Diseases of The Stomach and Duodenum
Gastritis
:Type A gastritis
This is an autoimmune condition in which there are circulating antibodies to the parietal cell. This results in the atrophy of the parietal cell mass, resulting in hypochlorhydria and ultimately achlorhydria. As intrinsic factor is also produced by the parietal cell there is malabsorption of vitamin B12, which, if untreated, may result in pernicious anaemia . Patients with type A gastritis are predisposed to the development of gastric cancer, and screening such patients endoscopically may be appropriate.
Type B gastritis : It is associationed with H. pylori infection. Most commonly, type B gastritis affects the antrum, causing peptic ulcer disease. Helicobacter-associated pangastritis is also a very common manifestation of infection. Patients with pangastritis seem to be most prone to the development of Intestinal metaplasia and gastric cancer
Intestinal metaplasia associated with dysplasia has significant malignant potential and, if this condition is identified, endoscopic screening may be appropriate.
Reflux gastritis
This is caused by enterogastric reflux and is particularly common after gastric surgery. Its histological features are distinct from those of other types of gastritis. Although commonly seen after gastric surgery, it is occasionally found in patients with no previous surgical intervention..
Bile-chelating or prokinetic agents may be useful in treatment and as a temporising measure to avoid the consideration of revisional surgery. Operation for this condition should be reserved for the most severe cases.
Erosive gastritis
This is caused by agents that disturb the gastric mucosal barrier; NSAIDs and alcohol are common causes. The NSAID-induced gastric lesion is associated with reduction of the production of cytoprotective prostaglandins in the stomach.
Stress gastritis
This is a common sequel of serious illness or injury and is characterized by a reduction in the blood supply to superficial mucosa of the stomach. Although common, it is not usually recognized unless stress ulceration and bleeding supervene, in which case treatment can be extremely difficult.
. Prevention of the stress bleeding by the routine use of H2-receptor antagonists, with or without barrier agents such as sucralfate, in patients who are in intensive care.
:Ménétrier’s disease
This is an unusual condition characterised by gross hypertrophy of the gastric mucosal folds, mucus production and hypochlorhydria. The condition is pre-malignant and may present with hypoproteinaemia and anaemia. There is no treatment other than a gastrectomy. The disease seems to be caused by overexpression of transforming growth factor alpha (TGF
Lymphocytic gastritis It is rare, characterised by the infiltration of the gastric mucosa by T cells
Eosinophilic gastritis appears to have an allergic basis and is treated with steroids and cromoglycate.. Phlegmonous gastritis is a rare bacterial infection of the stomach found in patients with severe illness.t intercurren :Peptic ulcer
Pathology : the pathogenesis of peptic ulcer involves a disturbance in the balance between the secretion of acid and pepsin by the stomach on the on hand and the mucosal barrier (a thick layer of mucus ) on the other . the normal stomach mucosa is adapted to contain the acid produced by the parietal (oxyntic) cells .when the mucosal defense is compromised , or nonexistent . the acid causes mucosal ulceration . ulcers also occur where acid attacks mucosa not specialized to deal with it.
:Sites of ulceration
Typical sites for peptic ulcers are the oesophagus(peptic oesophagitis ) ,stomach ,first part of duodenum ,at the stoma of a gastrojejunal anastomosis or adjacent to a meckels diverticulum when ectopic parietal cell are present .
:Aetiology
the vast majority of peptic ulcers are caused by infection with Helicobacter pylori. The stimuli to parietal cell function are neural (via the vagus nerve) and humoral (gastrin and histamine). Earlier treatments were therefore directed at reducing acid secretion by surgical denervation of the stomach (vagotomy) or removal of the parietal cells (partial gastrectomy) .more recently pharmacological control has been possible with histamine H2-receptor anatagonists (e.g. cimetidine and ranitidine ) and proton pump inhibitors (e.g. omeprazole).
H. pylori : it (previously called campylobacter pyloridis) is a spiral-shaped ,gram negative ,motile rod ,which is able to penetrate the viscid mucus layer lining the stomach . its potent urease activity splits any urea in the vicinity producing ammonia , thus neutralizing the pH in the local milieu surrounding the organism . many H. pylori strains also produce cytotoxins that possess protease and phospholipase activity allowing them to attack and damage mucosal membranes .this direct damage together with the resultant inflammation ,impairs the gastric mucosal barrier and allows further damage by gastric acid. Non-cytotoxin-producing strains explain asymptomatic carriage of the organism. H. pylori can be identified in almost all patients with duodenal ulcers and most patients with gastric ulcers.
