This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Chairman of Department of Medicine and Nephrology Consultant. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

IRON DEFICIENCY ANEMIA Presented By: Dr. Naif Al-Rowaily Medical Student 2009

ANEMIA - DEFINITION  REDUCTION OF HEMOGLOBIN CONCENTRATION BELOW REFERENCE VALUE

BLOOD PARAMETERS  Hemoglobin concentration (Hg) F: 12.1 –15.1; M: ,3 gm/dl (12-18 g/dl)  Erythrocytes count (RBC) F: 4.2-5,4; M: 4,7-6.1 x10 12 /l ( 4-6 x10 6 /  l) varies w altitude.  Hematocrit (Hct) F: ; M: ; (36-51%)  Platelet count (Plt) 150 – 450 x 10 3 /  l ( x 10 9 /l)  Leukocytes count (WBC) x 10 9 /l (4-10 x 10 3 /  l)

Erythrocytes parameters –Mean corpuscular volume (MCV) –N: fl –RDW(Red cell Distrubution Width) –Mean corpuscular hemoglobin (MCH) –N: pg –Mean corpuscular hemoglobin concentration (MCHC) –N: g/dl –Reticulocytes –0,5-2%

IRON DEFICIENCY ANEMIA  IRON METABOLISM –ABSORPTION IN DUODENUM –TRANSFERRIN TRANSPORTS IRON TO THE CELLS –FERRITIN AND HEMOSYDERIN STORE IRON  10% of daily iron is absorbed

 Most body iron is present in hemoglobin in circulating red cells  The macrophages of the reticuloendotelial system store iron released from hemoglobin as ferritin and hemosiderin  Small loss of iron each day in urine, faeces, skin and nails and in menstruating females as blood (1-2 mg daily)

IRON METABOLISM  Iron concentration (Fe) N:  g/dl  Total Iron Binding Capacity N:  g/dl  Transferrin saturation  Transferrin receptor concentration  Ferritin concentration N:  g/l

IRON DEFICIENCY ANEMIA  ETIOLOGY: CHRONIC BLEEDING MENORRHAGIA PEPTIC ULCER STOMACH CANCER ULCERATIVE COLITIS INTESTINAL CANCER HAEMORRHOIDS DECREASED IRON INTAKE INCREASED IRON REQUIRMENT (JUVENILE AGE, PREGNANCY, LACTATION)

IRON DEFICENCY - STAGES  Prelatent –reduction in iron stores without reduced serum iron levels Hb (N), MCV (N), iron absorption (  ), transferin saturation (N), serum ferritin (  ), marrow iron (  )  Latent –iron stores are exhausted, but the blood hemoglobin level remains normal Hb (N), MCV (N), TIBC (  ), serum ferritin (  ), transferrin saturation (  ), marrow iron (absent)  Iron deficiency anemia –blood hemoglobin concentration falls below the lower limit of normal Hb (  ), MCV (  ), TIBC (  ), serum ferritin (  ), transferrin saturation (  ), marrow iron (absent)

IRON DEFICIENCY ANEMIA  GENERAL ANEMIA’S SYMPTOMS: –FATIGABILITY –DIZZENES –HEADACHE –SCOTOMAS –IRRITABILITY –PALPITATION

CHARACTERISTICS SYMPTOMS –GLOSSITIS, STOMATITIS –DYSPHAGIA ( Plummer-Vinson syndrome) –ATROPHIC GASTRITIS –DRY, PALE SKIN –SPOON SHAPED NAILS, KOILONYCHIA, –BLUE SCLERAE –HAIR LOSS –PICA (APETITE FOR NON FOOD SUBSTANCES SUCH AS AN ICE, CLAY) –SPLENOMEGALY (10%) –INCREASED PLATELET COUNT

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IRON DEFICIENCY ANEMIA  MCV  MCH  MCHC N  Fe  TIBC  TRANSFERIN SATURATION  FERRITIN

