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PH-EN12

Thyroiditis

How autoimmunity, viruses, bacteria and fibrosis injure the thyroid follicles, why fast destruction leaks stored hormone (thyrotoxicosis with a low iodine uptake, then hypothyroidism), and how each form looks.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Explain why the thyroid’s store of hormone lets destruction cause thyrotoxicosis without any increase in production.
  • Contrast the mechanism and microscopy of Hashimoto, painless and postpartum, subacute granulomatous, acute suppurative and Riedel thyroiditis.
  • Explain why radioactive iodine uptake is low in destructive thyroiditis and why a hypothyroid phase usually follows.
  • Relate chronic thyroiditis to fibrosis, atrophy, compression of the neck and the risk of thyroid lymphoma.
  • Recognise the tests, classic appearances and numbers examiners ask for, and explain how each treatment acts on the mechanism.

What it is

Thyroiditis is inflammation of the thyroid gland. Its forms divide by cause and pace: autoimmune (chronic Hashimoto thyroiditis, and transient painless and postpartum thyroiditis), subacute granulomatous (de Quervain, after a viral illness), acute suppurative (bacterial), drug- or radiation-induced, and Riedel (fibrosing). Fast destruction releases stored hormone (destructive thyroiditis); slow destruction leads to hypothyroidism.

5 types to tell apart
Hashimoto thyroiditis
Chronic autoimmune destruction with lymphoid follicles and Hürthle cells; the commonest cause of hypothyroidism where iodine intake is adequate.
Painless (silent) and postpartum thyroiditis
A milder, transient autoimmune thyroiditis; postpartum thyroiditis follows childbirth. Thyrotoxic, then hypothyroid, then usually normal.
Subacute granulomatous (de Quervain) thyroiditis
A painful, tender gland weeks after a viral illness, with giant cells round escaped colloid; the same three-phase course.
Acute suppurative thyroiditis
A rare bacterial infection with pus or an abscess, often through a congenital fistula from the throat in children.
Riedel thyroiditis
Rare, dense fibrosis that replaces the gland and grows through its capsule into the neck; often part of IgG4-related disease.

Normal function

Follicles keep weeks of hormone in store

The thyroid is built of follicles: hollow spheres of round a store of , a gel of the protein thyroglobulin. The cells trap iodide from the blood in the , and the enzyme thyroid peroxidase attaches it to thyroglobulin, building thyroxine (T4) and a little triiodothyronine (T3) that stay bound in the colloid.

Release is a separate step controlled by thyroid-stimulating hormone (TSH): the cells take colloid back in, cut the hormone free and pass it to the blood. The hold weeks of hormone, so release and new production can come apart. That is the key to thyroiditis: if follicle walls break, the store escapes at once, whatever TSH is doing.

Trapping iodide needs healthy follicular cells driven by TSH. A small tracer dose of radioactive iodine therefore measures how hard the gland is making hormone, not how much hormone is in the blood. In a healthy gland only scattered lymphocytes lie in the tissue between the follicles.

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