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Achlorhydria
Model illustrating pathophysiology of achlorhydria and the development of gastric carcinoid tumours. With achlorhydria, the stimulatory effect of luminal acid on SST is lost. Consequently, SST secretion is decreased and its inhibitory restraint on gastrin secretion attenuated (disinhibition), resulting in hypergastrinaemia. Gastrin is not only a secretagogue but also a trophic hormone that induces growth of the oxyntic mucosa. If hypergastrinaemia is sustained for days, ECL cells will hypertrophy; if sustained for weeks to months, ECL cells become hyperplastic, dysplastic, and, in some patients, become carcinoid tumours.
From the collection of Professor Mitchell L. Schubert, with the acknowledgement of Mary Beatty-Brooks (medical illustrator)
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Achlorhydria
Classification of gastric carcinoid tumours
Hou W, Schubert, ML. Treatment of gastric carcinoids. Curr Treat Options Gastroenterol. 2007;10:123-133. Used with kind permission from Current Medicine Group LLC
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Achlorhydria
Model illustrating physiological regulation of gastric acid secretion by gastrin, histamine, somatostatin (SST), and luminal acid. Gastrin, released from antral G cells, is the main hormonal stimulant of acid secretion during meal ingestion. Gastrin acts directly on the acid-secreting parietal cells and, more importantly, indirectly by stimulating histamine secretion from enterochromaffin-like (ECL) cells. Histamine diffuses to adjacent parietal cells, where it binds to histamine H2 receptors coupled to stimulation of acid secretion. In the interdigestive phase, somatostatin (SST), released from antral D cells in response to luminal acid, tonically inhibits gastrin secretion from G cells, thereby maintaining acid secretion at an economically low level.
From the collection of Professor Mitchell L. Schubert, with the acknowledgement of Mary Beatty-Brooks (medical illustrator)
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