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Summary of Both Documents

These are clinical biochemistry exam case studies (MBBS level) - 10 minor cases (8 marks each) and 10 major cases (likely higher marks).

MINOR CASES (8 Marks Each)

Case 1 - Vitamin B12 Deficiency Anaemia (Post-Gastrectomy)

60-year-old female, post-partial gastrectomy | Hb 8g%, B12 150pg/mL, megaloblastic RBCs, hypersegmented neutrophils
  1. Diagnosis: Megaloblastic/pernicious anaemia due to Vitamin B12 deficiency
  2. Biochemical significance of gastric surgery: Partial gastrectomy removes parietal cells that produce Intrinsic Factor (IF). Without IF, B12 cannot be absorbed in the terminal ileum. B12 deficiency impairs DNA synthesis (needed for thymidylate synthesis via methyltetrahydrofolate), causing megaloblastic changes. B12 also needed for myelin synthesis - hence burning sensation in toes (subacute combined degeneration).
  3. Biochemical functions of B12:
    • Cofactor for methionine synthase (homocysteine → methionine, regenerates THF from methyl-THF)
    • Cofactor for methylmalonyl-CoA mutase (methylmalonyl-CoA → succinyl-CoA)
    • Required for normal myelin synthesis
    • Needed for DNA synthesis via folate metabolism
  4. Rich sources: Meat, liver, fish, eggs, dairy products (exclusively animal-based)

Case 2 - Iron Deficiency Anaemia

32-year-old female, koilonychia | Hb 8.7g%, microcytic hypochromic RBCs
  1. Diagnosis: Iron deficiency anaemia
  2. Common causes: Blood loss (menstruation, GI bleed), poor dietary intake, malabsorption, increased demand (pregnancy), hookworm infestation
  3. Biochemical significance: Iron is essential for haemoglobin (haem) synthesis. Deficiency impairs haemoglobin production → small pale RBCs (microcytic hypochromic). Iron also needed for myoglobin, cytochromes (energy production), hence fatigue. Koilonychia reflects iron-dependent enzyme deficiency in nail tissue.
  4. Rich dietary sources: Red meat, liver, green leafy vegetables (spinach), legumes, fortified cereals, jaggery

Case 3 - Metabolic Acidosis (High Anion Gap)

35-year-old AIDS patient, diarrhoea | pH 7.25, pCO2 27mmHg, HCO3 14mEq/L, Na 136, K 4, Cl 112
  1. Diagnosis: High anion gap metabolic acidosis
    • Anion gap = Na - (Cl + HCO3) = 136 - (112 + 14) = 10 mEq/L (borderline; actually this is normal anion gap). Given the clinical context (AIDS + diarrhoea), likely normal anion gap (hyperchloraemic) metabolic acidosis from diarrhoea (loss of HCO3).
    • pH 7.25 (acidotic), low HCO3 (14), compensatory low pCO2 (27) confirms metabolic acidosis with respiratory compensation.
  2. Normal ranges: pH 7.35-7.45, pCO2 35-45 mmHg, HCO3 22-26 mEq/L
  3. Respiratory compensation: Acidosis stimulates peripheral and central chemoreceptors → hyperventilation → increased CO2 exhalation → fall in pCO2 (Kussmaul breathing in severe cases) → partially corrects pH. Expected pCO2 = 1.5 × HCO3 + 8 ± 2 (Winter's formula) = 1.5 × 14 + 8 = 29 mmHg (observed 27 = adequate compensation).
  4. Causes:
    • Normal anion gap acidosis: Diarrhoea, renal tubular acidosis (RTA)
    • High anion gap acidosis: Diabetic ketoacidosis (DKA), lactic acidosis, uraemia, salicylate poisoning

Case 4 - Acute Renal Failure / Chronic Kidney Disease

27-year-old female, recurrent UTIs | Hb 6g%, creatinine 4.2mg/dL, urea 106mg/dL, haematuria, proteinuria
  1. Diagnosis: Acute-on-chronic renal failure (likely chronic pyelonephritis from recurrent UTIs leading to CKD)
  2. Biochemical finding indicating decreased GFR: Elevated serum creatinine (4.2 mg/dL; normal 0.6-1.2 mg/dL) and blood urea (106 mg/dL; normal 15-45 mg/dL). Creatinine is more specific as it is not affected by protein intake. Creatinine clearance directly reflects GFR.
  3. Cause of pedal oedema: Hypoproteinaemia from proteinuria → reduced oncotic pressure; also sodium and water retention due to reduced GFR → fluid accumulation in interstitium.
  4. Common causes of acute renal failure:
    • Pre-renal: Hypovolaemia, sepsis, cardiac failure
    • Renal (intrinsic): Glomerulonephritis, acute tubular necrosis, pyelonephritis
    • Post-renal: Urinary obstruction (stones, BPH)

