Clinical Pathology · MU Sofia

115. Thyroid epithelial hyperplasia. Hypothyroidism. Myxedema.

Covers the thyroid's structure and hormone release, then thyroid epithelial hyperplasia, including its causes, endemic and sporadic goitre, and diffuse versus multinodular forms with a gross specimen image. Goes on to hypothyroidism, its primary and secondary types and causes, and the clinical features of cretinism and myxedema. A mnemonic of six Ps summarises the features of cretinism.

Inside: 1 section · 1 labelled picture · 16 flashcards · 3 min

Topic 115 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 481 words (3 min of reading), with 16 flashcards.

In this note

  1. Thyroid epithelial hyperplasia. Hypothyroidism. Myxedema

Thyroid epithelial hyperplasia. Hypothyroidism. Myxedema

The thyroid gland has two lateral lobes connected by an isthmus. During embryological development it descends from the foramen cecum at the base of the tongue to its location on

the anterior of the neck. We mention this as you can get ectopic thyroid tissue along this path. The thyroid consists of lobules, which have follicles.

In response to Thyroid stimulating hormone (TSH) released from the pituitary, thyroxine (T₄) and triiodothyronine (T₃) are released. While T₄ is released in greater amounts, T₃ has a much greater level of affinity for the thyroid hormone receptor (TR), while in the periphery, T₄ is converted to T₃ as required, T₃ can be thought of as the active form of T₄, this allows the body to have consistently high levels of active hormone in the periphery as required, without the risk of toxicity. As the T₃ reacts with the TR, it controls the transcription of certain genes.

Thyroid epithelial hyperplasia

  • Note - in books this is referred to as Diffuse and Multinodular goiter
  • This is the enlargement of the thyroid and is the most common manifestation of thyroid disease
  • It is most often caused by iodine deficiency, causing impairment of hormone synthesis which increases TSH levels, in turn causing hypertrophy and hyperplasia of thyroid follicular cells and overall gross enlargement of the thyroid
  • In the vast majority of cases, the hyperplasia is sufficient compensation, and the T₃ and T₄ levels are steady, however where compensation fails, we have goitrous hypothyroidism
  • Goiters can be
  • Endemic (where there is low natural iodine in the diet, common in himalayas and Andes)
  • Sporadic (less common, more common in females around puberty)
  • Morphologically, hyperplasia can be diffuse or multinodular

Gross, multinodular goitre: the enlarged gland is full of nodules of different sizes filled with brown, glistening colloid and separated by fibrous bands.

Image: “Macro Thyroïde - Goitre 55-o.apatho-18a-thyroide” by Denis Desaulniers et Bernard Têtu, CC BY-SA 4.0, via Wikimedia Commons.

Hypothyroidism

  • Commonly divided into primary (an issue in the thyroid) or secondary (an issue of the pituitary which produces TSH)
  • Most common cause is low iodine leading to thyroid epithelial hyperplasia and goiter hypothyroidism (as above), other causes are listed below
  • Developmental abnormalities, iatrogenic, AI hypothyroidism, Hashimoto thyroiditis, Drugs, Pituitary failure (this is secondary form)
  • Clinical manifestations of hypothyroidism include:

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