Iron deficiency anemia is caused by iron loss exceeding iron absorption. It results in three stages: reduced iron stores, depleted iron stores impacting erythropoiesis, and manifest anemia with low hemoglobin. People at high risk include pregnant/menstruating women, children, and the elderly. Symptoms include fatigue, pale skin, and spoon nails. Diagnosis involves low serum ferritin and transferrin saturation below 10%, along with microcytic hypochromic anemia. Treatment aims to replace iron stores through oral or intravenous iron supplements.
Iron deficiency anemia is caused by iron loss exceeding iron absorption. It results in three stages: reduced iron stores, depleted iron stores impacting erythropoiesis, and manifest anemia with low hemoglobin. People at high risk include pregnant/menstruating women, children, and the elderly. Symptoms include fatigue, pale skin, and spoon nails. Diagnosis involves low serum ferritin and transferrin saturation below 10%, along with microcytic hypochromic anemia. Treatment aims to replace iron stores through oral or intravenous iron supplements.
Iron deficiency anemia is caused by iron loss exceeding iron absorption. It results in three stages: reduced iron stores, depleted iron stores impacting erythropoiesis, and manifest anemia with low hemoglobin. People at high risk include pregnant/menstruating women, children, and the elderly. Symptoms include fatigue, pale skin, and spoon nails. Diagnosis involves low serum ferritin and transferrin saturation below 10%, along with microcytic hypochromic anemia. Treatment aims to replace iron stores through oral or intravenous iron supplements.
Iron deficiency anemia is caused by iron loss exceeding iron absorption. It results in three stages: reduced iron stores, depleted iron stores impacting erythropoiesis, and manifest anemia with low hemoglobin. People at high risk include pregnant/menstruating women, children, and the elderly. Symptoms include fatigue, pale skin, and spoon nails. Diagnosis involves low serum ferritin and transferrin saturation below 10%, along with microcytic hypochromic anemia. Treatment aims to replace iron stores through oral or intravenous iron supplements.
Download as PPTX, PDF, TXT or read online from Scribd
Download as pptx, pdf, or txt
You are on page 1of 17
IRON DEFICIENCY ANAEMIA
DR MRS STELLA KANU
BMLS MBBS MSc OUTLINE INTRODUCTION/DEFINITION IRON DISTRIBUTION & TRANSPORT DIETARY IRON IRON ABSORPTION PATHOPHYSIOLOGY CAUSES OF IRON DEFICIENCY CLINICAL SIGNS AND DIAGNOSIS TREATMENT DEFINITION “Anaemia is decreased haemoglobin concentration, PCV or red cell mass, for age, sex and environment resulting in defective tissue oxygenation” Most commonly encountered problem in haematology More common in women, children & elderly Not a disease but an expression of underlying disease conditions Normal adult red cell value Iron deficiency is the end result of iron loss in excess of iron absorption. • There are three stages of iron deficiency: • The iron stores are reduced but are still sufficient for erythropoiesis. • The iron stores are depleted; then erythropoiesis is reduced. • Manifest iron deficiency anemia has developed (erythropoiesis reduced; hemoglobin has reduced to less than normal). On a worldwide basis, iron deficiency is among the most frequent causes of anemia. Persons with an increased iron demand, such as pregnant or menstruating women, or children in the stages of growth and development, are the first to develop an iron deficiency anemia. It is the most important cause of a microcytic hypochromic anaemia, in which the two red cell indices MCV (mean corpuscular volume) and MCH (mean corpuscular haemoglobin) are reduced and the blood film shows small (microcytic) and pale (hypochromic) red cells. . Children fed with cow’s milk often develop an iron deficiency because of the low iron content of this milk. In adults, iron deficiency is most often due to blood loss from the gastrointestinal or urogenital tract IRON DISTRIBUTION AND TRANSPORT Only a small amount of iron is gotten from dietary iron absorbed through the duodenum and jejunum. The transport and storage of iron is mediated by 3 proteins . Transferrin The transferrin Receptor-1 Ferritin. Transferrin