolysis • an anemic syndrome with a normochromal anemia; • a reticulocytosis; • a jaundice of a skin and mucosae; • hepato- and splenomegaly; • augmentation of the urobilinogen content in urine; • augmentation of the stercobilinogen content in a feces; • level of unconjugated bilirubin elevates; • low or absent levels of serum haptoglobin; • rising of a level serum iron; • the life span of RBC may be shortened; • erythroid hyperplasia of the bone marrow.

  40. Acquired hemolytic anemia

  41. Causes of immunohemolytic anemia

  42. Clinical manifistations • anemia, • spherocytosis, • splenomegaly, • venous thrombosis, • positive direct Coombs test

  43. Treatment

  44. Immune hemolysis due to cold-reactive antibodies • Antibodies that react with polysaccharide antigens are usually IgM and bind antigen better at temperatures lower than 37C, hence the name cold-reactive anyibodies. • IgM cold-reactive antibodies readily agglutinate RBC and are called cold agglutinins. • They arise in two clinical settings: 1) monoclonal antibodies, the product of lymphocytic neoplasma; and 2) polyclonal antibodies in response to infection.

  45. Immune hemolysis due to cold-reactive antibodies • Mycoplasmapneumoniae infection • Infectious mononucleosis • Viral infections

  46. Clinical manifistations • intravascular agglutination, (acrocyanosis) • hemolysis. • mild reticulocytosis, • agglutination on the blood film, • agglutination during analysis of the blood by particle analysis.

  47. Aplastic anemia • is a bone marrow failure syndrome characterized by peripheral pancytopenia and marrow hypoplasia.

  48. Epidemiology • The incidence of acquired aplastic anemia in Europeand Israel is 2 cases per million persons annually. • In Thailand andChina, rates of 5 to 7 per million have been established. • In general,men and women are affected with equal frequency, but there is a biphasicage distribution, with the major peak in the teens and twenties and a second rise in the elderly.

  49. Classification and etiology

  50. Drugs and chemicals associaed with aplastic anemia

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