May be use as a help

2. Anaemia: Definition of anaemia and prevalence of IDD
 Anaemia is defined as ‘a reduction of the
haemoglobin concentration, red-cell count, or packed
cell volume to below normal levels’.
 Some 2 billion people worldwide are affected by iron-
deficiency anaemia (IDD).
 IDD is widely prevalent in India, with
 20% of adult males,
 40% of children and adult non-pregnant females
 80% of pregnant females being affected.

3. Classification
The main groups of anaemias classified according to the
underlying cause
 Reduced red-cell production:
• Defective precursor proliferation
• Defective precursor maturation
• Defective proliferation and maturation
 Increased rate of red-cell destruction:
• Haemolysis
 Loss of red cells from the circulation:
• Bleeding

4. Distribution and loss of iron
1.The total amount of iron in the adult body is between 3 and 4 gm as haem
2. Haem is found as haemoglobin and myoglobin, although appreciable
quantities are found the liver, kidney and intestine
3. In a normal individual, the average red cell life span is 120 days. Thus,
0.8–1% of red cells turn over each day. Because each milliliter of red cells
contains 1 mg of elemental iron, the amount of iron needed to replace
those red cells lost through senescence amounts to 20 mg/d (assuming an
adult with a red cell mass of 2 L
Adult male 80 kg (mg) Adult female 60 kg (mg)
Haemoglobin 2500 1700
Myoglobin/ enzymes 500 300
Transferrin iron 3 3
Stores 600 to 1000 0 to 300

5. Recommended daily allowance for iron.
Current recommended dietary allowances of iron for
Indians:
 Boy 16-18yrs 50 (mg of iron/day)
 Girl 16-18 30
 Men >18 28
 Women >18 30
 Pregnant women 38
*Computed based on absorption rates of 3 per cent for males,5 percent for females

6. Causes of iron deficiency
Increased Demand for Iron
 Rapid growth in infancy or adolescence
 Pregnancy
 Erythropoietin therapy
Increased Iron Loss
 Chronic blood loss
 Menses
 Acute blood loss
 Blood donation
 Phlebotomy as treatment for polycythemia vera
Decreased Iron Intake or Absorption
 Inadequate diet
 Malabsorption from disease (sprue, Crohn's disease)
 Malabsorption from surgery (postgastrectomy)
 Acute or chronic inflammation

7. Absorption of iron from gut and homeostasis
 Iron absorption—this occurs in the duodenum and upper jejunum and
the following complex processes are involved:
(1) divalent metal transporter protein (DMT1)—essential for
uptake of ferrous ions by gut cells and erythron
(2) ferrireductase—reduces ferric form to ferrous
(3) uptake of haem by enterocytes—mediated by an unknown
membrane protein;
(4) ferroportin—mediates egress of ferric ions from enterocytes.
 Iron homeostasis—this is maintained by rigorous control of absorption
from the diet orchestrated by the peptide hormone, hepcidin, which is
synthesized by the liver and regulates the process by inhibiting efflux
of iron from enterocytes.

8. Iron metabolism and Haem synthesis
 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
haemosiderin
 They release iron to plasma, where it attaches to transferrin
which takes it to tissues with transferrin receptors –
especially the bone marrow – where the iron is
incorporated by erythroid cells into haemoglobin
 There is a small loss of iron each day in urine, faeces, skin
and nails and in menstruating females as blood (1-2 mg
daily) is replaced by iron absorbed from the diet.

9. Iron cycle
Fe
Fe
Fe
Fe
Fe Ferritin
Hemosiderin
slow
FeFe
Fe
Fe
Fe
Fe
Fe Fe
Fe
Ferritin Ferritin
TransferrinReceptor
RBC PRECURSOR
CIRCULATING RBCs
Fe
Fe
TRANSFERRIN
MONONUCLEAR
PHAGOCYTES

10. Stages in the development of iron deficiency*
 Prelatent :- the stage of negative iron balance
 reduction in iron stores without reduced serum iron
levels
 Latent:- stage of iron-deficient erythropoiesis
 iron stores are exhausted, but the blood haemoglobin
level remains normal
 Stage of Iron deficiency anemia
 blood haemoglobin concentration falls below the lower
limit of normal
*discussed in detail later

11. Approach to IDD will be considered under the
following heads:
 History
 Clinical features: general and specific
 Examination
 Blood tests
 Bone marrow picture
 Differential diagnosis
 Treatment

12. History
 In slowly developing anaemia, even at very low
haemoglobin levels, symptoms of anaemia may be absent.
 History of a sore tongue, dysphagia, dyspepsia, bleeding
from any site, and of symptoms suggestive of
malabsorption is important in cases of anaemia.
 Family history is important mainly in haemolytic anaemias
eg. thalassaemias in Sindhis, Kutchhis
Sickle cell disease in Patels
G-6-PD deficiency in Parsis

