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Iron Deficiency Anemia


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Iron Deficiency Anemia

  1. 1. Iron Deficiency Anemia Imran Shahzad Anjum,MD
  2. 2. Iron in human body  Total Iron in human body averages 4 to 5 grams which is distributed as: 1. 65% in form of Hb. 2. 4% in form of mayoglobin. 3. 1% in form of heme compunds whcih promote intracelluar oxidation. 4. 0.1% is combined with protein transferrin in blood plasma. 5. 15%−30% stored for later use,mainly in reticuloendothelial system of bone marrow and liver parenchymal cells, principally in form of ferritin
  3. 3. Iron transport & metabolism Fereitin hemosiderin heme Free Fe enzymes (Tissue:liver & RNC of BM) Transferrin−Fe Macrophages Degrading hemoglobin Free Fe Hemoglobin Red cells Blood loss−0.7mg daily In menses Fe absorbed (small intestine) Only regulation mechanism Fe excreted−0.6mg daily Bilirubin excreted
  4. 4. Iron absorption
  5. 5. Regulation of cellular & systemic Iron homeostasis hepcidin:25−amino acids peptide hormone secreted by liver Increase in Fe stores, infection, inflammation or malignancy ferroportin: sole known cellular Fe export channel Fe deficiency,hypoxia, increased erythropoiesis, Ineffective erythropoiesis Iron efflux into plasma from macrophages, heptocytes & intestinal enterocytes + − − + − +
  6. 6. Body Iron supply & storage
  7. 7. Iron deficiency  Iron deficiency is a decrease in the amount of body iron resulting from a sustained increase in iron requirements over iron supply.  Iron deficiency reduces the responsiveness of erythroid progenitors to erythropoitein,apparently through an Iron−aconitase−isocitrate pathway.  with a lack of Iron, decreased utilization for RBCs production helps preserve the supply of Iron for vital functions in other tissues.
  8. 8. Epidemiology  Iron deficieny is one of most prevalent forms of malnutition and so most common anemia worldwide.  Special groups:toddlers, adolescent girls, women of child−bearing age and some minority groups.  High prevalence of iron deficiency with or without anemia has been reported among patients with restless legs syndrome(akathisia).
  9. 9. Risk factors
  10. 10. Causes of Iron deficiency  Increased Iron requirements &/or hematopoiesis 1. Growth 2. Pregnancy & lactation 3. Erythropoietin therapy  Increased Iron loss/Blood loss Gastrointestinal tract, Genitourinary tract, respiratory tract, blood donation, phlebotomy as treatment for polychythemia vera  Decreased Iron intake or absorption 1. Dietary insufficiency of bioavailable Iron 2. Impaired absorption of Iron: intestinal malabsorption, gastric surgery,Iron−refractory Iron deficiency anemia 3. Acute or chronic inflammtion
  11. 11. Presenting forms 1. no signs or symptoms coming to medical attention only because of abnormalities noted on laboratory tests 2. features of underlying disorder responsible for development of iron dediciency 3. manifestations common to all anemias 4. one or more of signs and symtoms considered highly specific for iron deficiency,namely, pagophagia(variant of pica), koilonychia and blue sclerae.
  12. 12. Clinical presentation  It depends upon severity of Iron deficiency.  It produce signs & symptoms common to all anemias which are pallor, palpitations, tinnitus, headache, irritability, weakness, dizziness, easy fatigability and other vague & nonspecific complaints.  Iron deficiency produce clinical symptoms independent of anemia e.g. glosssitis, angular stomatitis, postcricoid esophageal web or stricture, gastric atrophy.  It has nonhematologic consequences, including impaired immunity and resistance to infection, diminished exercise tolerance and work performace and a variety of behavioral and neuropsychologic abnormalities.
