IDA is most common in south east asia and india , it is more common in pregnant and lactating female

1. DR SANTOSH KUMAR

2. BODY IRON
COMPARTMENTS
 Total body iron content – 3-5gms.
 Divided into Functional and storage
compartments.
 Functional forms (80%) –
hemoglobin, myoglobin,enzymes
(catalase, cytochromes, peroxidase)
 Storage forms (20%) – ferritin,
hemosiderin.
80%
20%
FUNCTIONAL
STORAGE

3. IRON ABSORPTION

4. REGULATION OF IRON
ABSORPTION
 Hepcidin, a small circulating plasma peptide
that is synthesized and released from the liver
serves as a communicator between iron stores
and intestinal absorption.
 Negative iron metabolism regulatory hormone.
 Downregulated in iron deficiency, increased
erythropoietic activity and hypoxia.
 Synthesis increased in iron overload.
Inflammation (anemia of chronic disease).
 Inflammatory cytokines like IL-6, LPS also rises
the hepcidin secretion.

5. TRANSPORT OF IRON
 Transferrin – a glycoprotein synthesized in
the liver. One molecule carries two atoms of
iron (diferric transferrin).
 The iron-binding sites of all the transferrin
present in the serum constitutes the total iron
binding capacity(TIBC).
 Carries the iron to erythroblasts in bone
marrow and other cells in the body and
delivers through the transferrin receptor (TfR)
present on the cell surface.

6. ERYTHROBLAST

7. STORAGE FORMS OF IRON
FERRITIN
• Soluble form
• Spherical Iron-protein
complex with protein shell
and iron core. It is found
in liver, spleen, bone
marrow and skeletal
tissues.
• In liver, stored
inparenchymaltissues
while in spleen and BM,
stored in macrophages.
HEMOSIDERIN
• Insoluble form
• Partly degraded protein
shells offerritinaggregate to
formhemosiderin.
• Stored in macrophages of
liver, spleen, bone marrow.
• Appears golden yellow or
browngranulaonH&E
stain.
• Iron inhemosiderinin
chemically reactive and
turns blue-black when
exposed to
potassiumferrocyanide,
which is basis of Prussian
blue stain.

8. IRON METABOLISM
Incorporation of
iron in
erythroblasts
Mature RBC in
circulation
Phagocytosisby
macrophages
Storage within
macrophages
asferritinandhemos
iderin
PlasmaTransferriniro
n
Intestinal
absorption
Skin, gut,
endEndometri
um
(1-2gm/day)

9. IRON BALANCE
 Only 10-15% of ingested iron is absorbed,
hence atleast 1mg of iron must be absorbed
from the diet in order to maintain a normal iron
balance.
 Heme iron in much more absorbable than
non-heme iron.
 Non-heme iron is influeneced by the other
dietary factors, such as ascorbic acid, citric,
aminoacid and sugars enhances absorption
while tannates, carbonates and oxalates
inhibits the absorption.

10. DAILY IRON REQUIREMENTS
 Infants upto 4 months –
0.5mg
 Infants 5-12 months and
children – 1mg
 Menstruating women – 3mg
 Pregnancy – 3-4mg
 Adult men and
postmenopausal women –
1mg

11. IRON DEFICIENCY
ANEMIA
 Deficiency of iron is the most common
nutritional disorder in the world.
 IDA develops when body iron stores are
depleted, level of circulating iron in reduced,
and insufficient iron available for
erythropoiesis.
 Occurs at all ages, but more common in
women of childbearing age.

12. PATHOGENESIS
 IDA develops when the supply of iron is
insufficient for the synthesis of hemoglobin.
 Three major factors contribute the
pathogenesis are,
Increased physiological demand for iron.
Pathological blood loss.
Inadequate iron intake
 Frequently more then 1 factor contributes to
anemia.

13. CAUSES OF IDA
 Dietary lack.
 Impaired absorption of iron (Celiac disease,
gastrectomy, H.pylori gastritis, PPIs.)
 Blood loss: physiological (menstruation) or
pathological (GI).
 Increased requirements due to rapid growth
in early childhood and adolescence and in
pregnancy.
 Rarely, genetic forms includes mutations in
TMPRSS6 gene causing iron refractory
IDA.

14. STAGES IN THE DEVELOPMENT OF
IDA
 Stage 1 – PRELATENT ( Storage Depletion)
- Lower than expected serum ferritin levels. Low
ferritin levels are the first sign that the body’s iron
stores are markedly depleted.
 Stage 2 – LATENT (Mild Deficiency)
- During the second stage, iron stores are
exhausted, but hemoglobin levels remain normal.
Transferrin decreases. It is often accompanied by a
reduction in size of RBCs.
 Stage 3 – OVERT (Iron Deficiency Anemia)
- Hemoglobin begin to drop in the final stage
which, at this stage RBCs are fewer in number, smaller
and contain less hemoglobin.

15. Depletion of iron stores
Iron
deficienterythropoiesis
Iron deficiency anemia
•Hb (N)
•MCV(N)
•Serum ferritin
(low)
•Transferrin
saturation (N)
•Hb (N)
•MCV(N)
•Serum ferritin
(low)
•Transferrin
saturation (low)
•TIBC (high)
•Hb (low)
•MCV (low)
•Serum ferritin
(low)
•Transferrin
saturation (low)
•TIBC (high)
PRELATENT
LATENT
OVERT

16. CLINICAL FEATURES
 Most common - Lethargy, weakness, fatigue,
dyspnoea on exertion & palpitation.
 Pallor of skin and mucous membrane.
 Epithelial tissue changes:
 Seen in long standing iron deficiency states.
 Koilonychia, atrophic glossitis, angular stomatitis,
dysphagia, esophageal web, gastritis.
 Pica
 Plummer-Vinson syndrome: chronic IDA,
dysphagia, glossitis, m/c in middle aged
women.

