Peptic Ulcer Disease: Pathophysiology
A peptic ulcer can be defined as "a focal mucosal defect with inflammatory cell infiltration and coagulation necrosis extending through the muscularis mucosae" (Halter, 1995, p. 2). Contrary to erosion, a peptic ulcer extends beyond the epithelial structures into that intestinal tract section that happens to be in constant contact with pepsin and acid-containing gastric juice (Halter, 1995). Peptic ulcers cause an imbalance between the gastro duodenal defense-influencing factors such as prostaglandin, bicarbonate and mucus, and those such as NSAID use, H. pylori, pepsin and gastric acid, which promote mucosal damage (Elsevier, 2012). If peptic ulcers keep recurring at the same site, the imbalance worsens, resulting in peptic ulcer disease (PUD).
Two types of peptic ulcers can be deduced from the explanation above; duodenal and gastric ulcers (Elsevier, 2012).
Gastric Ulcers: there are four major classifications of gastric ulcers: type I, type II, type III and type IV (Elsevier, 2012). The class differences are solely based on the location of the ulcers within the gastrointestinal tract. Type I and type IV ulcers arise and develop in the gastric body and cardia respectively, and have the effect of reducing a patient's basal output of acid (Elsevier, 2012). Type II and type III ulcers result in the hyper secretion of acid, and occur in the antrum and three centimeters from the pylorus respectively (Elsevier, 2012). The degree of acid secretion is, therefore, dependent upon an ulcer's closeness to the pylorus (Elsevier, 2012).
Duodenal Ulcers: these usually accompany type III gastric ulcers but, unlike them, have not been found to bear any malignant potential (Elsevier, 2012). They come about when the innate mucosa defenses are overwhelmed by abnormal secretions of acid (Elsevier, 2012). Duodenal ulcers, like type II and type III ulcers, result in acid hyper-secretion. In this case, however, these hyper-secretions are usually within what can be considered the normal range (Elsevier, 2012). The pathogenesis of duodenal ulcers results in exaggerated levels of endogenous gastrin (Elsevier, 2012).
Epidemiology
Between three and eight million people in the U.S. are affected by PUD, and 500,000 new cases (on average) are reported each year (Elsevier, 2012). Whereas there has been a significant decline in the incidence of DU in the recent past, that of GU has remained fairly stable, with only very slight increases (Halter, 1995). The trend portrayed by GU "is probably related to the large consumption of NSAIDs" and low-dose aspirin (Halter, 1995, p. 2, Elsevier, 2012). Therefore, in spite of the advancements in ulcer therapy such as PPIs and fiber optic endoscopy, PUD still continues to impose a significant burden on the U.S. economy (Elsevier, 2012).
Besides technological advancement, a number of other factors could have contributed to the decrease in the H. Pylori infection, as well as in the prevalence of DU. These include improved methods of food preparation, reduced family sizes, and improved sanitation (Elsevier, 2012). Men, and people of low socioeconomic status have, in this regard, been found to run higher risks of developing PUD (Elsevier, 2012). Older individuals too face an increased risk, because i) old age is associated with low levels of gastro duodenal defense-influencing factors (prostaglandin, bicarbonate and mucus), ii) conditions such as CVDs and arthritis, which are associated with old age, predispose the individual to the use of NSAIDs and aspirins, iii) elderly individuals "tend to have a higher rate of smoking and cumulative years of smoke exposure" (Elsevier, 2012).
PUD Risk Factors
H. Pylori Infection: More than three-quarters of all ulcers in the U.S. are associated with the H. Pylori bacterium (Elsevier, 2012). The microaerophilic rod-shaped bacterium attaches itself to the gastric epithelial cells, where it "lives within the gastric mucous layer" (Elsevier, 2012). The bacterium is transmitted from one person to another either through the fecal-oral or oral-oral routes (Elsevier, 2012). Experts hypothesize that H. Pylori disrupts the acid-regulating mechanism of the parietal cells, leading to acid-hyper-secretion (Halter, 1995). H. Pylori inhibits the duodenal mucosa's capacity to buffer gastric acid's caustic...
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