Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate, a crucial component of the mucosal-bicarbonate barrier, is vital in neutralizing stomach acid. A decline in bicarbonate production can tip the delicate balance, leading to an acidic environment within the stomach. This acidic milieu, in turn, inflicts injury upon the stomach lining, thereby setting the stage for the development of peptic ulcer disease.

Helicobacter pylori, a gram-negative bacillus, can further exacerbate the situation. This microbial invader interferes with somatostatin production, a hormone regulating acid secretion. As a result, there is an upsurge in gastric acid production and a simultaneous decrease in bicarbonate production, crippling the body's defense barrier. This tandem effect ultimately leads to the impairment of the mucosal-bicarbonate barrier and contributes to PUD development.

Prostaglandins, another essential player in this complex orchestra, support the gastric mucosa. They serve as champions of cytoprotection by increasing bicarbonate secretion and reducing gastric acid output. Their role is instrumental in maintaining the health and integrity of the gastric lining.

In pharmacotherapy, nonsteroidal anti-inflammatory drugs (NSAIDs) wield significant influence. While these medications are prized for their pain-relieving properties, they pose a risk to the mucosal-bicarbonate barrier. NSAIDs inhibit prostaglandin production, reducing gastric mucus secretion and mucosal blood flow. These alterations create an environment conducive to PUD development.

Chronic PUD often arises due to various disturbances in the gastrointestinal system. Factors such as duodenogastric reflux and atrophic gastritis can weaken the mucosal-bicarbonate barrier, rendering it vulnerable to the erosive effects of gastric acid and pepsin.