Iron is an essential nutrient that functions as a component of hemoglobin and proteins involved in oxygen transport and cellular respiration. Iron absorption occurs through three phases - luminal, mucosal, and basolateral - before entering the bloodstream. Hepcidin regulates iron levels by inhibiting absorption. Iron deficiency can cause microcytic hypochromic anemia while iron overload can damage organs like the liver, pancreas and skin if left untreated.

2. Important Functions:
• Forms a major component of important protein like
Hemoglobin and cytochromes.
• Present in Hemoglobin (major transfer protein)- O2 and CO2
• Compound of ETC – helps in cellular respiration.
• Helps in detoxification. Part of Cytochrome P450.
Recommended Dietary Allowance
• Adult: 20mg/day {out of which 1-2 mg is absorbed}
• Pregnancy and Lactation: 40mg/day
(creates an iron reserve in child as the child receives no iron input during breast feeding as milk
is a very poor source of iron)
• Growing children: 20-30 mg/day

4. Absorption, Transport And Storage of Iron (In Brief)
Absorption of Iron takes place in the intestine in 3 phases:
• Luminal Phase (Inside intestinal lumen)
• Mucosal cellular phase (Inside the duodenal enterocytes)
• Basolateral Phase (Release into portal blood stream)
And Finally the Extraluminal phase where is released into body
blood stream (Portal Circulation).

5. ABSORPTION,
TRANSPORT
&
STORAGE OF IRON

6. Fe+3
(Present in
food in our
diet)
Fe+2
(Absorbable
form of
Iron)
Gastric HCl, Vit C
DMT-1
Fe+2
Fe+3
(Stored as
Ferritin)
Duodenal
Enterocyte
Ferroportin Hephaestin
Fe+2 Ceruloplasmin Fe+3
Transferrin
Luminal Phase
Mucosal Cellular
Phase
Basolateral Phase
Blood/
Portal
Circulation

7. Transferrin
STORAGE FORM
Ferritin
Homosiderin
Also stored in :
Bone Marrow,
Spleen
Utilization:
Haemoglobin
Myoglobin
Cytochromes
Enzymes

9. REGULATION
IRON IS “ONE-WAY ELEMENT”
• REGULATION OF BODY IRON OCCURS AT ONLY AT LEVEL OF ABSORPTION AND NOT BY
EXCRETION.
• MOST OF THE BODY IRON STORED AND REUTILIZED.
•HEPCIDIN
• REGULATES IRON LEVEL - BY INHIBITING MEMBRANE PROTEIN:
• DMT-1 (DIVALENT METAL TRANSPORTER)
• FERROPORTIN
• INC: DURING ANAEMIA, HYPOXIA
• DEC: DURING INFLAMMATION (ACUTE PHASE PROTEIN), BODY IRON
STORES ARE FULL

10. IRON CONSERVATION
•HAPTOGLOBIN
• BINDS TO FREE HAEMOGLOBIN AFTER THE LYSIS OF RBC.
• PREVENTS EXCRETION THROUGH URINE
•HEMOPEXIN
• BINDS TO HEME MOLECULE AFTER REMOVAL FROM HAEMOGLOBIN
• PROTECTS THE BODY FROM ITS OXIDATIVE DAMAGE EFFECTS.

12. Iron Deficiency Anaemia
•CAUSES
•Nutritional deficiency of Iron
•Lack of absorption: due to Gastrectomy
•Hookworm infection: 1 worm can lead to 0.3mL blood loss per day.
•Repeated pregnancies: 1 g lost per parturition
•Chronic blood loss
•Lead poisoning

14. •MICROSCOPIC APPERANCE:
•Microcytic Hypochromic Anaemia
•LAB FINDINGS:
•Serum Iron Level : Decreases.
•Haemoglobin level: <10g/dL
•Ferritin level: <12µg/Dl
•TIBC (Total Iron Binding Capacity) : Increases

17. •CLINICAL MANIFESTATIONS:
• Apathy: patient becomes uninterested in surroundings (<10g, Body cells lack oxygen).
• Derangement in cellular respiration. (As Fe is part if cytochromes involved in cellular
respiration) Metabolic process becomes sluggish.
• Koilonychia : Spoon nail
• Achlorhydria: atrophy of gastric epithelium (dec abs. further aggravates the anaemia)
• Plummer-wilson syndrome:
• Atrophy of epithelium of oral cavity and oesophagus causes dysphagia.
• Difficult in swallowing due to epithelium degeneration of oral cavity and oesophagus
• Impaired attention, irritability, lowered memory (Very chronic case).
• Irreversible impairment of learning in children, apathy and poor scholastic performance.
In adults it leads to impairment in working capacity.

20. •TREATMENT:
• Oral Iron Supplement: 100 mg Iron + 500 µg Folic Acid (Pregnant Women)
20 mg Iron + 100 µg Folic Acid (Children)
• Iron Tablets + Vitamin C (For conversion of ferric to ferrous form)
• Along with additional Vit E supplement (To prevent Free-radical formation)

22. IRON OVERLOAD
•HOMOSIDEROSIS:
•CAUSES:
• Abnormal hepcidin-ferroportin complex
• Defective erythroid maturation
• Defective Iron transport
• Consequence of multiple RBC transfusion (common in early days)
• Hemosiderin pigments: accumulation in Liver and Spleen.
(Golden Brown granules)

23. •PRIMARY HEMOSIDEROSIS
• HEREDITARY HEMOCHROMATOSIS
• ABNORMAL GENE AT CHROMOSOME NO. 6 (SHORT HAND)
• CELLULAR DEFECT: INADEQUATE HEPCIDIN MEDIATED FERROPORTIN
DOWN REGULATION
• DIABETES MELLITUS- DUE TO DAMAGE TO BETA CELLS IN PANCREAS
• LIVER CIRRHOSIS
• SKIN DISCOLOURATION
• --- COLLECTIVELY CALLED BRONZE DIABETES

24. •SECONDARY HEMOSIDEROSIS
• DISORDER OF ERYTHROID MATURATION
• INEFFICIENT HEMPOESIS
•BANTU SIDEROSIS
• BANTU TRIBE IN AFRICA: MORE PRONE TO HEMOSIDEROSIS
• CONSUME HOME BREWED BEER IN LARGE QUANTITIES MADE FROM IRON POTS.
•TREATMENT
• DRAWING BLOOD REGULARALY
• DESFERROXAMINE- CHELATING AGENT – FE CHELATE WITH FE3+ TO FORM
FEROXAMINE WHICH IS EXCRETED IN URINE.