Growth hormone deficiency and excess — branching viva

Branch 1 — the short child (growth hormone deficiency)

The candidate is expected to justify growth hormone deficiency over a normal variant from the growth velocity and bone age, describe the stimulation test (clonidine or arginine; glucagon) with a peak below 6.7 to 10 ng/mL consistent with deficiency, and the pituitary magnetic resonance imaging and full axis panel that complete the work-up. [1] [3]

The examiner branches into therapy: the recombinant growth hormone dose of 0.045 to 0.050 mg/kg/day subcutaneous nocturnal titrated to the IGF-1, the monitoring of growth velocity, IGF-1, glucose, thyroid and adverse effects, and the two caviats — a sleep study before growth hormone in Prader-Willi syndrome because of upper-airway and sleep-apnoea risk, and the transition re-test at final height to decide whether adult growth hormone deficiency persists. [1]

Branch 2 — the overgrowing child (growth hormone excess)

The candidate is expected to explain gigantism versus acromegaly through the open versus fused state of the growth plates, confirm excess with the failure of growth hormone to suppress below 1 ng/mL after a 75-gram oral glucose load, and describe the pituitary magnetic resonance imaging, the formal visual field testing, and the genetic work-up. [10]

The examiner branches into management: endoscopic transsphenoidal resection as first-line, then a somatostatin analogue and the growth hormone receptor antagonist pegvisomant for residual disease — with the AIP-mutant resistant and the X-linked acrogigantism (GPR101 duplication) subtypes named as the higher-yield modern genetic diagnoses that guide pegvisomant use and family surveillance. [10] [12]