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Chapter: Biology of Disease: Disorders of the Gastrointestinal Tract, Pancreas, Liver and Gall Bladder

Disorders of the Stomach

Gastritis is the most common disorder affecting the stomach and is character-ized by inflammation and erosion of the gastric mucosa.

DISORDERS OF THE STOMACH

Gastritis is the most common disorder affecting the stomach and is character-ized by inflammation and erosion of the gastric mucosa. Gastritis is idiopathic in many cases but it can be caused by irritating foods, beverages, ingested poisons, aspirin and staphylococcal exotoxin . Gastritis may present acutely where the patient suffers from GIT bleeding, epigastric pain, that is pain on or over the stomach area, anorexia and hematemesis or vomit-ing of blood. Patients with chronic gastritis may have no symptoms except for epigastric pain. The possibility of exposure to irritating substances must be determined when assessing the patient’s clinical history. Gastroscopy, in which a tube with a camera on its end is passed into the stomach allowing a direct visualization of its wall, can be used to confirm the diagnosis by reveal-ing inflamed portions of the lining of the stomach. Relief from the symptoms of gastritis occurs following removal of the irritant substance or treatment of the underlying cause(s).

Atrophic gastritis is a degenerative stomach disorder characterized by chronic inflammation of the stomach with atrophy of its mucous membrane lining (Figure 11.26). This results in loss of gastric glandular cells and their eventual replacement by nonsecretory and fibrous tissues. Secretions of hydrochloric acid, pepsin and intrinsic factor are impaired, leading to digestive problems, vitamin B12 deficiency and megaloblastic anemia. Atrophic gastritis is the result of long-term damage to the gastric mucosa and is usually detected late in life. It can be caused by persistent infection with the bacterium Helicobacterpylori but it can also have an autoimmune origin.


Helicobacter pylori is able to bind to the stomach lining where the bacteriarelease urease, which hydrolyzes urea, releasing ammonia that neutralizes the stomach acid. This allows the bacterium to penetrate into the mucosal layer. The release of bacterial and inflammatory toxic products by Helicobacter pylori over time results in increasing gastric mucosal atrophy. Some glandular units develop an intestinal-type epithelium; others are simply replaced by fibrous tissue. The loss of gastric mucosa decreases the amount of acid secretion that increases the gastric pH and leads to a reduced ability to kill bacteria. Ingested bacteria can survive and reside in the stomach and the upper part of the small intestine. Infection is usually acquired during childhood and, if left untreated, progresses over the lifespan of the individual in one of two main ways that have different pathological consequences. The first is a gastritis that mainly affects the antrum of the stomach (Figure 11.9). This is the most frequently observed pattern in Western countries and individuals with peptic ulcers (seebelow) usually develop this pattern of gastritis. The second pattern is a morewidespread atrophic gastritis affecting, for example, the corpus, fundus and antrum with the loss of gastric glands and their partial replacement by an intestinal-type epithelium. This pattern is observed more often in developing countries and Asian individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis.

 


Autoimmune gastritis is associated with serum anti-intrinsic factor antibodies that reduce the amount of functioning intrinsic factor. This, in turn, decreases the availability of vitamin B12 and eventually leads to pernicious anemia in some patients. Cell-mediated immunity also contributes to the disease because T cell lymphocytes infiltrate the gastric mucosa and con-tribute to the epithelial cell destruction and resulting gastric atrophy.

Specific data on the incidence of atrophic gastritis are scarse. However, its prevalence mimics that of its two main causes. In both types, atrophic gastri-tis develops over many years and is detected later in life. Helicobacter pylori (Figure 11.27) infects approximately 20% of people younger than 40 years and 50% of those older than 60 years in the developed world. Infection is highly prevalent in Asia and in developing countries and it is estimated that 50% of the world’s population is infected. Thus chronic gastritis is probably extremely common. In contrast, autoimmune gastritis is a relatively rare condition, which is most frequently observed in patients of northern European descent


and in African Americans. The prevalence of pernicious anemia resulting from autoimmune gastritis is estimated to be 127 in 100 000 in the UK.

Chronic gastritis frequently is asymptomatic but can present as nonspecific abdominal pain. Since gastritis often occurs in severely ill, hospitalized peo-ple, its symptoms may be eclipsed by other, more severe symptoms.

Atrophic gastritis cannot be reliably diagnosed by gastroscopy but requires a microscopic examination of biopsy specimens. Helicobacter pylori infections are normally diagnosed using serological tests, breath tests or antigen tests of the feces. Pernicious anemia resulting from autoimmune atrophic gastritis usually presents in patients approximately 60 years of age.

Treatment of atrophic gastritis is directed at eliminating the causative agent, to correct complications of the disease and attempt to revert the atrophic process. When Helicobacter pylori is the causative agent, it can be eradi-cated using a combination of antimicrobial agents and antisecretory agents with a success rate of about 90%. Lack of patient compliance and antimi-crobial resistance are the most important factors influencing poor outcome. However, treatment of Helicobacter pylori infection may not lead to a reversal of existing damage unless started early but may block further progression of the disease. Some evidence suggests that A-carotene and/or vitamins C and E may reverse or reduce the risk of atrophic gastritis and/or gastric cancer. The major complication in patients with autoimmune atrophic gastritis is the development of pernicious anemia. This requires vitamin B12 replacement therapy.


