Chronic Gastritis - Assignment Example

Chronic Gastritis al affiliation Chronic Gastritis Gastritis is the inflammation of the stomach lining particularly the gastric mucosa. Usually, the stomach lining consists of special cells that produce digestive acid and enzymes. The lining also contains mucus, which prevents the acid from corroding the stomach walls. If an inflammation occurs, the stomach lining produces fewer enzymes, acid, and mucus. Since the mucus layer is too thin to protect the stomach walls from digestive acid, a painful sensation is frequently felt in the upper abdomen. Gastritis can either be acute or chronic. Acute gastritis occurs in the form of rapid inflammations on the stomach walls. It always last for a short period. On the other hand, chronic gastritis occurs in the form of stomach inflammations that last for a long time. If it not treated, chronic gastritis may last for a lifetime (National Institute of Health (NIH), 2010). Causes of Gastritis The major cause of gastritis is Helicobacter pylori (H. pylori) infection (Dai, Tang, & Zhang, 2011). H. pylori are forms of bacteria that infect the stomach walls. Their transmission mainly takes place from person to person. Contaminated water or food especially in places with poor sanitation also forms another mode of transmission (NIH, 2010). Gastritis can also be caused by the prolonged use of drugs that include ibuprofen and aspirin. When such anti-inflammatory drugs are used for some time, they trigger a gradual inflammation on the stomach lining. Some harmful chemical agents such as alcohol, radiation, and cocaine can also cause gastritis. If the gastric mucosa is exposed to harmful chemical agents, it accelerates the production of the gastric epithelium, potentially causing foveolar hyperplasia. Although most chemical-triggered gastropathies do not show any symptoms, multiple erosions and ulcers may develop, causing bleeding (NIH, 2010). Apart from H. pylori and anti-inflammatory drugs, gastritis can also be caused by autoimmune disorders, which attack healthy cells in the stomach lining. Such gastritis is usually restricted to the corpus. The autoimmune aggression targets parietal cells associated with anti-intrinsic factor antibodies and anti-parietal cell. Digestive disorders or diseases, viruses, fungi, parasites, and some bacteria other than H. pylori can also cause gastritis. For instance, duodenal reflux into the stomach may cause mucosal abrasions, which in turn trigger the inflammation of the gastric mucosa (Ruggea et al, 2011). Symptoms of Gastritis The most prevalent symptom of gastritis is dyspepsia, which includes nausea, vomiting, and upper abdominal pain. Many people having mild forms of the disease rarely have any symptoms. However, those who suffer from erosive gastritis often have ulcers, which can cause stomach bleeding. People with ulcers also have blood in their stool or vomit (NIH, 2010). Diagnostics Gastritis is usually diagnosed by endoscopy with a surgery of the stomach. The procedure involves the insertion of an endoscope, a device fitted with a tiny camera, through the nose or mouth into the stomach. Because it causes discomfort, it is always recommended that the patient is given some sedative to relieve the pain. The endoscope provides a view of the esophagus, stomach, and a section of the small intestines. The endoscope can also be applied in the removal tiny samples of abdominal tissues for laboratory examination (NIH, 2010). Apart from endoscopy, a test for H. pylori infection can also be used in the diagnosis of gastritis. In this case, the patient’s blood, stool, or even breath can be tested for infection. In addition, the presence of anemia can indicate gastritis infection. For instance, if the patient’s hemoglobin gets diminished, it could suggest bleeding in the stomach. The presence of blood in the stool could also suggest bleeding in the stomach, a sign of inflammation (Ruggea et al, 2011). H. pylori can be detected in the mucous layer on the gastric mucosa. However, in some instances, it may be tricky to detect particularly if there is extensive intestinal metaplasia. It may also be difficult to detect the bacterium during antisecretory therapy. In such situations, the infection is inferred by the manifestation of mononuclear and neutrophilic irritation (Ruggea et al, 2011). Lastly, upper gastrointestinal series test can also be performed. Here, the patient swallows barium. Barium makes the digestive tract more visible to X-rays. Thus, if an X-ray image is taken after swallowing barium, the digestive tract erosions or ulcers become more visible (NIH, 2010). Staging Gastritis Using the OLGA System The Operative Link for Gastritis Assessment (OLGA) proposes a multi-stage system for reporting gastritis. The system arranges the phenotypes of gastritis on a progressive scale of gastric cancer risk. It also considers gastric atrophy as the inflammation that indicates disease progression (Ruggea et al, 2011). Stage 0 Gastritis If the