GI System MCAT Practice Question
A 58-year-old man with a 15-year history of H. pylori infection presents with chronic epigastric pain and early satiety. Endoscopy reveals chronic atrophic gastritis with intestinal metaplasia. Laboratory studies show hypochlorhydria (pH 6.2) and elevated serum gastrin levels (180 pg/mL). Serologic testing confirms active H. pylori infection with positive IgG and IgA antibodies. Histopathology demonstrates infiltration of the gastric mucosa with lymphocytes and plasma cells, with marked atrophy of the gastric glands. Which of the following best explains the paradoxical reduction in gastric acid secretion in this patient despite initial H. pylori urease activity that should buffer gastric acid?
Answer choices
- AChronic Th1/Th17-mediated inflammation with cytokine-induced apoptosis and atrophy of parietal cells, reducing the functional mass of acid-secreting tissueCorrect answer
- BBacterial urease enzyme becomes permanently integrated into parietal cell membranes, directly blocking the H+/K+-ATPase pump
- CH. pylori lipopolysaccharide competitively inhibits histamine binding to H2 receptors on parietal cells
- DElevated gastrin levels cause chronic parietal cell stimulation leading to depletion of intracellular proton stores
- EIncreased ammonia production by urease neutralizes gastric acid faster than parietal cells can regenerate it
- FBacterial phospholipase damages the protective mucus layer, triggering a reflexive decrease in acid secretion by the stomach
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