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Iron Deficiency Anemia
 One of the most common medical problems
 Most common cause of anemia
 Iron deficiency anemia is the last step ;
 Iron depletion: absent or decreased iron stores
 Iron deficiency: depletion of stores + low serum iron and
ferritin
 Iron deficiency anemia: Anemia developing in an iron
deficient patient
Total amount of body iron:3-5 g
Iron Metabolism
 Iron is located at the center of Hem molecules
of Hb (amount:1.5-2 gr)
and it is also;
 Part of the myoglobin
 Takes place in the tissue enzymes
 Storage forms are
 Ferritin
 Hemosiderin
 Location: Bone Marrow, Liver, Spleen
 Transport iron is by transferrin.
Iron Metabolism
 Transferrin picks up iron from ;
1. The GI cells to deliver it to Hb forming cells
2. Storage parts as a step of iron recycling process
 Absorbtion + recycling provides the constant iron
supply of 1-2 mg/day necessary for Hb synthesis
Daily Iron Demands
Male 1 mg
Adolesc. 2-3 mg
Women in repr.age 2-3 mg
Pregnant 3-4 mg
Iron Metabolism
 Iron absorbtion is restricted to the needs of the body
 1mg of iron is lost each day
 Menstruation and pregnancy/lactation are other major
causes of iron loss and incresed demand in women
Iron Metabolism
 Normal diet contains about 14 mg of iron/day
 1/10 of ingested iron is absorbed
 Gastric acid releases iron from food
 Iron is absorbed in the reduced form
 Ascorbate increases absorbtion (by reducing)
 Phytates,phosphates , Tea, infection,,antacids
decrease absorbtion by making complexes with
iron
Iron Metabolism
 Main sites of absorbtion are;
 Duodenum
 Upper jejunum
 Malabsorbtive states or gastrojejunostomy prevent
absorbtion.
Iron Metabolism
Transport of iron
 Transferrin is the main iron carrier in plasma
 It is produced in liver cells with increased synthesis in
iron deficiency
 Transferrin binds 1-2 ferric iron molecules
 Transferrin-iron complex is endocytosed by Hb
producing cells after linking to receptors.
Iron Metabolism
 Total iron binding capacity and iron
 Transferrin is measured by quantifying the iron binding
sites available
 This is also called “Total iron binding capacity”
 TIBC is 1/3 saturated under normal conditions
Causes of iron deficiency
 Chronic blood loss
 Increased demand
 Malabsorbtion of iron
 Inadequate iron intake
 Intravascular hemolysis and hemoglobinuria-
hemosiderinuria
 Combinations
Increased demands
Pregnancy
Lactation
Rapid growth
Decreased intake
 Decreased iron in the diet
 Vegetarianism
 Decreased absorbtion
 Gastric surgery
 Sprue
 Pica
Increased iron loss
 Menorrhagia
 GIS hemorrhagia
•Colitis or imf. Bovel
disease
•Hemorrhoids
•NSAID use
•Parasites
•P.Ulcer
•Oesophagitis
•Varices
•Malignancy
Increased iron loss
 Bleeding disorder
 Pulmonary lesions with bleeding
 Hemoglobinuria – hemosiderinuria (chronic
intravascular hemolysis)
 Hematuria (chronic)
 Frequent donation
 250 mg iron /unit-blood
Clinical features
 General symptoms of anemia
 Fatigue may be disproportional to the degree of
anemia due to deficiency of tissue enzymes which
also need iron
 Glossitis
 Angular stomatitis
 Paterson-Kelly (Plummer Vinson) syndrome
(oesephageal web leading to disphagia)
Clinical features
 Gastric atroph
 Nail changes
 Brittle/fragility
 Koilonchia/spooning
 Splenomegaly
Clinical features
 Pica:Appetite for bizzare food/substances
 Geophagy (earth,clay)
 Pagophagia(ice)
 Amylophagia(starch)
 Developmental problems
 Splenomegaly
 Immun-deficiency
Lab. FeaturesWW
 Hb,Htc,RBC:Low
 MCV,MCH,MCHC:Low
 RDW: High
 Retics: Normal/Low
 Plt:Normal/Low/High
 WBC:Normal/Low
 Smear: Hypochromia,anisocytosis,microcytosis,
poikilocytosis
Lab.Features
 Serum Iron:  N: 2-4g/L
 TIBC:  40-75umol/L
 Serum Ferritin  male:40-340ug/l
 female:14-150ug/L
Lab.Features
 Transferrin saturation (Fe/TIBC):  (<15%)
<5%:definitely indicates iron deficiency
 Serum Transferrin Receptor: 
 Free Erythrocyte Protoporphyrin  (17 – 27 μg/dL)
 Bone marrow :
 Erythroid hyperplasia,
 Absence of hemosiderin
Differential diagnosis
 Microcytic anemias
 Iron deficiency anemia
 Thalassemia ,HbC,HbE etc
 Sideroblastic anemia
 Lead poisoning
 Anemia of chronic diseases (sometimes)
Important !!!!!!!
