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Hyperthyroidism

SNOMED: 34486009911 words•Updated 03/03/2026
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Exam Tips

  • Differentiate terms precisely: hyperthyroidism (overproduction) vs thyrotoxicosis (clinical hormone excess from any cause).
  • Interpret TFT patterns quickly: low TSH + high FT4/FT3 = overt primary hyperthyroidism; low TSH + normal FT4/FT3 = subclinical hyperthyroidism.
  • In Graves, TRAb positivity plus diffuse goitre/eye signs is high-yield for diagnosis.
  • In thyroiditis, uptake is low because hormone is released from damaged follicles rather than newly synthesized.
  • Always mention thionamide red flags in OSCEs: sore throat, fever, mouth ulcers -> stop drug and urgent FBC (agranulocytosis risk).
  • State key contraindications: radioiodine in pregnancy/breastfeeding; caution beta-blockers in asthma; pregnancy-specific choice of thionamide.

Definition

Hyperthyroidism is a biochemical disorder in which the thyroid gland synthesizes and secretes excess thyroid hormone, usually causing suppressed TSH with raised FT4 and/or FT3 in overt disease. It is one cause of thyrotoxicosis (the clinical state of thyroid hormone excess), but thyrotoxicosis can also occur without gland overproduction, such as in thyroiditis or exogenous hormone use.

Pathophysiology

Most UK cases are primary thyroid disease. Graves disease is a TSH-receptor antibody (TRAb)-mediated autoimmune process that drives diffuse thyroid hyperplasia and unregulated hormone synthesis; toxic multinodular goitre and toxic adenoma arise from autonomously functioning follicular tissue. Excess T3/T4 increases beta-adrenergic tone, thermogenesis, bone turnover, and myocardial oxygen demand, producing systemic hypermetabolism and cardiovascular risk. In contrast, thyroiditis causes release of preformed hormone (low uptake state) rather than increased synthesis. See Figure: hypothalamic-pituitary-thyroid negative feedback loop and Graves autoantibody mechanism in standard endocrine textbook thyroid chapters.

Risk Factors

  • Female sex (marked female predominance)
  • Family history of Graves disease or other autoimmune thyroid disease
  • Personal or family history of autoimmune disease (for example type 1 diabetes)
  • Smoking (dose-dependent risk of Graves disease and especially orbitopathy)
  • Older age (particularly toxic multinodular goitre/toxic adenoma)
  • Low iodine intake followed by iodine exposure
  • Iodine-containing drugs (for example amiodarone) or iodinated contrast exposure
  • Postpartum period (especially for postpartum thyroiditis)
  • Alemtuzumab therapy (increased risk of autoimmune thyroid disease)

Clinical Features

Symptoms

  • Weight loss despite normal or increased appetite
  • Heat intolerance and sweating
  • Palpitations, exertional breathlessness, reduced exercise tolerance
  • Tremor, anxiety, irritability, insomnia
  • Frequent stools/diarrhoea
  • Proximal muscle weakness and fatigue
  • Menstrual disturbance, reduced fertility, reduced libido
  • Neck swelling or pressure symptoms (dysphagia, dyspnoea) with large goitre
  • Eye discomfort, gritty eyes, diplopia in Graves orbitopathy

Signs

  • Sinus tachycardia or atrial fibrillation
  • Fine tremor, warm moist skin, hyperreflexia
  • Diffuse goitre (often with bruit in Graves) or nodular goitre
  • Lid retraction/lid lag; proptosis and ophthalmoplegia in Graves orbitopathy
  • Weight loss, proximal myopathy
  • Pretibial myxoedema and thyroid acropachy (less common Graves features)

