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Peptic ulcers are open sores or raw areas in the lining of the stomach (gastric ulcer) or upper part of the small intestine (duodenal ulcer). They result when the bacterium, Helicobacter pylori attaches itself to the lining of the stomach. Another cause of peptic ulcers are nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. The bacteria or NSAIDs weaken the protective mucus coating of the stomach and small intestines.
This process allows acid to get through to the sensitive lining. The irritation from the drugs or bacteria can cause the sensitive lining to become raw, which causes an ulcer to form. Peptic ulcers can also form when there is an imbalance between the digestive juices used by the stomach to break down food. The primary digestive juices, hydrochloric acid and pepsin, are very powerful substances that are necessary for breaking down food, which the body uses for energy. These acids are always present in the stomach in small amounts, except at meal times.
Incidence About 25 million people in the United States have had a peptic ulcer during their lifetime. At least 90 % of these cases are caused by H. pylori (Sonnenberg, 359). Patients who have duodenal ulcers are between the ages of 25 and 27. Gastric ulcers are less common with only 85, 000 cases diagnosed each year (Zone, 14). The patients who suffer from gastric ulcers are between the ages of 55 and 65.
Men are more prone to ulcers, but there has been a steady increase of women being diagnosed each year. Because the ulcer is caused predominantly by the H. pylori bacteria, those living in underdeveloped countries and those with low socioeconomic status are more likely to develop ulcers. H. pylori is believed to be transmitted through oral to oral contact, so those living in crowed areas are also more likely to become infected. History of Ulcer Diagnosis and Treatment Early 20 th Century Ulcers were believed to be caused mainly by stress and diet.
Treatment focused on primarily hospitalization, bed rest, and a diet of bland foods. Later on in the century, cause of the ulcer changed from stress and diet to gastric acid. The treatment then was a prescription for antacids and medications that blocked acid production. Even with treatment, there was a high recurrence rate. 1982 Robin Warren and Barry Marshall, Australian physicians, were the first to link H.
pylori to ulcers. This concluded that this bacterium was the cause of ulcers and not diet or stress (Munnangi, 1490). 1994 National Institutes of Health Consensus Development Conference concludes that there is a strong association between H. pylori and peptic ulcers. They recommended that patients with ulcers should be treated with antibiotics. 1995 Data show that about 75 percent of ulcer patients are still treated primarily with anti secretory medications, and only 5 percent receive antibiotic therapy. Consumer research by the American Digestive Health Foundation finds that nearly 90 percent of ulcer sufferers are unaware that H. pylori causes ulcers.
In fact, nearly 90 percent of those with ulcers blame their ulcers on stress or worry, and 60 percent point to diet (H. pylori in Peptic Ulcer Disease, 67). Pathophysiology In the stomach Pepsinogen, which is the precursor of pepsin, is activated to pepsin when there is hydrochloric acid present and the pH is in a range of 2 to 3. This pH is a highly favorable range of acidity for pepsin activity. Gastric ulcers only develop in the presence of an acid environment, however a large amount of gastric acid may not be present for an ulcer to develop. A person with a gastric ulcer normally has a regular level and even possibly even a lesser amount of gastric acidity compared to a person with a duodenal ulcer.
Some acid is necessary for an ulcer to erupt. In a normal stomach, the walls are protected from auto digestion by the gastric mucosal barrier. The mucosal barrier prevents the back diffusion of acid from the gastric lumen through the mucosal layers to the underlying tissue. The GI tract has an extreme cell turnover rate and the surface of the stomach is replace about every three days. Because of this, the mucosa is constantly repairing itself except when the cell breakdown is higher than the restoration rate. If the mucosal barrier becomes impaired, back-diffusion of the acid occurs and this causes the barrier to break.
With the breakage of the mucosal barrier, HCL acid can freely enter the mucosa and cause injuries to the tissue, which results in cellular destruction and inflammation. This causes the release of histamine. Histamines cause vasodilatation and an increase in capillary permeability, which then stimulates an even greater secretion of acid and pepsin. What Disrupts the Mucosal Barrier H. pylori is the number one cause of gastric ulcers. This bacterium causes a condition of chronic inflammation, which renders the mucosa.
