IM12.1-14 | Thyroid Dysfunction — Practice Quiz

Correct. The clinical picture — diffuse smooth goitre with a bruit, lid lag, and systemic thyrotoxicosis — is characteristic of Graves disease. The bruit over a diffuse goitre is virtually pathognomonic of Graves disease due to increased vascularity from TSH receptor stimulation. TRAb (TSH receptor antibody) confirms the autoimmune aetiology and differentiates Graves disease from toxic nodular goitre or other causes of suppressed TSH. Anti-TPO can be positive in Graves but is not aetiologically specific. TSH will be suppressed in all causes of thyrotoxicosis and does not distinguish aetiology.

The most critical distinction in thyroid evaluation is Graves disease versus other causes of thyrotoxicosis. Only Graves disease produces a thyroid bruit, exophthalmos, and pretibial myxoedema. TRAb confirms Graves aetiology and also predicts neonatal thyrotoxicosis risk in pregnancy.

The presence of a thyroid bruit with diffuse smooth goitre, lid lag, and systemic thyrotoxicosis strongly suggests Graves disease. TRAb is the specific antibody that drives the hyperthyroidism in Graves disease by binding and activating the TSH receptor. While TSH will be suppressed in all thyrotoxicosis, it does not identify the cause. Anti-TPO is non-specific. TRAb is the definitive aetiology test here.

Correct. This is primary hypothyroidism (elevated TSH with low FT4) caused by Hashimoto thyroiditis (positive anti-TPO). In primary hypothyroidism, the elevated TSH reflects intact pituitary feedback responding to insufficient thyroid hormone. Strongly positive anti-TPO confirms autoimmune thyroid destruction. Secondary hypothyroidism would show a low or inappropriately normal TSH with low FT4 — the opposite pattern. Subclinical hypothyroidism is defined as elevated TSH with NORMAL FT4.

Overt primary hypothyroidism = raised TSH + low FT4. Subclinical hypothyroidism = raised TSH + normal FT4. Secondary hypothyroidism = low/normal TSH + low FT4 (pituitary pattern). Anti-TPO positive in 90-95% of Hashimoto thyroiditis, the commonest cause of primary hypothyroidism in iodine-replete populations.

The TFT pattern here — raised TSH + low FT4 — defines overt primary hypothyroidism. The positive anti-TPO confirms Hashimoto thyroiditis as the cause. Secondary hypothyroidism (pituitary failure) shows a low or inappropriately normal TSH with low FT4. Subclinical hypothyroidism is raised TSH with normal FT4 — FT4 is below normal here, making it overt.

Correct. Propylthiouracil (PTU) is preferred in the FIRST trimester of pregnancy. Carbimazole and its active metabolite methimazole are associated with aplasia cutis, choanal atresia, and other embryopathies (carbimazole embryopathy) if used in the first trimester. PTU has a lower risk of teratogenicity and is therefore the drug of choice in the first trimester. However, PTU carries a risk of hepatotoxicity with prolonged use, so the standard practice is to switch from PTU to carbimazole/methimazole in the second trimester. Radioiodine is absolutely contraindicated in pregnancy.

Key pregnancy antithyroid drug rule: PTU in first trimester (carbimazole causes embryopathy), switch to carbimazole in second trimester (PTU causes hepatotoxicity). Radioiodine is absolutely contraindicated in pregnancy and for 6 months post-treatment. This is a high-yield exam trap.

PTU is preferred in the first trimester of pregnancy because carbimazole and methimazole are associated with a specific embryopathy (aplasia cutis, choanal atresia, oesophageal atresia — the carbimazole embryopathy). PTU is used in trimester 1, then switched to carbimazole in trimester 2 because PTU has hepatotoxicity risk with prolonged use. Radioiodine is absolutely contraindicated throughout pregnancy.

Correct. This is myxoedema coma — a life-threatening emergency defined by altered consciousness, hypothermia, bradycardia, and hypotension in severe hypothyroidism. The Burch-Wartofsky-equivalent management of myxoedema coma requires: (1) IV levothyroxine 200–400 µg loading dose (IV because enteral absorption is unpredictable in critical illness), (2) IV hydrocortisone 100 mg 8-hourly (concurrent adrenal insufficiency must be assumed and treated before large T4 doses, as thyroid hormone increases cortisol metabolism and may precipitate adrenal crisis), (3) active external rewarming, and (4) ICU admission for monitoring. Oral levothyroxine and passive rewarming are inadequate for this emergency.

