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?

Loss of mucus increases gastric motility which mechanically erodes the epithelium; therefore, prescribing prokinetic agents to slow gastric emptying is the primary therapy

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

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

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