Researchers studying gastrointestinal pathophysiology analyze hundreds of gastric mucosal biopsy specimens taken from patients who underwent endoscopy at a local tertiary care center. They notice that colonization of the gastric antrum with S-shaped, gram-negative bacteria is associated with a decreased number of somatostatin-producing antral cells. Depletion of these cells from the gastric antrum is most likely to cause which of the following conditions?

Question

Researchers studying gastrointestinal pathophysiology analyze hundreds of gastric mucosal biopsy specimens taken from patients who underwent endoscopy at a local tertiary care center.  They notice that colonization of the gastric antrum with S-shaped, gram-negative bacteria is associated with a decreased number of somatostatin-producing antral cells.  Depletion of these cells from the gastric antrum is most likely to cause which of the following conditions?

Quizplus · Accepted Answer

11ec160b_3959_a3d5_9249_cb51c2780109_MD0001_00 Helicobacter pylori is a motile, spiral-shaped, gram-negative bacteria found attached to the gastric mucosa or deep in the mucus layer overlying the gastric epithelium. It is protected from gastric acid by endogenous urease production: urease converts urea to ammonia, which alkalinizes the surrounding pH but injures gastric epithelial cells. Damage to the gastric mucosa is compounded by localized inflammation due to the immunologic response against H pylori. Chronic inflammation due to H pylori colonization in the gastric antrum leads to depletion of somatostatin-producing cells (delta cells), which are located mostly in the antrum. Somatostatin inhibits gastrin release from G-cells. In its absence, elevated gastrin levels act directly (via cholecystokinin B receptors) and indirectly (via histamine release by enterochromaffin-like cells) to increase acid secretion by parietal cells. In addition, H pylori releases cytotoxins that inhibit duodenal production of bicarbonate. The resultant increased acid load is emptied into the under-protected duodenum, leading to duodenal ulcer formation. In contrast, gastric ulcers occur when H pylori colonizes the gastric body (corpus) (Choice D). Chronic inflammation leads to multifocal atrophic gastritis and a reduction in the number of acid-producing parietal cells, which are located mostly in the gastric body. Delta cells in the antrum are not markedly reduced, therefore acid secretion is often low to normal. Gastric ulcer formation results from direct mucosal damage caused by bacterial products (eg, ammonia, cytotoxins) and the resultant inflammatory response. Unlike antral-predominant disease, corpus-predominant disease is associated with metaplasia and malignancies (eg, gastric lymphoma, adenocarcinoma) (Choice C). (Choice A) Chronic pancreatitis is not associated with H pylori infection. It is most frequently caused by chronic alcoholism or obstruction of the pancreatic ducts due to gallstones or malignancy. (Choice E) Vitamin B₁₂ deficiency can result from autoimmune gastritis. Autoimmune gastritis is characterized by autoantibodies against gastric parietal cells leading to inflammation of the gastric mucosa, parietal cell destruction, and achlorhydria. Its etiology is at least partially genetic. Educational objective: Helicobacter pylori antral gastritis is associated with the formation of duodenal ulcers due to increased gastric acid production. This increase in acidity is caused by unchecked gastrin production due to the destruction of somatostatin-secreting cells in the gastric antrum.

Researchers Studying Gastrointestinal Pathophysiology Analyze Hundreds of Gastric Mucosal Biopsy