Case 5 - Vitamin A Deficiency

3-year-old tribal child, xerophthalmia, Bitot's spots, corneal scarring, recurrent infections
  1. Diagnosis: Vitamin A (Retinol) deficiency
  2. Biochemical functions of Vitamin A:
    • Vision: 11-cis retinal is chromophore of rhodopsin (rod cells); deficiency → night blindness
    • Epithelial integrity: Retinoic acid regulates gene expression for epithelial differentiation
    • Immune function: Maintains mucosal barriers; supports lymphocyte function
    • Antioxidant (beta-carotene precursor)
    • Required for growth (IGF-1 signalling)
  3. RDA: 600 mcg RAE/day (children); 900 mcg/day (adult males)
  4. Rich sources: Liver (highest), fish liver oils, egg yolk, dairy, orange/yellow fruits and vegetables (beta-carotene: carrot, papaya, mango), dark leafy greens

Case 6 - Hypothyroidism

53-year-old female, weight gain, cold intolerance, constipation | TSH 20mIU/L (↑), FT4 4.0 pmol/L (↓)
  1. Diagnosis: Primary hypothyroidism
  2. Biochemical explanation for symptoms:
    • Thyroid hormones (T3/T4) regulate basal metabolic rate (BMR). Deficiency → reduced BMR → weight gain, fatigue, cold intolerance
    • Reduced Na/K-ATPase activity → myxoedematous changes (dry skin, coarse hair)
    • Reduced intestinal motility → constipation
    • Hyponatraemia and hypoalbuminaemia → dullness, aches
    • Anaemia (Hb 6.2g%) from reduced erythropoiesis (T3 stimulates EPO)
    • Diminished reflexes from delayed relaxation of deep tendon reflexes (myopathy)
  3. Common causes: Hashimoto's thyroiditis (autoimmune - most common), iodine deficiency, post-thyroidectomy, post-radioiodine therapy, drugs (amiodarone, lithium)
  4. Total vs Free T3/T4: Total T4/T3 includes protein-bound fractions (mainly TBG-bound); only free forms are biologically active. Pregnancy, liver disease, and drugs alter TBG → misleading total values. Free T4 (FT4) is better for evaluating thyroid function as it reflects the active unbound hormone.

Case 7 - Rickets (Vitamin D Deficiency)

4-year-old boy, bow legs, costochondral nodules (rachitic rosary), pigeon chest, poor muscle tone, convulsions
  1. Diagnosis: Rickets (Vitamin D deficiency in childhood)
  2. Role of Vitamin D:
    • Promotes intestinal absorption of calcium and phosphate
    • Promotes bone mineralisation (with PTH and calcitonin)
    • Renal reabsorption of calcium
    • Active form: 1,25-dihydroxycholecalciferol (calcitriol) - acts as a steroid hormone
    • Immunomodulation and cell differentiation (via VDR)
  3. RDA: 400-600 IU/day (10-15 mcg/day) for children; 600 IU for adults; 800 IU for >70 years
  4. Rich sources: Fatty fish (salmon, sardines), cod liver oil, fortified milk, egg yolk, sunlight (skin synthesis of D3 from 7-dehydrocholesterol)

Case 8 - Scurvy (Vitamin C Deficiency)

25-year-old male, perifollicular petechiae on legs, swollen bleeding gums, bloody stools - eating no fresh fruit/vegetables
  1. Diagnosis: Scurvy (Vitamin C / Ascorbic acid deficiency)
  2. Functions of Vitamin C:
    • Cofactor for prolyl and lysyl hydroxylase → collagen synthesis (hydroxylation of proline and lysine residues)
    • Antioxidant (reduces oxidative stress)
    • Enhances non-haem iron absorption (reduces Fe3+ to Fe2+)
    • Cofactor for dopamine-β-hydroxylase (noradrenaline synthesis)
    • Biosynthesis of carnitine, bile acids (cholesterol hydroxylation)
  3. RDA: 40-65 mg/day (India); 75-90 mg/day (WHO)
  4. Rich sources: Citrus fruits, guava, amla (Indian gooseberry - highest), capsicum, kiwi, tomatoes, broccoli