Zollinger-Ellison syndrome: this is a syndrome in which a non-insulin-secreting islet-cell tumour of the pancreas produces a potent gastrin-like hormone .it is an uncommon cause of peptic ulceration. In this syndrome the ulcers are often multiple and ulceration may be more wide-spread within the small bowel. Other factors in the aetiology of peptic ulceration .A number of other factors decrease the effectiveness of the mucosal defences against gastric juice. In particular, non- steroidal anti-inflammatory drugs (NSAIDs) inhibit the production of protective prostaglandins in the mucosa. Steroids also predispose to ulceration as do smoking and stress which are thought to have an effect on both acid secretion and mucosal defences.
The acute peptic ulcer
This may be single or multiple (multiple erosions). May occur without apparent cause or may be associated with ingestion of alcohol NSAIDs (aspirin and indomethacin are common culprits )steroid therapy, acute stress, a major operation , head injury (cushing’s ulcer) or severe burns (curling’s ulcer) . may present with sudden pain , haemorrhage or perforation. A proportion of acute ulcers probably go on to become chronic.
The chronic peptic ulcer
At least 80% of peptic ulcers occur in the duodenum. Duodenal ulcers may be occur at any age but especially in the thirties to forties ;about 80% occur in males. Females are relatively immune to duodenal ulceration before the menopause and especially during pregnancy. Gastric ulcers occur predominantly in males, but the sex preponderance is less marked, about 3:1 male to female. Any age may be affected but especially the forties to fifties (i.e. a decade later than the peak for duodenal ulceration).
:Clinical features
Physical signs in the uncomplicated case are absent or confined to epigastric tenderness. Clinical diagnosis depends on the careful history. the pain typically epigastric occurs in attacks that last for days or weeks and is interspersed with periods of relief. Pain that radiates into the back suggests a posterior penetrating ulcer. Peptic ulcer pain may come on immediately after a meal but more typically commences about 2hours after food so that the patient says it precedes a meal (‘hunger pain’) .characteristically ,it wakes the patient in the early morning so much so that patient may adopt the habit of taking a glass of milk or an alkali preparation to bed . However ,it is a myth to say that one can differentiate between a gastric and a duodenal ulcer merely on the time relationship of the pain. The pain is aggravated by spicy foods and relieved by milk and alkali although the relief is lost in deep and penetrating ulcers. they may be associated heartburn nausea and vomiting .the patient may lose weight because of the pain produced by food but often may gain weight because of the high intake of milk.
:Special investigations
*fibreoptic endoscopy : enables the oesophagus , stomach and duodenum to be examined. The ulcer can be identified and, particularly in the case of gastric lesion biopsy material to enable differentiation between a benign and malignant ulcer
*H. pylori detection.
a)endoscopic biopsy: Histological examination will confirm the presence of the organism and identify mucosal damage. A urease test where a biopsy sample is placed in a solution of urea together with a pH indicator is highly specific and sensitive for the organism . H. pylori splits urea releasing ammonia which changes the pH of the solution.
b) 13C –urea breath test. (c)serological testing. Infection with H. pylori results in generation of antibodies which may be detected. Antibody titre falls slowly after eradication . *Barium meals are seldom performed nowadays to diagnosis ulcers.
*Faecal occult blood examination in often positive in the presence of an ulcer.
:Treatment
Treatment of a peptic ulcer is medical in the first instance; surgery is indicated when complications supervene . the complications are chronicity , perforation , stenosis , hemorrhage and in the case of gastric ulcer , malignant change.
:Principles of medical treatment
The main principles of treatment are to eradicate H. pylori and to reduce and neutralize (using alkalis and milk) acid secretion. Failure to eradicate H. pylori by
Giving antacid therapy alone result in high relapse rates. H. pylori eradication: A two weeks course of antimicrobial therapy combined with acid reduction therapy will eradicate H. pylori .Acid reduction is usually afforded by a proton pump inhibitor (e.g. omeprazole , lanzoprazole) and the antimicrobial therapy is based either on clarithromycin or amoxicillin together metronidazole. the combination of to antibiotics recommended because of the high incidence of antibiotic resistance. Such protocols will eradicate H. pylori in over 90% of patients.
Synthetic prostaglandins (e.g. misoprostol) have been shown to have ulcer healing properties . the main use of this type of therapy is in the prevention of peptic ulceration in patients taking NSAIDs especially in those who give a past history of peptic ulcer or of bleeding while previously taking these preparations. Violent gastric acid stimulants such as alcohol should be avoided. Rest, sedation, avoidance of smoking and dealing with underlying anxiety states are helpful. Aspirin and other NSAIDs should be avoided wherever possible.