Ulcers are perforations of the GIT wall (Figure 11.28), particularly erosions of the mucosal layer related to cancer, that is, malignant ulcers, or to stomach acid, that is, peptic ulcers. Ulcers may also be named from their location, for example esophageal, gastric or stomach and duodenal ulcers. Esophageal ulcers are usually associated with hiatus hernias (see below) caused by acid splashing from the stomach into the lower esophagus. Gastric ulcers are rela-tively rare because the mucosal lining of the stomach is protected from the acid by a layer of alkaline mucus. They generally occur in patients older than 50 years of age. Duodenal ulcers are five times more common than gastric ulcers and generally occur in a younger population. More than 90% of ulcers occur in the duodenal wall, usually after it has been weakened by infection with Helicobacter pylori. It used to be thought that ulcers were caused by stress and excessive accumulation of HCl. However, it is now accepted that their commonest cause is infection with Helicobacter pylori (Figure 11.27) which can colonize and destroy the mucosal layer.

Peptic ulcers are linked to an increased production of acid and pepsin in gastric juice or to a reduced protection of the mucosa against gastric juice. Figure 11.29 illustrates diagrammatically the development of a peptic ulcer.Lesions that do not extend through the mucosal lining are referred to as ero-sions. Acute and chronic ulcers penetrate this layer and, in serious cases, may penetrate the stomach wall. In some patients, blood vessels in the GIT wall ulcerate and lead to heavy, and in some cases fatal, bleeding. Chronic ulcers have an associated basal scarring.


Patients with peptic ulcers present with epigastric pain but their diagnosis is made on clinical grounds, supported by endoscopy, laboratory tests for assessing acid and pepsin secretion and identification of Helicobacter pylori infection. Treatment is aimed at eradication of the Helicobacter pylori infec-tion and reducing acid output. Antibiotics that effectively sup-press symptoms include amoxycillin, clarithromycin, metronidazole and tetracycline, and they often cure the patient. Bismuth chelate and sucralphate may also be administered to decrease the synthesis of prostaglandins that stimulate inflammation. The resulting decrease in acid production by parietal cells and the increase in hydrogen carbonate production by mucus secreting epithelial cells have cytoprotective effects.

Zollinger-Ellison syndrome is a rare disorder that causes massive, multiple and recurrent peptic ulcers due to the excessive secretion of gastric juice from tumors affecting the pancreas or duodenum. Approximately 60% of the tumors are malignant. They are called gastrinomas because they secrete large amounts of gastrin, hence patients have an increased plasma gastrin concen-tration and rates of gastric acid secretion greater than 100 compared with nor-mal rates of less than 5 mmol h–1.

A diagnosis of Zollinger-Ellison syndrome usually requires demonstrating an increase in the concentration of gastrin in the patient’s serum, combined with an increased release of acid in the stomach. However, in about 30% of cases the plasma gastrin concentration is normal or only slightly above normal. The pentagastrin test is used to assess the acid output of the stomach. Pentagastrin is an analog of gastrin that stimulates the release of stomach acid. Acid output is assessed before and after intramuscular injection of pentagastrin. Patients with Zollinger-Ellison syndrome have a high basal acid output and pentagas-trin causes little further increase. Treatment of Zollinger-Ellison syndrome is by surgical removal of the gastrinoma.

A hernia is the protrusion of an organ or tissue out of the body cavity in which it is normally found. A hiatus hernia occurs when the upper part of the stom-ach is dislocated through the hole, called a hiatus, in the diaphragm, into the chest. Sliding hiatus hernias occur when the esophagus and stomach both move upwards so that the top end of the stomach protrudes through the gap in the diaphragm normally occupied by the esophagus (Figure 11.30 (A)) and these constitute 90% of cases. The remaining 10% are rolling hiatus hernias where a portion of the stomach curls upwards adjacent to the esophagus so that both it and an upper part of the stomach protrude through the gap (Figure 11.30 (B)). The causes of hiatus hernias are unknown but they may be due to intra-abdominal pressure or weakening of the gastroesophageal junc-tion caused by trauma or loss of muscle tone. Over 50% of individuals with hiatus hernia are asymptomatic, but when symptoms do occur, they include heartburn, which is aggravated by reclining, chest pain, dysphagia, belching, pain on swallowing hot fluids and a feeling of food sticking in the esophagus. Although hiatus hernia is not usually serious, it can cause inflammation of the lower end of the esophagus leading to a back flow of gastric juices; this is called reflux esophagitis, and it may cause bleeding (perhaps anemia) or a stricture. Cancer in a hiatus hernia is very rare, but there is a slight increased risk of it developing in the inflamed area.


Data on the incidence of hiatus hernia are few but the condition increases with age and is particularly common in overweight middle-aged women and can also occur during pregnancy. The contents of the GIT are often not clearly visible by X-rays and diagnosis requires confirmation with a barium meal. This consists of barium sulfate mixed with liquid and is usually flavored. The barium in the meal lines the inside of the GIT wall and is visible because barium is opaque to X-rays making this a useful method for detecting structural abnormalities of the GIT. The presence of a hiatus hernia can also be investigated by gastroscopy.

The aim of treatment is to alleviate the symptoms. Losing weight, reduc-ing smoking and coffee and alcohol intakes all help to relieve symptoms. The patient may be advised to avoid tight or restrictive clothing. Avoiding food intake before sleep and elevating the head of the bed help in reducing acid reflux. Medication such as antacids may be prescribed. Surgery is only used when there is strangulation of the hernia or the symptoms cannot be controlled.


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