BLOOD AND BONE MARROW SMEAR  BLOOD: –microcytosis, hipochromia, anulocytes, anisocytosis poikilocytosis  BONE MARROW –high cellularity –mild to moderate erythroid hyperplasia (25-35%; N 16 – 18%) –polychromatic and pyknotic cytoplasm of erythroblasts is vacuolated and irregular in outline (micronormoblastic erythropoiesis) –absence of stainable iron

Management  History and physical examination is sufficient to exclude serious disease (e.g pregnant or lactating women, adolescents) - CURE ANEMIA  History and/or physical examination is insufficient (e.g old men, postmenopausal women) - FIND ETIOLOGY OF ANEMIA AND CURE (CAUSAL TREATMENT) Gastroscopy Colonoscopy Gynaecological examination

ORAL IRON ABSORPTION TEST 1. baseline serum iron level mg of elemental iron orally 3. serum iron level 2-4 hours after ingestion

IRON DEFICIENCY ANEMIA CURE  ORAL –200 mg of iron daily 1 hour before meal (e.g. 100 mg twice daily) –How long? 14 days + (Hg required level – Hg current level) x 4 –half of the dose - 6 – 9 months to restore iron reserve –Absorption is enhanced: vit C, meat, orange juice, fish is inhibited: cereals, tea, milk

IRON DEFICIENCY ANEMIA CURE  PARENTERAL IRON SUBSTITUTION –Bad oral iron tolerance (nausea, diarrhoea) –Negative oral iron absorption test –Necessity of quick management – mg daily –I.v only in hospital (risk of anaphilactic shock) –I.m in outpatient department –iron to be injected (mg) = (15 - Hb/g%/) x body weight (kg) x 3

Iron Deficiency Anemia © 2007 American Academy of Family Physicians Iron Deficiency Anemia, Shersten Killip, M.D., M.P.H., John M. Bennett, M.D., M.P.H., and Mara D. Chambers, M.D.

TREATMENT  Transfusion should be considered for patients of any age with IDA complaining of symptoms such as fatigue or dyspnea on exertion. It also should be considered for asymptomatic cardiac patients with hemoglobin less than 10 g per dL (100 g per L).  However, oral iron therapy is usually the first-line therapy for patients with IDA.  Gastrointestinal absorption of elemental iron is enhanced in the presence of an acidic gastric environment. This can be accomplished through simultaneous intake of ascorbic acid (i.e., vitamin C).  Foods rich in tannates (e.g., tea) or phytates (e.g., bran, cereal), or medications that raise the gastric pH (e.g., antacids, proton pump inhibitors, histamine H2 blockers) reduce absorption and should be avoided if possible.

TREATMENT  Indications for the use of intravenous iron include chronic uncorrectable bleeding, intestinal malabsorption, intolerance to oral iron, nonadherence, or a hemoglobin level less than 6 g per dL (60 g per L).  The advantage of iron dextran is the ability to administer large doses (200 to 500 mg) at one time.  One major drawback of iron dextran is the risk of anaphylactic reactions that can be fatal.  Sodium ferric gluconate (Ferrlecit), a safer form of parenteral iron, was approved by the U.S. Food and Drug Administration in 1999.

TREATMENT  The risk of anaphylaxis is drastically reduced using sodium ferric gluconate.  In a study of 2,534 patients on hemodialysis, 0.04 percent receiving sodium ferric gluconate had life-threatening reactions compared with 0.61 percent receiving iron dextran.  Sodium ferric gluconate is usually administered intravenously in eight weekly doses of 125 mg for a total dosage of 1,000 mg. No test dose is required.  Another intravenous preparation, approved for use in the United States in 2000, is iron sucrose (Venofer). In iron deficiency not associated with hemodialysis, 200 mg is administered intravenously five times over a two-week period. Safety profiles are similar to sodium ferric gluconate, although published experience is more limited.