A patient develops an autoimmune gastritis that destroys mucus-secreting cells in the stomach mucosa. Which of the following best explains why this predisposes the patient to gastric ulcers and how treatment might address the pathophysiology?

• A. Loss of mucus increases gastric motility which mechanically erodes the epithelium; therefore, prescribing prokinetic agents to slow gastric emptying is the primary therapy
• B. Loss of mucus causes elevated bile reflux into the stomach which is the dominant cause of ulcers; the best approach is cholecystectomy to prevent bile production
• C. Loss of protective mucus exposes epithelial cells to low pH and pepsin, allowing autodigestion and ulceration; treatment should reduce acid production (e.g., proton pump inhibitors) and promote mucosal healing with sucralfate or prostaglandin analogs while addressing the autoimmune cause
• D. Decreased mucus causes overproduction of pepsinogen leading to systemic protease excess; the treatment is chronic high-dose enzyme inhibitors that block pepsinogen synthesis at the genetic level

Answer: (C)