MRCOG Part 1 · Endocrinology · Adrenal and Thyroid Glands and the Pancreas

Thyroid Gland: MRCOG Part 1 questions and key facts

The thyroid gland regulates basal metabolic rate and cellular metabolism through the secretion of thyroxine and triiodothyronine. Follicular hormone synthesis depends on secondary active iodide trapping via the basolateral sodium-iodide symporter, followed by peripheral deiodination requiring the trace element selenium. In the circulation, over 99% of thyroxine is protein-bound, leaving a minute free fraction that mediates biological activity. Thyroid disorders are distinguished biochemically: primary hypothyroidism displays a raised thyroid-stimulating hormone with low free thyroxine, most commonly caused, in iodine-sufficient countries, by Hashimoto's thyroiditis, whereas primary hyperthyroidism features a suppressed thyroid-stimulating hormone with elevated free thyroxine, predominantly driven by Graves' disease. Additionally, parafollicular C cells secrete calcitonin, which lowers circulating calcium.

The Uterio bank has 17 questions on this topic. 2 arebelow in full; the syllabus detail is in the Endocrinology study guide.

How the exam tests Thyroid Gland

  • Identifying autoimmune thyroid disorders, focusing on Hashimoto's thyroiditis as the principal cause of hypothyroidism and Graves' disease causing hyperthyroidism.
  • Interpreting TSH and free T4 together: primary hypothyroidism (high TSH, low free T4) versus secondary hypothyroidism (low or inappropriately normal TSH with low free T4).
  • The molecular mechanisms of follicular iodide uptake, including the stoichiometry and energy dependence of the sodium-iodide symporter.
  • Peripheral deiodination pathways, specifically the roles of deiodinase subtypes and their obligate requirement for selenium.
  • The extent of plasma protein binding of thyroxine and the main carrier proteins.

High-yield facts

  1. The sodium-iodide symporter moves one iodide ion into thyroid follicular cells coupled with the inward transport of two sodium ions.
  2. A basolateral sodium-potassium ATPase pump maintains the electrochemical sodium gradient driving secondary active transport via the sodium-iodide symporter.
  3. Over 99% of circulating T4 is protein-bound (mainly TBG, then transthyretin and albumin); under 1% is free and biologically active.
  4. Peripheral conversion of thyroxine to active triiodothyronine depends on deiodinase enzymes containing the trace element selenium as selenocysteine.
  5. Type 1 and type 2 deiodinases convert thyroxine to active triiodothyronine, whereas type 3 deiodinase produces inactive reverse triiodothyronine.
  6. Type 1 deiodinase is located in the liver, kidney, and thyroid, whereas type 3 deiodinase is expressed in the placenta, brain, and skin.
  7. Hashimoto's thyroiditis is the commonest cause of primary hypothyroidism in iodine-sufficient countries such as the UK (iodine deficiency is the commonest cause worldwide).
  8. Primary hypothyroidism causes raised TSH with low free T4 through compensatory feedback, whereas rare secondary hypothyroidism produces low or inappropriately normal TSH with low free T4.
  9. Graves' disease is the commonest cause of hyperthyroidism in the UK (about 60-80% of cases), caused by TSH-receptor-stimulating antibodies; toxic multinodular goitre and toxic solitary adenoma are less common.
  10. Subacute (de Quervain's) thyroiditis typically follows a viral illness, presenting with a painful goitre, transient thyrotoxicosis, and a subsequent hypothyroid phase.
  11. Calcitonin inhibits osteoclastic bone resorption and, to a lesser extent, increases renal calcium excretion, thereby lowering plasma calcium; it opposes parathyroid hormone.

Common pitfalls

  • Confusing the stoichiometry of the sodium-iodide symporter by assuming equimolar transport rather than two sodium ions per iodide ion.
  • Assuming circulating free thyroxine constitutes a substantial fraction, when actually more than 99% is protein-bound.
  • Choosing calcium, zinc, magnesium or chromium as the cofactor for peripheral T4-to-T3 conversion; the deiodinases require selenium (as selenocysteine).
  • Confusing Graves' disease (hyperthyroid, typically low TSH and high free T4) with Hashimoto's thyroiditis (hypothyroid, high TSH, low free T4), or mistaking subacute thyroiditis (painful goitre, transient thyrotoxicosis) for either.

