1 / 31

Iron Deficiency Anemia ( IDA )

Iron Deficiency Anemia ( IDA ). Liang Aibin, MD/PhD Dept. of Hematology TongJi Hospital of TongJi University. Ⅰ. Introduction to IDA. Iron deficiency is the state in which the content of iron in the body is less than normal.

gaetan
Download Presentation

Iron Deficiency Anemia ( IDA )

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Iron Deficiency Anemia ( IDA ) Liang Aibin, MD/PhD Dept. of Hematology TongJi Hospital of TongJi University

  2. Ⅰ. Introduction to IDA • Iron deficiency is the state in which the content of iron in the body is less than normal. • Iron Deficiency Anemia is resulting from lack of sufficient iron for synthesis of hemoglobin. • IDA is common nutritional and hematologic disorder worldwide, affecting an estimated 2 billion people. • IDA may occur as a result of many causes. • Despite improvement in diet and more effective and widespread use of well-absorbed forms of iron to fortify foods, IDA remains the most common cause of anemia of infancy & childhood.

  3. Ⅱ. Iron Metabolism A. Iron compounds in the body B. Iron kinetics C. Iron requirements

  4. Ⅱ. Iron Metabolism A. Iron compounds in the body

  5. Stores1000mg Tissue500 mg Red Cells2300 mg IRONBody Compartments - 75 kg man Absorption < 1 mg/dayExcretion < 1 mg/day 3 mg

  6. B. Iron kinetics (1) Iron sources:Dietary iron,recycled iron (2) Iron absorption,transport,use or storage and excretion

  7. Iron Absorption from duodenum • Iron absorption is increased in the presence of iron deficiency, and it decreases when there is iron overload. • At least nine proteins appear to be involved in this mechanism.

  8. INTRACELLULAR IRON TRANSPORT Fe+3 Transferrin Transferrin receptor H+ H+ Lysosome Fe+3 H+ H+

  9. CIRCULATING RBCs MONONUCLEARPHAGOCYTES Fe Fe Fe Fe Fe Fe Ferritin Fe Transferrin Receptor Fe Fe Fe Ferritin Fe Ferritin Fe slow Hemosiderin Fe Fe RBC PRECURSOR Fe Fe TRANSFERRIN

  10. C.Iron Requirements

  11. Ⅲ. Etiology & Pathogenesis 1. Causes of Iron Deficiency (1) Insufficient storage iron in fetus (2) Insufficient intake of iron (3) Rapid growth (4) Faulty or incomplete iron absorption (5) Excessive loss of iron

  12. 2. Pathogenesis Iron↓+Protoporphyrins↑→Heme↓+Globin→ HGB ↓ *Stages in development of iron deficiency ID.IDE:latent iron deficiency IDA:anemic stage

  13. Stages in Development of Iron Deficiency Ⅰ(ID) Loss of storage iron Ⅱ(IDE) Loss of circulating iron Ⅲ(IDA) Decreased HGB production SF(Serum Ferritin)↓ Bone marrow stainable iron: hemosiderin sideroblast ↓ FEP↑SI↓TIBC↑TS↓ HGB↓MCV↓ MCH↓MCHC↓ ID:Iron depletion IDE:Iron deficient erythropoiesis IDA:Iron deficiency anemia

  14. Ⅳ. Clinical Manifestation 1. Peak age: 6 mo~2 yr 2. Pallor,fatigue,weakness, etc 3. Extra-medullary hematopoiesis: hepatosplenomegaly

  15. 4. Nonhematologic manifestations (1) Cardiorespiratory system: tachypnea, tachycardia,CHF (2) Gastrointestinal effects:anorexia,pica,etc (3) Nervous system: irritability, spiritlessness, etc (4) Impaired WBC function and immunity: infection (5) Others: koilonychia,etc

  16. Ⅴ. Laboratory Findings 1. Blood Smear: Hb↓↓、RBC↓、 MCV↓、MCH↓、MCHC↓ → hypochromic, microcytic anemia Ret:N .↓ anisocytosis 2. Bone Marrow: hypercellular with erythro- hyperplasia. Cytoplasmic maturation lags behind nuclear maturation.

  17. 3. Tests Regarding Iron Metabolism (1) SF(Serum ferritin)↓ (2) FEP(free erythrocyte protoporphyrin) ↑ (3) SI(Serum iron) ↓,TIBC(total iron binding capacity)↑ (4) Bone marrow stainable iron: hemosiderin ↓, sideroblast <15%

  18. Ⅵ. Diagnosis & Differential Diagnosis 1. Diagnostic Criteria for IDA (1) Hypochromic, microcytic anemia: Hb↓, MCV<80 fl , MCH <26 pg , MCHC <0.31 (2) Definite cause(s) and / or manifestation(s) (3) SI<10.7 μmol/L (4) TIBC>62.7 μmol/L,TS<10-15% (5) BM stainable iron: hemosiderin↓or absent , sideroblast <15%

  19. (6) FEP>0.9 μmol/L (7) SF<16 μg / L (8) response to iron therapy 2. Differential Diagnosis IDA must be differentiated from several other hypochromic,microcytic anemias

  20. Ⅶ.Treatment 1. Correct the basic problem (eg. dietary, bleeding sources and similar problems) 2. Oral Iron

  21. (1) The recommended oral dose of elemental iron is 1.5~2 mg/kg 3 times between meals (4.5-6 mg/kg/d) (2) Various iron complex and concentrates are available e.g. Ferrous sulfate:20~30 mg/ kg/d (3) A Ret rise in 3~5 days and Hb increase in 1~2 wk after the initiation of iron therapy. After Hb becomes normal,treat for 2~3 more mo to replenish iron stores

  22. 3. Intramuscular Iron 4. Ascorbic Acid 5. Blood Transfusion Packed red blood cell transfusion for children with extremely low levels of Hb: 5-10 ml/kg /dose 6. Diet:improvement in the diet with reduction of milk intake, use of iron-fortified formulas, and an increase in iron-containing food such as meat, eggs, fortified infant cereals, and green vegetables

  23. * Failure to Correct Presumed IDA

  24. Responses to Iron Therapy in Iron Deficiency Anemia

  25. Ⅷ. Prevention IDA can be prevented by using iron-fortified infant formulas or supplemental iron-fortified solid foods *Recommended iron intake Full-term infants:1 mg/kg/d(0.5-3 yr) Preterm infants: 2 mg/kg/d (starting no later than 2 mo)

More Related