Histopharmacology of esophagus, stomach and duodenum
Histopharmacology of the esophagus, stomach and duodenum revolves around the treatment of peptic ulcer disease (which includes gastric and duodenal ulcers) and gastro-esophageal reflux disease (GORD) related to the physiology of lower esophageal sphincter.
Prevention/treatment of PUD and GORD involves the following
Acetylcholine from vagus nerve, histamine from ECL cells and gastrin from G cells of the stomach all help in the secretion of acid and hence treatment of hyperacidity must take this into consideration. The above all stimulate acid production and through receptors in the basolateral membrane of parietal cells which secrete acid.
Factors which assist the production of peptic ulcer disease include
Drugs for treatment of PUD and GORD
Neutralize hydrochloric acid in the stomach and help sufferers of peptic ulcer disease by allowing their wounds not to fester or become dangerously unhealing. Agents include magnesium trisilicate, aluminum hydroxide, sodium bicarbonate, alginic acid and dimeticone
But most antacids have large amounts of sodium and therefore not useful in patients with cardiac or renal diseases.
H2 receptor antagonists
By far the most widely used peptic ulcer disease drug are the H2 receptor antagonists. They bind selectively and competitively to the basolateral membrane of parietal cells thereby inhibiting acid secretion by these cells by histamine. They are best administered as a single evening dose and would cause healing of ulcer in about 8 weeks. Examples include cimetide (the first H2 antagonist) ranitidine, famotidine and nizatidine
Proton pump inhibitors
These drugs inactivates proton pump in parietal cells and hence reduce acid secretion. They include -omeprazole, esomeprazole, lansoprazolem pantoprazole and rabeprazole
Mucosal enhancers drugs
Drugs which increase mucosal resistance by cryprotection include bismuth chelate, sucralfate and misoprostol