delivers iron to tissues that have transferrin Receptors especially erythroblasts in the bone marrow which incorporate the iron into hemoglobin. At the end of th life span of red blood cells, they are broken down in the macrophages ,the iron is released from the hemoglobin ,enters plasma ad provides most of the iron on transferrin . IRON DISTRIBUTION Some iron is stored in the macrophages as ferritin and hemosiderin. Ferritin is a water soluble protein-iron complex which hemosiderin is an insoluble protein iron complex. Ferritin contains up to 20% of its weight as iron while hemosiderin contains 37% iron by weight . Ferritin is not visible by light microscopy while hemosiderin is visible in macrophages and other cells by light microscopy after straining my Perl's`(Prussian blue) reaction. Iron in ferritin and hemosiderin is in the ferric form, vitamin c being involved. A copper-containing enzyme , caeruloplasmin, catalyses oxidation of the iron to the ferric form for binding to plasma transferrin. Dietary iron Iron is present in food as ferric hydroxides, ferricprotein and haem-protein complexes. Both the iron content and the proportion of iron absorbed differ from food to food; in general, meat-in particular liver -is a better source than vegetables, eggs or dairy foods, The average Western diet contains 10-15 mg iron daily from which only 5-10% is normally absorbed, The proportion can be increased to 20-30% in iron deficiency or pregnancy Iron absorption • Factors reducing absorption • Factors favouring absorption • Inorganic iron • Haem iron • Ferric form (Fe3+) • Ferrous form (Fe2+) • Alkalis-antacids, pancreatic • Acids (HCl, vitamin C) secretions • Solubilizing agents (e.g. sugars, • Precipitating agents-phytates, amino acids) phosphates • Iron deficiency • Iron excess • Ineffective erythropoiesis • Decreased erythropoiesis • Pregnancy • Infection • Hereditary haemoc1uomatosis • Tea • Increased expression of DMT-1 • Decreased expression of DMT-1 and ferroportin and ferroportin • . in duodenal enterocytes • in duodenal enterocytes • Increased hepcidin. Iron absorption Organic dietary iron is partly absorbed as haem and partly broken down in the gut to inorganic iron. Absorption occurs through the duodenum. Haem is absorbed through a specific receptor, HCP-I, exposed on the apical membrane of the duodenal enterocytes.Haem is then digested to release iron. Inorganic iron absorption is favoured by and reduced by the above factors on the table. When a negative iron balance occurs, iron resorption first increases from the normal value of 5–10% to a maximum of 20%. If the iron stores are completely exhausted, as can be recognized by a decrease of the serum iron and ferritin and an increase in transferrin, then the erythropoiesis becomes defective. Abnormally small, poorly hemoglobinized (hypochromic) red blood cells are synthesized. After a few weeks, the total hemoglobin concentration decreases (manifest iron deficiency anemia). If the iron deficiency is more severe, the synthesis of other iron-dependent proteins (e.g., cytochromes, myoglobin, flavoproteins) is also impaired. Pathophysiology The normal body iron content is 3–5 g. This quantity is contained in hemoglobin, myoglobin, iron stores, and in the reticuloendothelial system (RES); a small amount is contained in serum as ferritin. Iron absorption and iron loss are normally kept constant during adult life. The daily iron demand is 1.3 mg for men and 1.8 mg for women (during the years of menstruation). Adolescents and pregnant women need more iron. Generally, the Western diet contains sufficient iron to compensate for the daily iron losses. Iron resorption takes place mainly in the duodenum and, to some extent, in the jejunum. The mucosal cells regulate intestinal iron absorption. Iron is either directly absorbed and transferred into the circulating blood or stored in the mucosal cells as ferritin. If serum iron is low, iron uptake from the gastrointestinal tract is rapid; if serum iron is elevated or normal, more iron is retained in the mucosal cells. The iron transport from blood to different sites of iron utilization or storage is then performed by transferrin, a specialized transport protein of the β-globulin fraction of human serum. One molecule of transferrin can bind two iron atoms. Normally, about 30% of the total iron-binding capacity is saturated with iron. In the next step, the transferring iron complex is bound to transferrin receptors on the surface of erythroblasts and other cells. Nonutilized iron is then either transported to different storage tissues and accumulated as ferritin or hemosiderin, or excreted via the kidneys. The total iron storage pool is about 800 mg in men and 400 mg in women CAUSES OF IRON DEFICIENCY
