See amoxicillin.
Causes It is likely that there is some abrasion, or break, in the lining membrane (or mucosa) of the stomach and/or duodenum, and that it is gradually eroded and deepened by the acidic gastric juice. The bacterium helicobacter pylori is present in the antrum of the stomach of people with peptic ulcers; 15 per cent of people infected with the bacterium develop an ulcer, and the ulcers heal if H. pylori is eradicated. Thus, this organism has an important role in creating ulcers. Mental stress may possibly be a provocative factor. Smoking seems to accentuate, if not cause, duodenal ulcer, and the drinking of alcohol is probably harmful. The apparent association with a given blood group, and the fact that relatives of a patient with a peptic ulcer are unduly likely to develop such an ulcer, suggest that there is some constitutional factor.
Symptoms and signs Peptic ulcers may present in di?erent ways, but chronic, episodic pain lasting several months or years is most common. Occasionally, however, there may be an acute episode of bleeding or perforation, or obstruction of the gastric outlet, with little previous history. Most commonly there is pain of varying intensity in the middle or upper right part of the abdomen. It tends to occur 2–3 hours after a meal, most commonly at night, and is relieved by some food such as a glass of milk; untreated it may last up to an hour. Vomiting is unusual, but there is often tenderness and sti?ness (‘guarding’) of the abdominal muscles. Con?rmation of the diagnosis is made by radiological examination (‘barium meal’), the ulcer appearing as a niche on the ?lm, or by looking at the ulcer directly with an endoscope (see FIBREOPTIC ENDOSCOPY). Chief complications are perforation of the ulcer, leading to the vomiting of blood, or HAEMATEMESIS; or less severe bleeding from the ulcer, the blood passing down the gut, resulting in dark, tarry stools (see MELAENA).
Treatment of a perforation involves initial management of any complications, such as shock, haemorrhage, perforation, or gastric outlet obstruction, usually involving surgery and blood replacement. Medical treatment of a chronic ulcer should include regular meals, and the avoidance of fatty foods, strong tea or co?ee and alcohol. Patients should also stop smoking and try to reduce the stress in their lives. ANTACIDS may provide symptomatic relief. However, the mainstay of treatment involves four- to six-week courses with drugs such as CIMETIDINE and RANITIDINE. These are H2 RECEPTOR ANTAGONISTS which heal peptic ulcers by reducing gastric-acid output. Of those relapsing after stopping this treatment, 60–95 per cent have infection with H. pylori. A combination of BISMUTH chelate, amoxycillin (see PENICILLIN; ANTIBIOTICS) and METRONIDAZOLE – ‘triple regime’ – should eliminate the infection: most physicians advise the triple regime as ?rst-choice treatment because it is more likely to eradicate Helicobacter and this, in turn, enhances healing of the ulcer or prevents recurrence. Surgery may be necessary if medical measures fail, but its use is much rarer than before e?ective medical treatments were developed.... duodenal ulcer
Acute gastritis is an in?ammatory reaction of the gastric mucosa to various precipitating factors, ranging from physical and chemical injury to infections. Acute gastritis (especially of the antral mucosas) may well represent a reaction to infection by a bacterium called Helicobacter pylori. The in?ammatory changes usually go after appropriate antibiotic treatment for the H. pylori infection. Acute and chronic in?ammation occurs in response to chemical damage of the gastric mucosa. For example, REFLUX of duodenal contents may predispose to in?ammatory acute and chronic gastritis. Similarly, multiple small erosions or single or multiple ulcers have resulted from consumption of chemicals, especialy aspirin and antirheumatic NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS).
Acute gastritis may cause anorexia, nausea, upper abdominal pain and, if erosive, haemorrhage. Treatment involves removal of the o?ending cause.
Chronic gastritis Accumulation of cells called round cells in the gastric mucosal characterises chronic gastritis. Most patients with chronic gastritis have no symptoms, and treatment of H. pylori infection usually cures the condition.
Atrophic gastritis A few patients with chronic gastritis may develop atrophic gastritis. With or without in?ammatory change, this disorder is common in western countries. The incidence increases with age, and more than 50 per cent of people over 50 may have it. A more complete and uniform type of ATROPHY, called ‘gastric atrophy’, characterises a familial disease called PERNICIOUS ANAEMIA. The cause of the latter disease is not known but it may be an autoimmune disorder.
Since atrophy of the corpus mucosa results in loss of acid- and pepsin-secreting cells, gastric secretion is reduced or absent. Patients with pernicious anaemia or severe atrophic gastritis of the corpus mucosa may secrete too little intrinsic factor for absorption of vitamin B12 and so can develop severe neurological disease (subacute combined degeneration of the spinal cord).
