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Iron deficiency anemia (IDA)

Iron deficiency anemia (IDA) 

▪ Iron deficiency is the commonest cause of anemia in every country of the world. 

▪ Also, it is the most important cause of microcytic hypochromic anemia. 

▪ IDA is characterized by a reduction in all three red cell indices. (MCV, MCH, MCHC) and peripheral blood film shows microcytic hypochromic red cells due to a defect in Hb synthesis. 

The metabolic aspect of iron 

▪Iron is the commonest element in the earth's crust. 

▪Yet IDA is the commonest cause of anemia, this is because the body has the limited ability to absorb iron, and excess loss of iron due to hemorrhage is frequent. 

Body iron distribution; iron compartment: 

▪1- Hemoglobin:

It contains four heme group linked to four globin chains and can bind four molecules of oxygen. It contains two-third of body iron; iron is incorporated from plasma transferrin into developing erythroblasts and reticulocytes in the BM. 

▪Transferrin obtains iron mainly from MQ, 

▪A small proportion of iron comes from dietary iron absorbed through the duodenum and jejunum. 

▪At the end of their life RBCs are broken down in the MQ of the RE system and their iron is released into the plasma, some of the iron is stored in the RE cells as hemosiderin and ferritin. 

2-storage iron: 

Ferritin is a water-soluble protein –iron complex, up to 20% of its weight is iron, it is not visible by light microscope. 

Hemosiderin is water is insoluble protein iron complex up to 37% of its weight is iron, visible in MQ by light microscope after staining with Perl’s reaction. 

Iron in ferritin and hemosiderin is in the ferric form Fe+3 before utilization it should be reduced to ferrous Fe+2 form. 

3- Iron also present in muscles as myoglobin. 

4-other tissue iron:

In most cells in iron-containing enzymes like cytochromes, enzymes of Krebs cycle, and enzymes required for the synthesis of DNA. 

5-labile iron pool:

Iron in the extravascular component of the intercellular fluid such as lymph or iron that rapidly exchanges between plasma and cystol. 

Amount of iron in the average adult 

▪Normally the concentration of iron in a human adult is 50mg/kg in males and 40mg/kg in females distributed as: 

1-Hb 66%. (2.000mg) 

2-Ferritin and hemosiderin 28%. (1.000mg) 

3-Myoglobin 3.5%(130mg) 

4-Haem enzymes (cytochromes), labile pool and other tissue iron 2.4%(88mg) 

5-Transferrin-bound iron 0.1%(3mg) 

Dietary iron and iron absorption 

▪Food is rich in iron; meat, liver. 

vegetables, eggs; legumes, cereals, flour, and dairy food also contain iron 

▪The average diet contains 10-15mg of iron of which 5-10% only absorbed, it can increase to 20-30% in IDA and pregnancy. 

▪Iron absorption mainly in the duodenum and jejunum. excess iron is combined with apoferritin to form ferritin. 

Factors favoring iron absorption 

1-ferrous form 

2-inorganic iron 

3-acid; Hcl and Vit.C 

4-solubilizing agents; sugars and amino acids 

5-iron deficiency 

6-increased erythropoiesis 


8-primary hemochromatosis. 

Factors reducing absorption 

1-ferric form. 

2-organic form. 

3-alkalis; antacids, and pancreatic secretions. 

4-precipitating agents; phytates and phosphate 

5-Iron excess 

6-Decreased erythropoiesis 

7- infections 


9- desferrioxamine. 

Utilization and catabolism of iron 

▪Normal erythrocytes remain in the circulation for about 4 months, then it destroyed and removed by phagocytic MQ of the reticuloendothelial system, 

▪Hb is digested and the amino acid reutilized 

▪the heme is degraded to bilirubin and excreted by the liver. 

▪the iron is recycled, firstly retained in the RES as storage iron, so about 20mg of the needed iron comes from hemoglobin catabolism, the rest comes from iron absorption and iron stores. 

Excretion of iron 

▪Very little iron is excreted by normal persons, 

▪healthy adult male excretes about 1mg each day mostly as Hb, storage iron in desquamated intestinal epithelial cells, and erythrocyte in feces, 

▪the negligible amount is excreted in sweat and urine and desquamated skin and nails. 

