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Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

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Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
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Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

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Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
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Gastritis-II: Pathophysiology01:17

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
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The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
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Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

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In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
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Gastrin pathophysiology: antisecretory drugs.

G Delle Fave1, B Annibale, L De Magistris

  • 1Cattedra di Gastroenterologia 1, Università La Sapienza, Roma, Italy.

The Italian Journal of Gastroenterology
|January 1, 1990
PubMed
Summary
This summary is machine-generated.

Long-term ranitidine therapy for duodenal ulcers can cause hypergastrinemia and increased relapse rates. This occurs in 20% of patients, linked to higher gastrin and gastric acid levels after treatment cessation.

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Area of Science:

  • Gastroenterology
  • Pharmacology
  • Internal Medicine

Background:

  • Peptic disease management involves antisecretory drugs.
  • Hypergastrinemia, a potential side effect, has trophic effects on gastric cells.
  • Long-term maintenance therapy requires careful consideration of hormonal changes.

Purpose of the Study:

  • To investigate the incidence of hypergastrinemia and gastric hypersecretion in duodenal ulcer patients on long-term ranitidine maintenance therapy.
  • To assess the relationship between hypergastrinemia, gastric acid increase, and ulcer relapse rates.

Main Methods:

  • A group of 55 duodenal ulcer patients received maintenance therapy with ranitidine 150mg/day for 3-5 years.
  • Gastrin levels and gastric acid secretion were evaluated one week after drug withdrawal.
  • Relapse rates were compared between patients who developed hypergastrinemia/hypersecretion and those who did not.

Main Results:

  • Twenty percent of patients developed hypergastrinemia and gastric hypersecretion after long-term ranitidine treatment.
  • The same 20% of subjects exhibited increased ulcer relapse rates.
  • A correlation was observed between elevated gastrin/gastric acid levels and higher relapse incidence.

Conclusions:

  • Long-term ranitidine maintenance therapy for duodenal ulcers is associated with a significant risk of hypergastrinemia and subsequent gastric hypersecretion.
  • The development of hypergastrinemia and gastric hypersecretion correlates with increased duodenal ulcer relapse rates.
  • Clinicians should consider the potential for hypergastrinemia and its impact on relapse when managing peptic disease with long-term antisecretory therapy.