Patients with atrophic gastritis often have bacterial colonisation of the upper alimentary tract, with increased concentration of nitrite and carcinogenic N-nitroso compounds. These, coupled with excess growth of mucosal cells, may be linked to cancer. In chronic corpus gastritis, the risk of gastric cancer is about 3–4 times that of the general population.
Postgastrectomy mucosa The mucosa of the gastric remnant after surgical removal of the distal part of the stomach is usually in?amed and atrophic, and is also premalignant, with the risk of gastric cancer being very much greater than for patients with duodenal ulcer who have not had surgery.
Stress gastritis Acute stress gastritis develops, sometimes within hours, in individuals who have undergone severe physical trauma, BURNS (Curling ulcers), severe SEPSIS or major diseases such as heart attacks, strokes, intracranial trauma or operations (Cushing’s ulcers). The disorder presents with multiple super?cial erosions or ulcers of the gastric mucosa, with HAEMATEMESIS and MELAENA and sometimes with perforation when the acute ulcers erode through the stomach wall. Treatment involves inhibition of gastric secretion with intravenous infusion of an H2-receptorantagonist drug such as RANITIDINE or FAMOTIDINE, so that the gastric contents remain at a near neutral pH. Despite treatment, a few patients continue to bleed and may then require radical gastric surgery.
Gastric ulcer Gastric ulcers were common in young women during the 19th century, markedly fell in frequency in many western countries during the ?rst half of the 20th century, but remained common in coastal northern Norway, Japan, in young Australian women, and in some Andean populations. During the latter half of this century, gastric ulcers have again become more frequent in the West, with a peak incidence between 55 and 65 years.
The cause is not known. The two factors most strongly associated with the development of duodenal ulcers – gastric-acid production and gastric infection with H. pylori bacteria – are not nearly as strongly associated with gastric ulcers. The latter occur with increased frequency in individuals who take aspirin or NSAIDs. In healthy individuals who take NSAIDs, as many as 6 per cent develop a gastric ulcer during the ?rst week of treatment, while in patients with rheumatoid arthritis who are being treated long term with drugs, gastric ulcers occur in 20–40 per cent. The cause is inhibition of the enzyme cyclo-oxygenase, which in turn inhibits the production of repair-promoting PROSTAGLANDINS.
Gastric ulcers occur especially on the lesser curve of the stomach. The ulcers may erode through the whole thickness of the gastric wall, perforating into the peritoneal cavity or penetrating into liver, pancreas or colon.
Gastric ulcers usually present with a history of epigastric pain of less than one year. The pain tends to be associated with anorexia and may be aggravated by food, although patients with ‘prepyloric’ ulcers may obtain relief from eating or taking antacid preparations. Patients with gastric ulcers also complain of nausea and vomiting, and lose weight.
The principal complications of gastric ulcer are haemorrhage from arterial erosion, or perforation into the peritoneal cavity resulting in PERITONITIS, abscess or ?stula.
Aproximately one in two gastric ulcers heal ‘spontaneously’ in 2–3 months; however, up to 80 per cent of the patients relapse within 12 months. Repeated recurrence and rehealing results in scar tissue around the ulcer; this may cause a circumferential narrowing – a condition called ‘hour-glass stomach’.
The diagnosis of gastric ulcer is con?rmed by ENDOSCOPY. All patients with gastric ulcers should have multiple biopsies (see BIOPSY) to exclude the presence of malignant cells. Even after healing, gastric ulcers should be endoscopically monitored for a year.
Treatment of gastric ulcers is relatively simple: a course of one of the H2 RECEPTOR ANTAGONISTS heals gastric ulcers in 3 months. In patients who relapse, long-term inde?nite treatment with an H2 receptor antagonist such as ranitidine may be necessary since the ulcers tend to recur. Recently it has been claimed that gastric ulcers can be healed with a combination of a bismuth salt or a gastric secretory inhibitor
for example, one of the PROTON PUMP INHIBITORS such as omeprazole or lansoprazole
together with two antibiotics such as AMOXYCILLIN and METRONIDAZOLE. The long-term outcome of such treatment is not known. Partial gastrectomy, which used to be a regular treatment for gastric ulcers, is now much more rarely done unless the ulcer(s) contain precancerous cells.
