Download iron deficiency anaemia

Dr. farhana zakaria
Dept of Pathology
 Anaemia refers to a decrease in the total number of
circulating red cells with decrease in haemoglobin
when compared with normal for that age group and
sex.
Iron deficiency anaemia
 Characterised by microcytic hypochromic red cells
with MCV < 80fl and MCH < 25pg.
 Morphologic changes of red cells appear as the iron
stores get depleted and iron is not available in
adequate amounts for haem synthesis.
Iron metabolism
 Iron is present in haemoglobin , myoglobin and iron
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containing enzymes of cytochrome system .
Body iron distribution is :
Haemoglobin – 2000-2500 mg
Myoglobin and enzymes – 400-500 mg
Iron stores – 500-1000 mg
Plasma iron – 2-3 mg
 Daily requirement :
 Diet should contain 10-15 mg of elemental iron and
with approx. 8-10% absorption , the net requirement
per day is 1 mg in males and 1.5mg in females in their
reproductive period.
Iron absorption
 Iron of the food in the presence of pepsin and low pH
(HCL) in stomach is broken into Fe² and Fe³ ions.
 At the mucosal cell surface Fe³ changes to Fe² and iron is
absorbed as Fe².
 Site of absorption : duodenum and upper jejunum.
 Mucosal block mechanism:
 Absorption of iron is controlled to a large extent by the
amount of iron stores.
 Iron is absorbed by the mucosal cell .
 There are three components of Fe absoption :
 It is transported across the cell into circulation
 Remains in the cell and is lost as the cell is shed off.
 Part of diet iron is not absorbed and lost in faeces.
 Mucosal cells control the amount of iron absorbed and
also the amount that is transferred into plasmaknown as mucosal block mechanism,
 When iron stores are nil or reduced in IDA –
absorption is enhanced and almost the whole iron is
put into circulation .
 When iron stores are increased as in haemosiderosis ,
major part of iron is not absorbed ; the part absorbed
remains in the cell and is lost as the cell is shed off;
very little absorbed part is transported into plasma.
Factors promoting Fe absorption
 HCl of the stomach
 Ascobic acid
 Haem iron is better absorbed.
• Alcohol
• Heme found in meat more readily absorbed than inorganic
iron
Factors hampering Fe absorption
 Phytates of cereals
 Tannates of tea
 Phosphates of diet and drugs
Transport of iron
 Iron in blood is carried all over the body by transferrin.
 Each molecule of transferrin carries 2 atoms of iron.
 Iron is released from transferrin in the marrow for
erythropoeisis and transferrin is reutilised to carry
iron.
Iron excretion
 A small amount of iron is lost in sweat and urine.
 Daily loss in males is about 1 mg and females about 2
mg.
Storage of iron
Iron is stored in the body in 2 forms:
 Haemosiderin
Golden brown granules in reticuloendothelial cells of
bone marrow, spleen and liver
Stains blue with Perls’ or Prussian blue reaction
 Ferritin
 Ferritin is present in circulation and serum ferritin
levels reflect the iron stores .
Bone marrow iron
 Normally bone marrow contains hemosiderin
 Inside macrophages
 Free pigment in the marrow and gives positive
prussian blue reaction.
 Assessment of iron stores in body –
 BM iron
 S.ferritin.
Grading of marrow iron
 Nil – no iron containing macrophage
 Decreased – occasional macrophage containing
haemosiderin.
 Normal – haemosiderin in macrophages and free
pigment
 Increased – abundant haemosiderin granules in
macrophages and free haemosiderin amongst marrow
cells.
Iron balance
 At the end of life of red cells , iron is released from
them and enters the plasma pool , from where it is
taken to reticuloendothelial cells of marrow for storage
.
Stages of iron deficiency
 Normal iron balance
 Negative iron balance
 Iron deficient erythropoeisis
 Iron deficiency anaemia
CAUSES of iron deficiency anaemia:
 Dietary lack
 Impaired absorption
 Increased requirement
 Chronic blood loss
 Uterine abnormalities
 GI bleeding
Pathogenesis
 Impaired Hb synthesis
 Impaired cellular proliferation
 Diminished iron containing proteins.
Clinical features
 Pallor of skin mucous membranes and sclerae
 Weakness, fatigue, dyspnoea on exertion, palpitation
 Angina, congestive heart failure
 Koilonychia, atrophic glossitis , angular stomatitis
 Plummer Vinson Syndrome –
Chronic iron deficiency anemia with Dysphagia
Diagnosis
 Peripheral blood findings:
 Haemoglobin reduced
 Mild, moderate, severe
 Mild : Hb 9-12gm/dl
 Moderate: 7-9gm/dl
 Severe: <7gm/dl
 RBC count reduced to a lesser degree
 Reticulocyte count – N / decreased / increased in
Hmg
 Mean cell volume (MCV): the average volume of an RBC,
expressed in femtoliters (cubic micrometers)
 Mean cell hemoglobin (MCH): the average content
(mass)o f Hb per RBC, expressed in picograms
 Mean cell hemoglobin concentration (MCHC): the average
concentration of Hb in a given volume of packed
RBCs, expressed in grams per deciliter
 RBC distribution width (RDW): the coefficient of variation
of RBC volume.
 Hb 12 – 15gm/dl
 Hematocrit :33-43%
 Reticulocyte count :0.5 to 1.5%
 P.smear
 MCV :82 – 96
 MCH :27-33pg
 MCHC: 33-47gm/dl
 RDW :11.5-14.5
 Haematocrit – reduced ( 13- 30%)
 MCV < 80 fl
 MCH < 25 pg
 MCHC < 27 g/dl
P.Smear
 Mild: microcytic hypochromic with normocytes
 Moderate: Predominantly Microcytic hypochromic
(Increased pallor)
 Severe: Microcyte hypochromic with
anisopoikilocytosis and polychromatophils
 Leukocytes and platelets are normal
 Increased marrow cellularity with erythroid
hyperplasia
Erythropoeisis – micronormoblastic
Leucopoesis and megakaryopoeisis is nomal
Depleted bone marrow iron – prussian blue staining
shows that the fragments are completely devoid of iron
and iron grade is 0 ( nil)
Assessment of iron status
 S. ferritin
 Indicates iron stores status
 Usually assessed by ELISA method
 <15 ug/L indicates nil iron stores .
 Normal levels 50-300 ug/L
 S. Iron in IDA is reduced to 10-15 ug/dL
 Normal 50-150 ug/dl
 TIBC is increased to 350-450 ug/dl
 Normal 310-340 ug/dl
 Transferrin saturation < 15% diagnostic of IDA.
 Normal is 30-40 %