Micronutrient Deficiencies
Community Medicine · Nutrition · lean revision notes
Micronutrient Deficiencies
Micronutrients are vitamins and minerals required in small amounts but indispensable for growth, immunity, vision, haematopoiesis and neurodevelopment. For NEET PG, this topic sits at the intersection of clinical medicine and Community Medicine — examiners love linking a single classic sign to its deficiency, then asking the prophylactic dose, treatment dose, or national programme schedule. Master the cut-offs, the grading systems, and the RCH/Anaemia Mukt Bharat doses.
Classification of micronutrients
Micronutrients are broadly divided into:
- Vitamins — fat-soluble (A, D, E, K; stored, toxicity possible) and water-soluble (B-complex, C; not stored except B12, daily intake needed).
- Minerals / trace elements — iron, iodine, zinc, fluorine, copper, selenium, chromium.
The "big four" public-health micronutrient deficiencies in India are iron, vitamin A, iodine and (increasingly) vitamin D and zinc. The National Nutritional Anaemia Prophylaxis Programme, National Programme for Prevention of Blindness, and National Iodine Deficiency Disorders Control Programme (NIDDCP) target the first three.
High-yield: The three classic "hidden hunger" deficiencies of public-health importance globally (WHO) are iron, vitamin A and iodine.
1. Iron Deficiency Anaemia (IDA)
Pathophysiology and stages
Iron deficiency is the commonest nutritional deficiency worldwide. It evolves through three sequential stages before frank anaemia appears:
| Stage | Name | First marker affected | Key findings |
|---|---|---|---|
| 1 | Iron depletion | ↓ Serum ferritin | Ferritin <15 µg/L; stores gone; Hb normal |
| 2 | Iron-deficient erythropoiesis | ↑ TIBC, ↓ transferrin saturation, ↑ FEP | Transferrin sat <16%; Hb still near-normal |
| 3 | Iron deficiency anaemia | ↓ Haemoglobin | Microcytic hypochromic anaemia, ↓ MCV, ↓ MCH |
High-yield: Serum ferritin is the earliest and most sensitive indicator of iron stores; the last to fall is haemoglobin. Ferritin is also an acute-phase reactant — falsely raised in infection/inflammation.
Clinical features
Fatigue, pallor, dyspnoea, koilonychia (spoon nails), angular stomatitis, glossitis, pica (pagophagia — craving ice), and Plummer-Vinson / Paterson-Brown-Kelly syndrome (IDA + dysphagia + post-cricoid oesophageal web; premalignant for oesophageal carcinoma).
Diagnosis
Peripheral smear: microcytic hypochromic RBCs, anisopoikilocytosis, pencil cells, target cells. Investigation of choice for body iron stores = serum ferritin; gold standard = bone marrow Prussian-blue (Perls) stain showing absent stainable iron (rarely done).
WHO Hb cut-offs (g/dL) for anaemia:
| Group | Anaemia if Hb < |
|---|---|
| Children 6–59 months | 11.0 |
| Children 5–11 yr | 11.5 |
| Children 12–14 yr / non-pregnant women | 12.0 |
| Pregnant women | 11.0 |
| Adult men | 13.0 |
Management & national programme
Treatment dose: oral ferrous sulphate giving elemental iron 3–6 mg/kg/day in children; adults ~100–200 mg elemental iron/day; continue 3 months after Hb normalises to replenish stores. Best response marker = reticulocytosis at 5–10 days; expected Hb rise ~1 g/dL per 2 weeks.
Anaemia Mukt Bharat (AMB) — 6×6×6 strategy prophylaxis (IFA):
- 6–59 months: IFA syrup 1 mL (20 mg iron + 100 µg folic acid) twice weekly.
- 5–9 years: 45 mg iron + 400 µg folic acid weekly (pink tablet).
- 10–19 years adolescents: WIFS — 60 mg iron + 500 µg folic acid weekly (blue tablet).
- Pregnant & lactating women: 60 mg elemental iron + 500 µg folic acid daily for 180 days antenatally and continued 180 days postpartum.
High-yield: Under AMB, the pregnant woman gets one IFA tablet daily for at least 180 days in pregnancy. Folic acid 400 µg (5 mg if high risk) is started periconceptionally to prevent neural tube defects.
