Ulcer Infection Assignment Report

Running head: ULCER INFECTION 1
Peptic Ulcer Disease
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ULCER INFECTION 2
Introduction
The stomach ulcer is also known as the gastric ulcer. The infection affects the normal
functioning of the muscularis mucosa, gastric mucosa, and the inner submucosa. The ulcers
occur along the digestive tract, such as the esophagus, duodenum, jejunum, and at the margin of
the gastroenterostomy. The infection can cause complications such as hemorrhages,
gastrointestinal blockage, perforations, and malignancy. The disease is a health problem
worldwide with high mortality and morbidity and differs with age, gender, and geographic
environment. The mucosa of the stomach controls the balancing between the aggressive and
protective factors. The hostile elements include; pepsin, alcohol usage, anomalous motility,
nonsteroidal anti-inflammatory drugs (NSAID), gastric acid, bile salts, and infections related to
helicobacter pylori (H. Pylori) and other microorganisms. The protecting factors include
secretion of mucus, production of gastro-protective prostaglandin, normal tissue
microcirculation, and bicarbonate production. This essay will discuss the pathogenesis, causes,
symptoms, treatment functions of the protective factors.
Gastric Defensive Factors
The stomach is lining is composed of intricate epithelium that creates a discriminatory
barrier between the lumen and the body. The epithelium consists of pre-epithelial mucus-
bicarbonate, Subepithelial, components). It folds into several tube-like intestinal glands with
several branching that extends to muscularis mucosa. The gastric epithelial performs its diverse
functions in an aggressive luminal environment that can accommodate around 150 mm of HCL
and other aggressive proteases. These aggressive proteases have the ability to digest a variety of
toxic pathogens and stomach tissue itself. Many defensive mechanisms under normal conditions
prevent local destruction of the mucosal integrity from maintaining its structural functions

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despite exposure to the injurious factors. The gastric protective mechanism has a stomach
mucosal obstruction, which is a multilayered system that consists of a pre-epithelia mucus
barrier, the epithelial barrier which connects to tight junctions and sub-epithelial components that
compose nerves and the blood flow (Chai, 2011).
Peptic Ulcer Pathology
Erosions are superficial mucosal defects. The erosion defects in the ulcers outspread
through the musularis mucosa, up to the muscularis propria. Acute lesions are caused by aspirin
injury. They are many and shallow, occurring with minimal surrounding fibrosis or
inflammation, thus heal very fast. On the other hand, chronic ulcers occur singly, surrounded by
inflammation and fibrosis.
Causes and Pathophysiology
Acid secretion, reactive oxygen species, bacteria, NSAID, and other aggressive factors
impair the mucosal defense, thus altering the epithelial barrier, and this leads to the formation of
mucosal injury. The impacts of the gastric obstruction show the pathogenesis mechanism of
gastric ulcers, gastric disease, and long-lasting gastritis. These mechanisms are generated by the
imbalance between the defensive and the aggressive factors. Recent studies have shown that
familial and genetic factors in the duodenal ulcer and the increase of acid-pepsin secretion is due
to a response to several stimuli. The duodenal ulcer is characterized by duodenitis and H. pylori
contagion, and in several incidences, the secretion of compromised duodenal bicarbonate in the
face of controlled acid and peptic activity. These facts show that increased peptic activity is
accompanied by the reduced duodenal buffering capability that leads to increased mucosal injury
and may result in gastric metaplasia. The presence of antral H. pylori can lead to colonization

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and inflammation of the gastric metaplasia. This inflammation disrupts the mucosal defensive
mechanism or the regeneration that may result in ulceration (Zatorski, 2017).
The reoccurrence of inflammation and further injuries with loss of regeneration
framework may lead to a chronic ulcer. The gastric ulcers can occur due to decreased activity of
the peptic acid, and this shows that the mucosal defensive damage is more crucial. The
combination of the p defensive inflammation and a regulated amount of pepsin and acid may
initiate ulceration. Several questions are yet to be understood concerning the pathophysiology of
the mucosal regeneration and the mechanism by which the inflammation and H. pylori bacteria
interrupt the normal functioning of the gastrointestinal. Some of the causes that initiate and can
worsen the peptic ulcer disease include; alcohol use, reactive oxygen species, bacteria, and their
products, acid secretion, NSAIDs, and other different acidic chemical compounds (Berg &
McCallum 2016).
Source: https://www.medicinenet.com/peptic_ulcer/article.htm