13. Symptoms of anaemias in general
 Can be classified as per each system:
 Fatigue
 Dizziness, light headedness
 Headache
 Insomnia
 Tinnitus
 Palpitation
 Dyspnoea
 Lethargy
 Disturbances in menstruation, reduced libido
 Impaired growth in infancy

14. Symptoms of IDD
 Irritability
 Poor attention span with lack of interest in
surroundings
 Poor work performance
 Behavioural disturbances
 Pica (geophagia. pagophagia, abnormal food cravings)
 Defective structure and function of epithelial tissue
 especially affected are the hair, the skin, the nails, the tongue,
the mouth, the hypopharynx and the stomach
 Increased frequency of infection.

15. Pica (perverted eating habits)
 The habitual ingestion of unusual substances
 earth, clay (geophagia)
 laundry starch (amylophagia)
 ice (pagophagia)
 Usually is a manifestation of iron deficiency and is
relieved when the deficiency is treated
 It is dangerous because it can lead to helmenthiasis
(hookworm)

16. Abnormalities in physical examination
 Pallor - of skin, lips, nail beds and conjunctival mucosa
 Nails - flattened, fragile, brittle,
-koilonychia( hollow nail) due to retarded growth of nail plate.
3 stages: brittleness, platynychia and spooning
 Tongue and mouth
 Atrophic glossitis, angular cheiliosis, stomatitis
 Dysphagia
 Stomach
 atrophic gastritis, (reduction in gastric secretion,
malabsorption)
 The cause of these changes in iron deficiency is uncertain,
but may be related to the iron requirement of many
enzymes present in epithelial and other cells

17. KOILONYCHIA
&
ATROPHIC
GLOSSITIS

18. Angular
cheiliosis

19. Laboratory investigations
 The single most important investigation is a careful examination of a
good-quality Romanowsky-stained peripheral smear (PS).
 Some common morphologic abnormalities of the red cells seen on PBS
in IDD are as follows :
Abnormality Significance
Hypochromia (Defective haemoglobinisation) iron-deficiency anaemia,
thalassaemias
Microcytosis (Defective haemoglobinisation) iron-deficiency anaemia,
thalassaemias
Anisocytosis (Variation in size of cells) iron-deficiency anaemia,
thalassaemias
haemoglobinopathies
Pencil cells and target cells are amongst others to be seen and both are the
result of defective haemoglobinisation and/or excess membrane

20. Normocytic Normochromic and Microcytic
Hypochromic PBS: A compraison

21. Pencil cells: Oval to elongated, ellipsoid shape with central
area of pallor and hemoglobin at both ends of cell
Significance: Iron deficiency anaemia (Elongated cells)
Vitamin B12 deficiency anaemia (Oval Cells)

22. Anisocytosis
RBC show abnormal size variation
Significance: Iron deficiency
Vit B12 deficiency

23. Target Cells:
Characterised by thin “bulls-eye” shape and an increase in the surface
membrane area to volume ratio due to a decrease in Hb
Significance: Iron Deficiency Anaemia,
Vit B12 deficiency Anaemia and
other disorders (eg Liver Disorders, Thalassemia)

24. Reticulocyte count: (N= upto 2%)
 This gives an estimate of the adequacy of the marrow
response to the anaemia.
 Reticulocytes are young red cells with presence of
nuclear remnants in the cytoplasm
 Reticulocytopenia occurs in nutritional deficiency
anaemias and aplastic anaemia

25. Laboratory findings (1)
 Blood tests
 erythrocytes
 hemoglobin level 
 packed cell volume (PCV) 
 RBC 
 MCV and MCH 
 Retic count 
 anisocytosis
 poikilocytosis
 Hypochromia
 leukocytes
 normal
 platelets
 usually normal or thrombocytosis

26. Iron studies
 Serum Iron - the amount of circulating iron bound to
transferrin(normal range is 50–150 g/dL)
 Total Iron-Binding Capacity(TIBC) - an indirect measure of the
circulating transferrin (normal range is 300–360 g/dL)
 the serum ferritin level correlates with total body iron stores; thus,
is the most convenient laboratory test to estimate iron stores. The
normal value for ferritin in Adult males 100 g/L, while adult females
30 g/L.
 Red cell protoporphyrin : reflects an inadequate iron supply to
erythroid precursors to support hemoglobin synthesis. Normal
values are <30 g/dL of red cells. In iron deficiency, values in excess
of 100 g/dL are seen.
 Serum Levels of Transferrin Receptor Protein: because transferrin
receptor protein (TRP) is released by cells into the circulation,
serum levels of TRP reflect the total erythroid marrow mass.
Normal values are 4–9 g/L

27. Laboratory findings (2)
 Iron metabolism tests
 serum iron concentration 
 total iron-binding capacity 
 saturation of transferrin 
 serum ferritin levels 
 sideroblasts 
 serum transferrin receptors 

28. Bone marrow examination
 Staining of iron stores in the bone marrow with Perls’s
reagent where it appears blue.
 Examination of the amount of iron provides useful
information as to the appropriateness of iron therapy for
hypochromic anaemia eg. In CKD, Chronic inflammation.