 The diagnostic procedure is not complete until the
underlying pathology is disclosed.
Treatment
 Replace iron and treat underlying disease.
 Oral route is preferred for replacement.
 Response can be followed by retic. increase in 1-2
weeks (5-7 days)
 Hb response to treatment
 half normal by a month
 returns to normal by 2-4 months
 Replacement therapy is prolonged by 6-12 months
to replenish stores of iron.
 Ongoing bleeding may cause indefinite therapy.
Treatment
Oral iron therapy:
dose (mg) elemental
iron(mg)
Fe fumarate 200 65
Fe gluconate 300 37
Fe sulphate 200 67
Treatment
Oral iron therapy:
Total daily dose:150-200 mg elemental iron
Give in 3-4 divided doses,
Each one hour before meals.
Do not prefer enteric coated forms.
In case of GIS intolerance;
 Change the route of administration or
 Change the preparation or
 Reduce dose
Treatment
Non responding patient:
 possible causes
 Misdiagnosis
 Patient does not take the medicine
 Continuing blood loss
 Malabsorbtion
 Change the drug
 Change the route of administration
 Underlying disease /comorbidity
 Combined deficiency
Treatment
 Parenteral iron therapy:
Routine use is not justified,
Response is not faster than oral replacement.
Indications
 Malabsorbtion
 Intolerance to oral replacement
 Colitis/enteritis
 Needs in excess of amount that can be given orally
 Patient uncooperative/poor compliance
 Autologous blood donation setting
 Hemodialysis
Treatment
Parenteral iron therapy:
Total iron dose: (15-patient Hb) x bw x 3
– Iron Dextran: 50 mg/ml (iv/im)
 Max daily dose is 100 mg im
– Ferric gluconate:
 A test dose of 25 mg elemental iron (2 mL) must be
given in 50 mL saline over 60 minutes
– Ferric-hydroxy-sucrose (100 mg/5mL)
– 2.5 ml first day
– 5ml third day
– 2x5 ml/week
Parenteral replacement therapy may cause
 allergic reactions,
 local pain or induration,
 serum sickness like disease,
 lymphadenomegaly,
 arthralgia,
 myalgia etc.
Treatment
preventive iron supplementation
 Pregnants ( at 20-24 weeks Hb< 11 g/dL, Ferritin ).
 Lactation.
 Frequent blood donation.
 Autologous blood donation settings.
 Gastrectomised patients.
 High dose asprin treatment.

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5. Iron deficiency anemia (1).ppt66666666

  • 1.
  • 2. Iron Deficiency Anemia  One of the most common medical problems  Most common cause of anemia  Iron deficiency anemia is the last step ;  Iron depletion: absent or decreased iron stores  Iron deficiency: depletion of stores + low serum iron and ferritin  Iron deficiency anemia: Anemia developing in an iron deficient patient
  • 3. Total amount of body iron:3-5 g
  • 4. Iron Metabolism  Iron is located at the center of Hem molecules of Hb (amount:1.5-2 gr) and it is also;  Part of the myoglobin  Takes place in the tissue enzymes  Storage forms are  Ferritin  Hemosiderin  Location: Bone Marrow, Liver, Spleen  Transport iron is by transferrin.
  • 5. Iron Metabolism  Transferrin picks up iron from ; 1. The GI cells to deliver it to Hb forming cells 2. Storage parts as a step of iron recycling process  Absorbtion + recycling provides the constant iron supply of 1-2 mg/day necessary for Hb synthesis
  • 6. Daily Iron Demands Male 1 mg Adolesc. 2-3 mg Women in repr.age 2-3 mg Pregnant 3-4 mg
  • 7. Iron Metabolism  Iron absorbtion is restricted to the needs of the body  1mg of iron is lost each day  Menstruation and pregnancy/lactation are other major causes of iron loss and incresed demand in women
  • 8. Iron Metabolism  Normal diet contains about 14 mg of iron/day  1/10 of ingested iron is absorbed  Gastric acid releases iron from food  Iron is absorbed in the reduced form  Ascorbate increases absorbtion (by reducing)  Phytates,phosphates , Tea, infection,,antacids decrease absorbtion by making complexes with iron
  • 9. Iron Metabolism  Main sites of absorbtion are;  Duodenum  Upper jejunum  Malabsorbtive states or gastrojejunostomy prevent absorbtion.
  • 10. Iron Metabolism Transport of iron  Transferrin is the main iron carrier in plasma  It is produced in liver cells with increased synthesis in iron deficiency  Transferrin binds 1-2 ferric iron molecules  Transferrin-iron complex is endocytosed by Hb producing cells after linking to receptors.