Case 9 - Hypocalcaemia / Tetany

10-year-old strict vegan boy, muscle cramps, spasms | Serum Ca 4 mg/dL (↓; normal 8.5-10.5 mg/dL)
  1. Diagnosis: Hypocalcaemia causing tetany (likely nutritional, with possible Vitamin D deficiency contributing)
  2. Functions of Calcium:
    • Muscle contraction (sliding filament mechanism via troponin C)
    • Neurotransmitter release (Ca2+ triggers vesicle fusion)
    • Bone and teeth mineralisation (as hydroxyapatite)
    • Blood coagulation (factor IV; multiple clotting steps)
    • Second messenger (via calmodulin and IP3 pathways)
    • Enzyme activation (lipase, ATPase)
  3. Causes of hypocalcaemia: Hypoparathyroidism, Vitamin D deficiency, malabsorption, chronic renal failure (reduced 1α-hydroxylation), hypoalbuminaemia, pancreatitis, hypomagnesaemia
  4. RDA: 800-1000 mg/day (children and adults); 1200 mg/day (adolescents and pregnant women)

Case 10 - Respiratory Acidosis

36-year-old chronic smoker, cough, wheeze, dyspnoea | pH 7.26 (note: "2.26" in document is likely a typo for 7.26), pCO2 52 mmHg, HCO3 26 mEq/L
  1. Diagnosis: Acute respiratory acidosis (likely acute exacerbation of COPD/chronic bronchitis from smoking)
    • pH < 7.35 (acidic), pCO2 > 45 mmHg (CO2 retention), HCO3 near normal (no metabolic compensation yet, acute event)
  2. Other causes of respiratory acidosis: Pneumonia, pulmonary oedema, neuromuscular disorders (GBS, myasthenia gravis), CNS depression (opioids, barbiturates), severe asthma, airway obstruction
  3. Normal ABG ranges: pH 7.35-7.45 | pCO2 35-45 mmHg | HCO3 22-26 mEq/L
  4. Role of respiratory system in acid-base balance: Lungs regulate CO2 (carbonic acid). CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3- (via carbonic anhydrase). By changing rate/depth of breathing, the respiratory system adjusts CO2 levels within minutes - hyperventilation reduces H+ (corrects acidosis), hypoventilation retains CO2 (corrects alkalosis).

MAJOR CASES

Case 1 - Gout (Hyperuricaemia)

40-year-old male, post-alcohol party, acute monoarthritis of ankle | Uric acid 10 mg/dL (↑), normal RBS/urea/creatinine
a) Diagnosis: Acute gouty arthritis b) Common drug & biochemical basis:
  • Colchicine (acute): Inhibits microtubule polymerisation → prevents neutrophil migration and phagocytosis of urate crystals → reduces inflammation
  • Allopurinol (chronic prevention): Structural analogue of hypoxanthine → competitive inhibitor of xanthine oxidase → reduces uric acid production
  • NSAIDs/Indomethacin (acute): Inhibit COX enzymes → reduce prostaglandin-mediated inflammation c) Increased uric acid: Alcohol metabolism increases NADH → promotes lactate production (lactic acidosis reduces uric acid excretion) and increases purine synthesis/degradation. Alcohol also dehydrates, increasing urate concentration. Final product of purine catabolism in humans (lack uricase) is uric acid via xanthine oxidase. d) Conditions associated with hyperuricaemia: Gout, Lesch-Nyhan syndrome (HGPRT deficiency), Von Gierke disease (glucose-6-phosphatase deficiency), polycythaemia vera, leukaemia (high cell turnover), renal failure, diuretic use (thiazides), obesity

Case 2 - Diabetic Ketoacidosis (DKA)

Known diabetic, unconscious, Kussmaul breathing, acetone breath | BSL 526 mg/dL, pH 7.1, Benedict's and Rothera's positive
e) Diagnosis: Diabetic ketoacidosis (DKA) f) Cause of decreased pH: Insulin deficiency → uncontrolled lipolysis → excess free fatty acids → hepatic β-oxidation → acetyl-CoA excess (TCA cycle saturated) → ketone body synthesis (acetoacetate, β-hydroxybutyrate, acetone). Acetoacetate and β-hydroxybutyrate are organic acids → accumulate → consume HCO3 → fall in pH (metabolic acidosis) g) Purpose of Rothera's test: Detects ketone bodies (acetoacetate and acetone) in urine. Sodium nitroprusside + ammonium sulphate gives purple/violet ring in positive test. Used to confirm ketosis/ketonuria in DKA. h) Ketone bodies: (1) Acetoacetate (2) β-hydroxybutyrate (3) Acetone. Synthesised in liver from acetyl-CoA, utilised by extrahepatic tissues (brain, muscle) as fuel. i) Detection of acetone by physical examination: Fruity/sweet odour on the breath (acetone is volatile and exhaled). Detected by smelling the patient's breath.

