A patient undergoing treatment for esophageal reflux disease is given a proton pump inhibitor. What effect does this drug have on parietal cells?

A proton pump inhibitor primarily works by inhibiting the H+/K+ ATPase enzyme found in the parietal cells of the stomach. This enzyme is responsible for the final step in gastric acid production, which involves the exchange of potassium ions for hydrogen ions, effectively secreting hydrogen ions into the gastric lumen and contributing to the acidity of gastric juice. By blocking this enzyme, proton pump inhibitors reduce the secretion of gastric acid, leading to decreased acidity in the stomach.

In the context of a patient with esophageal reflux disease, the inhibition of acid secretion provides therapeutic benefits by reducing the amount of acid that can reflux into the esophagus, thereby alleviating symptoms and preventing damage to the esophageal lining caused by acidic content.

Other options do not accurately depict the mechanism or effect of proton pump inhibitors on parietal cells or gastric function. For instance, stimulating acid secretion would counteract the therapeutic goals of managing esophageal reflux, while increasing pepsin secretion does not occur as pepsin is activated in the presence of acid rather than provided by the proton pump inhibitors. Enhancing bicarbonate production is not a primary mechanism of action of proton pump inhibitors; while there might be indirect effects on the duodenum’s bicarbonate secretion due to lower