atrophy score is zero in both the oxyntic and mucosecreting compartments, the OLGA stage is known as zero. In this stage, there is no standard biopsy sample that can reveal atrophy. Although the inflammatory score remains independent of this stage, there are some exceptions particularly when the fluid infiltrate prevents the assessment of any loss of glands (Ruggea et al, 2011). Stage I Gastritis The stage is characterized by the presence of patchy atrophic lesions, which are only found in some biopsy samples. In most cases, the atrophy is found in angularis incisura samples. The detection of H. pylori in patients using proton pump inhibitors is extremely difficult. However, the coexisting inflammatory wounds may suggest the presence of H. pylori (Ruggea et al, 2011). Stage II Gastritis The stage results from a combination of different atrophy scores. In most cases, atrophy can be detected in the distal mucosa biopsy samples. In addition, duodenal ulcers are more common than gastric ulcers (Ruggea et al, 2011). Stage III Gastritis In this stage, a metaplastic variation of atrophy can be detected consistently. In addition, gastric peptic ulcer can be identified more often than in the first three OLGA stages (Ruggea et al, 2011). Stage IV In this stage, the detection of H. pylori infection in patients is hindered by extensive metaplastic transformation (Ruggea et al, 2011). Treating Gastritis Most of the treatments of gastritis focus on the reduction of the quantity of acid in the stomach. Digestive acid causes severe pain in the upper abdomen because the stomach lining is inflamed. However, if the quantity of the acid is reduced, the symptoms can be relieved. The stomach lining also heals when there is less acid. Thus, the use of antacids such as Maalox, Rolaids, Alka-Seltzer, Mylanta, and Rio-pan is recommended. The antacids work by neutralizing the acid that has already been produced in the stomach (NIH, 2010). The quantity of acid can also be reduced if their production is slowed down or even stopped. The production of stomach acid is considerably slowed down by histamine 2 blockers such as ranitidine and famotidine. If histamine 2 blockers become ineffective, proton pump inhibitors can be used. Proton pump inhibitors are more effective than histamine 2 blockers. They are obtainable in various brands such as lansoprazole, omeprazole, esomeprazole, rabeprazole, pantoprazole, and dexlansoprazole (Ruggea et al, 2011). Recommended Plan of Action In the treatment of gastritis, the recommended plan of action depends on the cause of the disease. For example, if the cause is a prolonged use of anti-inflammatory drugs, the patient can be advised to stop using the drug, reduce the quantity taken, or even switch to a different class of medication. If the cause is stress, proton pump inhibitors can be used especially if the patient is critically ill (NIH, 2010). If the cause of gastritis is H. pylori infection, a patient may not experience the symptoms in many cases. However, it does not mean that the patient is safe from related dangers. While treating gastritis caused by H. pylori, focus is placed on killing the bacteria and also reducing stomach acid. If the quantity of stomach acid is not reduced, the gastritis may lead to ulcers or cancer in the stomach or small intestines. Moreover, if the H. pylori bacteria are not killed, more inflammation of the stomach lining would occur. Therefore, a triple therapy is recommended for patients with gastritis caused by H. pylori. Proton pump inhibitors would reduce the production of acid while amoxicillin and clarithromycin kills the bacteria. The use of bismuth subsalicylate eliminates H. pylori bacteria effectively from the digestive tract (NIH, 2010). Frequent medical checkups are also necessary for the treatment of gastritis caused by H. pylori. The checkups are important because of the absence of symptoms, which may mislead the patient into believing that the disease has healed completely. If the bacterium is eliminated entirely from the digestive tract, there will be no risks of other gastrointestinal diseases. A successful elimination of the bacteria is indicated by a rapid disappearance of neutrophils. However, if the treatment fails, it can be detected by the persistence of mononuclear infiltrate or neutrophils (Ruggea et al, 2011) References Dai, Y., Tang, Z., & Zhang, Y. (2011). How to assess the severity of atrophic gastritis. World Journal of Gastroenterology. 17(13): 1690-1693. Retrieved November 19, 2014 from http://www.wjgnet.com/1007-9327/pdf/v17/i13/1690.pdf National Institute of Health. (2010). Gastritis. Retrieved November 19, 2014 from http://digestive.niddk.nih.gov/ddiseases/pubs/gastritis/Gastritis_508.pdf Ruggea, M., Penelli, G., Pilozzi, E., Fassan, M., Ingravallo, G., Russo, M.V., & Mario, D.F. (2011). Gastritis: the histology report. Retrieved November 19, 2014 from http://www.siapec.it/content/file/2874/gastritis%20the%20histology%20report%20M%20Rugge%20et%20al.pdf Read More