NBME-style questions › Small Bowel Disorders
Small Bowel Disorders · Biochemistry and Molecular Biology · NBME-Style

Small Bowel Disorders — NBME-style practice question

A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.

A 62-year-old man comes to the emergency department because of right-sided back pain, nausea, and dark urine. He reports alternating episodes of decreased urine output followed by a temporary increase in urine output for the past 2 days. In the past year, he has had two urinary tract infections. He has Crohn disease and underwent a small bowel resection 5 years ago. He currently takes mesalamine and a multivitamin. His father had recurrent kidney stones. His vital signs are within normal limits. Examination shows right costovertebral angle tenderness. Urinalysis shows 70 RBC/hpf and envelope-shaped crystals. A CT scan of the abdomen shows a 6-mm stone in the proximal right ureter and two 4-mm stones in the left kidney. Which of the following factors has most likely contributed most to this patient’s current condition?

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Answer: C. This man has Crohn disease with prior small-bowel resection and now develops nephrolithiasis with envelope-shaped crystals — diagnostic of calcium oxalate stones. The mechanism is enteric hyperoxaluria: in Crohn disease with terminal-ileum disease or resection, bile salts and free fatty acids are malabsorbed. Free fatty acids preferentially bind luminal calcium (forming soaps that are excreted), leaving dietary oxalate unbound. Unbound oxalate is then freely absorbed across the colon and excreted in the urine, where it precipitates with calcium to form oxalate stones. This is why patients with fat malabsorption (Crohn, short bowel, chronic pancreatitis, bariatric surgery with Roux-en-Y) are at high risk for calcium oxalate stones. Management: low-oxalate diet, oral calcium supplementation (binds intestinal oxalate before it can be absorbed), and treatment of the underlying malabsorption. Key distinctions: parathyroid adenoma (primary hyperparathyroidism) causes hypercalcemia and calcium-phosphate or calcium-oxalate stones but is not the unique pathway here. Vitamin D toxicity also causes hypercalcemia/hypercalciuria. High urine pH favors calcium phosphate or struvite (Mg-ammonium-phosphate) stones, not oxalate. **Why each option:** **A.** Parathyroid adenoma causes primary hyperparathyroidism with hypercalcemia and hypercalciuria — but the specific mechanism in this Crohn patient is enteric hyperoxaluria from fat malabsorption. **B.** Vitamin D toxicity causes hypercalcemia/hypercalciuria but is not the mechanism in a Crohn patient with bowel resection — fat malabsorption explains the calcium-oxalate stone formation. **C.** Correct. Malabsorption of fatty acids in Crohn disease binds luminal calcium, freeing oxalate for colonic absorption and producing enteric hyperoxaluria with calcium-oxalate stones. **D.** High urine pH favors calcium phosphate (RTA) or struvite (urea-splitting infections) stones; calcium-oxalate stones form preferentially in acidic-to-neutral urine.

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