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peptic ulcer disease, GERD, irritable bowel syndrome, inflammatory bowel disease |
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acid producing cells in the stomach |
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-directly stimulate gastric acid secretion, -increasing the release of histamine from ECL cells -increasinf the release of gastrin from Gcells |
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most potent inducer of acid secretion via CNS, local distention, & components of gastric content |
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gastrin stimulates acid by |
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-indirectly inducing the release of histamine from ECL cells -directly on parietal cells |
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-made by antral D cells -released when gastric lumen becomes more acidic pH<3 -inhibit gastric acid secretions by supressing gastrin release in negative feedback loop |
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meds to treat acid hyper-secretion |
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antacids H2 receptor blockers proton pump inhibitors |
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Sodium Bicarbonate calcium carbonate aluminum hydroxide magnesium hydroxide |
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excessive doses of sodium bicarbonate and calcium carbonate |
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may lead to metabolic alkalosis, hypercalcemia, renal insufficiency |
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magnesium hydroxide adverse effect |
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aluminum hydroxide adverse effect |
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anatacid drug interaction |
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-Al and Mg known to chelate other drugs in the GI tract-form insoluble complexes -due to gastric and urinal pH changes may affect rates of disslution, absorption, bioavailability and renal elimination of several drugs (thyroid hormones, allopurinol, imidazole antifungals, drugs that need acid for absorption) |
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H2 receptor blocker examples |
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cimetidine, ranitidine, famotidine, nizatidine |
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block the release of acid by inhibiting H2 receptors of ECL cells from binding histamine |
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pharmacdynamics of H2 receptor blcokers |
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-highly effective in reducing nocturnal acid secretion -highly selective, competive inhibitors of h2 receptors at parietal cells |
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