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

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Inhibition of secretion of acidity/hyperacidity

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Enhancement of mucosal defences against hyperacidity

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Neutralization of gastric acidity in hyperacidity

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Removal or eradication of Helicobacter pyloris

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Stop smoking

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

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Hyperacidity of the stomach in sufferers

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Infection with H pylori

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Use of non steroidal anti-inflammatory agents (NSAID)

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Smoking

Drugs for treatment of PUD and GORD

Antacids

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

Others

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Eradication of Helicobacter pylori infection

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Withdrawal of NSAID

 

Fresh stomach Fixed stomach Model stomach Diagramatic stomach Stomach interior 1
Stomach interior 2 Blood supply stomach Nerve to anterior stomach Nerve to posterior stomach Stomach ulcer

 

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