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بسم الله الرحمن الرحیم

بسم الله الرحمن الرحیم. А nemia – pathologic state , accompanied by decrease in the level of hemoglobin and the quantity of erythrocytes per unit of volume of the blood.

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بسم الله الرحمن الرحیم

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  1. بسم الله الرحمن الرحیم

  2. Аnemia– pathologic state,accompanied by decrease in the level ofhemoglobin and the quantity of erythrocytes per unit of volume of the blood.

  3. Erythrocytes - less informative index of anemia than the level of hemoglobin therefore, in the general practice the basic criterion of severity is precisely Hb: Light degree of anemia - Hb 110-90 g / l, The average degree of severity - Hb 90-70 g / l, Severe anemia - Hb below 70 g / liter

  4. Laboratory Definition of Anemia • Hgb: • Women: <12.0 • Men: < 13.5 • Hct: • Women: < 36 • Men: <41

  5. RBC Life Cycle • In the bone marrow, erythropoietin enhances the growth of differentiation of burst forming units-erythroid (BFU-E) and colony forming units-erythroid (CFU-E) into reticulocytes. • Reticulocyte spends three days maturing in the marrow, and then one day maturing in the peripheral blood. • A mature Red Blood Cell circulates in the peripheral blood for 100 to 120 days. • Under steady state conditions, the rate of RBC production equals the rate of RBC loss. • Erythropoetin role

  6. Classification of Anemia • I. Anemias resulting from acute blood loss • II. Anemias resulting from a deficit of erythropoesis 1) At the expense of maturation (mainly microcyte): • violation of absorption and utilization of iron (iron) • violation of transportation of iron (atransferrinemia) • violation of recycling iron (thalassemia, sideroblastic anemia ) • violation of reutilization of iron (anemia of chronic disease);

  7. Anemia (continued) 2) At the expense of differentiation (essentially normal): • aplastic anemia (congenital and acquired) 3) At the expense of proliferation (mainly macrocytes) • B12-DEFICIENCY anemia • Folic-DEFICIENCY anemia.

  8. Anemia (continued) • Anemias resulting from increased destruction of erythroid series cells - haemolytic: • 1) caused by internal defects of erythrocytes membranopathy, enzimopathy, haemoglobinopathies; • 2) the external (extracllular) effects: • autoimmune, traumatic, etc. • Classification D. Nathan, F. Oski, 2003, (book «Anemias in children», NA Finogenova et al, 2004.):

  9. The clinical value of blood

  10. Measurements of Anemia • Hemoglobin = grams of hemoglobin per 100 mL of whole blood (g/dL) • Hematocrit= percent of a sample of whole blood occupied by intact red blood cells • RBC = millions of red blood cells per microL of whole blood • MCV = Mean corpuscular volume • If > 100→ Macrocytic anemia • If 80 – 100 → Normocytic anemia • If < 80 → Microcytic anemia • RDW = Red blood cell distribution width • = (Standard deviation of red cell volume ÷ mean cell volume) × 100 • Normal value is 11-15% • If elevated, suggests large variability in sizes of RBCs

  11. Anemia due to Decreased Response to Erythropoietin • Iron-Deficiency • Vitamin B12 Deficiency • Folate Deficiency • Anemia of Chronic Disease

  12. Iron Deficiency • Can result from: • Pregnancy/lactation • Normal growth • Blood loss • Intravascular hemolysis • Gastric bypass • Malabsorption • Iron is absorbed in proximal small bowel; decreased abosrption in celiac disease, inflammatory bowel disease • May manifest as PICA • Tendency to eat ice, clay, starch, crunchy materials • May have pallor, koilonychia of the nails, beeturia • Peripheral smear shows microcytic, hypochromic red cells with marked anisopoikilocytosis.

  13. Iron Deficiency Anemia - koilonychia

  14. Iron in the Body

  15. Serum Transferrin(Beta-globulin). • Main function - transport of absorbed iron in the depot (liver, spleen), into the medullaryerythroid predecessors and into the reticulocytes. • Basic place of synthesis - liver. • An increase in the content of transferrin with lowering in the level of iron of serum is characteristic for the iron-deficiency state. • A decrease in the level of transferrin can be with the damage of the liver (different genesis) and with the loss of protein (for example, in nephrotic syndrome). • The level of transferrin is increased in the last term of pregnancy.

  16. Transferrin LIMITATION • The concentration of TF is subjected to the daily variations • Acute inflammation contributes to lowering the TF level CLINICAL SIGNIFICANCE • Basic clinical index for the differentiation between the iron-deficiency ([TF]↑) and hemolytic anemia ([TF]↓) • More precise index than total iron binding capacity • After the liberation of iron from the complex, TF ion of Fe3+ must be restored into Fe2+

  17. Ferritin • water-soluble complex of iron hydroxide with the protein apoferritin. • It is located in cells of the liver, spleen, bone marrow, in the reticulocytes. • Ferritin is the basic protein in human which deposits iron and concentration of ferritin in the serum reflects the reserve of iron in the organism.

