MBBS viva · Endocrinology / General Medicine
Thyroiditis & Goitre — thyrotoxicosis interpretation and the painful thyroid viva
A final-prof viva on interpreting a thyrotoxic TFT panel, using radioactive iodine uptake and antibodies to separate destructive thyroiditis from Graves and toxic multinodular goitre, and defending the phase-specific management of subacute thyroiditis. Examiner expects the low-vs-high RAIU rule, dose-level detail and the storm bundle.
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Interpretation
The examiner hands you a panel showing TSH less than 0.05 mIU/L, free T4 32 pmol/L, free T3 raised, and a note that the patient has a painful, tender thyroid, a fever and a recent sore throat, with ESR 76 mm/h. The examiner asks: "Interpret these results, give the diagnosis, and outline the management."
- Interpretation: the suppressed TSH with raised free T4/T3 confirms thyrotoxicosis; the painful tender thyroid, fever, raised ESR and preceding viral illness localise this to subacute (De Quervain, granulomatous) thyroiditis.[1]
- The decisive discriminator the examiner will probe: radioactive iodine uptake (RAIU) is LOW in subacute thyroiditis (and all destructive thyroiditides) because the gland is leaking preformed hormone — versus HIGH and diffuse in Graves and high and patchy/focal in toxic multinodular goitre/adenoma.[1][2]
- Contrast patterns the examiner will test: Graves (diffuse goitre, bruit, eye signs, TRAb positive, high diffuse uptake); toxic MNG (nodular, no eye signs, TRAb negative, high patchy uptake); postpartum/silent thyroiditis (painless, anti-TPO positive, normal ESR, low uptake).[2]
Key points
The examiner will probe each; be ready to defend them at viva depth:
- The low-vs-high RAIU rule — destructive thyroiditis (subacute, postpartum, silent, amiodarone type 2) and iodine-induced Jod-Basedow all have low uptake (leak, not synthesis); Graves and toxic nodular disease have high uptake (active synthesis).[1]
- Why the thyrotoxic phase of thyroiditis is NOT treated with antithyroid drugs — the hormone is leaking from a damaged gland, not being synthesised; carbimazole/PTU and radioiodine are ineffective. Use a beta-blocker (propranolol).[1]
- Subacute thyroiditis management reproduced verbatim — NSAIDs first-line; oral prednisolone 40 mg daily, tapered over 2-4 weeks, if pain is severe or NSAIDs fail; beta-blocker for the thyrotoxic phase; levothyroxine only if the hypothyroid phase is symptomatic. It is self-limiting.[1]
- Hashimoto thyroiditis — commonest cause of hypothyroidism/goitre in iodine-sufficient areas; anti-TPO positive; painless firm rubbery goitre; lifelong levothyroxine ~1.6 mcg/kg/day; small increased risk of thyroid (B-cell) lymphoma.[3]
- Amiodarone — iodine-rich (37.5 percent iodine); Wolff-Chaikoff effect → hypothyroidism; Jod-Basedow → thyrotoxicosis. Type 1 = synthetic (underlying nodular goitre, increased vascularity; thionamide + potassium perchlorate) vs type 2 = destructive (normal gland, decreased vascularity; prednisolone 40-60 mg).[7]
- Goitre classification — diffuse (Graves, Hashimoto, iodine deficiency, puberty) vs multinodular (hyperplasia; toxic or compressive); Pemberton sign = retrosternal goitre; stony-hard goitre = Riedel (IgG4-related, steroids/tamoxifen).[2]
- Thyroid storm — hyperpyrexia + AF/heart failure + CNS signs → PTU 500-1000 mg load then 250 mg every 4 h + iodine (≥1 h after thionamide) + hydrocortisone 100 mg every 8 h + propranolol, in ICU; PTU preferred (blocks T4-to-T3).[2]
References
- Wiersinga WM, et al. Hyperthyroidism. Lancet Diabetes Endocrinol 2023.[1]
- Ross DS, et al. 2016 ATA Hyperthyroidism guideline. Thyroid 2016.[2]
- Ralli M, et al. Hashimoto thyroiditis update. Autoimmun Rev 2020.[3]
- Macchia PE, Feingold KR. Amiodarone Induced Thyrotoxicosis. Endotext.[7]
References4ShowHide
- [1]Wiersinga WM, et al. Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis. Lancet Diabetes and Endocrinology, 2023.PMID 36848916
- [2]Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid, 2016.PMID 27521067
- [3]Ralli M, et al. Hashimoto's thyroiditis: an update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation. Autoimmunity Reviews, 2020.PMID 32805423
- [7]Macchia PE, Feingold KR. Amiodarone Induced Thyrotoxicosis. Endotext, 2000.PMID 25905259