Hyperthyroidism and thyroid nodule: the Australian GP guide

What hyperthyroidism is

Hyperthyroidism occurs when the thyroid gland produces more hormone than the body needs, elevating circulating thyroxine (T4) and triiodothyronine (T3) while suppressing TSH through feedback inhibition. In Australian general practice it is encountered at roughly 1–2 new diagnoses per 1,000 patients per year, with a strong female predominance (F:M approximately 5–10:1 for Graves’ disease).

Graves’ disease — autoimmune, driven by TSH-receptor antibodies (TRAb) — accounts for 60–70% of cases in Australia, peaks in women aged 20 to 40, and is the only cause that produces extra-thyroidal features: thyroid eye disease (Graves’ orbitopathy), pretibial myxoedema, and thyroid acropachy. Smoking is the single most important modifiable risk factor for eye disease progression.

Toxic multinodular goitre and toxic adenoma account for most remaining cases, particularly in older adults and those from areas of historical iodine deficiency. Thyroiditis — post-viral (subacute, de Quervain’s), postpartum, or drug-induced (amiodarone, immune checkpoint inhibitors) — causes transient thyrotoxicosis through release of stored hormone rather than excess synthesis. It is characterised by low radioiodine uptake and usually self-resolves.

Subclinical hyperthyroidism (TSH below the reference range with normal T4 and T3) is frequently found incidentally. Persistent suppression below 0.1 mIU/L raises the risk of atrial fibrillation, bone loss, and cardiovascular mortality — particularly in adults over 65 — and warrants treatment consideration.

A. Core clinical — the AU general-practice framework

The diagnostic ladder

Therapeutic Guidelines (eTG) and Australian Medicines Handbook (AMH) recommend a structured investigation sequence:

First-line: TSH. A suppressed TSH is the sensitive screening test. If TSH is below the reference range, add free T4 and free T3. T3 toxicosis (isolated T3 elevation with normal T4) occurs early in Graves’ disease and with toxic adenoma.

Second-line (suppressed TSH): TRAb (TSH receptor antibody) — sensitivity approximately 98% for Graves’ disease; anti-TPO supports autoimmune basis. Baseline FBC and LFTs before starting antithyroid drugs. ECG to screen for atrial fibrillation.

Imaging: Thyroid ultrasound distinguishes diffuse vascularity (Graves’) from a multinodular gland or single nodule. Thyroid scintigraphy (Tc-99m or I-123 uptake scan) shows diffuse uniform uptake in Graves’, patchy nodular in toxic MNG, focal hot in toxic adenoma, and low uptake in thyroiditis or exogenous thyroid hormone.

Pitfalls: Biotin supplements cause spurious TSH suppression and apparent FT4 elevation through immunoassay interference — advise patients to withhold biotin at least 48 hours before thyroid function tests. Apathetic hyperthyroidism in older adults presents with weight loss, atrial fibrillation, and depression rather than the agitation expected in younger patients — the Endocrine Society of Australia emphasises this is easily missed without a TSH.

Clinical features to elicit

Classic hyperthyroidism: weight loss with preserved or increased appetite, heat intolerance, excessive sweating, palpitations, tremor, anxiety, hyperdefecation, and menstrual irregularity. On examination: tachycardia (sinus or atrial fibrillation), widened pulse pressure, fine tremor, warm moist skin, diffuse or nodular goitre, and lid lag. In Graves’ disease: proptosis, lid retraction, conjunctival injection, and periorbital oedema.

Treatment hierarchy

Three definitive options exist, chosen by shared decision between patient and endocrinologist:

1. Antithyroid drugs (ATDs) — first-line in many Australian centres, particularly for Graves’ disease where medical remission is achievable.
2. Radioactive iodine (RAI, I-131) — definitive; most patients develop hypothyroidism within 12 months and require lifelong levothyroxine.
3. Thyroidectomy — for large goitre, suspicious nodule, ATD intolerance, or patient preference.

Beta-blockers (propranolol 20–80 mg three times daily, or atenolol 25–100 mg daily) control symptoms while definitive treatment takes effect and also block peripheral T4-to-T3 conversion at higher doses.

