Endocrine and diabetes medicines — formative SAQs

SAQ 1 — Diabetic ketoacidosis: the insulin and fluid prescribing sequence (10 marks)

A 7-year-old with previously undiagnosed type 1 diabetes presents drowsy with deep sighing respirations. Bedside glucose is 24 mmol per L, blood ketones 6.2 mmol per L, and venous pH 7.08. She is 7 percent dehydrated but not in shock. [4] [9]

Questions

1. Outline the immediate fluid and insulin prescribing sequence for her resuscitation, including the insulin rate, the timing of insulin relative to fluids, and the rule on insulin boluses. (6 marks) [4]
2. Explain the pharmacological rationale for why insulin is the definitive treatment of DKA, and why a steep glucose fall is avoided. (4 marks) [4] [9]

Model answer

Fluid and insulin sequence (6). First restore intravascular volume: an isotonic saline bolus of 10 to 20 mL per kg is given only if the child is in shock; otherwise begin a calculated deficit replacement over 24 to 48 hours with isotonic saline, as she is dehydrated but not shocked. Only after intravascular volume is restored, start a continuous intravenous insulin infusion at 0.05 to 0.1 unit per kg per hour using soluble or rapid-acting insulin. Do not give an intravenous insulin bolus at any point, because a bolus drives a steep osmolar fall that contributes to cerebral oedema. Replace potassium once insulin starts and urine output is established, and add dextrose to the fluids when the glucose falls to around 11 to 14 mmol per L to keep the glucose fall gradual. Transition to subcutaneous insulin only when ketones have cleared, the pH has normalised, and the child is eating. [4] [9]

Rationale (4). DKA is an insulin-deficient state: without insulin, glucose cannot enter cells and lipolysis runs unchecked, flooding the liver with free fatty acids that it converts to ketone bodies, producing acidosis. Insulin reverses both arms at once — it restores glucose uptake, suppressing hyperglycaemia, and it switches off lipolysis, stopping ketogenesis — which is why insulin (not fluids or bicarbonate) is the definitive treatment. A steep glucose fall is avoided because it generates a rapid osmolar shift that, alongside the cerebral hypoperfusion of dehydration, contributes to cerebral oedema, the leading cause of DKA-related death in children. Gradual glucose control with dextrose support protects the brain. [4] [9]

SAQ 2 — Neonatal levothyroxine and growth hormone prescribing (10 marks)

A neonate's newborn thyroid screen returns positive for congenital hypothyroidism, confirmed on a venous sample on day 8. Separately, an 8-year-old boy with confirmed growth hormone deficiency is about to start recombinant growth hormone. [6] [12]

Questions

1. State the levothyroxine starting dose, the timing, the administration advice, and the recheck schedule for the neonate, and explain why the first two years are critical. (6 marks) [6] [7]
2. State the recombinant growth hormone dose, route and timing for the 8-year-old, and describe the monitoring and the safety surveillance. (4 marks) [12]

Model answer

Levothyroxine (6). Start levothyroxine immediately at 10 to 15 microgram per kg per day, given once daily and ideally on an empty stomach (avoid co-administration with calcium or iron), and begun within the first two weeks of life because thyroid hormone is essential for brain myelination in infancy and a delayed or under-dosed start costs IQ points that do not return. Recheck TSH and free T4 at 2 and 4 weeks, then every 1 to 3 months in the first two years and every 3 to 6 months thereafter, titrating to a TSH in the age-appropriate range. The first two years are the critical neurodevelopmental window, so consistent administration and a dose that grows with the baby are non-negotiable; a trial off therapy for suspected transient disease happens later, never now. [6] [7]

Growth hormone (4). Start recombinant human growth hormone (somatropin) at 0.045 to 0.050 mg per kg per day, equivalent to about 0.15 to 0.17 IU per kg per week, given as a once-daily subcutaneous injection, usually at bedtime to mirror the physiological overnight growth hormone pulse. Titrate to an IGF-I in the age-appropriate reference range and to the growth response, reviewing every 3 to 6 months. Run the safety surveillance at each visit: ask about headache and visual change (intracranial hypertension), examine for limp (slipped capital femoral epiphysis), and check glucose and thyroid function. Continue to near-adult height, then reassess for adult growth hormone deficiency at transition. [12]