A stomach ulcer refers to an lesion in the inner lining of the stomach and the adjoining intestinal tract called the duodenum. The ulcer located in the stomach is known as a gastric ulcer, and that located in the duodenum is called a duodenal ulcer. Usually, both are grouped together and termed as stomach ulcer.
The stomach is an organ of the digestive system, located in the abdomen just below the ribs and on the left. Swallowed food is squeezed down the oesophagus and pushed through a sphincter (small muscle ring) into the stomach, where it is mixed with powerful gastric juices containing enzymes and hydrochloric acid. The stomach is a muscular bag, so it can churn the food and break it down mechanically as well as chemically. Once the food is the consistency of smooth paste, it is squeezed through a second sphincter into the first part of the small intestine (duodenum). The lining of the stomach – the mucosa or gastric epithelium – is layered with multiple folds. Ulcers occur in this lining.(as in the above picture)
A stomach ulcer or Gastric ulcer is a break in the tissue lining the stomach. The term ‘peptic ulcer’ refers to those that occur in either the stomach or the first part of the small intestine that leads out of the stomach, called the duodenum. It was once commonly thought that stress, smoking and diet were the principal causes of stomach ulcers. However, the Helicobacter pylori (H. pylori) bacterium is now known to be responsible for most duodenal ulcers and 60 per cent of stomach ulcers. The H. pylori bacterium also prompts many symptoms of dyspepsia, or indigestion. Treatment for stomach ulcers includes the use of antibiotics to kill the infection, and acid-suppressing drugs.
Some stomach ulcers are asymptomatic. The symptoms of a stomach ulcer can include:
Abdominal pain just below the ribcage
Loss of appetite
Altered blood present in the vomit or in the bowel motions (occasionally)
Symptoms of anaemia, such as light-headedness.
A variety of causes:
A stomach ulcer can be caused by a variety of factors, including:
*Helicobacter pylori – these bacteria is thought to be responsible for around 60 per cent of stomach ulcers and at least 90 per cent of duodenal ulcers.
Certain medications – including aspirin, taken regularly to help prevent heart attack or stroke, and drugs for arthritis. Anti-inflammatory medications (NSAIDS) are thought to cause around two fifths of stomach ulcers.
*Cancer – stomach cancer can present as an ulcer, particularly in older people.
Helicobacter pylori…..click & see
The Helicobacter pylori bacterium (H. pylori) is the main cause of peptic ulcers. The discovery of this micro-organism in 1983 revolutionised many aspects of gastroenterology, including the treatment of stomach ulcers. It is thought that about one in three people over the age of 40 years are infected with this strain of bacteria in Australia. The germs live in the lining of the stomach, and the chemicals they produce cause irritation and inflammation. H. pylori directly causes one third of stomach ulcers, and is a contributing factor in around three fifths of cases. Other disorders caused by this infection include inflammation of the stomach (gastritis) and dyspepsia (indigestion). Researchers believe the germ could also play a contributing role in the development of stomach cancers. The infection is more common among poor or institutionalised people. The mode of transmission is so far unknown, but is thought to include sharing food or utensils, coming into contact with infected vomit, and sharing of water (such as well water) in undeveloped populations.
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.
A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes (i.e. settles there after entering the body) the antral mucosa. The immune system is unable to clear the infection, 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 acid 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.
There is debate as to whether Stress in the psychological sense can influence the development of peptic ulcers (see Stress and ulcers). 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.
Overuse of Laxatives are also known to cause peptic ulcers.
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.
Stress and ulcers:
Despite the finding that a bacterial infection is the cause of ulcers in more than 75% of cases, bacterial infection does not appear to explain all ulcers and researchers continue to look at stress as a possible cause, or at least a complication in the development of ulcers.
An expert panel convened by the Academy of Behavioral Medicine research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role. Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid.
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 behavior that causes a risk to health. Unravelling the aetiology of peptic ulcer will make an important contribution to the biopsychosocial model of disease.
A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor .
A study on mice showed that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers
*Perforated ulcer (anterior. Surface) with sudden onset of the pain, a chemical peritonitis followed by bacterial peritonitis.
*Posterior penetration (posterior. Surface), maybe to pancreas=>increased amylase-pain=>radiating to back, unrelated to meals.
*Hemorrhage (post. Surface), bleeding from Gasteroduodenal artery.
*Gastric Outlet Obstruction (Goo) which happens usually because of edema or scarring, most often occurs in the setting of duodenal or pyloric channel ulcers.
*A severe, untreated ulcer can sometimes burn through the wall of the stomach, allowing digestive juices and food to leech into the abdominal cavity. This medical emergency is known as a perforated ulcer. Treatment generally requires immediate surgery.
Diagnosing a stomach ulcer is done using a range of methods, including:-
*Endoscopy – a thin flexible tube is threaded down the oesophagus into the stomach under light anaesthesia. The endoscope is fitted with a small camera so the physician can see if there is an ulcer.
*Barium meal – a chalky liquid is drunk and an x-ray is performed, showing the stomach lining. These tests are less common nowadays, but may be useful where endoscopy is unavailable.
*Biopsy – a small tissue sample is taken during an endoscopy and tested in a laboratory. This biopsy should always be done if a gastric ulcer is found.
*C14 breath test – to check for the presence of H. pylori. The bacteria convert urea into carbon dioxide. The test involves swallowing an amount of radioactive carbon (C14) and testing the air exhaled from the lungs. A non-radioactive test can be used for children and pregnant women.
*An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. 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:
*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.
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.
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
Modern Treatment options:
Special diets are now known to have very little impact on the prevention or treatment of stomach ulcers. Treatment options can include:
Medications – including antibiotics, to destroy the H. pylori colony, and drugs to help speed the healing process. Different drugs need to be used in combination; some of the side effects can include diarrhoea and rashes. Resistance to some of these antibiotics is becoming more common.
Subsequent breath tests – used to make sure the H. pylori infection has been treated successfully.
Changes to existing medications – the doses of arthritis medications, aspirin or other anti-inflammatory drugs can be altered slightly to reduce their contributing effects on the stomach ulcer.
Reducing acid – tablets are available to reduce the acid content in the gastric juices.
In Ayurveda it is a disease of tri-doshic nature i.e. Vata, Pitta, Kapha. But aggravation of pitta is noted in all cases.
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Diet: Since hyperacidity is the villain of the piece which ultimately leads to stomach ulcers, the first step is to withhold all foods which aggravate the condition. Fried food and spices, specially chillies, should be totally prohibited. Milk should be freely taken, at intervals of 3 to 4 hours during a day, because the pain of the ulcer occurs at times when the stomach is empty. Milk, wheat, and ghee should be taken in adequate quantities.
Lifestyle modifications – such as quitting cigarettes, since smoking reduces the natural defences in the stomach and impairs the healing process.: In addition to the above, the patient must be advised to keep himself free from worry and stresses of life which are likely to exacerbate the ulcer pain. He must take sufficient rest and sleep for an hour or so during the day. His below movement must be ensured because constipation can only contribute to worsening of the condition.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.