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Q1: Recognition and sources (2 min)
A 3-year-old with developmental regression, pica, and peeling paint at home — what is your diagnosis and how do you confirm it? List five sources of lead exposure, and explain why children absorb more lead than adults.
Expected: Suspect lead poisoning; confirm with whole venous blood lead level (capillary is screening only). Sources: lead paint/dust, lead pipes/water, industry (battery/smelting/ammunition), surma/kohl and sindoor, Ayurvedic Bhasmas, ceramic glazes, moonshine, retained bullets, leaded-petrol soil. Children absorb ~50% of ingested lead vs ~10% in adults (higher GI absorption, pica behaviour, developing blood-brain barrier, calcium/iron deficiency increases absorption).
Q2: Pathophysiology (3 min)
Explain the haematological and neurological mechanisms of lead toxicity. What is basophilic stippling, and which two enzymes does lead inhibit? How does lead's calcium-mimicry explain its distribution and its effects on bone, teeth, and the fetus?
Expected: Lead inhibits ALA dehydratase (urinary ALA rises) and ferrochelatase (iron cannot insert into protoporphyrin IX → zinc protoporphyrin accumulates) → sideroblastic microcytic anaemia with basophilic stippling (aggregated degenerated ribosomes). Neurotoxicity: disrupts synaptogenesis, NMDA-receptor and neurotransmitter function, induces neuronal apoptosis → irreversible IQ loss, encephalopathy. Lead mimics calcium — deposits in bone/teeth (metaphyseal 'lead lines'), crosses BBB and placenta. Bone holds >90% of body burden in adults (half-life years-decades), mobilised in pregnancy/lactation/osteoporosis.
Q3: Chelation (3 min)
Describe the three chelating agents used in lead poisoning — drug, dose, route, indication. What is the specific sequence in lead encephalopathy, and why? Name two important contraindications and adverse effects.
Expected: Succimer (DMSA, oral) — moderate, over 45 micrograms/dL (children): 10 mg/kg every 8h for 5d then every 12h for 14d. CaNa2 EDTA (IV) — moderate-severe, over 70: 1000–1500 mg/m2/day infusion for 5 days. Dimercaprol (BAL, IM) — severe/encephalopathy: 75 mg/m2 deep IM every 4h for 5d. Encephalopathy sequence: BAL IM FIRST, then EDTA IV 4h later — BAL crosses BBB and chelates brain lead; EDTA alone mobilises bone lead and raises brain lead, worsening encephalopathy. Always CaNa2 EDTA — disodium EDTA causes fatal hypocalcaemia. Contraindications: BAL in G6PD deficiency (haemolysis) and peanut allergy (peanut-oil vehicle). Adverse: EDTA nephrotoxicity; succimer transaminitis/neutropenia; all deplete zinc/copper/iron; rebound after chelation.
Q4: Pitfalls, prognosis, and prevention (2 min)
Why is the developmental prognosis guarded despite successful chelation? What is the single most common management failure, and how does it relate to public-health prevention?
Expected: Established neurodevelopmental harm (IQ loss) is irreversible — the TLC Trial showed succimer lowers blood lead but does not improve long-term IQ. Prognosis therefore depends on prevention. Commonest management failure: re-exposure when the source is not remediated — never discharge a child to an unremediated home. Prevention: no safe blood lead level in children (CDC reference value 3.5 micrograms/dL, 2021); leaded-petrol ban (completed globally 2021), lead-paint bans, water-pipe replacement, screening of high-risk children, and abatement by certified contractors are the effective public-health interventions.