B. Antithyroid drugs — evidence and safety

Per eTG Endocrinology and AMH:

Carbimazole first-line outside pregnancy: start 15–45 mg daily (divided or once daily), titrate to euthyroid over 4–8 weeks, then maintain at 5–15 mg daily. In Graves’ disease, treat for 12–18 months then trial cessation — approximately 50% achieve sustained remission. Extended treatment (≥5 years) achieves higher sustained remission rates per Azizi et al 2019 and is a reasonable option for patients who tolerate the drug and prefer to defer definitive treatment.

The critical safety warning — agranulocytosis: Carbimazole causes agranulocytosis in approximately 0.3% of patients; PTU in approximately 0.5%. Risk peaks in the first three months. Every patient starting an antithyroid drug must be counselled explicitly: fever, sore throat, or mouth ulcers means stop the medication immediately and present for an urgent FBC. Document this conversation. Delay in stopping the drug can be fatal. Additional side effects: hepatotoxicity (more common with PTU — check LFTs at baseline and months one, three, and six), rash, and rare ANCA-associated vasculitis with long-term PTU.

PTU is preferred over carbimazole in two settings: first-trimester pregnancy (carbimazole T1 teratogenic risk: aplasia cutis, choanal and oesophageal atresia) and thyroid storm (PTU also blocks peripheral T4-to-T3 conversion). In all other contexts carbimazole is favoured.

Monitoring on ATDs: TFTs at four weeks, then 6–8 weekly until stable, then 3-monthly. FBC and LFTs at baseline, then at months one, three, six, and twelve.

C. Thyroid nodule — TIRADS risk stratification

Thyroid nodules are common — palpable in approximately 5% of adults, detectable by ultrasound in up to 50%. Only approximately 5% are malignant. Structured risk stratification, not blanket biopsy, is the standard approach recommended by the Australian and New Zealand Thyroid Society.

TIRADS (Thyroid Imaging Reporting and Data System) classifies nodules by ultrasound features (composition, echogenicity, shape, margin, echogenic foci):

TIRADS class	Features	FNA threshold
TR1	Benign (simple cyst)	Not indicated
TR2	Not suspicious	Not indicated
TR3	Mildly suspicious	≥2.5 cm
TR4	Moderately suspicious	≥1.5 cm
TR5	Highly suspicious	≥1.0 cm

FNA cytology is classified by the Bethesda system (I–VI). Bethesda II (benign) is reassuring; V–VI (suspicious/malignant) warrants surgical referral.

Clinical features prompting earlier referral regardless of TIRADS grade: rapid nodule growth, firm or hard consistency, hoarse voice (vocal cord palsy), cervical lymphadenopathy, family history of thyroid cancer, age under 20 or over 70, prior neck radiation, or concurrent clinical hyperthyroidism suggesting a toxic adenoma.

Ultrasound operator expertise matters. Specialised thyroid ultrasound significantly improves sensitivity for deep or infiltrating lesions compared with general radiology. The Australian and New Zealand Thyroid Society recommends referral to operators with specific thyroid expertise for nodules requiring detailed characterisation.

D. Australian operations

PBS drugs: Carbimazole (Neo-Mercazole) and PTU are on the general schedule. Beta-blockers (propranolol, atenolol, metoprolol) and levothyroxine (for post-RAI or post-thyroidectomy replacement) are also general schedule. Selenium 100 mcg tablets are available over the counter. Teprotumumab (Tepezza) — TGA-approved 2025 for moderate-to-severe thyroid eye disease — has evolving PBS status; verify current listing before prescribing.

MBS items relevant to general practice: TSH (66716), free T4 (66717), free T3 (66719), TRAb (66622), FBC (65070), LFTs (66512), UEC (66500), ECG (11707), thyroid ultrasound (55050), ultrasound-guided FNA (55054), DXA for bone density (12306). Standard consultation items 23, 36, 44. GPCCMP items 965/967 for chronic hyperthyroidism with comorbidity (atrial fibrillation, osteoporosis, mental health) — allied health referral pathway. MHCP 2715/2717 for comorbid anxiety or depression. ATSI Health Assessment (715); 75+ Health Assessment (705).

Driving: Per Austroads — Assessing Fitness to Drive, uncontrolled hyperthyroidism with arrhythmia restricts driving — document clinical status and treatment response.

Euthyroid before elective surgery: Anaesthetic complications in uncontrolled hyperthyroidism are significant — ensure euthyroid state is documented pre-elective procedure.

Telehealth: suitable for stable medication follow-up with pathology results available; in-person required for thyroid eye disease examination and goitre assessment.

