Today’s acute diagnostic thread is porphyria. Acute hepatic porphyria may present with severe diffuse abdominal pain that appears disproportionate to the examination, particularly when imaging remains unrevealing. Nausea, constipation, tachycardia, hypertension, neuropsychiatric symptoms, seizures, proximal weakness and hyponatraemia strengthen the pattern. Repeatedly normal investigations should prompt diagnostic reconsideration rather than labelling the presentation as psychosomatic or drug-seeking.

A random urine sample for aminolevulinic acid and porphobilinogen is the key screening investigation during a suspected acute attack; a 24-hour collection is not required. Urine porphyrins alone are less useful because mild elevations can occur in other conditions and do not directly measure the neurotoxic precursors. The sample should be collected during symptoms and, where possible, before haem treatment, although treatment must not be delayed in a severely unwell patient.

Management includes removing triggers, ensuring carbohydrate intake, correcting fluid and electrolyte disturbance carefully and selecting analgesics, antiemetics, anticonvulsants and antihypertensives from a reliable porphyria-safety source. Common precipitants include fasting, alcohol, infection, hormonal change and CYP-inducing medicines. Severe attacks require specialist input and intravenous haemin. Motor neuropathy can progress to respiratory weakness, making bedside respiratory assessment and escalation important when weakness develops.

The psychiatry episode challenges the assumption that every adult presenting with poor concentration has ADHD. ADHD is a neurodevelopmental disorder, so assessment should establish symptoms before the age of 12, a persistent longitudinal pattern and meaningful impairment in current life. Increased demands may expose previously compensated difficulties, but new midlife inattention still requires a broad differential. Sleep deprivation, obstructive sleep apnoea, substance use, concussion, menopause, excessive social-media use and occupational overload may all produce similar complaints.

Retrospective childhood histories need careful interpretation. Daydreaming, uneven school performance or missed deadlines are common experiences and should not automatically be reframed as evidence of childhood ADHD. School reports, family collateral and longitudinal records may be useful when recall is vague. Good academic performance does not exclude ADHD, but neither does current stress combined with a few non-specific childhood memories establish the diagnosis. The episode also reviews antipsychotic-associated weight gain, with semaglutide producing the greatest weight-loss effect in the analysis discussed and metformin offering additional metabolic benefits.

Rickets provides the paediatric clinic thread. Defective mineralisation at growing bones may cause delayed walking, poor growth, bone pain, swollen wrists, bowed legs, knock knees, rachitic rosary and pathological fractures. Assessment should include sunlight exposure, diet, supplementation, skin pigmentation, malabsorption symptoms and chronic kidney disease. Examination should look deliberately for skeletal deformity rather than relying on reported pain alone.

Serum 25-hydroxyvitamin D is the preferred test for vitamin D status. Calcium, phosphate, alkaline phosphatase and parathyroid hormone help define the wider metabolic disturbance. Normal serum calcium does not exclude rickets because secondary hyperparathyroidism may maintain circulating calcium by mobilising it from bone. Wrist or knee radiographs can confirm active disease through growth-plate and metaphyseal changes. Treatment includes colecalciferol and adequate calcium, with specialist referral when clinical deformity, an alternative metabolic cause or hereditary hypophosphataemic rickets is suspected.