GI System MCAT Practice Question
A 58-year-old man with hypertension has been taking furosemide 40 mg daily for 3 months. Laboratory studies show serum potassium of 2.9 mEq/L, serum sodium of 138 mEq/L, and serum glucose of 94 mg/dL (fasting). He reports fatigue and mild muscle weakness. On small intestinal biopsy, enterocytes show normal SGLT1 expression at the apical membrane. The patient's glucose absorption is found to be impaired despite normal fasting blood glucose and intact transporter expression. Which of the following best explains the mechanism of impaired glucose absorption in this patient?
Answer choices
- AHypokalemia decreases the electrochemical gradient across the enterocyte basolateral membrane, reducing driving force for Na+ exit
- BHypokalemia reduces Na+/K+-ATPase activity, diminishing the inward sodium gradient required for SGLT1-mediated glucose cotransportCorrect answer
- CHypokalemia inhibits apical membrane expression of SGLT1 through reduced phosphatidylinositol signaling
- DHypokalemia increases intracellular calcium in enterocytes, competitively inhibiting glucose binding to SGLT1
- EHypokalemia impairs intestinal blood flow, reducing glucose delivery to the portal circulation despite normal absorption
- FHypokalemia shifts the small intestine toward alkalosis, ionizing glucose and preventing SGLT1 recognition
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