Lansoprazole, proton pump

Prevacin Lansoprazole Proton pump inhibitor 3.5 5 Norvasc Amlodipine Calcium antagonist 5 -0.5... 

The proton pump inhibitors are contraindicated in patients who have hypersensitivity to any of the drags. Omeprazole (Pregnancy Category C) and lansoprazole, rabeprazole, and pantoprazole (Pregnancy Category B) are contraindicated during pregnancy and lactation. The proton pump inhibitors are used cautiously in older adults and in patients with hepatic impairment. 

H2 receptor antagonists (Cimetidine, famotidine, nizatidine, ranitidine) Proton pump inhibitors Lansoprazole Omeprazole Pantoprazole Rabeprazole... 

The histamine2-receptor antagonists or H2RAs (cimetidine, famotidine, nizatidine, and ranitidine) and proton pump inhibitors (omeprazole, esomeprazole, lansoprazole, pantopra-zole, and rabeprazole) reduce the amount of acid secreted into the stomach by gastric parietal cells. These agents are also helpful for nausea and vomiting related to gastric acid secretion. 

Proton pump inhibitors (PPIs), such as omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole, are commonly prescribed to treat symptoms of heartburn, acid reflux, chest pain, dyspepsia, and chronic cough. PPIs inhibit the transfer of protons into the stomach lumen. Pharmacological acid suppression is thus used to treat gastroesophageal reflux disease (GERD) and esophagitis, peptic ulcers, and Helicobacter pylori infection as well as to prevent ulcer development with concurrent nonsteroidal anti-inflammatory drug use. 

Omeprazole (p. 167) can cause maximal inhibition of HCl secretion. Given orally in gastric juice-resistant capsules, it reaches parietal cells via the blood. In the acidic milieu of the mucosa, an active metabolite is formed and binds covalently to the ATP-driven proton pump (H+/K+ ATPase) that transports H+ in exchange for IC into the gastric juice. Lansoprazole and pantoprazole produce analogous effects. The proton pump inhibitors are first-line drugs for the treatment of gastroesophageal reflux disease. 

Omeprazole is an antiulcer drug. It is a proton pump inhibitor. This substituted benzimidazole inhibits gastric acid secretion to help acid/peptic disorders and duodenal ulcers. It interferes with the proton pump in the mucous lining of the stomach, the last stage of acid production. It can turn off stomach acid in as little as one hour. Lansoprazole (no. 12) has a similar structure. 

C. Visible oesophageal inflammation, ulcer or stricture Proton pump inhibitors e.g., omeprazole 20-40 mg daily, lansoprazole 30 mg daily, pantoprazole 40 mg daily, rabeprazole 20 mg daily... 

Proton pump inhibitors lansoprazole omeprazole magnesium pantoprazole sodium rabeprazole sodium... 

Other proton pump inhibitors e.g., lansoprazole is more potent than omeprazole and has higher bioavailability, rapid onset of action and longer duration of action. Pantoprazole is the new H+K+ATPase inhibitor with similar properties and action to omeprazole. 

These agents are second generation proton pump inhibitors. Their mode of action is similar to omeprazole. Structural differences give more rapid absorption and greater bioavailability of lansoprazole. Lansoprazole has less effect on P-450 enzymes, while interaction with pantoprazole is insignificant. Lansoprazole has a significant antibacterial effect on Helicobacter pylori. 

Five proton pump inhibitors are available for clinical use omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole. All are substituted benzimidazoles that resemble H 2 antagonists in structure (Figure 62-3) but have a completely different mechanism of action. Omeprazole is a racemic mixture of R- and S-isomers. Esomeprazole is the S-isomer of omeprazole. All are available in oral formulations. Esomeprazole and pantoprazole are also available in intravenous formulations (Table 62-2). 

Proton pump inhibitors (PPIs), eg, omeprazole, lansoprazole Irreversible blockade of H +, K+-ATPase pump in active parietal cells of stomach Long-lasting reduction of stimulated and nocturnal acid secretion Peptic ulcer, gastroesophageal reflux disease, erosive gastritis Half-lives much shorter than duration of action low toxicity reduction of stomach acid may reduce absorption of some drugs and increase that of others... 

Proton pump inhibitors -prazole Omeprazole, lansoprazole Gastric ulcers (27)... 

Pantoprazole sodium, a substituted benzimidazole derivative, is an irreversible proton pump inhibitor, and was developed for the treatment of acid-related gastrointestinal disorders. As with other drugs of its class (e. g. omeprazol or lansoprazole), pantoprazole reduces gastric acid secretion through inhibition of the portion on the gastric parietal cell. In combination with other drugs, pantoprazole can be used for the initial treatment of H. Pylori infection [1],... 

Li XQ, Andersson TB, Ahlstrom M, et al. Comparison of inhibitory effects of the proton pump-inhibiting drugs omeprazole, esomeprazole, lansoprazole, pan-toprazole, and rabeprazole on human cytochrome P450 activities. Drug Metab Dispos 2004 32 821-827. 

Omeprazole [om ME pary zol] is the first of a new class of drugs that binds to the H7K+-ATPase enzyme system (proton pump) of the parietal cell, suppressing secretion of hydrogen ions into the gastric lumen. The membrane-bound proton pump is the final step in the secretion of gastric acid (see Figure 24.3). A second proton pump inhibitor, lansoprazole [Ian SOP ra zol], is also available. 

There are currently four racemic PPIs available on the market omeprazole, lansoprazole, pantoprazole, and rabeprazole. (More recently, enantiomerically pure versions have also been studied and developed, e.g., S-omeprazole, marketed by AstraZeneca as esomeprazole see Chapter II-2.) Proton pump inhibitors share the same core structure, the substituted pyridylmethyl-sulfmyl-benzimidazole, but differ in terms of substituents on this core structure. The absolute requirements of the core structure for the activity of PPIs was not understood until it became clear that the active PPIs are derived from inactive prodrugs the prodrugs are transformed, in the acid-secreting parietal cells, by a unique cascade of chemical structural transformations leading to the active principle, a cyclic sulfenamide species. Inhibition of acid secretion in turn is then achieved by formation of covalent disulfide bonds with key cysteines of the (H+/K+)-ATPase. 

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