Case 3 - Pre-hepatic (Haemolytic) Jaundice

Post-malaria treatment | Total bilirubin 2.5 mg/dL, direct 0.4 mg/dL, indirect 2.1 mg/dL, SGOT/SGPT normal, ALP normal, urine urobilinogen +, bile pigments absent
a) Diagnosis: Pre-hepatic (haemolytic) jaundice - likely malaria-induced haemolysis b) Cause of increased bilirubin: Malaria causes RBC lysis → excess haemoglobin released → converted to haem → biliverdin → unconjugated bilirubin by reticuloendothelial system. Liver conjugation capacity overwhelmed → unconjugated (indirect) bilirubin rises predominantly. c) Test for serum bilirubin estimation: Van den Bergh reaction (diazotisation reaction with diazonium sulphanilic acid). Direct bilirubin reacts immediately (aqueous); indirect needs methanol (Van den Bergh indirect/total reaction). d) Reason for increased urobilinogen: Excess bilirubin delivered to intestine → gut bacteria convert it to urobilinogen (increased quantity) → absorbed into portal circulation → excreted in urine (urobilinogen). Some urobilinogen is oxidised to urobilin (gives dark urine/stool). e) Urinary urobilinogen detected by: Ehrlich's aldehyde test (p-dimethylaminobenzaldehyde in HCl → cherry red colour)

Case 4 - Alkaptonuria

Child, urine darkens on air exposure, napkin stains dark | Benedict's positive, GOD-POD negative, ferric chloride transient blue
a) Diagnosis: Alkaptonuria (Ochronosis) b) Enzyme defect: Homogentisate oxidase (homogentisic acid oxidase) deficiency - in the tyrosine/phenylalanine catabolism pathway c) Urine darkens on air exposure: Homogentisic acid accumulates in urine. On exposure to air, it undergoes oxidative polymerisation to a dark brownish-black melanin-like pigment (alkapton). This is the hallmark. d) Benedict's positive, GOD-POD negative: Benedict's test detects all reducing sugars AND other reducing substances (including homogentisic acid, which is a reducing compound). GOD-POD (glucose oxidase-peroxidase) is specific only for glucose. Homogentisic acid is not glucose → GOD-POD negative. e) Useful biochemical investigation: Urine homogentisic acid measurement by HPLC or colorimetric method; paper chromatography for urine; ferric chloride test (transient blue-green colour, fades quickly); urine on alkali turns dark rapidly.

Case 5 - Multiple Myeloma

30-year-old male (ex-radiology technician), back pain, bone density decrease | Total protein 10 g/dL (↑), albumin 2.8 g/dL (↓), Bence Jones protein in urine, M-band on electrophoresis
a) Diagnosis: Multiple myeloma (plasma cell dyscrasia) b) Cause of increased total protein: Monoclonal proliferation of plasma cells → massive overproduction of a single class of immunoglobulin (M-protein/paraprotein) → raised total protein despite low albumin (reversed A:G ratio) c) Past history of radiation exposure: X-ray technicians have prolonged low-dose ionising radiation exposure, which is a known risk factor for multiple myeloma (DNA damage/mutations in plasma cell precursors). Yes, occupational history is relevant. d) Bence Jones proteins: Monoclonal free light chains (kappa or lambda) produced in excess by myeloma cells. They are small enough to pass through glomerular filtration → excreted in urine. Classically precipitate at 50-60°C and redissolve at boiling (heat test). Detected by urine protein electrophoresis/immunofixation. e) Conditions with M-band (monoclonal band) on electrophoresis: Multiple myeloma, Waldenström's macroglobulinaemia, MGUS (monoclonal gammopathy of undetermined significance), primary amyloidosis, heavy chain disease, solitary plasmacytoma

