

Iron deficiency anemia

Muhammad Asif Zeb
Lecturer Hematology
Khyber Medical university
Peshawar
 
Anemia is a medical
condition in which the
hemoglobin concentration is
less than normal
(for the age and sex of the individual)
 Severity

 Mild anemia
 With hemoglobin level 9-12 g/dl

 Moderate anemia
 With hemoglobin level 6-9g/dl

 Severe anemia
 With hemoglobin level <6g/dl
 
 Iron deficiency anemia is the most common form of anemia
caused from too little iron in the body

 About 20% of women,

 90% of pregnant women,
 and 3% of men
do not have enough iron in their body.

 Body Iron Distribution

 Most body iron is present in haemoglobin in circulating red
cells
 The macrophages of the reticuloendotelial system store iron
released from haemoglobin 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 distribution

 Iron Metabolism

 an adult male
ingest about 15 mg of iron of which only 10% will be
absorbed, giving him 1.5
mg/day of iron that can be used for red cell production or
stored in the reticuloendothelial system (RES)

 iron ingestion

duodenum

10% if ingested iron is absorbed

conversion of iron from the Fe3

(ferric) to the Fe2(ferrous)

transportation of iron from GI tract to bone

marrow via transferrin(mono ferric\di ferric)
 1 gram of transferrin binds 1.4 mg of iron
(total iron binding capacity)

iron

in bone marrow for the developing

normoblast for use of hemoglobin synthesis

erythrocytes

macrophages
reticuloendothelial system


 Iron Storage

 Iron is stored mainly in the liver in reticuloendothelial
system as
 Hemosiderin
 Ferritin
 Hemosiderin is the major long term storage form of iron ;
release slowly,
 Ferritin is the primary storage form of soluble iron ;release
readily at time of need.
 Ferritin
 Iron storage protein


 In humans, it acts as a buffer against iron deficiency and
iron overload
 Consists of:
 Apoferritin – protein component
 Core- ferric, hydroxyl ions and oxygen

 Largest amount of ferritin-bound iron is found in:

 Liver hepatocytes (majority of the stores)
 BM
 Spleen
 Excess dietary iron induces increased ferritin production
 Partially digested ferritin= HAEMOSIDERIN- insoluble
and can be detected in tissues (hepatocytes) using Perl’s
Prussian blue stain
 Hemosidrin

 Water insoluble protien iron complex
 Visible by light microscope
 It has higher iron to protein ration up to 37% than
ferritin up to 20%
 Formed by partial digestion of ferritin aggregates by
lysosomal enzymes.
 Hemosidrin is present predominately in
macrophages rather than hepatocytes.
 Transferrin (Tf)

 Transports iron from palsma to erythroblast
 Mainly synthesized in the liver
 Fe3+ (ferric) couples to Tf
 Apotransferrin = Tf without iron
 Contains sites for max 2 iron molecules
 Synthesis is inversely proportional to iron store
 Pathophysiology of IDA

Iron deficiency anaemia develops in three stages
 iron depletion
 Iron deficient erythropoiesis
 iron deficiency anaemia
 Iron Depletion

 Iron stores are exhausted as indicated by decreased serum
ferritin, serum iron normal
 No anaemia
 Erythrocyte morphology is normal
 Iron Deficient Erythropoiesis

 There is insufficient iron to insert into the protoporphyrin
ring to form heme,
 Serum iron is also depleted.
 Anaemia and hypochromia are still not detectable
 Erythrocytes may became slightly microcytic
 Iron Deficiency Anemia

 Long standing negative flow leads to IDA
 Blood loss significantly shorten this stage
 Classic microcytosis and hypochromia
 The situation represents advanced stage of severely
deficient body iron
 Causes of Iron Deficiency
Anemia

 Blood Loss
 Gastrointestinal Tract
 Menstrual Blood Loss
 Urinary Blood Loss (Rare)
 Blood in Sputum (Rarer)
 Increased Iron Utilization
 Pregnancy
 Infancy
 Adolescence
 Polycythemia Vera
 
 Malabsorption
 Tropical Sprue
 Gastrectomy
 Chronic atrophic gastritis
 Dietary inadequacy
 Parasitic infection
 Hook worm
 Sign and Symptoms

• Fatigability
• Dizziness
• Headache
• Irritability
• Dry, pale skin
• Spoon shaped nails, Koilonychias
• Pica (Appetite for non food substances such as clay)
• Splenomegaly (10%)
• Increased platelet count
 

Laboratory Diagnosis
 Complete Blood Count

 Rbc count normal-decrease
 Hemoglobin decreased
 Wbc conut normal
 Palatelets normal-increase(in chronic bleeding)
 RDW increased
 (is the first sign to appear even before microcytosis of the
cell occurs in the iron depletion stage of anemia )
 Red cell Indices


 PCV decreased
 MCV decreased
 MCH decreased
 MCHC decreased
 Peripheral Film

 DLC normal-increase(in chronic infections)
 RBC morphology
 Anisocytosis
 microcytosis
 Hypochormia
 Poikilicytosis
 Tear drop cells
 Elliptocytes
 Target cells


 Reticulocyte Count

 Normal- rdeuced-slightly
 Iron Profile

 Serum iron low
 Serum ferritin low
 TIBC(total iron binding capacity) inreased
 Tansferrin saturation % low
 Bone Marrow

 Bone marrow is hyper cellular with polychromatic
normoblast predominance
 Erythroid series is small and have tiny projection from the
cytoplasm
 Iron stain; Negative



 Investigations Occasionally
Required

 Feaces examination for parasites
 LFT in case if liver damage

 Prussian-blue Stain

 Iron is released from the hemosidrine molecules by treating
the slide with weak acid solution .the free iron combines
with potassium ferrocynide to produce ferric Ferro cyanide.
Free iron will appear greenish blue
Procedure 
 Air dry film
 Fix with methanol 10-20min
 Place slide in solution of 10g /l potassium Ferro cyanide
in 0.1 mol/l HCL for 30 min
 Wash in running tap water for 1 min
 Rinse in distilled water
 Counter stain with neutral red for10-15 sec
Differential diagnosis
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 
Thank You