  • 11. Iron Metabolism  Total iron binding capacity and iron  Transferrin is measured by quantifying the iron binding sites available  This is also called “Total iron binding capacity”  TIBC is 1/3 saturated under normal conditions
  • 12. Causes of iron deficiency  Chronic blood loss  Increased demand  Malabsorbtion of iron  Inadequate iron intake  Intravascular hemolysis and hemoglobinuria- hemosiderinuria  Combinations
  • 14. Decreased intake  Decreased iron in the diet  Vegetarianism  Decreased absorbtion  Gastric surgery  Sprue  Pica
  • 15. Increased iron loss  Menorrhagia  GIS hemorrhagia •Colitis or imf. Bovel disease •Hemorrhoids •NSAID use •Parasites •P.Ulcer •Oesophagitis •Varices •Malignancy
  • 16. Increased iron loss  Bleeding disorder  Pulmonary lesions with bleeding  Hemoglobinuria – hemosiderinuria (chronic intravascular hemolysis)  Hematuria (chronic)  Frequent donation  250 mg iron /unit-blood
  • 17. Clinical features  General symptoms of anemia  Fatigue may be disproportional to the degree of anemia due to deficiency of tissue enzymes which also need iron  Glossitis  Angular stomatitis  Paterson-Kelly (Plummer Vinson) syndrome (oesephageal web leading to disphagia)
  • 18. Clinical features  Gastric atroph  Nail changes  Brittle/fragility  Koilonchia/spooning  Splenomegaly
  • 19. Clinical features  Pica:Appetite for bizzare food/substances  Geophagy (earth,clay)  Pagophagia(ice)  Amylophagia(starch)  Developmental problems  Splenomegaly  Immun-deficiency
  • 20. Lab. FeaturesWW  Hb,Htc,RBC:Low  MCV,MCH,MCHC:Low  RDW: High  Retics: Normal/Low  Plt:Normal/Low/High  WBC:Normal/Low  Smear: Hypochromia,anisocytosis,microcytosis, poikilocytosis
  • 21. Lab.Features  Serum Iron:  N: 2-4g/L  TIBC:  40-75umol/L  Serum Ferritin  male:40-340ug/l  female:14-150ug/L
  • 22. Lab.Features  Transferrin saturation (Fe/TIBC):  (<15%) <5%:definitely indicates iron deficiency  Serum Transferrin Receptor:   Free Erythrocyte Protoporphyrin  (17 – 27 μg/dL)  Bone marrow :  Erythroid hyperplasia,  Absence of hemosiderin
  • 23. Differential diagnosis  Microcytic anemias  Iron deficiency anemia  Thalassemia ,HbC,HbE etc  Sideroblastic anemia  Lead poisoning  Anemia of chronic diseases (sometimes)
  • 24. Important !!!!!!!  The diagnostic procedure is not complete until the underlying pathology is disclosed.
  • 25. Treatment  Replace iron and treat underlying disease.  Oral route is preferred for replacement.  Response can be followed by retic. increase in 1-2 weeks (5-7 days)  Hb response to treatment  half normal by a month  returns to normal by 2-4 months  Replacement therapy is prolonged by 6-12 months to replenish stores of iron.  Ongoing bleeding may cause indefinite therapy.
  • 26. Treatment Oral iron therapy: dose (mg) elemental iron(mg) Fe fumarate 200 65 Fe gluconate 300 37 Fe sulphate 200 67
  • 27. Treatment Oral iron therapy: Total daily dose:150-200 mg elemental iron Give in 3-4 divided doses, Each one hour before meals. Do not prefer enteric coated forms. In case of GIS intolerance;  Change the route of administration or  Change the preparation or  Reduce dose
  • 28. Treatment Non responding patient:  possible causes  Misdiagnosis  Patient does not take the medicine  Continuing blood loss  Malabsorbtion  Change the drug  Change the route of administration  Underlying disease /comorbidity  Combined deficiency
  • 29. Treatment  Parenteral iron therapy: Routine use is not justified, Response is not faster than oral replacement. Indications  Malabsorbtion  Intolerance to oral replacement  Colitis/enteritis  Needs in excess of amount that can be given orally  Patient uncooperative/poor compliance  Autologous blood donation setting  Hemodialysis
  • 30. Treatment Parenteral iron therapy: Total iron dose: (15-patient Hb) x bw x 3 – Iron Dextran: 50 mg/ml (iv/im)  Max daily dose is 100 mg im – Ferric gluconate:  A test dose of 25 mg elemental iron (2 mL) must be given in 50 mL saline over 60 minutes – Ferric-hydroxy-sucrose (100 mg/5mL) – 2.5 ml first day – 5ml third day – 2x5 ml/week
  • 31. Parenteral replacement therapy may cause  allergic reactions,  local pain or induration,  serum sickness like disease,  lymphadenomegaly,  arthralgia,  myalgia etc. Treatment
  • 32. preventive iron supplementation  Pregnants ( at 20-24 weeks Hb< 11 g/dL, Ferritin ).  Lactation.  Frequent blood donation.  Autologous blood donation settings.  Gastrectomised patients.  High dose asprin treatment.

Editor's Notes

  1. Ferous sulphate Ferous fumarate