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Chapter 26: Stomach

The consistently largest artery to the stomach is the

A. Right gastric

B. Left gastric

C. Right gastroepiploic

D. Left gastroepiploic

Answer: B

The consistently largest artery to the stomach is the left gastric artery, which usually arises directly from the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature. Approximately 20% of the time, the left gastric artery supplies an aberrant vessel that travels in the gastrohepatic ligament (lesser omentum) to the left side of the liver. Rarely, this is the only arterial blood supply to this part of the liver, and inadvertent ligation may lead to clinically significant hepatic ischemia in this unusual circumstance. (See Schwartz 10th ed., p. 1037.)

Which of the following inhibits gastrin secretion?

A. Histamine

B. Acetylcholine

C. Amino acids

D. Acid

Answer: D

Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion. The latter effect is predominantly mediated in a paracrine fashion by somatostatin released from antral D cells. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal mediator of gastrin-stimulated acid production is histamine from mucosal enterochromaffin-like (ECL) cells. Acetylcholine released by the vagus nerve leads to stimulation of ECL cells, which in turn produce histamine. (See Schwartz 10th ed., p. 1045.)

Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via

A. Antral alkalinization leading to inhibition of somatostatin release

B. Direct stimulation of gastrin release

C. Local inflammation with autoimmune response

D. Upregulation of parietal cell acid production

Answer: A

Helicobacter pylori possess the enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach. H. pylori infection is associated with decreased levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. These effects are probably mediated by H. pylori-induced local alkalinization of the antrum (antral acidification is the most potent antagonist to antral gastrin secretion), and H. pylori-mediated increases in other local mediators and cytokines. The result is hypergastrinemia and acid hypersecretion, presumably leading to the parietal ...

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