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Stomach Ulcers Concept and Problem Essay

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Updated: Jun 4th, 2020


Stomach ulcer is a major health problem whose effects are seen in the erosion of a patient’s stomach lining. This leads to fatigue, unintentional weight loss, potential bleeding, vomiting of blood, nausea and massive abdominal pain among other gastrointestinal symptoms. Studies indicate that stomach ulcers can severely disintegrate the lining of an individual’s stomach by interfering with the mucous coating that prevents stomach acid from coming into contact with the stomach wall. Lacy and Rosemore are quite categorical that with the passage of time, the acid eats through the stomach lining and thereby occasioning the exposure of capillaries that are located beneath the walls of the stomach (2789). The end result of this erosion of mucus coating is incessant pain due to bleeding in addition to perforations and subsequent health problems related to peritonitis and sepsis especially if the condition is not addressed promptly.

Etiology of the lesion

Malfertheiner, Chan and McColl indicate in their article Peptic Ulcer Disease that before 1990, stomach ulcer was a health problem believed to be mainly caused by poor diet and long term stressful circumstances as well as depression (1449). These factors were assumed to interfere with mucus production and therefore giving room to corrosive stomach acids which then eroded the lining of the stomach wall. Many researchers today are still emphatic that the possible cause of peptic ulcer and its development is stress. They argue that head trauma, burns and psychological stress lead to ulcers with its main etiology being stress related. Lacy and Rosemore agree in part that stress can indeed lead to production of stomach acid. The latter undisputedly provides a favorable environment where Helicobacter Pylori can thrive (2789). However, in a quick rejoinder, they argue that that ulcer is not an infectious disease in addition to the fact that a psychological factor like stress has less significant role to play.

Besides stress, another cause of stomach ulcers is a bacterium known as Helicobacter Pylori which is responsible for 90% of duodenal ulcers and 60 % of gastric ulcers. This bacterium as Zelickson points out can spread to humans via contaminated water and food (1054). It is important to note that an individual’s immune system and its antibodies are not able to fight and clear the bacteria and its infections. If this bacteria is not properly managed, it may further cause a type B gastritis which is a chronic active gastritis that affects the regulation and production of gastrin. Needless to say, early detection and control of this harmful bacterium is indeed crucial since it may lead into other chronic and deadly infections.

In addition, the use of non-steroidal anti-inflammatory drugs (NSAIDs) and other medicines such as ibuprofen and aspirin can cause ulcers. Smith and Stabile indicate that prostaglandins stimulate the production of a layer of mucus to protect the stomach wall from gastric acid (799). The use of NSAIDs inhibits the functions of glucocorticoids and the production of cycloxygenase 1 (Cox-1). The latter is an important component that aids in the production of prostaglandins. Other inhibitors like Rofecobix and celecobix among other anti-inflammatories also inhibit the roles played by Cox-2 leading to gastric ulceration.

Credible studies relate other causes of stomach ulcers to factors such as smoking, diet, blood type and use of certain or excessive spices in food. While these may be contributing factors, Dino et al clarify that they may not be classified as causes unless they are linked to an infection by H. Pylori (17). Alcohol consumption may also be a factor when associated with the bacteria.

Macroscopic and microscopic findings

Ulcers in the stomach are normally localized in areas of lesser curvatures. Macroscopically, ulcers have a parietal defect that is either round or oval. They have perpendicular borders, smooth bases and a diameter of between 2-4 centimeters. The borders of the ulcers vary depending on how intense they are. As such, the borders can be regular or irregular. Microscopically, an acid-pepsin aggression causes a mucosal defect which severely affects the muscularis propria and muscularis mucosae resulting into gastric peptic ulcers. Lacy and Rosemore are of the opinion that their margins indicate chronic gastritis and are perpendicular (2792). The authors observe that when gastric peptic ulcers reach their active phases, they appear to have four zones showing fibrous tissue, granulation tissue, fibrinoid necrosis and inflammatory exudates. The bases of the fibres may have thrombosis or vessels with thickened walls. Both the microscopic and macroscopic findings on stomach ulcers are integral in understanding the etiology, prevention and treatment of the condition.

Symptoms, signs and laboratory findings caused by the lesion

Physicians normally use characteristic symptoms as a base for establishing the diagnosis of stomach ulcers. The diagnosis of stomach ulcers can be made through a gastroscopy whereby a direct visual identification is done to determine the severity and location of the ulcer. Besides, a Helicobacter Pylori can be diagnosed via histological examination, stool antigen test, measurement of antibodies, rapid urease test and urea breath test. Stomach ulcers mainly affect the nerves which surrounds the stomach. This agitates the nerves causing massive pains. If this is left unattended for some significant period of time, it may spread and tear the stomach wall and cause peritonitis.

Some of the common symptoms are burning pains in the stomach mostly interpreted as hunger, indigestion or heartburn. Other symptoms include fatigue, nausea, bloating, feeling sick and retching. It may also cause complications such as serious perforations and bleeding ulcers.

Treatment and prognosis

The treatment of stomach ulcers before the process of gastroscopy can be done by administering H2 antagonists or antacids and bismuth compounds. The latter are effective in clearing or reducing the presence of Helicobacter Pylori. For patients using NSAIDs, prevention of its side effects which manifest in peptic ulcers can be treated using misoprostol or a prostaglandin analogue. Zelickson points out that the effective elimination of Helicobacter Pylori can be achieved by combining 1 proton pump inhibitor (PPI) with an antibiotic such as Metronidazole, Tetracycline, amoxicillin or clarithromycin. As such, the first line treatment would be a pantoprazole (a PPI), a metronidazole and an amoxicillin (1054). In addition, in order to obtain relief from excess stomach acid, indigestion, heartburn and peptic ulcers, physicians recommend the use of a ranitidine. The latter drug acts as a general pain killer.

Relevance to dental practice

Stomach ulcers and dental problems are mainly caused by bacterial infections. This is a factor that calls for medical experts especially in the field of dental health to encourage proper dental care. This will be critical in reducing possible strain to an individual’s immune system due to peripheral infections related to stomach ulcers. Dental practitioners should be able to aid their patients in the application of preventative measures aimed at fostering good health and limiting infections.

Works Cited

Dino Vaira, Luigi Gatta, Chiara Ricci, Andrea Tampieri, Maurizio Cavina and Veronica, Be. “Peptic ulcer and Helicobacter Pylori.” Postgraduate medicine, 117.6 (2005): 17-23. Print.

Lacy, Brian and Justin, Rosemore. “Helicobacter Pylori: ulcers and more: the beginning of an era.” The Journal of nutrition 131.10 (2001): 2789-2793. Print.

Malfertheiner Peter, Francis Chan and Kenneth, McColl. “Peptic ulcer disease.” The Lancet, 374.9699 (2009): 1449-1461. Print.

Smith, Brian and Bruce, Stabile. “Emerging Trends in peptic ulcer disease and damage control surgery in the H. Pylori era.” The American Surgeon, 71.9 (2005): 797- 801. Print.

Zelickson, Marc. “Helicobacter Pylori is not the predominant etiology for peptic ulcers requiring operation.” The American Surgeon, 77.8 (2011): 1054-1060. Print.

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