29. Laboratory findings (3)
 Bone marrow examination
 high cellularity
 mild to moderate erythroid hyperplasia
 bone marrow shows absence of stainable iron

30. Stages in the development of iron deficiency
 Prelatent :- the stage of negative iron balance
 reduction in iron stores without reduced serum iron levels
 Hb (N), MCV (N), iron absorption (), transferin saturation (N),
serum ferritin (), marrow iron ()
 Latent:- stage of iron-deficient erythropoiesis
 iron stores are exhausted, but the blood haemoglobin level
remains normal
 Hb (N), MCV (N), TIBC (), serum ferritin (), transferin saturation
(), marrow iron (absent)
 Stage of Iron deficiency anemia
 blood haemoglobin concentration falls below the lower limit
of normal
 Hb (), MCV (), TIBC (), serum ferritin (), transferin saturation
(), marrow iron (absent)

31. Differential diagnosis
Tests Iron Deficiency Inflammation Thalassemia Sideroblastic
Anemia
Smear Micro/hypo Normal
micro/hypo
Micro/hypo with
targeting
Variable
Sr.Iron <30 <50 Normal to high Normal to high
TIBC >360 <300 Normal Normal
Percent
saturation
<10 10–20 30–80 30–80
Ferritin (g/L) <15 30–200 50–300 50–300
Hemoglobin
pattern on
electrophoresis
Normal Normal Abnormal with
thalassemia; can
be normal with
thalassemia
Normal

32. Management of iron deficiency anemia
Correction of the iron deficiency
 Orally
 Blood transfusion
 intravenously
Treatment of the underlying disease

33. Blood tranfusion (PRC’s)
 Indications:
Symptoms of anemia
Cardiovascular instability
Continued and excessive blood loss from whatever source
Advantages:
1. Transfusions correct the anemia acutely
2. Transfused red cells provide a source of iron for
reutilization (assuming they are not lost through
continued bleeding.)

34. Oral iron therapy
 The optimal daily dose - 300 mg of elemental ironOral iron preparations
Generic Name Tablet (Iron Content) in mg
and % of absorption
Ferrous sulfate 325 (65) 20% ( Fefol, Fesovit, Orofer)
Ferrous fumarate 325 (107) 33% (Vitcofol. Livogen, Enzofer)
Ferrous gluconate 325 (39) 12%
Polysaccharide iron 150 (150) 100%

35. Oral iron: additional points
 continue treatment for 3 - 6 months after the anemia is
relived
 side effects
 heartburn, nausea, abdominal cramps, diarrhoea
 iron absorption
 is enhanced: vitC, meat, orange juice, fish
 is inhibited: cereals, tea, milk (tannin, phylates and
phosphates)

36. Failure of oral therapy
 Incorrect diagnosis
 Complicating illness
 Failure of the patient to take prescribed medication
 Inadequate prescription (dose or form)
 Continuing iron loss in excess of intake
 Malabsorption of iron

37. Parenteral iron therapy (1)
 Is indicated when the patient
 intolerance to oral iron
 loses iron (blood) at a rate to rapid for the oral
intake
 is unable to absorb iron from gastrointestinal
tract

38. Parenteral iron therapy (ii)
 Preparations and administration
iron - dextran complex (50mg iron /ml)
 intramuscularly or intravenously
 necessary is the test for hypersensitivity, no longer
used
newer iron complexes such as sodium ferric gluconate
(Ferrlecit) and iron sucrose (Venofer) have lower rates
of adverse effects.
iron to be injected (mg) = (15-pts Hb/gm%) x body weight
(kg) x2.3 + 1000(for stores)

39. Side effects
 Local:
pain at the injection site, discoloration of the skin,
lymph nodes become tender for several weeks, pain in
the vein injected, flushing, metallic taste
 Systemic:
 Immediate: hypotension, headache, malaise,
urticaria, nausea, anaphylactoid reactions
 Delayed: lymphadenopathy, myalgia, arthralgia,
fever

40. Thank You.