Iron transport 

▪Iron is transported in plasma bound to B-globulin, transferrin, which is synthesized in the liver, has a half-life of 8-10 days, it binds two atoms of iron per molecule, normally it is one-third saturated. 

▪cell membranes especially erythrocyte precursors contain transferrin receptors that bind Fe 3+ -transferrin. 

▪Transferrin gains iron from the MQ of the RE system. 

▪The transport iron compartment is estimated by measurement of the serum iron concentration. 

▪The transferrin concentration in plasma is estimated by measurement of the total iron-binding capacity (TIBC). 

Iron requirements 

▪The amount of iron required each day to compensate for losses from the body and growth varies with age and sex, highest during pregnancy, lactation, menstruation, and adolescence, so these groups are particularly likely to develop iron deficiency. 

▪For Example, the iron requirement in an adult male is 0.5-1 mg/day while in pregnant lady it is 1.5-3 mg/day. 

Iron deficiency anemia (IDA) 

▪When IDA is developing the RE stores (ferritin and hemosiderin) become completely depleted before anemia occurs. 

▪In early-stage Patients usually have no symptoms. 

▪Symptoms are those of low Hb like palpitations, dyspnea, headache, and dizziness. 

▪Pt can show painless glossitis, angular stomatitis, brittle spoon nails (Koilonychia), dysphagia due to pharyngeal web, and pica. 

▪all these epithelial cell changes are due to a reduction in iron-containing enzymes. 

Prevalence of iron deficiency 

▪Third of the world population is believed to be iron deficient. 

▪IDA mostly occurs in children, poor socioeconomic class, and women of all ages. 

Adverse effects of iron deficiency 

▪Iron is important in the function of many cells in addition to oxygen transport, so if the iron is deficient it will result in: 

1-immunologic and cellular mechanisms against infection are impaired, also phagocytosis and killing of bacteria. 

2-brain and motor function; there is impaired exercise tolerance. In neonates, it is associated with disturbances in motor function and attention. 

3-epithelial changes; the buccal and oral epithelium exhibits thinning and dyskeratotic changes, these epithelial changes may cause fissuring at the corners of the mouth and glossitis and web formation at the cricoid level of the hypopharynx. 

4-koilonychia; (spoon nail); it also reflexes the reduction of tissue iron. 

Causes of IDA 

1-chronic blood loss; usually uterine or GI bleeding and rarely urinary bleeding. 

2-increased demands; pregnancy, growth, and childbearing. 

3- Malabsorption; gastrectomy or celiac disease. 

4- Poor diet. 

What further details are important in clinical history? 

▪Dietary intake of iron 

▪Symptoms of malabsorption/weight loss 

▪Overt GI blood loss 



▪Oral iron therapy 

▪Bleeding history/ family history of bleeding disorder 

Laboratory findings 

▪CBC; red cell indices and PBF; shows hypochromic, microcytic cells with target cells, pencil-shaped cells. 

▪Platelets are often moderately raised. 

▪BMA is not essential to assess IDA except in complicated cases, increased erythropoiesis and the erythroblasts are small and have ragged cytoplasm. 

▪Prussian, blue-stained specimen of bone marrow confirms iron depletion. 

▪Serum iron and total iron-binding capacity (TIBC); the serum iron is low, and TIBC is high. 

▪Serum ferritin; very low. 

▪Investigation for the causes of IDA; clinical history, physical and rectal examination, upper GIT endoscopy, sigmoidoscopy, searching for hookworm ova, urine for hematuria. 


▪ Correct the underlying cause. 

▪Iron is given to correct the anemia and replenish iron stores. 

▪Prophylactic iron therapy; in cases of pregnancy, hemodialysis, and premature babies. 

▪Parenteral iron only if oral iron is ineffective as severe malabsorption and late pregnancy. 

Causes of failure to respond to oral iron 

▪Continuing hemorrhage. 

▪Failure to take tablets 

▪Wrong diagnosis 

▪Mixed deficiency 

▪Another cause of anemia; malignancy or inflammation. 


▪Use of slow-release preparation.