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Paeds Vivasendocrinology-diabetes-and-growth

Paeds Vivas · endocrinology-diabetes-and-growth

Hyperthyroidism and Graves disease — branching viva

Branching viva on distinguishing thyrotoxicosis from hyperthyroidism, confirming Graves disease through a suppressed TSH, raised free T4 and a positive TSH-receptor antibody, delivering the beta-blocker bridge and carbimazole-first-line strategy, holding propylthiouracil for thyroid storm and first-trimester pregnancy, recognising transient neonatal thyrotoxicosis, and reaching definitive radioactive iodine or surgery for relapse.

branching clinical structured oral3 min readVerification in progress

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
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Study tools

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
Prompt
A thirteen-year-old girl presents with palpitations, tremor, weight loss despite an increased appetite, heat intolerance, anxiety, declining school performance and prominent eyes, with a diffuse goitre and a bruit. Her thyroid function shows a suppressed TSH, a raised free T4 and a positive TSH-receptor antibody. The examiner asks: what is the diagnosis, how does the antibody produce the clinical and biochemical picture, how do you confirm it, what is the first-line management and why is propylthiouracil avoided — then branches to a two-week-old infant of a mother with a burnt-out Graves disease who is tachycardic and failing to thrive, and asks you to explain the neonatal mechanism, the natural history and the surveillance rule, before closing on a thyrotoxic adolescent who has stopped taking her tablets and presents febrile and confused.

Opening framework

My framework has three layers. First, the recognition — a suppressed TSH with a raised free T4 confirms thyrotoxicosis, and a positive TSH-receptor antibody confirms Graves disease and makes the radioiodine scan unnecessary in most children. Second, the mechanism — a stimulating antibody switches on the TSH receptor without any pituitary brake, driving hormone synthesis and the beta-adrenergic storm that defines the clinical picture. Third, the management — a beta-blocker bridges the symptoms while carbimazole or methimazole controls the gland, and propylthiouracil is held for thyroid storm and first-trimester pregnancy because of fulminant hepatotoxicity in children. [1]

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References6ShowHide
  1. [1]Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid, 2016.PMID 27521067
  2. [3]Wiersinga WM, Poppe KG, Effraimidis G. Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis. Lancet Diabetes Endocrinol, 2023.PMID 36848916
  3. [5]Kaguelidou F, Alberti C, Castanet M, Guitteny MA, Czernichow P, Léger J. Predictors of autoimmune hyperthyroidism relapse in children after discontinuation of antithyroid drug treatment. J Clin Endocrinol Metab, 2008.PMID 18628515
  4. [6]Léger J, Carel JC. MANAGEMENT OF ENDOCRINE DISEASE: Arguments for the prolonged use of antithyroid drugs in children with Graves' disease. Eur J Endocrinol, 2017.PMID 28381452
  5. [9]Rivkees SA, Mattison DR. Propylthiouracil (PTU) Hepatoxicity in Children and Recommendations for Discontinuation of Use. Int J Pediatr Endocrinol, 2009.PMID 19946400
  6. [11]Polak M. Hyperthyroidism in early infancy: pathogenesis, clinical features and diagnosis with a focus on neonatal hyperthyroidism. Thyroid, 1998.PMID 9920374
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