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Goitre: diffuse and multinodular

  • Lesion

A goitre is an enlarged thyroid. It usually grows because the gland struggles to make enough hormone, most often for lack of iodine.

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What it is

Goitre is the commonest thyroid disease. When hormone synthesis is impaired, TSH rises and drives follicular hyperplasia; over time cycles of hyperplasia and involution turn a diffuse goitre into a nodular one. Endemic goitre reflects dietary iodine deficiency in mountainous inland regions, including parts of the Andes; sporadic goitre is commoner in women and has many causes.

Structure

  • Diffuse goitre: symmetric enlargement; early, hyperplastic crowded cells; later, distended follicles with flattened cells and abundant colloid.
  • Multinodular goitre: asymmetric, may weigh many times normal; nodules of colloid-rich follicles without a complete capsule.
  • Secondary changes: old haemorrhage (haemosiderin), scarring, calcification, cysts.
  • Substernal extension (plunging goitre) can compress the trachea or superior vena cava.

Step by step

  1. Iodine deficiency or a synthesis defect lowers hormone output.
  2. TSH rises and stimulates follicular growth.
  3. Hyperplasia restores hormone at the price of a larger gland.
  4. Repeated cycles of stimulation and involution create heterogeneous nodules.
  5. Some nodules gain autonomy (often TSHR or GNAS mutations) and can make the patient thyrotoxic.

Clinical notes

  • Mass effects: dysphagia, airway compression, superior vena cava syndrome.
  • A dominant nodule needs ultrasound and often fine-needle aspiration to exclude carcinoma.
  • Colombia and the Andean countries: iodised salt sharply reduced endemic goitre.

Test yourself

Think of the answer, then tap the question to see it.

What drives thyroid enlargement in iodine deficiency?

Low hormone output raises TSH, which stimulates follicular cell hyperplasia and hypertrophy.

What distinguishes toxic multinodular goitre from Graves disease?

Autonomous nodules cause the hyperthyroidism, there are no TSH-receptor antibodies, and there is no ophthalmopathy or dermopathy.

Which secondary changes are typical of multinodular goitre?

Haemorrhage, haemosiderin, fibrosis, calcification and cystic degeneration.

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Goiter (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.