The activation of<unk> s<unk> s act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric<unk> <unk>  of the gastric parietal cells. The<unk> <unk>  is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion. Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%. Decreasing the acid in the stomach can aid the healing of duodenal ulcers and reduce the pain from indigestion and heartburn. However, stomach acids are needed to digest proteins, vitamin B12, calcium, and other nutrients, and too little stomach acid causes the condition hypochlorhydria. The<unk> s are given in an inactive form, which is neutrally charged (lipophilic) and readily crosses cell membranes into intracellular compartments (like the parietal cell canaliculus) with acidic environments. In an acid environment, the inactive drug is<unk> ated and rearranges into its active form. As described above, the active form will covalently and irreversibly bind to the gastric<unk> <unk> , deactivating it. In H. pylori eradication,<unk> s help by increasing the stomach pH, causing the bacterium to shift out of its coccoid form which is resistant to both acids and antibiotics.<unk> s also show some weaker additional effects in eradication.
Proton-pump inhibitor
Antisialagogue
Mucoactive agent
Prokinetic agent
Galactagogue
Cholagogue
Antacid
Caloric restriction mimetic