  13. 13. Laboratory evaluation of iron status Direect measures Indirect measures Fe deficiency Fe overload BM Aspirate& biopsy MRI Non−inv Q. Flebotomy Liver biopsy 1. Serum ferritin 2. Serum iron &TIBC 3. Transferrin saturation 4. RBC protoporphyrin 5. Serum level of TRP no single indicator or combination of indicators is Ideal for evaluation of iron status in all clinical circumstances
  14. 14. Stages of Iron deficiency  Negative iron balance/iron depletion: demands for or loss of iron exceed the body´s ability to absorb iron from diet and starts Iron store depletion.  Iron deficient erythropoiesis: after the depletion of Iron store,once transferrin saturation falls to 15−20%, Hb synthesis becomes impaired.  Frank Iron deficiency anemia: both Iron store and serum Iron depleted and Hb & hematocrit begin to fall, reflecting iron deficiency anemia,transferrin saturation at this poit is 10−15% with hypochromia/microcitosis.
  15. 15. Classification of Iron deficiency  un−complicated Iron deficiency: the characteristic patterns of indicatores of body iron status because hepcidin production is regulated only by Fe−stores in a healthy person.  complicated Iron deficiency: the characteristic pattern of indicators of body iron status is lost because hepcidin production is controled by a lot of factors and serum ferritin acute phase reactant.
  16. 16. Tests normal −ve IB IDE IDA BM store 1−3+ 0 −1+ 0 0 S. ferritin (µg/dl) 50−100 <20 <15 <15 TIBC (µg/dl) 300−360 360˃ 380˃ 400˃ SI (µg/dl) 50 −150 NL <50 <30 Sat:SIx100/TIBC 30−50% NL <20 <10 Sideroblas%(BM) 40−60 NL <10 <10 Protoporfrin(µg/dl) 30−50 NL 100˃ 200˃ RBCs Morphology NL NL NL Micocytic/h ipocromic un−complicated iron deficiency
  17. 17. Pheripheral blood smear
  18. 18. Bone marrow aspirate
  19. 19. Assessment of Iron store on bone marrow aspirate
  20. 20. un−complicated iron deficiency  Transferrin saturation% : <18%  Serrum ferritin : <15 µg/dl  Red cell protoporphyrin level : 100 µg/dl˃  Serum levels of TRP: 9 µg/dl˃  RBCs morphology: microcytic/hypochromic  Iron deficiency can give reactive thrombocitosis but leukocyte normal.
  21. 21. Complicated iron deficiency  Individualizied the patients because not have specific pattern of iron depletion due to following reasons. 1. Depending upon clinical circumstances,the effects of inflammation or erythropoiesis on hepatic hepcidin synthesis may predominate over those of iron body stores. 2. Malignancy also stimulate hepcidin production. 3. Hypoxia and increased erythropoitic demand inhibit the stimulus. 4. Liver disease and malnutrition may also impair hepcidin expression. 5. Plasma ferritin:acute phase reactant, concentration increase by fever,acute Infection, rheumatoid arthitis,liver & other tissue damge. 6. Only 2 conditions that may lower plasma ferritin concentration independtly of decrease of iron stores are hypothyrodism and ascorbate deficiency. serum TRP is less affected by inflammation, its measurement usually can determine whether iron store are absent.
  22. 22. Differential diagnosis of microcytic hypochromic anemia  decreased body Iron stores 1. Iron deficiency anemia  Normal or increased body iron stores 1. Anemia of chronic disease 2. Defective absorption,transport/use of iron 3. Disorders of globin synthesis: thalassemia, other microcytic hemoglobinopathies 4. Disorders of heme synthesis: sideroblastic anemias(hereditary & acquired) 5. Iron refractory,iron deficiency anemia 6. Atransferrinemia 7. Aceruloplasminemia 8. Divalent metal transporter hemochromatosis with impaired iron export (type 4A) 9. Heme oxygenase 1 deficiency
  23. 23. Diagnosis of microcytic anemia Tests Iron def. inflammati on thalassemia siderobla stic smear Micro/ hypo Normal,mi cro/hypo Micro/hypo with targeting variable SI <30 <50 Normal−hig Norma−h TIBC 360˃ <300 Normal normal Saturation% <10 10−20 30 −80 30 −80 Ferritin(µg/dl) <15 30−200 50 −300 50 −300 Hb pattern norma normal abnormal normal
  24. 24. Diagnosis of microcytic anemia  Diagnosis of Iron deficiency often is confirmed by outcomes of a therapeutic trail of Iron.  The unequivvocal diagnostic response consists of 1. A reticulocytosis,which begin approximately 3−5 days after adequate Iron therapy is instituted, reaches a maximum on days 8 to 10 and then declines. 2. Increase in Hb concentration which should begin shotly after reticulocyte peak, is invariably present by 3 weeks after iron therapy is begun and persists untill Hb concentation is restored to normal.  Therapeutic trail merely aids in establishing presence of Iron deficiency, search for underlying causes of iron deficiency must continue despite a positive response to therapy.  Difficulties in evaluation of microcytic hypochromic disorders usually arise when direct assessment of BM iron is unavailable and diagnosis depends on indirect indicators of Iron status.