Cancer of the stomach Cancer of the stomach is common and dangerous and, worldwide, accounts for approximately one in six of all deaths from cancer. There are marked geographical di?erences in frequency, with a very high incidence in Japan and low incidence in the USA. In the United Kingdom around 33 cases per 100,000 population are diagnosed annually. Studies have shown that environmental factors, rather than hereditary ones, are mainly responsible for the development of gastric cancer. Diet, including highly salted, pickled and smoked foods, and high concentrations of nitrate in food and drinking water, may well be responsible for the environmental effects.
Most gastric ulcers arise in abnormal gastric mucosa. The three mucosal disorders which especially predispose to gastric cancer include pernicious anaemia, postgastrectomy mucosa, and atrophic gastritis (see above). Around 90 per cent of gastric cancers have the microscopic appearance of abnormal mucosal cells (and are called ‘adenocarcinomas’). Most of the remainder look like endocrine cells of lymphoid tissue, although tumours with mixed microscopic appearance are common.
Early gastric cancer may be symptomless and, in countries like Japan with a high frequency of the disease, is often diagnosed during routine screening of the population. In more advanced cancers, upper abdominal pain, loss of appetite and loss of weight occur. Many present with obstructive symptoms, such as vomiting (when the pylorus is obstructed) or di?culty with swallowing. METASTASIS is obvious in up to two-thirds of patients and its presence contraindicates surgical cure. The diagnosis is made by endoscopic examination of the stomach and biopsy of abnormal-looking areas of mucosa. Treatment is surgical, often with additional chemotherapy and radiotherapy.... stomach, diseases of
Shigellosis This form is usually caused by Shigella dysenteriae-1 (Shiga’s bacillus), Shigella ?exneri, Shigella boydii, and Shigella sonnei; the latter is the most benign and occurs in temperate climates also. It is transmitted by food and water contamination, by direct contact, and by ?ies; the organisms thrive in the presence of overcrowding and insanitary conditions. The incubation is between one and seven days, and the severity of the illness depends on the strain responsible. Duration of illness varies from a few days to two weeks and can be particularly severe in young, old, and malnourished individuals. Complications include perforation and haemorrhage from the colo-rectum, the haemolytic uraemic syndrome (which includes renal failure), and REITER’S SYNDROME. Diagnosis is dependent on demonstration of Shigella in (a) faecal sample(s) – before or usually after culture.
If dehydration is present, this should be treated accordingly, usually with an oral rehydration technique. Shigella is eradicated by antibiotics such as trimethoprimsulphamethoxazole, trimethoprim, ampicillin, and amoxycillin. Recently, a widespread resistance to many antibiotics has developed, especially in Asia and southern America, where the agent of choice is now a quinolone compound, for example, cipro?oxacin; nalidixic acid is also e?ective. Prevention depends on improved hygiene and sanitation, careful protection of food from ?ies, ?y destruction, and garbage disposal. A Shigella carrier must not be allowed to handle food.
Entamoeba histolytica infection Most cases occur in the tropics and subtropics. Dysentery may be accompanied by weight loss, anaemia, and occasionally DYSPNOEA. E. histolytica contaminates food (e.g. uncooked vegetables) or drinking water. After ingestion of the cyst-stage, and following the action of digestive enzymes, the motile trophozoite emerges in the colon causing local invasive disease (amoebic colitis). On entering the portal system, these organisms may gain access to the liver, causing invasive hepatic disease (amoebic liver ‘abscess’). Other sites of ‘abscess’ formation include the lungs (usually right) and brain. In the colo-rectum an amoeboma may be di?cult to di?erentiate from a carcinoma. Clinical symptoms usually occur within a week, but can be delayed for months, or even years; onset may be acute – as for Shigella spp. infection. Perforation, colo-rectal haemorrhage, and appendicitis are unusual complications. Diagnosis is by demonstration of E. histolytica trophozoites in a fresh faecal sample; other amoebae affecting humans do not invade tissues. Research techniques can be used to di?erentiate between pathogenic (E. dysenteriae) and non-pathogenic strains (E. dispar). Alternatively, several serological tests are of value in diagnosis, but only in the presence of invasive disease.
Treatment consists of one of the 5nitroimidazole compounds – metronidazole, tinidazole, and ornidazole; alcohol avoidance is important during their administration. A ?ve- to ten-day course should be followed by diloxanide furoate for ten days. Other compounds – emetine, chloroquine, iodoquinol, and paromomycin – are now rarely used. Invasive disease involving the liver or other organ(s) usually responds favourably to a similar regimen; aspiration of a liver ‘abscess’ is now rarely indicated, as controlled trials have indicated a similar resolution rate whether this technique is used or not, provided a 5-nitroimidazole compound is administered.... dysentery
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