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Folio edition · Set in Instrument Serif & Archivo

Paeds Vivasendocrinology-diabetes-and-growth

Paeds Vivas · endocrinology-diabetes-and-growth

Acquired hypothyroidism and Hashimoto thyroiditis — viva

Branching structured oral on acquired hypothyroidism and Hashimoto thyroiditis.

branching clinical structured oral
On this page & tools

Target exams

RACP DCEMRCPCH Clinical

Target exams

RACP DCEMRCPCH Clinical
Prompt
A growth chart shows a 13-year-old girl whose height has crossed from the 50th to the 25th centile over eight months while her BMI has risen. She is tired, constipated and her grades have slipped. A firm, bosselated goitre is present. You are the paediatric registrar in clinic.

Opening (must-hit)

"I will confirm the diagnosis with venous TSH and free T4 and anti-TPO antibodies, classify it as overt, subclinical or central, start weight-based levothyroxine for overt primary disease, recheck at six weeks titrating to a normal TSH, and screen for the associated autoimmune conditions — type 1 diabetes, coeliac disease, and in Down or Turner syndrome the annual surveillance that should already be running." [1][3]

Branch A — Recognition and classification

Examiner: What is the most likely diagnosis and how do you classify it? Candidate: Acquired hypothyroidism from Hashimoto thyroiditis — the commonest cause in iodine-sufficient children. I classify by anatomical level (primary here — TSH raised, free T4 low), by aetiology (autoimmune, anti-TPO positive) and by severity (overt, symptomatic). The growth slowdown with rising BMI is the cardinal early signal. [1][3]

Branch B — Investigations

Examiner: Which bloods do you send, and do you need an ultrasound? Candidate: Venous TSH and free T4 confirm the axis and the level; anti-TPO antibodies confirm the autoimmune cause in about 90%. Ultrasound is reserved for an asymmetric, nodular, tender or hard gland with nodes — the picture here is typical, so I do not image routinely. I also screen coeliac serology and, if any polyuria, HbA1c. [4][6]

Branch C — Subclinical disease

Examiner: Her TSH is only mildly raised and her free T4 is normal. Walk me through that. Candidate: That is subclinical hypothyroidism. Up to a third of children normalise spontaneously, so I re-test TSH and free T4 in four to eight weeks before treating. I treat when there is a goitre, symptoms, a steadily rising TSH, or anti-TPO positivity — all predictors of progression to overt disease. [5]

Branch D — Treatment and dosing

Examiner: She is overt and weighs 45 kg. What do you start and how? Candidate: Levothyroxine sodium once daily, weight-based: for an adolescent over 12, 2–3 mcg/kg/day, so about 90 to 135 mcg — I would start around 100 mcg once daily. I give it on an empty stomach 30–60 minutes before breakfast, separated from calcium, iron, soy and PPIs by at least four hours. I recheck TSH and free T4 at six weeks, then every four to six months, targeting a TSH of 1 to 5 mU/L. [2][7]

Branch E — Adherence and the non-responder

Examiner: Six weeks later her TSH is still high. What is the commonest reason? Candidate: Non-adherence or an absorption-reducing interaction — iron, calcium, soy or a PPI taken together, or dosing with food. Before raising the dose I confirm how and when she actually takes it, offer a liquid formulation if tablets fail, and link dosing to a fixed daily anchor. Only then do I escalate. [2][7]

Branch F — Central hypothyroidism trap

Examiner: Suppose her TSH was low with a low free T4. What changes? Candidate: That is central hypothyroidism. I check morning cortisol and exclude adrenal insufficiency before starting thyroxine, because T4 accelerates cortisol clearance and can precipitate adrenal crisis. I image the pituitary and involve endocrinology the same day. [4]

Branch G — Associated conditions and surveillance

Examiner: She also has Down syndrome. How does that change the plan? Candidate: It makes the thyroid an annual, mandatory review from infancy — lifetime hypothyroidism risk is 15 to 30%, often silent. I screen TSH and free T4 yearly regardless of symptoms, and I extend the same surveillance logic to Turner syndrome and type 1 diabetes. [3][4]

Branch H — Severe decompensation

Examiner: The child becomes hypothermic, bradycardic and drowsy. What is this and what do you do? Candidate: Myxoedema coma. I manage in intensive care: intravenous levothyroxine with intravenous hydrocortisone given first to cover possible adrenal insufficiency, gentle warming, cautious sodium correction, and treatment of the precipitant. [4]

Examiner traps

  • Treating symptoms without venous TSH and free T4 confirmation.
  • Missing coeliac serology, HbA1c and the Down/Turner/T1DM annual surveillance. [3]
  • Starting T4 in central disease without checking cortisol first.
  • Declaring the disease lifelong at the first visit — a minority remit; plan a supervised withdrawal trial. [1]
  • Calling a nodular, hard, node-bearing gland "Hashimoto" — that is cancer until proven by ultrasound and FNA. [3]
  • Forgetting pregnancy counselling: L-T4 needs rise 25 to 30%. [2]

References

  1. [1]Bhattacharyya SS Acquired Hypothyroidism in Children. Indian Journal of Pediatrics, 2023.PMID 37256446
  2. [2]Rodriguez L, et al. Treatment of hypothyroidism in infants, children and adolescents. Trends in Endocrinology and Metabolism, 2022.PMID 35537910
  3. [3]Hanley P, Lord K, Bauer AJ Thyroid Disorders in Children and Adolescents: A Review. JAMA Pediatrics, 2016.PMID 27571216
  4. [4]Diaz A, Lipman Diaz E Hypothyroidism. Pediatrics in Review, 2014.PMID 25086165
  5. [5]Salerno M, et al. Management of endocrine disease: Subclinical hypothyroidism in children. European Journal of Endocrinology, 2020.PMID 32580145
  6. [6]Caturegli P, De Remigis A, Rose NR Hashimoto thyroiditis: clinical and diagnostic criteria. Autoimmunity Reviews, 2014.PMID 24434360
  7. [7]Jonklaas J, et al. Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid, 2014.PMID 25266247