Nutritional Diseases

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Nutritional diseases arise when macronutrient (protein, carbohydrate, fat) or micronutrient (vitamins, minerals) intake is deficient, excessive, or imbalanced relative to bodily demand. The Pathology syllabus tests two recurrent clinical poles: Protein-Energy Malnutrition (PEM) in children and single-vitamin deficiency syndromes in adults.

Marasmus = chronic calorie + protein deficit → muscle wasting, no oedema, growth failure (<18 months).
Kwashiorkor = acute protein deficit with near-normal calories → oedema, fatty liver, hypoalbuminaemia, flaky-paint dermatitis, after weaning.
Rickets (children) vs Osteomalacia (adults): both from vitamin D deficiency causing defective mineralisation.
Pellagra = niacin (B3) deficiency → the 3 D’s: Dermatitis, Diarrhoea, Dementia.
Scurvy = vitamin C deficiency → bleeding gums, perifollicular haemorrhages, corkscrew hairs.

BMI cut-off (WHO Asia-Pacific)	Category
< 18.5	Underweight
18.5–22.9	Normal
≥ 23	Overweight
≥ 25	Obese

Use the Asia-Pacific thresholds for Indian INI CET stems; obesity drives T2DM, NAFLD, and hypertension.

🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

PEM spectrum and clinical differentiation

INI CET questions usually present a malnourished child and ask you to label the syndrome. Marasmus is a chronic adaptive state: weight-for-age < 60%, loss of subcutaneous fat, “old-man” facies, normal serum albumin, absent oedema. Kwashiorkor is an acute decompensation: oedema (often starting in the feet), hepatomegaly from fatty change (apolipoprotein B synthesis fails → hepatic triglyceride accumulation), hypoalbuminaemia (< 3 g/dL), depigmented, sparse hair, and angular stomatitis. Laboratory distinction centres on serum albumin, transferrin, and the essential amino acid index, all markedly depressed in kwashiorkor but preserved in marasmus.

Vitamin deficiency syndromes — clinical signatures

Each B-complex vitamin produces a near-pathognomonic picture tested in image- or vignette-based MCQs.

Vitamin B1 (thiamine): Beriberi — dry (symmetric peripheral neuropathy, wrist/foot drop) and wet (high-output cardiac failure, dilated chambers); also Wernicke-Korsakoff in alcoholics (ophthalmoplegia, ataxia, confabulation).
Vitamin B3 (niacin): Pellagra — Casal’s necklace dermatitis, diarrhoea, dementia.
Vitamin B12 + folate: Megaloblastic anaemia with hypersegmented neutrophils; B12 additionally causes subacute combined degeneration of dorsal columns and lateral corticospinal tracts.
Vitamin C: Scurvy — defective hydroxylation of proline/lysine in collagen → bleeding gums, perifollicular haemorrhages, corkscrew hairs, subperiosteal bleeds, impaired wound healing.

Deficiency	Syndrome	Hallmark lesion
Vitamin A	Xerophthalmia	Bitot spots, keratomalacia
Vitamin D	Rickets / Osteomalacia	Rachitic rosary, Looser zones
Vitamin K	Haemorrhagic disease	↑ PT/INR, prolonged clotting
Niacin (B3)	Pellagra	Casal’s necklace dermatitis
Vitamin B12	Megaloblastic anaemia + SCD	Hypersegmented neutrophils

Obesity — Indian cut-offs matter

BMI = weight (kg) / height (m)². For Indian populations, WHO Asia-Pacific thresholds (≥ 23 overweight, ≥ 25 obese) are the standard INI CET answer because of higher metabolic risk at lower BMI. Adipocyte hypertrophy (adult-onset) vs hyperplasia (childhood-onset) has therapeutic implications — hyperplasia is largely irreversible. Appetite regulation centres on the leptin–melanocortin axis in the arcuate nucleus; MC4R mutations cause monogenic obesity.

🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Mechanisms linking nutrient imbalance to tissue injury

Micronutrients are not merely “good for you” — each has a defined biochemical role whose failure explains the lesion. Vitamin C is the cofactor for prolyl/lysyl hydroxylase, so its loss produces collagen that cannot cross-link, manifesting as the vascular fragility of scurvy. Vitamin D’s active hormone, 1,25-(OH)₂-D₃, drives intestinal Ca²⁺ absorption via calbindin; in children, the unmineralised osteoid plus cartilage at the physis produces the widened, cupped metaphyses and rachitic rosary of rickets, whereas in adults only the osteoid seam thickens — the histology of osteomalacia. Niacin (B3) is the precursor of NAD⁺/NADP⁺, so deficiency impairs ATP synthesis and redox cycling, explaining the high-turnover tissues affected (skin, gut, brain).

Energy equations used in clinical stems

BMR (Mifflin–St Jeor): 10·kg + 6.25·cm − 5·age + 5 (men) or − 161 (women) kcal/day.
TEE = BMR × PAL, where PAL ranges 1.2 (sedentary) to 1.9 (very active).
Nitrogen balance = (protein g / 6.25) − (urinary urea N + 4); positive in growth, negative in catabolic PEM.
Devine ideal body weight: 50 kg (men) or 45.5 kg (women) + 2.3 kg per inch over 5 ft — used to dose chemotherapeutics and estimate caloric needs.

Adjacent links and common traps

Hypervitaminosis A is teratogenic (craniofacial, cardiac malformations) and causes pseudotumour cerebri; hypervitaminosis D causes hypercalcaemia, nephrocalcinosis, and metastatic soft-tissue calcification.
Plummer–Vinson triad (iron deficiency + oesophageal webs + dysphagia) predisposes to post-cricoid squamous carcinoma.
Endemic cretinism has two forms — neurological (deaf-mutism, spastic diplegia, normal stature) and myxoedematous (short stature, hypothyroidism) — both from in-utero iodine deficiency.

Trap: A child with oedema is not marasmus, even if severely wasted — kwashiorkor dominates when protein deficit is acute and recent, regardless of BMI.

Practice prompts

A 2-year-old weaned child presents with bilateral pitting oedema, hepatomegaly, hypopigmented hair, and serum albumin 1.8 g/dL. Name the syndrome and the hepatic lesion.
A chronic alcoholic with confusion, ataxia, and ophthalmoplegia after IV glucose — identify the deficiency, the syndrome, and the brainstem nuclei most affected.

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Nutritional Diseases