  25. 25. Treatment of Iron deficiency anemia  Generally iron therapy can be defered untill the underlying cause of iron lack has been identified.  The goal of therapy is to supply sufficient iron to repair Hb deficit and replenish storage iron.  For patients with unusual blood loss or malabsortion, specific diagnostic tests and appropriate therapy take priority.  Types of therapies: oral,parenteral,RBC tranfusion  Types of therapies: oral,parenteral,RBC tranfusion  Adverse reaction of therapies: hemochromatosis (iron overload)
  26. 26. Choice of therapy  The severity and cause of iron deficiency anemia will determine the appropriate approach to treatment.  Oral iron is the treatment of choice for most patients because of its effectiveness, safety and economy and should always be given perference over parenteral iron for initial treatment.  Parenteral therapy with risk of adverse reactions should be reserved for exceptional patient who 1. Remains intolerant of oral iron despite repeated modifications in dosage regimen. 2. Has iron needs that cannot be met by oral therapy because of either chronic uncontrollable bleeding or other sources of blood loss such as hemodialysis or coexisting chronic inflammatory state. 3. Malabsorbs iron.  Transfusion therapy is reserved for individuals who have symptoms of anemia, cardiovascular instability, continued and excessive blood loss from whatever source and require immediate intervention.
  27. 27. Oral Iron therapy  Oral Iron preparations: ferrous sulfate, ferrous fumarate, ferrous gluconate, polysaccharide iron.  Therapy should begin with ferrous iron salt, ferrous sulfate is most widely used either as tablets containing 60−70mg of iron for adults or as liquid preparation for children.  Taken separately from meals in 3 or 4 divided doses and supplying a daily of 150 to 200 mg of elemental iron in adults or 3 mg per Kg of body weight in children.  Administration between meals maximize absorption.  For milder anemia a single dose of 60mg per day may be adequate.
  28. 28. Oral Iron therapy  Sustained treatment for a period of 6−12 months after correction of anemia will be necessary to achieve stores of at least 0.5−1.0 g of iron.  An increase in Hb concentration of at least 2 g/dl after 3 weeks of therapy generally is used as criterion for an adequate therapeutic response.  Most patients are able to tolerate oral iron without difficulty but 10%−20% may have symptoms attributable to iron,most common side effects are gastrointestinal.
  29. 29. Parenteral Iron therapy  Parenteral preparations: higher and lower molecular weight iron dextran, sodium ferric gluconate complex, iron sucrose & ferumoxytol.  Amount of iron need by an individual patient: Body weight(kg)x2.3x(15−patient´s Hb,g/dl)+500 or 1000mg(for store)  Infrequent immediate life theatening anaphylactic reactions constitute the most serious risk associated with use of either IM or IV iron preparations,may have fatal outcomes.  Delayed but severe serum sickness−like reactions may also develop with fever, urticaria, denopathy, myalgias and arthralgias.
  30. 30. Red cell transfusion  not only do transfusion correct anemia acuetly but transfused red cells provide a source of iron for reutilization,assuming they are not lost through continued bleeding.
  31. 31. Bibliography  Basic Principles & practice of Hematology 2013 by Hoffman  Harrison´s principles of internal medicine  Robbins Basic Pathology  Guyton & Hall Text of Medical Physiology