Iron is an essential trace element required for oxygen transport and many enzymatic processes. Women and children have higher iron requirements. Dietary sources like jaggery are rich in iron while milk is poor. Factors like calcium, phytates and oxalates inhibit iron absorption in the duodenum and jejunum, while vitamin C and cysteine enhance absorption. Iron is important for carrying oxygen via hemoglobin, acting as an enzyme cofactor, and supporting brain and cell functions. Iron deficiency anemia results from low intake or increased losses and is characterized by low hemoglobin and red blood cell changes. It is commonly seen in pregnant women and treated with oral or parenteral iron supplements.

1. Iron (Fe)

2. • Trace Element: daily req. < 100mg
• Adult man & postmenopausal women:10 mg
• Premenopausal women: 15 to 20 mg
• Pregnant women: 30 to 60 mg
Women require greater amount due to physiological loss during
menstruation.

3. Source

4. • Jaggery is rich source of Iron
• Milk is poor source of Iron.

5. Factors influencing Iron Absorption
• Dietary factors inhibiting iron absorption
Iron is abs. in upper part of Duodenum and Jejunum.
• Calcium, Phosphates, Copper and Lead.
• Phytates and Oxalates
Cereals Green leafy Veg.

6. Dietary factors enhancing iron absorption
•Ascorbic acid
•Cysteine
•H+

7. •Why Fe is important for body?

8. Role of iron:
1. To carry O2 as part of HB.
2. As part of enzymes like oxidases, catalases, peroxidases, cytochromes,
ribonucleotide reductase, aconitase, Nitric oxide synthase→ required for DNA, RNA
synthesis, ETC ,cell proliferation.
3. Formation of myelin & dendritic cells →so required for brain function such
as learning & memory.
4. Supports transcription of certain genes → cell cycle & differentiation.

10. Iron S. centers

11. Iron in our body:
Iron has critical functions but body must protect itself from free
Iron bcz participates in rxns generating free radicals such as
singlet O2 or OH-.

12. Iron cycle

13. Iron absorption:
Heme transporter
Duod. Cyt b
Vit C
Divalent metal transporter

14. Non heme dietary iron : Fe++
& Fe+++ salts & organic
complexes.
Fe3+ converted to Fe2+ by vit
C & apical membrane
Ferrireductase, inc duodenal
cytochrome b
Acid microclimate at brush border
provides an H+ potential gradient
to drive Fe2+ transport via
Divalent Metal ion transporter
DMT-1 into enterocyte
heme
Endocytosis: protein involved is
heme carrier protein 1
Fe2+ liberated I n
lysosome/endosome. Basolateral
export of Fe2+ mediated by
Ferroportin in a/w Hephaestin,
Heme Oxygenase & Diferric
Transferrin

15. Iron Transport

16. Role of Transferrin

17. Hephaestin and Ceruloplasmin
• Ferroxidase activity.
• It oxidizes iron as part of the transmembrane transfer process
&/or the process of loading iron onto plasma Tf.
• Ceruloplasmin has same action
in circulation

18. Transferrin receptor

19. Body Fe stores
: storage form of Fe
• Intestinal mucosal cells, liver, spleen, bone
marrow
• It can bind to 4000 Fe atoms / molecule
• Plasma Ferritin levels body Fe stores
• Acute Phase reactant

21. Hemosiderin (iron overload)

22. • Deposition of hemosiderin is HEMOSIDEROSIS.
• BRONZE DIABETES :
1.deposition of hemosiderin in Pancreas lead to decreased insulin and
hyperglycemia.
2. deposition in liver Cirrhosis
3. Deposition under skin bronze skin colour

24. Hemochromatosis
• Excess iron abs. from intestine.
• AR
• Mutation of HFE gene on C-6.
• Gene product DMT 1 transporter & hepcidin synthesis
• Iron absorption from intestines
Lab Investigation:
Serum iron
Transferrin Saturation & Se Ferritin

25. Treatment
• Phlebotomy - every 3 month
• Chelation therapy – Desferroxamine
Complications-
• Cirrhosis / cancer
• Diabetes

26. •Clinical Significance:

28. CAUSES OF IDA
Increased Requirements
Growing infants and children
Menstruating women
Pregnancy,Lactation
Multiparity,Parturition
Decreased Intake
Low socioeconomic status
Vegetarian diet
Lack of balanced diet or poor
intake
Alcoholism ,Elderly
Increased Loss
GI bleeding
Regular blood donors
Post-operative patients with
significant blood loss.
Hematuria
Intestinal parasites (travel or
immigration from an endemic
area)
Intravascular hemolysis:
hemoglobinuria)
Decreased Absorption
Upper GI Pathology: Chronic
gastritis,Gastric
lymphoma,Celiac
disease,Crohn's disease
Medications that decrease
gastric acidity or bind iron
Gastrectomy or intestinal
bypass
Duodenal pathology

29. Evolution of IDA:

30. Investigations:
Hb-↓
Red cell indices-
↓MCV,↓MCH,
↓MCHC
PL- ↑/N
WBC-N/
granulocytopenia
Ret-N/↑
CH
HYPOCHROMIC , MICROCYTIC CELLS WITH PENCIL CELLS,
TEAR DROP CELLS, & OCCASIONAL TARGET CELLS.