Case 6 - Beta-Thalassaemia Major

6-month-old child, consanguineous parents | Hb 3g%, MCV 45fL, microcytic hypochromic, target cells, anisocytosis, poikilocytosis | Hb electrophoresis: ↑HbA2, ↑HbF, fused bands; HbS solubility negative, unstable Hb test positive
a) Diagnosis: Beta-thalassaemia major (Cooley's anaemia) b) Biochemical defect: Mutations in the beta-globin gene (chromosome 11) → absent or severely reduced beta-globin chain synthesis. Excess alpha chains precipitate → damage RBC membrane → haemolysis. Compensatory ↑HbF (α2γ2) and ↑HbA2 (α2δ2). c) Why HbF and HbA2 increased: Absence of beta chains leads to compensatory increased production of gamma (γ) chains (forming HbF = α2γ2) and delta (δ) chains (forming HbA2 = α2δ2) to use the excess alpha chains. This is a compensatory gene switching back to fetal programmes. d) Why Hb, PCV, MCV are decreased (not increased - likely a typo in the question): Severe anaemia from haemolysis of abnormal RBCs containing excess alpha chain precipitates, ineffective erythropoiesis, and destruction of RBC precursors in bone marrow. Microcytic (low MCV) due to reduced haemoglobin content per cell. e) Treatment: Regular blood transfusions (every 2-4 weeks to maintain Hb >9g/dL), iron chelation therapy (desferrioxamine or deferasirox to prevent iron overload), folic acid supplementation, splenectomy (if hypersplenism), bone marrow/stem cell transplantation (curative), hydroxyurea (increases HbF)

Case 7 - Kwashiorkor (Protein Energy Malnutrition)

2.5-year-old girl, low socioeconomic family | Hb 5g%, total protein 5.2g/dL, albumin 2g/dL (↓), generalised oedema, distended abdomen, no urine protein, ↓Cu, ↓Mg, ↓K
a) Diagnosis: Kwashiorkor (protein-energy malnutrition with predominant protein deficiency) b) Normal levels:
  • Total protein: 6-8 g/dL
  • Albumin: 3.5-5.0 g/dL
  • Globulin: 2.3-3.5 g/dL
  • A:G ratio: 1.5-2.5:1 c) Conditions with decreased total serum protein: Kwashiorkor, nephrotic syndrome, liver cirrhosis (reduced synthesis), malabsorption, chronic infections, protein-losing enteropathy, burns, starvation d) Daily protein requirement: 0.8-1.0 g/kg/day (adults); 1.5-2.0 g/kg/day (children); 1.1 g/kg/day (pregnancy) e) Cause of generalised oedema: Severe hypoalbuminaemia → reduced plasma oncotic pressure → fluid shifts from intravascular to interstitial space (decreased Starling forces for fluid retention) → generalised pitting oedema and ascites. No urinary protein loss (urine protein negative) distinguishes this from nephrotic syndrome.

Case 8 - Glycogen Storage Disease (Von Gierke's / GSD Type Ia vs Type III)

3-month-old girl, liver/muscle glycogen accumulation 6%, hepatomegaly, fasting hypoglycaemia, hyperlipidaemia, ketoacidosis | pH 7.25, SGOT/SGPT normal
a) Diagnosis: Glycogen storage disease - given muscle and liver involvement with normal transaminases, most consistent with GSD Type III (Cori's disease / debranching enzyme deficiency), though Type Ia (Von Gierke) also fits liver features. Type I (Von Gierke) classically has liver only (not muscle) and very high lactate; Type III involves both liver and muscle. b) Morning hypoglycaemia and hyperlipidaemia: In GSD, glycogenolysis and gluconeogenesis are impaired → cannot maintain blood glucose during fasting → hypoglycaemia. Hypoglycaemia triggers lipolysis → elevated free fatty acids → hyperlipidaemia (also impaired glucose uptake by adipose drives continued fat mobilisation). c) Biochemical defect:
  • Type Ia: Glucose-6-phosphatase deficiency (liver/kidney)
  • Type III: Amylo-1,6-glucosidase (debranching enzyme) deficiency d) Ketoacidosis: Hypoglycaemia + impaired glucose utilisation → cells shift to fat oxidation → excess acetyl-CoA → ketone body overproduction → ketoacidosis (pH 7.25, low CO2) e) Treatment: Frequent high-carbohydrate feedings, raw cornstarch (slow-release glucose), avoid fasting, nasogastric feeds overnight, liver transplantation (for severe Type I), high-protein diet (in Type III, protein can provide gluconeogenic substrates)

