What are the symptoms of a stomach ulcer? How can they be cured? What foods should be avoided?

Answer 1

Stomach ulcers are caused by bacteria. Go to your doctor and cure it now instead of wasting time and money on Tums and other crap.

http://www.netdoctor.co.uk/diseases/facts/pepticulcer.htm

http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Stomach_ulcer?OpenDocument

http://news.bbc.co.uk/2/hi/health/4304290.stm

Answer 2

Hi! Well, it looks like the former answers have already gone into what an ulcer is. Of course, avoid spicy foods and foods that irritate your stomach in particular. You should avoid mints as well if you get reflux with it, as mints can prolong it.
Licorice root is a specific for curing ulcers, and I use it in combination with Marshmallow root which is also wonderfully soothing. However, if you have heart issues as well, take Cinnamon instead in combination with the Marshmallow and avoid the Licorice root. I am at windstarhealing.com if you have any questions! Have a great day.

Answer 3

Symptoms of a peptic ulcer can be:

Abdominal pain, classically epigastric with severity relating to mealtimes (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
Bloating and abdominal fullness
Waterbrash (bitter regurgitation)
Nausea, and sometimes vomiting
Loss of appetite and weight loss;
Hematemesis (vomiting of blood);
Melena (tarry, foul-smelling feces due to oxidised iron from hemoglobin);
Rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.
A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than 2 weeks of the above symptoms the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest mostly before the meal — when acid (production stimulated by hunger) is passed into the duodenum.

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Stress and ulcers
Despite the finding that a viral infection is the proximate cause of ulcers in 75% of cases, support for the theory that stress causes ulcers has not disappeared.

The experts looked over the evidence and concluded that ulcers are not merely an infectious disease and that psychological factors do play a significant role. [2]
One researcher said,

Having a positive attitude seems to correlate with an increased ability of the immune system in fighting diseases.[3]
According to research physician Susan Levenstein,

I have a suspicion that one reason the medical establishment wiped stress off the charts so fast was that it didn't feel comfortable with psychological explanations. They were happier when they could label ulcers as an infectious disease. It's easy to fall into either-or thinking: either ulcers are caused by stress or they're caused by Helicobacter. The truth is much more complicated and, I think, more exciting. Since peptic ulcer is one of the few 'infectious' diseases in which stress plays an important role, it gives us a great model for understanding how psychological factors can tip the balance toward disease, in the uneasy equilibrium we all live in with a whole variety of infectious agents. [4]
The discovery that Helicobacter pylori is a cause of peptic ulcer has tempted many to conclude that psychological factors are unimportant. But this is dichotomised thinking. There is solid evidence that psychological stress triggers many ulcers and impairs response to treatment, while helicobacter is inadequate as a monocausal explanation as most infected people do not develop ulcers. Psychological stress probably functions most often as a cofactor with H pylori. It may act by stimulating the production of gastric acid or by promoting behaviour that causes a risk to health. Unravelling the aetiology of peptic ulcer will make an important contribution to the biopsychosocial model of disease. [5]
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Pathophysiology
Tobacco smoking, blood group, spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.[1]

A major causative factor (75% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori, a spirochaete that colonizes (i.e. settles there after entering the body) the antral mucosa. The immune system is unable to clear the infection[2], despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion is increased. Gastrin, in turn, stimulates the production of gastric acid by parietal cells. The acids erodes the mucosa and causes the ulcer.

Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucous, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. Newer NSAIDs (celecoxib, rofecoxib) only inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

Glucocorticoids lead to atrophy of all epithelial tissues. Their role in ulcerogenesis is relatively small.

Stress in the psychological sense has not been proven to influence the development of peptic ulcers.[3] Burns and head trauma, however, can lead to "stress ulcers", and it is reported in many patients who are on mechanical ventilation.

Smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia.

A family history is often present in duodenal ulcers, especially when blood group O is also present. Inheritance appears to be unimportant in gastric ulcers.

Gastrinomas (Zollinger Ellison syndrome), rare gastrin secreting tumors, cause multiple and difficult to heal ulcers.

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Diagnosis
In patients in whom peptic ulcer is suspected, the correct test is esophagogastroduodenoscopy (EGD), a form of endoscopy, sometimes known as just gastroscopy. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

The diagnosis of Helicobacter pylori can be by:

Biopsy during EGD;
Breath testing (does not require EGD);
Direct culture from an EGD biopsy specimen;
Direct detection of urease activity in a biopsy specimen;
Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy.
The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the greater (large) curvature of the stomach; most are also a consequence of chronic H. pylori infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

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Macroscopical appearance
Gastric ulcer is most often localized on the lesser curvature of the stomach. It is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irreguliar as in gastric cancer - ulcerative form. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.

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Microscopical appearance
Gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. 1

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Treatment
Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even clear organisms.

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Erythromycin, Ampicillin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI). An effective combination would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of Helicobacter usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. And most bleeding ulcers require endoscopy urgently to stop bleeding with cautery or injection.

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Epidemiology
In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third world countries. Transmission is by food and human contact, sharing food utensils etc.

A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort, abdominal pain or gastritis.

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History
In 1997, the Centers for Disease Control and Prevention, with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. This campaign reinforced the news that ulcers are a curable infection, and the fact that health can be greatly improved and money saved by disseminating information about H. pylori.[4]

Helicobacter pylori was rediscovered in 1982 by two Australian scientists Robin Warren and Barry Marshall[5]. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food as had been assumed before[6].

John Lykoudis was a general practitioner in Greece who treated patients from peptic ulcer disease with antibiotics long before it was commonly recognized that bacteria were a dominant cause for the disease[7].

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References
^ For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids. National Digestive Diseases Information Clearinghouse
^ Blaser MJ, Atherton JC. Helicobacter pylori persistence: biology and disease. J Clin Invest 2004; 113: 321-33. Full text at PMC: 14755326
^ The majority of peptic ulcers are caused by the H. pylori bacterium. Many of the other cases are caused by NSAIDs. None are caused by spicy food or stress. [1]
^ Ulcer, Diagnosis and Treatment - CDC Bacterial, Mycotic Diseases
^ Marshall BJ (1983). "Unidentified curved bacillus on gastric epithelium in active chronic gastritis". Lancet 1 (8336): 1273–1275. PMID 6134060.
^ Marshall BJ, Warren JR (1984). "Unidentified curved bacilli in the stomach patients with gastritis and peptic ulceration". Lancet 1 (8390): 1311–1315. PMID 6145023.
^ Basil Rigas, Efstathios D. Papavasassiliou. John Lykoudis. The general parctitioner in Greece who in 1958 discovered the etiology of, and a treatment for, peptic ulcer disease. in Barry Marshall (editor), Helicobacter Pioneers. Firsthand accounts from the scientists who discovered helicobacters, 1892-1982, 2002, ISBN 0867930357