31. • MICROCYTOSIS IN IFA:
• Erythrocyte division in the bone marrow is governed by the
hemoglobin concentration. Cell division stops when a critical
hemoglobin concentration has been reached. Therefore, if
hemoglobin production is defective (as occurs in iron
deficiency), erythrocytes continue to divide until that
hemoglobin concentration is reached. With each division they
become successively smaller.
• Hypochromia is caused by impairments in
Fe uptake and metabolism
Heme synthesis
Globin synthesis

32. • Serum Ferritin:
• Storage form of Fe
• Present in all tissues
• Water soluble
• Protein shell apoferritin→ forms hollow shell &
have ferroxidase activity→ takes up /release Fe
quickly.
• Adult males= 100 μg/L
• Adult females= 30 μg/L
• Iron stores depleted < 15 μg/L
HEMOSIDERIN: other
storage form
Present in
macrophages
Water insoluble

33. • Ferritin levels ↓ in IDA but↑by inflammation & cancers
which ↓its sensitivity for detection of Fe deficiency
coexisting with anemia of chronic inflammation.
• Serum Iron & Total Iron binding capacity:
• Normal S. Iron=50-150μg/dl ( diurnal variation- more in
morning )
• TIBC= 300-360 μg/dl
• Transferrin saturation = S.Ironx100/TIBC
• { normally 25-50%, <18% in IFA, > 50% in Fe
overload}

34. Evaluation of Bone Marrow Iron Stores:
• bone marrow aspirate or biopsy also helpful. Marrow iron
stain shows effective delivery of iron to developing
erythroblasts( sideroblasts)
• Normally 20-40% sideroblasts have visible ferritin granules
in their cytoplasm.

35. • IDA in Pregnancy and Parturition
• In pregnancy, the average iron loss resulting from
diversion of iron to the fetus, blood loss at delivery
(equivalent to an average of 150 to 200 mg of iron),
and lactation is altogether approximately 900 mg; in
terms of iron content, this is equivalent to the loss of
more than 2 L of blood.
• Approximately 30 mg of iron may be expended
monthly in lactation.
• Because most women begin pregnancy with low iron
reserves, these additional demands frequently result
in iron-deficiency anemia. Iron depletion has been
reported in some 85 to 100 percent of pregnant
women.

36. TREATMENT
• Treatment of cause.
• Diet: green leafy vegetables
• ( e.g. spinach) beans, lentils or
• red meat,
• Iron therapy:
• A) oral preparations:
• Fe sulphate 200mg ( 60 mg elemental- best
absorbed),
• ferrous gluconate 300mg( 35mg elemental-better
tolerated)

37. • Requirement : upto 200-300 mg of elemental Fe/day
of which about 50 mg is absorbed. Recent research
suggests the replacement dose of iron, at least in the
elderly with iron deficiency, may be as little as 15 mg
per day of elemental iron.
• Replacement : continue tablets for 6 months to
replenish stores( upto 0.5-1.0g stores should be
present)
• Side effects: nausea, vomiting, abdominal pain,
constipation, diarrhoea, black stools.
• Response: reticulocyte count ↑ by 4-7days, peak at
10 day.

38. • Fortification with ascorbic acid increases
bioavailability in both presence and absence of
inhibiting substances, but is subject to deterioration
from moisture or heat..
• Microencapsulation with lecithin binds and protects
the iron particles from the action of inhibiting
substances. The primary benefit over ascorbic acid is
durability and shelf life
• Using an iron amino acid chelate, such as NaFeEDTA,
similarly binds and protects the iron particles

39. • B) PARENTERAL :
• Indications: intolerance to oral iron
• Rapid replenishment needed
• Impaired iron absorption
• preparations
For i.m.
(stretch skin, insert needle
deep IM, release skin &
then inject to prevent skin
discolouration)
Iron dextran( Imferon)
Iron Sorbitol citrate(
Uniferon)
For IV
(In 5% dextrose or NS)
Iron dextran-Imferon
Iron gluconate-Ferrlecit

40. • Dose calculation:
• Test dose 25 mg before injection is essential.
• Complications: anaphylaxis, injection abscess,
discoloration of skin.
• C) BLOOD TRANSFUSION:
• PCV given in ↑↑blood loss, CHF, urgent
replenishment. Diuretics & antihistaminics given
to prevent fluid overload & allergy. Hb rises in 3
day. 1 unit PCV increases hematocrit by 3%.
2.38 X body wt(kg) X 15-Hb(g/dl) + 500mg or
1000mg for stores

41. Iron-Refractory iron deficiency anemia:
• Iron-refractory iron deficiency anemia (IRIDA) is an
autosomal recessive disorder characterized by iron
deficiency anemia unresponsive to oral iron treatment but
partially responsive to parenteral iron therapy. IRIDA has
recently been shown to be caused by mutations in the gene
TMPRSS6, which encodes a transmembrane serine
protease (also known as matriptase-2) expressed by the
liver. IRIDA patients show inappropriately elevated levels of
hepcidin, a circulating hormone produced by the liver that
inhibits both iron absorption from the intestine and iron
release from macrophage stores.

42. • Recent studies suggest that TMPRSS6 normally acts to
downregulate hepcidin expression by cleaving hemojuvelin,
a membrane-bound protein that promotes hepcidin
signaling in hepatocytes.
• Genes related to iron-refractory iron deficiency anemia :
• 1 TMPRSS6 transmembrane protease, serine 6
• 2 TMPRSS11A transmembrane protease, serine 11A
• 3 EPO erythropoietin.

43. Anemia due to other deficiencies