Synopsis
Recognise autonomous nodular hyperthyroidism, define structural and functional risk, and choose durable radioiodine or surgical treatment while controlling cardiovascular consequences.
- Toxic multinodular goitre contains several autonomously functioning areas, whereas toxic adenoma is a single dominant autonomous nodule suppressing the surrounding gland.
- Both become more common with age and often present gradually through atrial fibrillation, heart failure, weight loss or osteoporosis rather than classic Graves features.
- Biochemistry shows suppressed TSH with raised free T4 and/or free T3; T3-predominant disease is particularly common in nodular autonomy.
Key red flags
New atrial fibrillation, worsening angina, exertional dyspnoea, ankle swelling or high-output failure may be the main manifestation and deserves urgent cardiovascular assessment according to stability.
Investigation priorities
Confirm overt or subclinical hormone excess and identify T3 predominance.
Management branches
Suppressed TSH occurs with a palpable nodule or multinodular gland.
- Measure free T4 and free T3, examine the neck and nodes, and review Graves signs, iodine exposure, amiodarone and pregnancy possibility.
- Use TRAb and endocrinology-directed scintigraphy to establish autonomy; obtain ultrasound for structural characterisation when the nodule or goitre meets a clinical indication.
Key medicines
Carbimazole for autonomous hyperthyroidismChoose a BNF-listed initial total commonly within 15 to 40 mg daily according to free-hormone elevation, then titrate through endocrinology while definitive treatment is planned.
Beta blocker for nodular thyrotoxic symptomsUse an individual BNF-checked oral beta-blocker regimen, for example propranolol 10 to 40 mg three or four times daily when appropriate, titrated to pulse and tolerance.