skip to main content

Lithium Hyperparathyroidism — MRCPsych Paper B MCQ

Instant feedback + full explanation. One question, done properly.

HardMood DisordersLithium HyperparathyroidismMRCPsych Paper B

A 52-year-old man with bipolar I disorder has taken lithium for 8 years. Routine tests show an adjusted serum calcium of 2.72 mmol/L, raised parathyroid hormone and low phosphate. His eGFR is normal and he is vitamin D replete. Which alteration in parathyroid physiology most specifically explains this lithium-associated hyperparathyroidism?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: A — Reduced calcium-sensing receptor sensitivity, raising the calcium set-point for PTH suppression

Explanation lettering: B = shown as A · A = shown as B · D = shown as C · E = shown as D · C = shown as E

B is correct. Lithium reduces the sensitivity of parathyroid calcium-sensing receptor signalling, shifting the calcium–PTH suppression curve to the right. A higher extracellular calcium concentration is therefore required to suppress PTH, resulting in an inappropriately raised PTH despite hypercalcaemia. Chronic exposure may additionally promote parathyroid hyperplasia or reveal adenomatous disease. Option A would enhance, rather than impair, PTH suppression. Options C and E describe secondary hyperparathyroidism, which usually occurs with low or normal calcium and is inconsistent with the normal renal function and adequate vitamin D stated. Increased calcitonin secretion in option D is not the established lithium mechanism and would not explain persistent PTH-dependent hypercalcaemia. NICE recommends measuring calcium every 6 months during lithium treatment.

Reference: Haden ST et al. Alterations in parathyroid dynamics in lithium-treated subjects. Journal of Clinical Endocrinology & Metabolism. 1997;82:2844–2848. https://pubmed.ncbi.nlm.nih.gov/9284708/