1. Chronic blood loss
2. Increased demands during infancy, adolescence pregnancy, lactation and menstruation. 3. Malabsorption as seen in gastrectomy gluten-induced enteropathy 4. Poor diet especially in infants &children. Clinical Signs and Diagnosis The symptoms of iron deficiency anemia depend on its severity. Patients are easily fatigued, may have dyspnea on exertion and have pale skin and pale mucous membranes. An atrophic glossitis, spoon nails (koilonychia), or an angular stomatitis develop. In very severe cases, the patients have dysphagia due to esophageal webs (Plummer-Vinson syndrome). Some patients also develop atrophic gastritis. An early event in iron deficiency is a decrease in serum ferritin, the major iron storage protein. Normal serum concentration of ferritin is 40–350 ng/mL in men and 20–150 ng/mL in women. The serum values reflect the body iron stores in the reticuloendothelial system. The next laboratory sign of iron deficiency to develop is a decrease in the hemoglobin concentration. At this point the number of red blood cells can still be normal. If the iron deficiency persists, abnormalities of red cell morphology can be recognized (e.g., poikilocytosis, anisocytosis, hypochromasia). The reticulocytes are generally decreased and the red cell indices (e.g., mean corpuscular volume [MCV], mean corpuscular hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC]) are below normal. The bone marrow morphology shows nonspecific changes. The stainable iron, usually seen in bone marrow macrophages after staining with Prussian blue, is decreased or absent. In iron deficiency, the transport protein transferrin is usually increased. The serum iron concentration is generally low, but is not a reliable indicator of the degree of iron deficiency. The transferrin saturation (serum/total iron-binding capacity) is typically less than 10%. A new parameter for estimating iron deficiency is the measurement of the serum transferrin receptors. In contrast to ferritin, the levels of serum transferrin receptors are usually not influenced by acute or chronic infections. The normal values (as measured by ELISA) are 4–9 μg/L. In iron deficiency, the levels of serum transferrin receptors increase proportionally to the degree of iron deficiency. Early iron deficiency can also be diagnosed by measuring the red blood cell protoporphyrin. The normal value is approx 30 μg/dL of red cells. In iron deficiency, the value increases to greater than 100 μg/dL. Increased levels are also found in lead poisoning and some sideroblastic anemias and porphyrias. Treatment The first step is to identify and treat the underlying cause of the iron deficiency. It is especially important that an underlying malignancy is not overlooked. The standard treatment of iron deficiency is oral ferrous sulfate. One tablet (100 mg, containing 67 mg as ferrous iron) is given before meals and should be continued until the iron deficiency is corrected and the iron stores are replenished (3–4 mo in severe iron deficiency). In severe cases, two or three tablets daily can be given. An increase in reticulocytes should be seen 7–10 d after the iron substitution is begun if the iron is being adequately absorbed. A prophylactic iron treatment should he given during pregnancy or for premature newborns. Parenteral iron should only be given when oral iron is not effective or cannot be tolerated. Parenteral iron is preferable when gastritis or a duodenal ulcer leads to pronounced side effects or if a severe malabsorption precludes the resorption. Parenteral iron always carries the risk of a hypersensitivity reaction and therefore should be given under close medical supervision.