검색어: irreversibly (영어 - 인도네시아어)

the most potent suppressors of gastric acid secretion are inhibitors of the gastric h+,k+-atpase (proton pump) (figure 36–2a). in typical doses, these drugs diminish the daily production of acid (basal and stimulated) by 80% to 95%. five proton pump inhibitors are available for clinical use: omeprazole (prilosec, rapinex, zegerid) and its s-isomer, esomeprazole (nexium), lansoprazole (prevacid), rabeprazole (aciphex), and pantoprazole (protonix). these drugs have different substitutions on their pyridine and/or benzimidazole groups but are remarkably similar in their pharmacological properties (see appendix ii). omeprazole is a racemic mixture of r- and s-isomers; the s-isomer, esomeprazole (s-omeprazole), is eliminated less rapidly than r-omeprazole, which theoretically provides a therapeutic advantage because of the increased half-life. despite claims to the contrary, all proton pump inhibitors have equivalent efficacy at comparable doses. proton pump inhibitors are prodrugs that require activation in an acid environment. after absorption into the systemic circulation, the prodrug diffuses into the parietal cells of the stomach and accumulates in the acidic secretory canaliculi. here, it is activated by proton-catalyzed formation of a tetracyclic sulfenamide (figure 36–2), trapping the drug so that it cannot diffuse back across the canalicular membrane. the activated form then binds covalently with sulfhydryl groups of cysteines in the h+,k+-atpase, irreversibly inactivating the pump molecule. acid secretion resumes only after new pump molecules are synthesized and inserted into the luminal membrane, providing a prolonged (up to 24- to 48-hour) suppression of acid secretion, despite the much shorter plasma half-lives (0.5 to 2 hours) of the parent compounds. because they block the final step in acid production, the proton pump inhibitors are effective in acid suppression regardless of other stimulating factors. the most potent suppressors of gastric acid secretion are inhibitors of the gastric h+,k+-atpase (proton pump) (figure 36–2a). in typical doses, these drugs diminish the daily production of acid (basal and stimulated) by 80% to 95%. five proton pump inhibitors are available for clinical use: omeprazole (prilosec, rapinex, zegerid) and its s-isomer, esomeprazole (nexium), lansoprazole (prevacid), rabeprazole (aciphex), and pantoprazole (protonix). these drugs have different substitutions on their pyridine and/or benzimidazole groups but are remarkably similar in their pharmacological properties (see appendix ii). omeprazole is a racemic mixture of r- and s-isomers; the s-isomer, esomeprazole (s-omeprazole), is eliminated less rapidly than r-omeprazole, which theoretically provides a therapeutic advantage because of the increased half-life. despite claims to the contrary, all proton pump inhibitors have equivalent efficacy at comparable doses. proton pump inhibitors are prodrugs that require activation in an acid environment. after absorption into the systemic circulation, the prodrug diffuses into the parietal cells of the stomach and accumulates in the acidic secretory canaliculi. here, it is activated by proton-catalyzed formation of a tetracyclic sulfenamide (figure 36–2), trapping the drug so that it cannot diffuse back across the canalicular membrane. the activated form then binds covalently with sulfhydryl groups of cysteines in the h+,k+-atpase, irreversibly inactivating the pump molecule. acid secretion resumes only after new pump molecules are synthesized and inserted into the luminal membrane, providing a prolonged (up to 24- to 48-hour) suppression of acid secretion, despite the much shorter plasma half-lives (0.5 to 2 hours) of the parent compounds. because they block the final step in acid production, the proton pump inhibitors are effective in acid suppression regardless of other stimulating factors.
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