Peptic Ulcer Disease
Peptic ulcer disease (PUD) is defined as a defect in the lining of the gastrointestinal mucosa, with appreciable depth or involvement of the submucosa [1]. The development of peptic ulceration is a result of an imbalance between factors potentially damagi
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Introduction to Peptic Ulcer Disease Peptic ulcer disease (PUD) is defined as a defect in the lining of the gastrointestinal mucosa, with appreciable depth or involvement of the submucosa [1]. The development of peptic ulceration is a result of an imbalance between factors potentially damaging the gastric mucosa (aggressive) and protective (defensive) factors. The former include endogenous factors (e.g., gastric acid and pepsin) and exogenous factors including chronic Helicobacter pylori (Hp) infection, use of nonsteroidal anti-inflammatory drugs (NSAIDs), consumption of alcohol, smoking, and exposure to stress [2]. The latter comprise pre-epithelial defense (secretion of mucus and bicarbonates), epithelial defense (epithelial restitution and replication, extracellular buffers including bicarbonates), and post-epithelial defense (mucosal microcirculation, tissue acidbase balance). Sometimes the definitive cause of the ulcer cannot be established (“idiopathic ulcer”). The
P.C. Konturek (*) Second Department of Internal Medicine, Thuringia Clinic Saalfeld, Rainweg 68, Saalfeld/Saale 07318, Germany e-mail: [email protected] S.J. Konturek Institute of Physiology, Jagiellonian University Cracow, Grzegorzecka Str. 16, Krakow 31-525, Poland e-mail: [email protected]
possible pathogenetic factors associated with this rare peptic ulceration are older age, multimorbidity, recent surgery, underlying sepsis, and medication (other than NSAIDs ulcerogenic drugs). Peptic ulcer is typically localized in the stomach (gastric ulcer) and duodenum (duodenal ulcer), most commonly in the duodenal bulb (the part of the duodenum closest to the stomach) due to the high exposure to gastric acid. Small areas of the duodenum colonized by Hp, called duodenal gastric metaplasia, may additionally contribute to the pathogenesis of PUD in duodenum [3]. The most common symptoms of PUD are abdominal pain, vomiting, hematemesis (vomiting of blood), and melena (the passage of dark stools stained with altered blood). In contrast, older patients (>80 years) often lack abdominal pain. Pain occurs typically during the night, when gastric acidity is increased (due to circadian changes) and buffering food intake is minimal [4]. Complications of PUD include bleeding, perforation of stomach or duodenum, and gastric outlet obstruction (i.e., an obstructed pylorus) that could be fatal if untreated [5]. More often, gastric outlet obstruction is caused by neoplasia, however. Duodenoscopy is the current standard for diagnosis of PUD revealing its localization and possible complications (especially bleeding). In addition, endoscopy allows obtaining biopsies from gastric mucosa for detection of Hp infection [6].
E. Lammert, M. Zeeb (eds.), Metabolism of Human Diseases, DOI 10.1007/978-3-7091-0715-7_21, © Springer-Verlag Wien 2014
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Pathophysiology of Peptic Ulcer Disease and Metabolic Alterations Among the endogenous aggressive factors, gastric acid and pepsin play a crucial role, as shown by Schwartz’ dictum: “no acid, no ulcer” [7]
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