The consistently largest artery to the stomach is the:
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.
Which of the following inhibits gastrin secretion?
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 ofECL cells, which in turn produce histamine.
Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via:
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. pylorimediated increases in other local mediators and cytokines. The result is hypergastrinemia and acid hypersecretion, presumably leading to the parietal cell hyperplasia seen in many patients with duodenal ulcer. Other mechanisms whereby H. pylori can induce gastroduodenal mucosal injury include the production of toxins (vacA and cagA), local elaboration of cytokines (particularly interleukin-8) by infected mucosa, recruitment of inflammatory cells and release of inflammatory mediators, recruitment and activation of local immune factors, and increased apoptosis.
The effect of erythromycin on gastric emptying is through its function as a:
Erythromycin is a common prokinetic agent used to treat delayed gastric empting, and works as a motilin agonist. Domperidone and metoclopramide, two other commonly used medications, function as dopamine antagonists.
Drugs that accelerate gastric emptying:
Which of the following is secreted by gastric parietal cells?
Activated parietal cells secrete intrinsic factor in addition to hydrochloric acid. Presumably the stimulants are similar, but acid secretion and intrinsic factor secretion may not be linked. Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B 12 deficiency can be life-threatening, and patients with total gastrectomy or pernicious anemia require B12 supplementation by a nonenteric route.
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