Case 9 - Acute Myocardial Infarction (in a Diabetic)

60-year-old diabetic male, chest pain, sweating | Glucose 300, Cholesterol 350, SGOT 50 (↑), SGPT 10 (normal), LDH 10 (low/normal), CK-MB 40 (↑)
a) Diagnosis: Acute myocardial infarction (AMI) with underlying Type 2 diabetes mellitus and hypercholesterolaemia b) Normal ranges:
  • Serum cholesterol: < 200 mg/dL (desirable)
  • SGOT (AST): 10-40 IU/L
  • SGPT (ALT): 7-56 IU/L
  • LDH: 140-280 IU/L
  • CK-MB: < 5% of total CK (< 25 IU/L); elevated in AMI within 4-8 hours, peaks at 12-24h c) LDH isoenzymes in AMI: Yes - LDH1 (H4 tetramer) predominates in heart muscle; in AMI, LDH1 > LDH2 ("flipped LDH ratio"). Normally LDH2 > LDH1. This flip is diagnostic. LDH rises 24-48h after AMI, peaks at 3-6 days, useful for late diagnosis when troponin window is missed. d) CK isoenzymes:
  • CK-MM: skeletal muscle (predominant)
  • CK-MB: cardiac muscle (diagnostic marker for AMI - rises 4-8h, peaks 24h, returns to normal 48-72h)
  • CK-BB: brain
  • CK-MB elevated in: AMI (most specific), myocarditis, cardiac surgery, Duchenne muscular dystrophy (also skeletal muscle damage) e) Why cholesterol increased: Diabetes → insulin deficiency/resistance → increased VLDL synthesis → hyperlipidaemia. Also reduced LPL activity (insulin-dependent) → impaired VLDL clearance → elevated triglycerides and LDL.

Case 10 - Nephrotic Syndrome

4-year-old boy, facial and generalised oedema | Total protein 3g/dL (↓↓), cholesterol 600mg/dL (↑↑), urea 80mg/dL (↑), creatinine 4.5mg/dL (↑), urine protein ++++
a) Diagnosis: Nephrotic syndrome (most likely minimal change disease at this age) b) Cause of hypoproteinaemia: Massive proteinuria (urine protein ++++) - glomerular basement membrane loses its negative charge and size-selectivity → proteins (especially albumin, small size ~69 kDa) leak into urine → severe hypoalbuminaemia → reduced total protein c) Cause of oedema: Hypoalbuminaemia → reduced plasma oncotic pressure → fluid moves from intravascular to interstitial space → generalised oedema (face, ankles, ascites) d) Reason for hyperlipidaemia: Hypoalbuminaemia → liver compensatory response: increased lipoprotein synthesis (especially VLDL and LDL) to maintain plasma oncotic pressure by producing other proteins. Reduced catabolism of lipoproteins (low LPL activity due to low albumin). Cholesterol-carrying lipoproteins spill into blood → hypercholesterolaemia (+ lipiduria/oval fat bodies in urine). e) Increased blood urea and creatinine: Reduced renal blood flow (due to hypovolaemia from low oncotic pressure) → reduced GFR → accumulation of nitrogenous waste products (urea from protein catabolism, creatinine from muscle metabolism) in blood. Also, progression of glomerular disease can directly impair filtration.
Quick Reference - Diagnoses at a Glance:
FileCaseDiagnosis
Minor1Vitamin B12 deficiency anaemia (post-gastrectomy)
Minor2Iron deficiency anaemia
Minor3Metabolic acidosis (normal anion gap, from diarrhoea)
Minor4Acute/chronic renal failure (from recurrent UTI/pyelonephritis)
Minor5Vitamin A deficiency (xerophthalmia)
Minor6Primary hypothyroidism
Minor7Rickets (Vitamin D deficiency)
Minor8Scurvy (Vitamin C deficiency)
Minor9Hypocalcaemia / Tetany
Minor10Respiratory acidosis (acute exacerbation of COPD)
Major1Acute gouty arthritis
Major2Diabetic ketoacidosis (DKA)
Major3Pre-hepatic (haemolytic) jaundice (post-malaria)
Major4Alkaptonuria
Major5Multiple myeloma
Major6Beta-thalassaemia major
Major7Kwashiorkor
Major8Glycogen storage disease (Type I/III)
Major9Acute myocardial infarction (in diabetic)
Major10Nephrotic syndrome
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