Practice questions: Thyroid Gland

Single best answer, exactly as the exam asks. Commit to an option before opening the explanation.

Question 1

Endocrinology

A 45-year-old woman presents with fatigue, cold intolerance, weight gain, and constipation. Her serum TSH is elevated, and her free T4 is low. Which of the following is the MOST likely diagnosis?

  1. AGraves' disease
  2. BHashimoto's thyroiditis
  3. CSubacute thyroiditis
  4. DToxic multinodular goitre
  5. ESecondary hypothyroidism
Show answer and explanation

Correct answer: B. Hashimoto's thyroiditis

Key takeaway

Elevated TSH and low free T4, combined with symptoms of hypothyroidism, point to a diagnosis of primary hypothyroidism, with Hashimoto's thyroiditis being the most common cause in adults in iodine-sufficient regions.

The classic picture of hypothyroidism can be seen here: fatigue, cold intolerance, weight gain, and constipation. The blood results reveal an elevated thyroid-stimulating hormone (TSH) and a low free thyroxine (T4) level, which clearly indicates primary hypothyroidism.

Hashimoto's thyroiditis is an autoimmune condition and the most common cause of primary hypothyroidism in iodine-sufficient regions (worldwide, iodine deficiency remains the leading cause). The autoimmune process leads to destruction of the thyroid gland, resulting in decreased thyroid hormone production (low free T4) and a compensatory rise in TSH from the pituitary gland.

The other conditions listed present differently.

Graves' disease is an autoimmune condition and is the most common cause of hyperthyroidism, the opposite of this clinical picture.

Subacute thyroiditis (de Quervain's thyroiditis) is usually a self-limiting condition that commonly follows a viral infection. It typically causes initial thyrotoxicosis (and therefore high T4 and low TSH), due to inflammation and hormone release, followed by a hypothyroid phase. Clinically, it usually presents with a painful goitre.

Toxic multinodular goitre causes hyperthyroidism.

Secondary hypothyroidism is rare and is caused by pituitary failure: free T4 is low while TSH is low or inappropriately normal (occasionally mildly raised but biologically less active). A clearly raised TSH with this clinical picture points instead to primary thyroid failure.

Question 2

Endocrinology

The thyroid gland concentrates iodide using a transporter that simultaneously moves it along with:

  1. AOne Na+
  2. BOne K+
  3. CTwo Na+
  4. DTwo Cl-
  5. ETwo HCO3-
Show answer and explanation

Correct answer: C. Two Na+

Key takeaway

The thyroid's sodium-iodide symporter uses the energy from the sodium gradient to concentrate iodide; it co-transports iodide with two Na+ ions.

The thyroid gland has a powerful mechanism to concentrate iodide, which is essential for thyroid hormone synthesis. This mechanism is a secondary active transport using a protein called a sodium-iodide symporter (NIS).

The sodium-iodide symporter moves iodide into the thyroid follicular cells against its concentration gradient. It does this by coupling iodide transport with the movement of sodium down its concentration gradient. Specifically, two sodium ions (2Na+) are transported inwards for every one iodide ion (I-) transported inwards.

The gradient for sodium is maintained by a Na+/K+-ATPase pump, which is an example of primary active transport, on the basolateral membrane. This uses ATP to move sodium out of the cell into the blood and potassium in. This also creates an electrochemical gradient that drives the symporter.

One Na+ understates the coupling: NIS carries two sodium ions with each iodide, so each cycle moves one net positive charge into the cell, and this electrogenic coupling is what allows iodide to be accumulated against its gradient. One K+ is wrong because potassium is not carried by NIS; it enters the cell through the basolateral Na+/K+-ATPase that maintains the sodium gradient. Two Cl- and Two HCO3- confuse the basolateral uptake step with the apical efflux step: iodide leaves the cell for the colloid in part through pendrin, an apical anion exchanger that swaps iodide for chloride or bicarbonate rather than co-transporting iodide with them.

15 more thyroid gland questions in the bank

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What the syllabus covers under thyroid gland

  • Thyroid Hormone Synthesis and Secretion
  • Actions of Thyroid Hormones
  • Thyroid Disorders

Read the full section in the Endocrinology guide, or check the next exam dates.