Hyperthyroidism

Hyperthyroidism refers specifically to overactivity of the thyroid gland, whereas thyrotoxicosis is the clinical state of tissue exposure to excessive thyroid hormones. Graves' disease accounts for 75-80% of cases in the UK and is characterised by the presence of TSH-receptor antibodies (TRAb). Other common causes include Toxic Multinodular Goitre (Plummer's disease) and Toxic Adenoma (solitary hot nodule). Rare causes include de Quervain's (subacute) thyroiditis, which is a transient self-limiting condition following a viral infection. Untreated thyrotoxicosis increases the risk of atrial fibrillation, osteoporosis, and in extreme cases, 'Thyroid Storm'—a life-threatening hypermetabolic state. The diagnosis is confirmed biochemically by a suppressed TSH and elevated free T4/T3. Subclinical hyperthyroidism is defined by a low TSH with normal T4/T3. Management is tailored to the underlying cause: Graves' is often treated with an 18-month course of carbimazole, while toxic nodules are more likely to require definitive therapy (radioactive iodine or surgery). Cardiovascular symptoms are managed with beta-blockers, typically propranolol, which also inhibits the peripheral conversion of T4 to the more active T3.

The thyroid gland produces thyroxine (T4) and triiodothyronine (T3) under the control of Thyroid Stimulating Hormone (TSH) from the anterior pituitary. In Graves' disease (Type II Hypersensitivity), B-cells produce IgG autoantibodies (TRAb) that mimic TSH and bind to the TSH receptor on thyroid follicular cells, causing unrestrained synthesis and release of thyroid hormones. In Toxic Multinodular Goitre, certain areas of the gland become autonomous of TSH control. Excessive T3/T4 binds to nuclear receptors in almost all tissues, leading to an increased basal metabolic rate. Actions include upregulating beta-adrenergic receptors (causing sympathetic symptoms), increasing gluconeogenesis and lipolysis, and increasing bone turnover. Subacute thyroiditis (de Quervain's) involves the release of pre-formed hormone due to inflammation of the follicles, typically following a viral illness, presenting with a painful goitre.

Symptoms: Heat intolerance, weight loss (despite increased appetite), palpitations, anxiety, irritability, diarrhoea, and oligomenorrhea. Signs: Tachycardia (often AF), fine tremor, warm/moist skin, and brisk reflexes. Graves'-specific features: Diffuse painless goitre with a bruit, Exophthalmos (proptosis, lid lag, lid retraction), Pretibial Myxoedema (non-pitting oedema with orange-peel texture), and Thyroid Acropachy (clubbing/periosteal new bone formation). A 'Thyroid Storm' presents with fever (>38.5C), severe tachycardia, confusion, and vomiting—this requires emergency treatment with high-dose antithyroid drugs, Lugol's iodine, steroids, and beta-blockers.

Medical: 1. Beta-blockers (Propranolol) for immediate symptom control. 2. Antithyroid drugs (ATD): Carbimazole is first-line. Two regimes: 'Dose titration' (start high, reduce as T4 falls) or 'Block and Replace' (high dose carbimazole to stop all production + Levothyroxine). Propylthiouracil is used in the 1st trimester of pregnancy or if carbimazole is not tolerated. Radioactive Iodine (I-131): Often definitive treatment for nodules or recurrent Graves'. Requires 6 months of contraception following treatment and carries a high risk of permanent hypothyroidism. Surgical: Total/subtotal thyroidectomy for large goitres, suspected malignancy, or when other treatments fail/are contraindicated. Complications include recurrent laryngeal nerve damage and hypoparathyroidism.