High-yield: Parenteral iron (iron sucrose / ferric carboxymaltose) is reserved for intolerance, malabsorption, or non-compliance — never to "speed up" routine cases.
2. Vitamin A Deficiency (VAD) & Xerophthalmia
Function and pathophysiology
Retinol is needed for rhodopsin synthesis (rod vision) and maintenance of epithelial/conjunctival integrity. Deficiency causes both ocular signs and increased infection-related child mortality (measles, diarrhoea, respiratory infection).
WHO Xerophthalmia classification (must memorise order)
| Code | Sign | Reversible? |
|---|---|---|
| XN | Night blindness (earliest symptom) | Yes |
| X1A | Conjunctival xerosis | Yes |
| X1B | Bitot's spot (foamy triangular patch, temporal conjunctiva) | Yes |
| X2 | Corneal xerosis | Yes |
| X3A | Corneal ulceration / keratomalacia <1/3 cornea | Partly |
| X3B | Keratomalacia ≥1/3 cornea | No (blinding) |
| XS | Corneal scar | — |
| XF | Xerophthalmic fundus | — |
Flow of progression: XN → X1A → X1B → X2 → X3A → X3B → XS
High-yield: Night blindness (XN) is the earliest sign; Bitot's spot (X1B) is the earliest specific clinical sign. Keratomalacia is the commonest cause of nutritional childhood blindness in India.
High-yield: Bitot's spots are due to keratinised epithelium + Corynebacterium xerosis, classically on the temporal conjunctiva, and may persist even after treatment (so not a good prevalence indicator beyond age 6).
Diagnosis
Clinical signs + serum retinol <0.70 µmol/L (20 µg/dL) indicates deficiency; <0.35 µmol/L is severe. Conjunctival impression cytology and dark adaptometry are supportive.
Treatment & prophylaxis (National Prophylaxis Programme Against Nutritional Blindness)
WHO treatment of xerophthalmia / measles (oral vitamin A):
- <6 months: 50,000 IU
- 6–12 months: 100,000 IU
- >12 months: 200,000 IU
Give on day 0, day 1, and day 14 (three doses).
Prophylactic schedule (India): first dose 1,00,000 IU at 9 months with measles vaccine, then 2,00,000 IU every 6 months up to 5 years (total 9 doses). Pregnant women should not exceed 10,000 IU/day (teratogenic in excess).
High-yield: Megadose vitamin A toxicity → pseudotumour cerebri (raised ICP), bulging fontanelle in infants, dry skin, hepatotoxicity. Hence dose by age and never exceed recommended schedule.
3. Iodine Deficiency Disorders (IDD)
Spectrum
Iodine is essential for thyroid hormone (T3/T4) synthesis. Deficiency produces a spectrum well beyond goitre:
- Fetus: abortions, stillbirth, congenital anomalies.
- Neonate: neonatal hypothyroidism, cretinism (neurological: deaf-mutism, squint, spastic diplegia, mental retardation; myxoedematous type: dwarfism, hypothyroid features).
- Child/adolescent: goitre, impaired mental function, retarded growth.
- Adult: goitre, hypothyroidism, ↓ work capacity.
High-yield: Iodine deficiency is the most common preventable cause of mental retardation worldwide. The most damaging consequence is on the developing fetal brain.
Diagnosis & assessment indicators
Median urinary iodine concentration (UIC) is the best population indicator of recent iodine intake:
| Median UIC (µg/L) | Iodine status |
|---|---|
| <20 | Severe deficiency |
| 20–49 | Moderate deficiency |
| 50–99 | Mild deficiency |
| 100–199 | Optimal (adequate) |
| 200–299 | Above requirement |
| ≥300 | Excessive |
Goitre prevalence (palpation/USG) and neonatal TSH (>5 mIU/L in >3% of newborns suggests IDD) are also used.
Prophylaxis — NIDDCP
- Universal salt iodisation is the cornerstone.
- Iodine content: at production level ≥30 ppm; at consumer level ≥15 ppm (parts per million).
- Annual requirement of iodine ≈ 150 µg/day (adult), 250 µg in pregnancy/lactation.
- Iodised oil (oral/injectable) for areas where salt iodisation is impractical.
- NIDDCP target: reduce IDD prevalence to <10%.
