skip to main content

Lithium-Thiazide Interaction — MRCPsych Paper B MCQ

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

HardMood DisordersLithium-Thiazide InteractionMRCPsych Paper B

A 55-year-old woman with bipolar disorder has been stable on an unchanged dose of lithium carbonate. Her correctly timed 12-hour serum lithium concentration has remained approximately 0.7 mmol/L. Bendroflumethiazide is started for hypertension. Three weeks later, despite unchanged lithium dosing, salt and fluid intake, renal function and sampling time, her lithium concentration is 1.3 mmol/L. Which mechanism best explains this change?

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

Reveal the answer and explanation

Correct answer: A — Distal sodium reabsorption is inhibited, causing sodium loss and compensatory proximal reabsorption of sodium and lithium

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

B is correct. Bendroflumethiazide inhibits sodium-chloride reabsorption in the distal convoluted tubule. The resulting natriuresis and mild extracellular-volume contraction promote compensatory proximal tubular sodium reabsorption. Lithium is handled alongside sodium in the proximal nephron, so its reabsorption increases and renal lithium clearance falls. This can substantially raise the serum concentration despite unchanged lithium dosing and renal function. Thiazides do not increase gastrointestinal lithium absorption (A), and lithium is not cleared by metabolism. The interaction is not caused by competition for tubular secretion because lithium is principally filtered and reabsorbed rather than actively secreted (C). Reverse accumulation of bendroflumethiazide due to lithium is not the established mechanism (D). A clinically important pharmacokinetic interaction does exist, excluding E.

Reference: Bergsland KJ et al. Role of proximal tubule in the hypocalciuric response to thiazide of patients with idiopathic hypercalciuria. American Journal of Physiology-Renal Physiology. 2013;305:F592–F599. https://pubmed.ncbi.nlm.nih.gov/23720347/