17. LABORATORY FINDINGS
 Peripheral blood smear
 RBC- initially normocytic normochromic, later
shows microcytosis and hypochromia.
Anisocytosis is an important early sign.
Poikilocytosis mainly elongated and tailed forms
(pencil cells).
 WBC- normal or mildly reduced.
 Platelets- often increased in cases of anemia
due to chronic blood loss, however decreased in
acute blood loss.
 Reticulocyte count – normal/ reduced

19. RED CELL INDICES
 MCV – reduced.
 MCH – reduced.
 MCHC – reduced
in severe or long
standing cases.
 RDW – increased.

20. IRON STUDIES
1. SERUM FERRITIN
 Most specific in diagnosis of IDA.
 Normal range : 15-300 mcg/L.
 Value <12 mcg/L strongly indicates iron
deficiency.
 Since it is acute phase reactant, it lacks
sensitivity and its normal value does not
reliably exclude iron deficiency.
 Not suitable in pts with infectious or
inflammatory diseases.

21. 2. SERUM IRON
 Normal range : 50-150 mcg/dL.
 Usually <50mcg/dL in IDA.
 Reflects iron bound to transferrin.
3. TOTAL IRON BINDING CAPACITY
 Normal range : 300-400 mcg/dL.
 Increased in IDA >400 mcg/dL.
 Serum Iron and TIBC normal, IDA is
excluded.
 If Sr. Iron is low and TIBC is high, IDA is
confirmed.
 If Sr. Iron is low and TIBC is low, indicate
anemia of chronic disease.

22. 4. TRANSFERRIN SATURATION
 Ratio of serum iron to TIBC
 Indicates proportion of transferrin to which
iron is bound.
 Normal value : 30%
 In IDA usually <15%.
Transferrin saturation = Serum Iron *100
TIBC

23. 5. SERUM TRANSFERRIN RECEPTOR ASSAY
(TfR)
 Serum Transferrin receptors are derived from
proteolysis of cell membrane transferrin
receptors when RBCs undergoes maturation.
 In IDA, transferrin receptors on erythroid cells
increases, hence serum levels also increases.
 Useful in ;
 Differentiating IDA from Anemia of chronic
disease.
 Diagnosing IDA in patients with chronic
inflammation.

24. ERYTHROCYTE ZINC
PROTOPOROHYRIN
 Combination of protoporphyrin with iron to
form heme occurs in mitochondria of erythroid
precursors.
 Failure of this step occurs in IDA.
 An alternate ligand in the form of zinc is
inserted in the protoporphyrin ring with the
formation of zinc protoporphyrin(ZPP).
 Increased levels ZPP are seen in IDA.
 Useful in differentiating IDA from thalassemia.
 Can be applied to large-scale screening
programs in public health surveys.

25. BONE MARROW
 Decreased or absence of stainable iron in
bone marrow on Perl’s Prussian blue stain
is characteristic finding in bone marrow
aspirate.
 Micronormoblasts are seen in which cells
are smaller than normal with reduced
amount of cytoplasm that is vacuolated
and has rugged borders.
 Shows increased erythroid precursor cells.

26. Micronormoblasts

27. D/D OF HYPOCHROMIC
ANEMIA
 Majority of cases of microcytic hypochromic
anemia is IDA.
 However, hypochromic anemia is
encountered in disorders in which
morphological abnormality is due to
unavailability of iron.
 Therefore, establishment of accurate
diagnosis is of great importance in ensuring
correct treatment.

28. TESTS IRON
DEFICIENCY
ANEMIA OF
CHRONIC
DISEASE
THALASSEMIA
MINOR
SIDEOBLASTIC
ANEMIA
MCV Low Normal/low Low Low
RDW High High/ normal Nomal/ high Normal/ high
RBC
morphology
Micro, hypo &
anisocytosis
Micro, hypo/
Normo,normo
Micro, hypo &
target cells
Dimorphic
RBC count Low Low Normal Normal
Serum Iron Low Low/ normal Normal/ high Normal/ high
TIBC High Low Normal Normal
Transferrin
saturation
Low Low/ normal Normal/ high Normal/ high
Ferritin Low High/ normal Normal Normal
Serum TfR High Normal High Normal
Free
erythrocyte
protoporphyrin
High High Normal Increased
Hb pattern on
electrophoresis
Normal Normal Abnormal
HbA2 >3.5%
normal
Marrow Iron Low/ absent Normal/ high Normal Ring sideroblasts

29. TREATMENT
 Management of IDA includes
 Correction of underlying cause of anemia.
 Administration of iron.
 Oral / parenteral iron can be used.
 Ferrous sulphate usually preferred
preparation, 1 tablet (200mg) contains 60mg
of elemental iron, given thrice daily.

30.  Following initiation therapy, increase in
reticulocyte count develops within 3-7
days and peaks between 8th-10th day.
 Hb should rise by 1gm/dl in 4 weeks
(known as Response to iron therapy).
 About 6-8 weeks are needed for
restoration of Hb level, treatment
continued for further 4 months to replenish
the body iron stores.

31.  Causes of poor response to oral therapy
includes ;
 Patient non-compliance.
 Inadequate dosage.
 Malabsorption.
 Continued excess bleeding.
 Coexistent Vitamin B12/ folate deficiency.
 Concurrent infections, inflammatory or
neoplastic diseases.
 Iron refractory iron deficiency anemia.

32.  Indication of parenteral iron therapy
are GI intolerance to oral iron,
advanced stage of pregnancy with
severe anemia, malabsorption of iron.
 IV preparations available for use are,
 Iron dextran.
 Sodium ferrous gluconate.
 Iron sucrose.