High-yield: Goitrogens (cabbage, cauliflower, tapioca/cassava, soybean) and the cyanogenic glycoside in cassava worsen iodine deficiency. Excess iodine can paradoxically cause iodine-induced hyperthyroidism (Jod-Basedow).
4. Vitamin D Deficiency — Rickets & Osteomalacia
Pathophysiology
Vitamin D (cholecalciferol, D3) is synthesised in skin via UV-B, then hydroxylated in liver → 25(OH)D (storage form, best status marker) and kidney → 1,25(OH)₂D (calcitriol) (active form). It promotes intestinal calcium and phosphate absorption. Deficiency → ↓ Ca/PO₄ → defective bone mineralisation.
| Feature | Rickets (children) | Osteomalacia (adults) |
|---|---|---|
| Defect | Unmineralised growing epiphyseal cartilage | Unmineralised osteoid in mature bone |
| Signs | Craniotabes, frontal bossing, rachitic rosary, Harrison's sulcus, bow legs/knock knees, widened wrists, delayed dentition/fontanelle closure, double malleoli | Bone pain, proximal myopathy, waddling gait, pseudofractures |
| X-ray | Cupping, splaying, fraying of metaphysis | Looser's zones (pseudofractures), Milkman lines |
Diagnosis
Investigation of choice = serum 25-hydroxyvitamin D. Cut-offs: deficiency <20 ng/mL (<50 nmol/L), insufficiency 20–30 ng/mL, sufficiency >30 ng/mL. Biochemistry in nutritional rickets: ↓/normal Ca, ↓ PO₄, ↑ alkaline phosphatase (ALP — earliest), ↑ PTH (secondary hyperparathyroidism).
Treatment
Vitamin D ("stoss" or daily) — e.g. cholecalciferol 2000 IU/day for 6 weeks or 60,000 IU/week × 6 weeks, then maintenance, plus adequate calcium. Sunlight exposure for prevention.
High-yield: Rachitic rosary = beading at costochondral junctions; scorbutic rosary (vitamin C) is sharper/angular with a step-off and sternum depressed inward. Don't confuse the two.
5. B-complex & Vitamin C deficiency syndromes
| Vitamin | Deficiency disease | Classic features / triad |
|---|---|---|
| B1 (thiamine) | Beriberi; Wernicke-Korsakoff | Wet beriberi (high-output cardiac failure, oedema), dry beriberi (peripheral neuropathy); Wernicke triad: ophthalmoplegia + ataxia + confusion; infantile beriberi (aphonic cry) |
| B2 (riboflavin) | Ariboflavinosis | Angular stomatitis, cheilosis, glossitis (magenta tongue), photophobia |
| B3 (niacin) | Pellagra | 3 D's: Dermatitis (Casal's necklace, photosensitive), Diarrhoea, Dementia (+4th D Death). Seen in maize-eaters, Hartnup disease, INH therapy, carcinoid |
| B5 (pantothenic acid) | Burning feet syndrome | Paraesthesia of feet |
| B6 (pyridoxine) | Peripheral neuropathy, sideroblastic anaemia, seizures (infants) | INH-induced neuropathy prevented by pyridoxine |
| B7 (biotin) | Dermatitis, alopecia | Raw egg white (avidin) ingestion |
| B9 (folate) | Megaloblastic anaemia, NTDs | Glossitis; NO neurological signs |
| B12 (cobalamin) | Pernicious/megaloblastic anaemia; subacute combined degeneration | Glossitis, neuropathy, dorsal column signs; methylmalonic acid + homocysteine ↑ |
| C (ascorbic acid) | Scurvy | Perifollicular haemorrhage, corkscrew hairs, swollen bleeding gums, subperiosteal haemorrhage, poor wound healing; scorbutic rosary |
High-yield: Pellagra = niacin (B3) deficiency, classically in populations subsisting on maize/jowar (niacin is bound, low tryptophan). Casal's necklace = photosensitive dermatitis around the neck.
High-yield: B12 vs folate — both cause megaloblastic anaemia, but only B12 deficiency causes neurological damage (SACD). Giving folate alone to a B12-deficient patient corrects anaemia but worsens neuropathy — always check B12 first.
High-yield: Always give thiamine BEFORE glucose in suspected Wernicke's / alcoholics — glucose first precipitates acute Wernicke encephalopathy.