E. Special populations

Thyroid eye disease (Graves’ orbitopathy): Smoking cessation is the most important modifiable factor — smokers have markedly higher risk of progression. Mild disease: selenium 100 mcg twice daily for six months (Marcocci NEJM 2011 showed improvement in mild active TED), artificial tears, and prism glasses for diplopia. Moderate-to-severe active disease: IV methylprednisolone (~4.5 g cumulative). Severe or refractory: orbital decompression surgery, orbital radiotherapy, or teprotumumab (specialist referral). RAI may worsen active thyroid eye disease — use cautiously in moderate-to-severe disease.

Pregnancy: PTU in the first trimester; switch to carbimazole from the second trimester. Check TRAb in the second-to-third trimester — antibodies cross the placenta and can cause fetal and neonatal hyperthyroidism. Joint obstetric and endocrinology management. Postpartum thyroiditis (~5–10% of postpartum women) runs a biphasic course — transient hyperthyroidism followed by hypothyroidism; most resolve within 12 months.

Thyroid storm: A rare, life-threatening emergency — high fever, tachyarrhythmia, delirium, vomiting, diarrhoea, and multi-organ failure; mortality 10–30%. Immediate ED transfer. Management includes PTU 200 mg four-hourly, IV propranolol, Lugol’s iodine (≥1 hour after PTU to block hormone release), hydrocortisone 100 mg IV 8-hourly, active cooling, and treatment of the precipitant.

Subclinical hyperthyroidism in older adults: Persistent TSH below 0.1 mIU/L warrants treatment consideration in patients over 65, those with atrial fibrillation, osteoporosis, or postmenopausal women — per eTG Endocrinology. Watchful waiting with 3–6 monthly TFTs is appropriate for mild suppression without risk factors.

Drug-induced thyrotoxicosis: Amiodarone-induced thyrotoxicosis (AIT) Type 1 (iodine-driven Graves’ on susceptible thyroid) versus Type 2 (destructive thyroiditis) requires specialist differentiation — management differs substantially. Immune checkpoint inhibitors (pembrolizumab, nivolumab) increasingly cause thyroiditis in oncology patients — screen TFTs at baseline and at each cycle.

When to escalate

Urgent ED or immediate specialist call:

• Suspected thyroid storm — fever plus tachyarrhythmia plus agitation or altered consciousness.
• Thyroid eye disease with visual threat — corneal exposure, optic nerve compression.
• Atrial fibrillation with haemodynamic compromise.
• Worsening hyperthyroidism in pregnancy.

Same-week endocrinology referral:

• Newly diagnosed hyperthyroidism in adults.
• Pregnancy with thyrotoxicosis.
• Suspicious thyroid nodule (TR4–TR5 on TIRADS).
• Antidepressant- or checkpoint-inhibitor-induced thyrotoxicosis.

Routine referral:

• Planning radioactive iodine or thyroidectomy.
• Moderate thyroid eye disease for ophthalmology assessment.
• Refractory or recurrent Graves’ disease after completing an ATD course.
• Complex polypharmacy (amiodarone, immune checkpoint inhibitors).

What this article is and is not

This is general health information drawn from current Australian general practice guidelines — Therapeutic Guidelines (eTG), AMH, Endocrine Society of Australia, Australian and New Zealand Thyroid Society — and the American Thyroid Association 2016 Hyperthyroidism Guideline where Australian primary-tier guidance is silent. It is not personal medical advice and does not create a doctor–patient relationship. Specific treatment decisions — including antithyroid drug choice, radioactive iodine, and thyroidectomy — are made with your own GP and treating specialists.

For consumer-friendly information: HealthDirect — Hyperthyroidism, Better Health Channel — Thyroid gland, Australian Thyroid Foundation.

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Sources cited

1. Therapeutic Guidelines (eTG) — Endocrinology: Thyroid
2. Australian Medicines Handbook (AMH)
3. Endocrine Society of Australia
4. Australian and New Zealand Thyroid Society
5. RACGP
6. TGA
7. Austroads — Assessing Fitness to Drive
8. HealthDirect — Hyperthyroidism
9. Better Health Channel — Thyroid gland
10. Australian Thyroid Foundation
11. American Thyroid Association — 2016 Hyperthyroidism Guideline
12. Marcocci C et al — Selenium and mild Graves’ orbitopathy (NEJM 2011)
13. Azizi F et al — Extended antithyroid drug treatment (Eur Thyroid J 2019)