Myxoedema coma management: IV levothyroxine 200–400 µg bolus + hydrocortisone 100 mg IV (always give steroids first or concurrently — thyroid hormone increases cortisol metabolism and can trigger adrenal crisis) + active rewarming + ICU. Precipitants: infection, cold exposure, drugs (sedatives, opioids), non-compliance.

Myxoedema coma is a medical emergency requiring IV thyroid hormone replacement (levothyroxine 200–400 µg IV bolus), mandatory IV hydrocortisone (adrenal insufficiency must be assumed), active rewarming, and ICU care. Oral levothyroxine has unpredictable absorption in critically ill patients. Hydrocortisone must precede or accompany thyroid hormone to avoid precipitating adrenal crisis. Passive rewarming alone is inadequate.

Correct. Toxic multinodular goitre (TMNG) is the most likely diagnosis. The key features are: (1) overt thyrotoxicosis (suppressed TSH + elevated FT4), (2) multinodular goitre without bruit or eye signs, (3) TRAb negative (ruling out Graves disease), (4) older patient — TMNG typically presents in individuals over 50 with longstanding nodular goitre. Graves disease would show TRAb positivity, a diffuse smooth goitre with bruit, and frequently eye signs. Subacute thyroiditis causes a painful thyroid and is typically transient. A TSH-secreting pituitary adenoma would show an elevated or inappropriately normal TSH, not suppressed TSH.

Toxic multinodular goitre (TMNG) vs Graves disease: TMNG — older patient, multinodular goitre, no bruit, no eye signs, TRAb negative, RAIU shows patchy hot nodules. Graves — younger, diffuse smooth goitre + bruit, exophthalmos possible, TRAb positive, RAIU diffusely elevated. Treatment of TMNG: radioiodine or surgery (thionamides control but do not cure).

The combination of suppressed TSH + elevated FT4 + multinodular goitre + no bruit + no eye signs + negative TRAb in an older patient points to toxic multinodular goitre. Graves disease requires TRAb positivity and typically shows a diffuse bruit-bearing goitre with ophthalmopathy. Subacute thyroiditis is painful and transient. TSH-secreting pituitary adenoma shows a paradoxically normal or elevated TSH alongside raised FT4.

Correct. The Burch-Wartofsky Point Scale (BWPS) is the standard diagnostic scoring system for thyroid storm. Interpretation: score ≥45 = thyroid storm likely; score 25–44 = impending storm; score <25 = storm unlikely. A score of 55 firmly indicates thyroid storm — a life-threatening emergency. Treatment requires immediate multi-drug protocol: (1) PTU 500–1000 mg loading (blocks synthesis and peripheral T4-to-T3 conversion), (2) iodine (Lugol's) given 1 hour AFTER PTU (blocks hormone release), (3) beta-blocker (propranolol IV for rate and to inhibit peripheral T4-to-T3 conversion), (4) hydrocortisone IV (reduces peripheral conversion, addresses relative adrenal insufficiency), and (5) treatment of the precipitant.

Thyroid storm Burch-Wartofsky Point Scale: ≥45 = storm. Treatment sequence: PTU 500–1000 mg load FIRST → Lugol iodine 1 hour later (iodine before PTU causes Jod-Basedow worsening) → IV propranolol → IV hydrocortisone → treat precipitant. Common precipitants: infection, surgery, trauma, radioiodine, iodinated contrast.

Burch-Wartofsky Point Scale: ≥45 = thyroid storm (immediate treatment required), 25–44 = impending storm (close monitoring and treat), <25 = unlikely. A score of 55 mandates ICU-level emergency treatment. The multi-drug protocol is: PTU first (blocks synthesis + T4→T3 conversion), then Lugol iodine 1 hour later (blocks hormone release), plus IV propranolol (rate control + blocks T4→T3 conversion), IV hydrocortisone, and treat the precipitant (here: surgery/infection).

Correct. This is T3 thyrotoxicosis — characterised by suppressed TSH, NORMAL FT4, and ELEVATED FT3. This pattern is seen in early Graves disease, toxic nodular goitre, and sometimes after radioiodine treatment. The critical diagnostic error is to stop at the normal FT4 and conclude the patient is subclinically thyrotoxic without checking FT3. Subclinical hyperthyroidism would show suppressed TSH with both FT4 and FT3 normal. The teaching point from the SDL is that this is one of the most dangerous diagnostic errors in thyroid testing.