Also, NSAIDs, such as aspirin, inhibit the production of mucus and prostaglandins, which results in a dysfunctional permeability. Corticosteriods also reduce the rate of mucous cell renewal. Lipid-soluble cytotoxic drugs are able to pass through the barrier and thereby destroy it. After the disruption of the mucosal barrier, there is an increase in blood flow. The increase in blood flow is due to the prostaglandin and histamines acting as vasodilators.
As the flow increases in the affected mucosa, hydrogen ions are removed from the area, and then buffers are sent to try and neutralize the hydrogen ions that are still present. With the help of nutrients the rate of mucosal cell reproduction is increased. If this process cannot be carried out and blood flow is not increased, ulcers result. Another factor that can disrupt the mucosal barrier is hyper secretion of HCL acid. Stress causes an increased stimulation of the vagal nerve, which signals secretion of HCL acid.
Duodenal ulcers are the result of increased acid content where as gastric ulcers are a result of H. pylori or over use of NSAIDs. Gastric Ulcers Gastric ulcers can form in any part of the stomach. The most common site is the lesser curvature, close to the antral junction. The lesions of a gastric ulcer are superficial with smooth margins and are round, oval or cone-shaped. The primary cause of gastric ulcers is H.
pylori. This bacterium secretes urease, which buffers the area around the bacteria and protects it from destruction due to the acidic environment of the stomach. In cases of gastric ulcers, there is a normal or even a decrease in the amount of acid secretions. Duodenal Ulcers Duodenal ulcers are formed the same way gastric ulcers are, mainly by a H. pylori infection. Duodenal ulcers, however, are located mainly in the first 1 - 2 centimeters of the duodenum.
These ulcers are penetrating. Duodenal ulcers account for 80 % of all ulcers (Lewis, 1112). In cases of duodenal ulcers, there is a greater amount of hydrochloric acid secretion. Causes of Peptic Ulcers Helicobacter pylori (H.
pylori) H. pylori is the number one cause of peptic ulcers. Before the discovery of H. pylori, the stomach was thought to be a sterile environment. H.
pylori is able to penetrate the mucous membrane of the stomach and attach itself there. This causes the immune system to allow it to survive for a persons entire life. It lives off the acid in the stomach by producing the enzyme urease, which generates ammonia. The ammonia then neutralizes the acid and ensures the survival of the bacteria. H. pylori, however produces a number of toxins that cause the inflammation and damage to the sensitive lining of the stomach and small intestine.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Using NSAIDs for a long period of time is the second highest cause of peptic ulcers. NSAIDs include aspirin, ibuprofen, and naproxen. These drugs reduce pain and inflammation by blocking the enzyme cyclooxygenase, which is involved in the production of prostaglandins. Since NSAIDs reduce prostaglandins they impair the defense system to the intestine and increase the danger of damaging the mucous layer, which causes ulcers. Some NSAIDs can even be injected intravenously, but they still reach the stomach at one point through the bloodstream.
Ulcers form if an NSAID is taken for a long period of time. Zollinger-Ellison Syndrome This is the least common cause of peptic ulcers. This is a tumor in the pancreas that produces excessive amounts of gastrin. Gastrin is a hormone that stimulates gastric acid formation. The excessive production of gastric acid leads to the irritation of the mucous lining, and eventually an ulcer will form. Other Causes Other conditions such as alcohol abuse, stress, and smoking may cause ulceration to the lining of the stomach or intestine.
These practices are thought to cause ulcers because they cause irritation to the GI mucosa. Genetics also may play a role in the development of ulcers. This is because of the increased vulnerability to H. pylori within close living quarters.
Symptoms of Peptic Ulcers It is quite common for people with peptic ulcers to have no pain or even show signs of symptoms (Medinfo, 1). When there is pain, a duodenal ulcer is described as a burning or a hunger feeling located in a small area between the breastbone and navel. The pain may even be felt during sleep and become intense enough to awaken the person in the middle of the night (Peptic Ulcers, 1). These pains usually occur spontaneously and about one to two hours after eating or when the stomach is empty and sometimes even right after eating. Food can even aggravate the ulcer more if it has eroded through the gastric mucosa. Gastric ulcer pain may occur in the same place or slightly higher up (Peptic Ulcers, 1).
The sensation may even be that of feeling full, indigestion...
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