  18. Iron Deficiency Anemia – Lab Findings • Serum Iron • LOW (< 50 micrograms/dL) • Total Iron Binding Capacity (TIBC) • HIGH ( > 360 micrograms/dL) • Serum Ferritin • LOW (< 20 nanograms/mL) • Can be “falsely”normal in inflammatory states

  19. Treatment of Iron Deficiency Anemia • Oral iron salts • Ferrous sulfate – 325 mg(50 mg absorption) • Side effects: constipation, black stools, positive hemmoccult test • Vitamin C can facilitate iron absorption.

  20. Treatment of Iron Deficiency Anemia • Diet: meat, liver, yeast, fish • Oral preparations: recovery rate Hb does not differ from parenteral introduction, side effects are less, excessive introduction does not lead to hemosiderosis. - Dosage : 1 hour prior to the meal in the evening time (absorption increase in the second-half of a day)

  21. Possibilities : dark colour of stool and transitory dyspeptic disorders (nausea, diarrhea or watery stool) Check analysis of the blood: in 7-10 days – reticulocyte reaction; 4 weeks - increase Hb and Ht - Iron tolerance test(2 tablet-2 h-100 micro/dl During the normalization of the indices of the blood – reduce the dose of preparation

  22. in exceptional cases in severe iron deficiency anemia intolerance of oral preparations (after repeated replacement and reduction in the dose) diseases of gastro-intestinal tract syndrome of the disrupted intestinal absorbtion after the extensive resection of the small intestine continuous blood loss Parenteral Introduction of Iron

  23. Complications of Parenteral Introduction • Local reactions (pains, phlebitis) • General reactions (anaphylaxis, fever, head and articulate pains, vomiting, rash, bronchospasm). Preparations: Venofer - for the intravenous introduction, Maltofer, Ferrum-Lek - intramuscular

  24. Overdose of Iron In the first 6-8 hours - epigastral pains, nausea, vomiting (including with the blood), diarrhea, pallor, sleepiness, acrocyanosis) For 12-24 hours - metabolic acidosis, leukocytosis, there can be spasms, coma, after 2-4 days - necroses of the liver and kidneys. Treatment: emetic means, stomach lavage, the method of milk with the egg white, Deferoksamin, Desferal, symptomatic therapy.

  25. Iron Overload Syndrome • Human does not have special mechanism of the excretion of iron! Its excessive introduction leads to hemosiderosis. Clinical manifestations: Gradual increase of the dimensions of the liver, spleen, cardiopathy, suprarenal insufficiency, diabetes mellitus Laboratory signs: • Increase in serum iron (more than 30 mmol/liter), percentage of saturation transferrin by iron it is more than 50%, ferritin of serum it is more than 1000 ng/ml

  26. Megaloblastic Anemia • A subclass of macrocytic anemia (under morphologic classification) Or • A subclass of anemias due to defective DNA synthesis (pathogenetic classification)

  27. Vit.B12 • Average diet contains 5 – 30g Vit. B12 daily • The amount of Vit. B12 in the body is about 2 – 5 mg. • Most of it is in the liver. • The store is sufficient for 3-6 years in case of impaired absorbtion. • The storage form is mainly adenosylcobalamin.

  28. B12 in diet R-Binder Parietal cell IF R - B12 stomach Duodenum and jejunum Pancreas enzymes R- B12 Enterohepatic circulation B12 B12 IF B12 TC II B12 Ileum cells IF - B12 İleum

  29. Functions of Vit.B12 2- Methyl FH4FH4 HomocysteinMethioninSAM B12 Methionin synthase

  30. Vit.B12 • Food sources rich in Vit.B12 • Liver • Kidney • Muscle • Egg • Milk ,Cheese and other diary products • Seafood

  31. Folic acid Daily requirements Age • 0 - 10 3.6g /kg • > 10 3g /kg • Pregnants 500 g • Lactation +100 g • Diet contains 100 - 500 g folate/day.

  32. Folate absorbtion • Mainly jejunum. • In the form of monoglutamate . • Methyltetrahydrofolate monoglutamate is the form it is found in serum .

  33. Folate levels: Normal ranges • Serum: 6 – 21 g/L (RBC volume) • Red cell: 160 – 640 g/L (RBC volume) Folate deficiency • Serum folate : <4g /L • Red cell folate: <140g /L

  34. Folate stores • Total body folate: 5 – 20 mg • Storage place : Liver • Storage form: Methyl-FH4 polyglutamate

  35. Thymidylate synthase Deoxyuridilate DNA-thymine Thymidilate Methylene THFA Dihydrofolate THFA Dihydrofolate reductase serine Methyonine glycine B12 Homocystein Methyl THFA

  36. Tissues or organs other than bone marrow are also affected • Skin,GIS, female genital system mucosal epithelium • Congenital abn.(neural tube defects) • Neurologic changes(Vit.B12 deficiency) • Peripheral neuropathy • Subacute combined degeneration of spinal cord • Cerebral -Mental changes • Hyperhomocysteinemia

  37. Clinical findings(1) • Anemia: Symptoms of anemia + palor+slight icterus • Glossitis : Sore tongue, poor taste sensation, pain Papill. atrophy-beefy tongue

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