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Gastritis and peptic ulcer disease<br />

MEGAN L. FIX AND STEPHEN H. THOMAS<br />

n Agents<br />

n Antacids<br />

n Belladonna alkaloids plus phenobarbital<br />

n Viscous lidocaine<br />

n H2-receptor antagonists<br />

n Proton pump inhibitors<br />

n Sucralfate<br />

n Prokinetics<br />

n Evidence<br />

<strong>This</strong> chapter groups the clinically distinct, but similarly treated, entities of<br />

gastritis and peptic ulcer disease (GPUD). While some patients with endoscopically<br />

confirmed ulcers or gastritis present to the ED with refractory pain,<br />

in most cases it is not easy to distinguish between the various GI causes of<br />

epigastric pain. In fact, endoscopy trials show that neither clinical gestalt nor<br />

multivariate modeling (using ED-available information) can reliably distinguish<br />

between organic and functional dyspepsia. 1 Consequently, even in<br />

those ED cases for which a GI origin for epigastric pain can be assumed,<br />

diagnostic uncertainty is common. Clinicians treating epigastric pain may<br />

find useful information in some other chapters (e.g. those on biliary tract pain<br />

or gastroesophageal reflux disease [GERD]).<br />

The diagnostic imprecisions of the ED population prompt additional caveats.<br />

First, acute care clinicians trying to apply the literature on epigastric<br />

pain therapy should keep in mind that the typical clinical study subject is one<br />

in whom there is an endoscopically characterized diagnosis – a luxury the<br />

acute care provider must often do without. Second, the interpretation of<br />

dyspepsia studies is influenced by the fact that only since the mid-1990s<br />

has there been a full appreciation of the role of Helicobacter pylori in GPUD<br />

213

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