Vibrio cholerae produces secretory diarrhoea without mucosal invasion. The intracellular mechanism responsible is:

• A Inhibition of the basolateral Na-K-ATPase causing loss of transepithelial gradients
• B Direct blockade of the apical Na-H exchanger on enterocytes
• C Activation of phospholipase C raising intracellular calcium and opening calcium activated potassium channels
• D ADP ribosylation of Gs alpha causing sustained adenylyl cyclase activity, raised cAMP, and opening of apical CFTR chloride channels ✓

Explanation

Cholera toxin binds GM1 receptors, its D subunit enters the cell and ADP ribosylates the alpha subunit of Gs, locking it in the GTP bound state. Adenylyl cyclase stays active, cAMP rises persistently, and PKA phosphorylates and opens the apical CFTR chloride channel. Chloride secretion drives sodium and water into the lumen. The Na-H exchanger is not blocked, the Na-K pump is intact, and the cAMP rather than the calcium pathway is engaged.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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