Investigations

Serum TSH:Suppressed in primary overt and subclinical hyperthyroidism; inappropriately normal/high suggests rare central causes (for example TSH-secreting adenoma).
Free T4 and Free T3:Overt disease: FT4 and/or FT3 above reference range; subclinical disease: FT4/FT3 normal with low TSH; T3-predominant thyrotoxicosis can occur.
TSH receptor antibody (TRAb):Positive supports Graves disease and helps distinguish from thyroiditis/nodular disease.
Thyroid peroxidase antibodies (TPOAb):May be positive in autoimmune thyroid disease but less specific than TRAb for Graves.
Radioisotope thyroid uptake scan (if diagnosis uncertain):Diffuse high uptake in Graves, focal/patchy uptake in toxic nodular disease, low uptake in thyroiditis or exogenous hormone use.
Thyroid ultrasound with Doppler:Useful for nodules/goitre characterization; increased vascularity may support Graves.
ECG:Sinus tachycardia or atrial fibrillation, especially in older adults.
Baseline full blood count and liver function tests:Required before antithyroid drugs to identify pre-existing neutropenia or liver dysfunction and for treatment safety monitoring.
Pregnancy test (if relevant):Essential before radioiodine and to guide antithyroid drug choice in pregnancy.

Management

Lifestyle Modifications

  • Strong smoking cessation advice (major modifiable risk factor for Graves orbitopathy progression and poorer treatment response).
  • Avoid excess iodine intake (for example kelp supplements) and review iodine-rich medications with specialists.
  • Counsel on adherence and safety-netting: urgent FBC if sore throat, fever, or mouth ulcers while on thionamides.
  • Address cardiovascular risk, bone health, and symptom burden; discuss fertility/pregnancy plans early.

Pharmacological Treatment

Thionamides (reduce thyroid hormone synthesis)

  • Carbimazole oral 20-40 mg once daily initially (titrate to maintenance usually 5-15 mg daily)
  • Propylthiouracil oral 100-150 mg three times daily initially (used when carbimazole unsuitable, including specific pregnancy contexts)

Main first-line therapy for Graves in UK practice. Major safety warnings: agranulocytosis (stop immediately and check urgent FBC if infection symptoms), hepatotoxicity (particularly severe with propylthiouracil), and rash/arthralgia. Carbimazole is associated with congenital malformations when used in early pregnancy; propylthiouracil is often preferred in first trimester, then many specialists switch back to carbimazole later to reduce maternal liver risk.

Symptomatic beta-blockade

  • Propranolol oral 10-40 mg three to four times daily
  • Alternative if needed: atenolol oral 25-50 mg once daily

Improves tremor, palpitations, and anxiety while definitive control is achieved. Contraindications/cautions: asthma or bronchospasm, bradycardia, heart block, and decompensated heart failure.

Definitive non-surgical therapy

  • Radioiodine (I-131), individualized activity per specialist protocol

Effective for Graves and toxic nodular disease; commonly leads to hypothyroidism requiring lifelong levothyroxine. Contraindicated in pregnancy and breastfeeding; conception should be deferred after treatment per local protocol. May worsen Graves orbitopathy, especially in smokers; steroid prophylaxis may be considered by specialists.

Surgical / Interventional

  • Total or near-total thyroidectomy for large/compressive goitre, suspected malignancy, relapse/intolerance to drugs, or patient preference.
  • Pre-operative optimization usually includes thionamide therapy and often beta-blockade to achieve euthyroid state.
  • Key risks to counsel: hypocalcaemia from hypoparathyroidism, recurrent laryngeal nerve injury, bleeding/haematoma, and lifelong thyroid hormone replacement.

Complications

  • Graves orbitopathy, including sight-threatening dysthyroid optic neuropathy or severe corneal disease
  • Thyroid storm (life-threatening decompensated thyrotoxicosis)
  • Atrial fibrillation, tachyarrhythmia, and heart failure
  • Osteoporosis and fragility fracture risk from prolonged untreated excess thyroid hormone
  • Proximal myopathy and reduced quality of life
  • Compressive symptoms from large goitre (dysphagia, airway compromise)
  • Adverse pregnancy outcomes if poorly controlled thyrotoxicosis

Prognosis

Prognosis is generally good with timely diagnosis and appropriate treatment, but relapse is common after antithyroid drugs (particularly in Graves), so long-term biochemical follow-up is essential. Definitive therapy (radioiodine or surgery) usually controls thyrotoxicosis but frequently results in hypothyroidism requiring lifelong levothyroxine. Morbidity rises when disease is untreated or undertreated, especially from cardiovascular complications, bone loss, and severe orbitopathy.

Sources & References

💊BNF Drug References(50)

✅NICE Guidelines(1)

📖Textbook References(10)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1210)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1210)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1207, 1208)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1208)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 939)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 938)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 939)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 936)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 939)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 939)[context]

Sources

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