Mnemonics:
- Pellagra → "4 D's: Dermatitis, Diarrhoea, Dementia, Death."
- Wernicke → "COAT": Confusion, Ophthalmoplegia, Ataxia, Thiamine.
- Fat-soluble vitamins → "ADEK."
Zinc & other trace elements (quick facts)
- Zinc: acrodermatitis enteropathica, growth retardation, hypogonadism, poor wound healing, impaired taste (hypogeusia). Zinc + ORS is now standard in childhood diarrhoea — 10–14 days, 10 mg/day (<6 months) or 20 mg/day (≥6 months) — reduces duration and recurrence.
- Fluorine: deficiency → dental caries; excess → dental & skeletal fluorosis (>1.5 ppm in water; optimal ~0.5–0.8 ppm in Indian climate).
- Copper: Menkes (deficiency, kinky hair), anaemia/neutropenia; selenium: Keshan disease (cardiomyopathy), Kashin-Beck disease.
High-yield: WHO/UNICEF diarrhoea management = low-osmolarity ORS + zinc for 14 days. This is a favourite single-best-answer.
Key differentials at a glance
- Microcytic anaemia: IDA vs thalassaemia trait (normal/raised RBC count, ↑ HbA2, normal ferritin) vs anaemia of chronic disease (↑ ferritin, ↓ TIBC) vs sideroblastic.
- Night blindness: Vitamin A deficiency vs retinitis pigmentosa vs congenital stationary night blindness.
- Bowing of legs: nutritional rickets vs hypophosphataemic (vitamin-D-resistant) rickets (↓PO₄, normal Ca/PTH, X-linked) vs renal osteodystrophy vs physiological bowing.
- Glossitis/stomatitis: B2, B3, B6, B12, folate, iron — examiners combine signs to point at one.
Recently asked / exam angle
- Earliest indicator of iron deficiency → serum ferritin (not Hb). Repeatedly tested.
- Xerophthalmia grading — match XN/X1B/X3B to the lesion; "earliest sign" = night blindness; "earliest specific sign" = Bitot's spot.
- Vitamin A dosing by age (50k / 100k / 200k IU) and the 9-month + measles prophylactic dose.
- Iodine in salt: ≥15 ppm at consumer level and median UIC 100–199 µg/L = optimal.
- Pellagra = niacin; 3 D's; pellagra in Hartnup, INH, carcinoid.
- Zinc dose in diarrhoea (10/20 mg × 14 days) and AMB IFA pregnancy dose (60 mg iron, 180 days).
- Looser's zones = osteomalacia; rachitic rosary vs scorbutic rosary.
- Thiamine before glucose; B12 before folate. Classic "trap" MCQs.
- Most sensitive vitamin-D status test = 25(OH)D; earliest biochemical change in rickets = ↑ ALP.
Rapid revision
- Iron deficiency stages: ferritin ↓ first → transferrin sat ↓ → Hb ↓ last.
- Pregnant woman anaemia cut-off = Hb <11 g/dL; AMB gives 60 mg iron + 500 µg folate daily × 180 days.
- Plummer-Vinson = IDA + dysphagia + oesophageal web (premalignant).
- Vitamin A: XN (night blindness) earliest, X1B (Bitot's spot) earliest specific, X3B keratomalacia → irreversible blindness.
- Vitamin A treatment: <6 mo 50k, 6–12 mo 100k, >12 mo 200k IU on days 0, 1, 14.
- Iodine: salt ≥15 ppm consumer level, median UIC 100–199 µg/L optimal; deficiency = top preventable cause of mental retardation.
- Cretinism (neurological type): deaf-mutism, squint, spastic diplegia, mental retardation.
- Vitamin D: best marker 25(OH)D <20 ng/mL = deficient; earliest biochemical change ↑ ALP; Looser's zones in osteomalacia.
- Pellagra = niacin (B3); 3 D's; Wernicke = thiamine; ophthalmoplegia + ataxia + confusion.
- B12 deficiency causes SACD; folate does not — never give folate alone in B12 deficiency.
- Zinc + low-osmolarity ORS for 14 days in childhood diarrhoea (10/20 mg).
- Scurvy (vitamin C): corkscrew hairs, perifollicular & subperiosteal haemorrhage, bleeding gums, scorbutic rosary.