Explanations for the fast rise in occurrence of EAC involve the increasing prevalence of gastroesophageal reflux and obesity as well as the declining incidence of Helicobacter pylori infection. Helicobacter pylori infection is correlated with hypergastrinemia, the excess of gastrin in the blood. Gastrin is a hormone that is secreted by G cells situated in the gastric antrum and works on the parietal cells to trigger the production of hydrochloric acid. Constant hypergastrinemia due to daily PPI therapy contributes to the raised gastric acid-secretory capacity that is not obvious throughout PPI therapy, but that emerges quickly when the drug is stopped. Increased acid production due to hypergastrinemia poses a risk factor for development of
Helicobacter pylori (H. pylori) is a human pathogen that is responsible for ulcers and stomach inflammation. The organism had been researched by several scientists around the world since 1875; however none of them was successfully culture it. Until 1982, Dr. Barry Marshall and Dr. Robin Warren succeeded in observing the colonies, and thus became the first scientists to discover this bacterium. By self-testing, Dr. Marshall drank a liquid that contained H. pylori culture. A few days later, he got sick with many symptoms such as vomiting and nausea. After ten days, by undergoing endoscopy, he was able to confirm the role of H. pylori in causing gastritis. Then he and Dr. Warren also demonstrated the effect of
For one, gastric cancer affects many people. In 2011, an estimated 74,035 people in the US had been inflicted with gastric cancer ("SEER Stat Fact," 2013). Additionally, this year, an estimated 22,220 additional people will receive the diagnosis of the stomach cancer ("Stomach (Gastric Cancer)," 2014). Though these numbers may not seem to indicate much of a problem in the United States when compared to prostate cancer's 233,000 estimated new cases and breast cancer's 232,670 estimated new cases, gastric cancer has a significant impact worldwide, being the cancer with the second highest mortality rate ("New Targeted Drug," 2014; "SEER Stat Fact," 2013).
Description/Synopsis: Proton pump inhibitors (PPIs) are used for the treatment of gastroesophageal reflux disease (GERD) and Laryngopharyngeal reflux (LPR) due to their potential to inhibit gastric acid production. Unfortunately, high doses of PPIs are associated with adverse health outcomes. The use of PPIs has been shown to affect the absorption of minerals and vitamin-like calcium, iron and vitamin B12. Not only the risk of other severe conditions like hyperparathyroidism, diarrhea and pneumonia increases upon the long-term use of PPIs but the negative effects also extend to coronary heart disease and atherosclerotic diseases. PPIs reduce the efficacy of the drug clopidogrel which inhibits platelet activation thereby contributing to coronary heart disease and myocardial
According to XX, common causes of epigastric tenderness include; gastritis, esophagitis, esophageal spasms, epigastric hernia, GERD, peptic ulcer disease, with or without bleeding, pancreatitis and hiatal hernia. A gastric ulcer is an ulceration or breakdown in the stomach or duodenal lining. The symptoms of a gastric ulcer include dull and burning recurrent abdominal pain in the epigastric region which can be exacerbated by food. Antacids or milk may relieve the pain. In the additional history, it states that the patient describes his pain as burning. The epigastric pain is relieved by eating, especially drinking milk, but returns two hours after eating. In this case scenario, food intake, especially milk is a relieving factor, not an exacerbating factor. The patient history states he denies early satiety, anorexia or weight loss. He states he has had dyspepsia in the past, but his present symptoms are much worse. The factors that damage the gastric mucosal barrier include use of non-steroidal anti-inflammatory drugs (NSAIDs), cigarette smoking, glucocorticoids, H. Pylori, alcohol consumption and stress. The patient states he has been taking an NSAID (Tylenol) for two months due to a knee injury. He smokes a pack a day, drinking three mixed drinks a day and has increased stress due to a recent job change. .So, he has many exacerbating factors for the development of a gastric or duodenal ulcer. The bacteria Helicobacter
Gastroesophageal reflux disease is characterized by a variety of symptoms, including the common “heartburn” and acid regurgitation, as well as the not so common chest pain (unrelated to the heart), chronic cough, hoarseness, and throat irritation. It is more familiarly known as GERD and is one of the most common chronic and rapidly growing diseases of today; yet, the underlying cause is still unclear. There seem to be many different theories on what causes GERD, but the most common treatment is the Proton Pump Inhibitor (PPI).
One common cause of gastritis is H. Pylori. H. Pylori is a bacteria found worldwide, but especially in developing countries, where up to 10% of children and 80% of adults are likely to have had an H. pylori infection. However, patient usually are without any symptoms (Pilotto & Franceschi, 2014). The human host is the only known reservoir. Transmission occurs by person-to-person contact, by both fecal-oral and oral-oral routes therefore, infection is most likely acquired in childhood (Go,2003).
