Peptic Ulcer Disease Research Paper

Length: 5 pages Sources: 3 Subject: Sports - Drugs Type: Research Paper Paper: #9266154 Related Topics: Pathophysiology, Arthritis, Chronic Disease, Smoking Cessation
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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).


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...


H. Pylori inhibits the duodenal mucosa's capacity to buffer gastric acid's caustic effects by inducing an inflammatory reaction that interferes with the epithelial cells' ability to secrete bicarbonate (Elsevier, 2012).

NSAIDs: this is the second-most significant PUD risk factor (Elsevier, 2012). More than 60% of Americans aged above 65 use NSAIDs every week, and 34% everyday (Elsevier, 2012). Each year, approximately 15%-20% of new PUD cases are associated with arthritis patients. Even the very low dosages of aspirin have been found to increase the risk of PUD (Elsevier, 2012). NSAIDs are believed to suppress the production of prostaglandin (Elsevier, 2012). Two enzymes control the synthesis of prostaglandin; cyclooxygenase-2 and cyclooxygenase-1 (Elsevier, 2012). NSAIDs cause tissue inflammation, thereby inhibiting the activity of cyclooxygenase-1 (Elsevier, 2012). This reduced activity causes the homeostatic functions of gastrin to decrease. As a result, inadequate levels of bicarbonate and mucus are produced, increasing the epithelial cells' vulnerability to damage by pepsin and hydrochloric acid (Elsevier, 2012).

Smoking, Alcohol, Stress and Cocaine: these have been found to increase the risk of PUD, though the mechanisms behind their operations are still unclear (Elsevier, 2012). Alcohol is hypothesized to increase the permeability of the mucosal cells, whereas smoking inhibits the production of prostaglandin and bicarbonate (Elsevier, 2012). However, "a direct cause-effect relationship has yet to be demonstrated" in these cases (Elsevier, 2012).

The At-Risk Population and Screening

Cocaine users, cigarette smokers, and alcohol drinkers run a higher risk of developing PUD (Elsevier, 2012). The elderly, individuals from families with PUD history, and patients who are frequently exposed to intensive care treatment settings run a high risk as well (Elsevier, 2012). One of two tests could be used in the diagnosis of an ulcer: upper endoscopy or upper GI (UMMC, 2013). In upper endoscopy, a thin tube fitted with a camera on one end is driven into the GI tract, through the mouth (UMMC, 2013). In the GI test, a patient is made to drink barium, after which they are exposed to several x-ray tests (UMMC, 2013). Both tests require H. Pylori screening. However, routine screening for the bacterium is not recommended (Elsevier, 2012). Moreover, "H. Pylori infection does not necessarily lead to PUD. Only 15% to 20% of infected individuals will develop PUD in their lifetime" (Elsevier, 2012).

PUD Prevention and Treatment


The treatment mechanism for an NSAID-induced ulcer differs from that caused by H. Pylori infection (UMMC, 2013). The treatment for a H. Pylori-induced ulcer is a combination of H. Pylori-killing antibiotics, PPIs, and bismuth (UMMC, 2013). An NSAID-induced ulcer is, on the other hand, treated using a PPI (UMMC, 2013). Many agents have been found to be equally effective for the treatment of PUD. This remains the case, despite the variations in the drugs' modes of action (Halter, 1995). Due to this, investigators are beginning to shift their attention from aggressive mechanisms to more defensive ones (Halter, 1995).


PUD resulting from the use of NSAIDs can be prevented by limiting the use of the same (Elsevier, 2012). These medications should only be taken for brief, rather than routine courses, so as to prevent the acute inflammation of tissues; a situation that increases the gastro-intestinal tract's vulnerability to damage by hydrochloric acid (Elsevier, 2012). Moreover, acetaminophen could be used as an alternative to NSAIDs and aspirin (UMMC, 2013). Medical advice should be sought if one has to use NSAIDs continuously over a long period. In such situations, the practitioner could either test for H. Pylori, prescribe an acid blocker or PPI to limit the NSAID effect, or offer misoprostol (UMMC, 2013).

Therapy aimed at controlling prophylactic acid levels could be administered to patients who run a high risk of developing GI tract complications due to NSAID use (Elsevier, 2012). This group includes persons who are aged above 60, have histories of prior GI tract complications (perforation, bleeding, PUD), suffer from serious chronic illnesses such as diabetes,…

Sources Used in Documents:


Elsevier. (2012). Peptic Ulcer Disease. Clinical Key Elsevier. Retrieved from

Halter, F. (1995). Pathophysiology of Peptic Ulcer Disease. In D. Hollander & G. Tytgat (Eds.), Sucralfate: from Basic Science to the Bedside (Ch. 10). New York: Plenum Press.

UMMC. (2013). Peptic Ulcer. The University of Maryland Medical Center. Retrieved from

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