T3 thyrotoxicosis: suppressed TSH + normal FT4 + elevated FT3. This is an examination trap. Always measure FT3 when TSH is suppressed and FT4 is normal to exclude T3 toxicosis. Failure to check FT3 is one of the two most dangerous diagnostic errors in thyroid testing per the SDL.

This is T3 thyrotoxicosis: suppressed TSH + normal FT4 + elevated FT3. The error is stopping at normal FT4 and concluding subclinical thyrotoxicosis without checking FT3. Subclinical hyperthyroidism = suppressed TSH + normal FT4 AND normal FT3. Overt hypothyroidism = raised TSH + low FT4. Secondary hypothyroidism = low/normal TSH + low FT4. Always check FT3 when TSH is suppressed and FT4 is normal.

Correct. The TSH of 2.1 mIU/L is within the normal range (0.4–4.0 mIU/L), indicating that the levothyroxine dose is appropriate. In newly started levothyroxine, TSH takes 6–8 weeks to stabilise after a dose change, and some residual symptoms may persist while tissues adapt to restored thyroid hormone levels. The correct response is to confirm euthyroidism by rechecking TFTs at 6 weeks on the same dose — not to increase the dose arbitrarily in response to residual symptoms. Increasing the dose would risk over-replacement (suppressed TSH, risk of atrial fibrillation and osteoporosis). Adding T3 is not standard practice for uncomplicated hypothyroidism.

Levothyroxine monitoring: check TFTs at 6–8 weeks after any dose change. Target TSH: 0.4–4.0 mIU/L for most adults; 0.1–2.5 mIU/L in pregnancy. Do not dose-escalate based on symptoms when TSH is already in range — over-replacement causes AF and osteoporosis. Annual TFT monitoring once stable.

TSH 2.1 mIU/L is within the target therapeutic range for levothyroxine in hypothyroidism (TSH 0.4–4.0 mIU/L). The appropriate action is to confirm stability at this dose by rechecking TFTs in 6 weeks. Residual symptoms with a normal TSH may reflect slow tissue adaptation rather than under-replacement. Dose increases should only follow a documented persistently elevated TSH, not symptoms alone when TSH is already in range.

Correct. Under India's NIDDCP, iodised salt must contain at least 30 ppm iodine at the point of production and at least 15 ppm iodine at the consumer level (to account for losses during storage, cooking, and transport). The national mandate requires that all edible salt sold in India be iodised. This programme is one of India's most successful public health interventions, reducing endemic goitre and cretinism. The Food Safety and Standards Authority of India (FSSAI) enforces the 15 ppm consumer-level standard.

NIDDCP iodised salt standard: 30 ppm at production, 15 ppm minimum at consumer level. India mandates universal salt iodisation under Prevention of Food Adulteration Act and FSSAI. Iodine deficiency is the commonest preventable cause of hypothyroidism and cretinism worldwide. Goitre belt in India: sub-Himalayan states + peninsular endemic zones.

The NIDDCP mandates 30 ppm iodine at the production/packing level and 15 ppm at the consumer level (losses occur during storage and cooking). The 15 ppm consumer-level standard is the enforceable minimum. This programme has been central to controlling iodine deficiency disorders, including endemic goitre and cretinism, across India.

Correct. Predictors of sustained remission after a standard 12–18-month course of antithyroid drug therapy for Graves disease include: (1) small thyroid gland (normal or near-normal size at end of treatment), (2) TRAb negative or very low titre at end of treatment (TRAb persistence predicts relapse), (3) mild biochemical thyrotoxicosis at presentation, and (4) female sex and non-smoking status. Large goitre, persistently elevated TRAb, and young age are associated with higher relapse rates. Overall, 50–70% of Graves disease patients relapse after stopping thionamides — hence definitive therapy (radioiodine or surgery) is preferred for patients with risk factors for relapse.

Graves disease remission predictors after thionamide withdrawal (18 months course): favourable — small gland, TRAb negative, mild initial disease; unfavourable — large goitre, high TRAb, young age, male sex, smoker. Overall relapse 50–70%. Consider radioiodine or thyroidectomy for relapse or high-risk features.

Remission predictors for Graves disease after thionamide withdrawal: small gland, negative or low TRAb, mild initial thyrotoxicosis, and non-smoker status favour remission. Large goitre, high TRAb, and young age predict relapse. Overall 50–70% relapse — which is why definitive therapy is recommended for patients with large goitres, high TRAb, or recurrence.