Prior to the isolation of Helicobacter pylori (H. pylori} by Robin Warren and Barry Marshall in 1982, it was theorized that peptic ulceration, an ailment first described in 1857 by William Brinton, stemmed from poor diet, tobacco use, and stress due to the failure to definitively identify a causative agent as well as the belief that the inhospitable environment within the human stomach resulted in its sterility (Tanenbaum 2005). Because physicians were ignorant to the existence of H. pylori, individuals suffering from peptic ulcerations underwent ineffective treatments for over a century. The successful isolation of H. pylori and identification of its role in gastric diseases earned Warren and Marshall a joint Nobel Prize in Physiology or Medicine in 2005 (The Nobel Prize 2005). Despite the passage of thirty-two years, modern medicine has been unable to definitively eradicate H. pylori, but research continues in hopes of developing a more permanent cure as well as effective methods of preventing initial peptic ulceration, as occurrence is linked to an increased risk of developing gastric carcinomas.
Gastritis is a common disorder of stomach. In gastritis, lining of stomach gets inflamed Or eroded. It is commonly caused by Helicobacter Pylori and use of non steroidal anti-inflammatory drugs. Radiation therapy, smoking, autoimmune problems, alcohol, crohn disease and cocaine are its less common causes. The person suffering from gastritis is presented with abdominal pain, vomiting, nausea, heartburn and loss of appetite. People having gastritis are more likely to have any anxiety disorder.
Even though more people are getting treated, there are MORE cases of GERD, NOT LESS! Stomach acid is a critical component of good digestion. If you suffer from low stomach acid or take drugs that suppress your stomach acid, you would be contributing to the development of digestion issues such as GERD. The stomach acid needs to be around a PH of 3. This prevents an overgrowth of bacteria. If your stomach acid becomes too weak and alkaline, bacteria can begin to thrive and take over.
Some common disorders associated with gastric acid secretion are gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and gastritis. For example, in gastroesophageal reflux disease, high gastric contents enter and remain in the lower part of the esophagus due to weakened esophageal sphincter, abdominal pressure, hiatal hernia, alcohol consumption or cigarettes smoking. Usually, the lower esophageal sphincter maintains enough pressure around the lower end of the esophagus to close it and prevent reflux (McPhee and Hammer, 2012). Sometimes the pressure in the stomach exceeds the pressure in the esophagus, causes the sphincter to open and gastric contents penetrate the esophagus which cause pain and irritation. Peptic ulcer diseases (PUD) and gastritis disorders, however; are primarily caused by bacterial infection with helicobacter pylori and acid secretions also play a major role (McPhee and Hammer, 2012). Direct alteration of signal transduction in mucosal and immune cells by H pylori infection may cause an increase in acid secretion and diminish mucosal defenses (McPhee and Hammer,
The discovery of H. pylori by Warren and Marshall in 1983 has changed the concept of gastro duodenal ulcer disease [67]. Studies over the past suggest a strong relation of H.pylori to peptic ulcers [68]. Infection with H. pylori results in certain series of events, ultimately resulting in the development of gastric diseases. The initial acute gastritis is followed by atrophy, intestinal metaplasia and dysplasia that can lead to carcinoma of gastric mucosa. Almost all individuals infected with H. pylori develop gastritis. This series of events was first time suggested by Correa et al. and has since been supported by many other studies [18].
N: Gastric ulcer is the painful sores that are found inside the lining of the stomach. It can be caused by H.pylori or medications (ASA, NSAIDs, biphosphonates). Lifestyle such as smoke, alcohol and spicy foods can increase the risk of gastric acid development. Symptoms of gastric ulcer are stomach pain, nausea, bloating, feeling fullness and/or heartburn. If it is left untreated, it can develop to gastric bleeding, severe
A question of bias also arises when considering that Gyte, an author of this review, published research in 2006 regarding the efficacy of pharmaceuticals to manage gastric regurgitation, with data from the study being used to collaborate this review (Gyte, & Richens, 2006).
reflux events in turn may aggravate apnoeic episodes and increase its severity.11,17 Valipour et al. found that 70% of
Sample size: n = 244, age 40-69, living in the region that has the highest mortality rate of gastric cancer, no history of gastric cancer or gastric surgery or liver cancer or cirrhosis or other cancer within 5 years before the research, no abnormal liver function, no β-carotene or vitamin C supplementation, living in the study area for one year during the research,