The stomach, which varies considerably in size, is divided into the upper portion (the fundus), the mid-region or body, and the antrum, which extends into the pyloric region.
There are two sphincters, the gastro-oesophageal sphincter and the pyloric sphincter; the latter is largely made up of a thickening of the circular muscle layer. The muscle wall of the stomach has three layers-an outer longitudinal, an inner circular, and an innermost oblique layer of smooth muscle.
The duodenum has outer longitudinal and inner smooth muscle layers. It is C-shaped and the pancreas sits in the concavity. It terminates in the jejunum at the duodenojejunal flexure. The mucosal lining of the stomach, particularly in the greater curvature, is thrown into thick folds or rugae. The upper two-thirds of the stomach contains parietal cells, which secrete hydrochloric acid, and chief cells, which secrete pepsinogen. The junction between the body and the antrum of the stomach can often be seen macroscopically, but can be confirmed by measuring surface pH. The antrum contains only mucus-secreting and G cells, which secrete gastrin. There are two major forms of gastrin, G17 and G34, depending on the number of amino-acid residues. G17 is the major form found in the antrum.
The duodenal mucosa contains Brunner’s glands, which secrete alkaline mucus. This, along with the pancreatic and biliary secretions, helps to neutralize the acid secretion from the stomach when it reaches the duodenum.
The factors controlling acid secretion. Secretion is under neural and hormonal control. Both stimulate acid secretion through the release of histamine, which acts on the parietal cells either directly or via immunocytes. Other major gastric functions
• Reservoir for food
• Emulsification of fat and mixing of gastric contents
• Secretion of intrinsic factor
• Absorption (of only minimal importance) Gastric emptying epends on many factors. There are osmoreceptors in the duodenal mucosa that control gastric emptying by local reflexes and the release of gut hormones. In particular, intraduodenal fat delays gastric emptying by negative feedback through duodenal receptors.
There is no universally accepted classification of this condition partly because there is a poor correlation between clinical, pathological and endoscopic findings. Acute gastritis, acute ulceration and erosions.
In acute gastritis there is an acute inflammatory infiltrate in the superficial gastric mucosa predominantly with neutrophils, This is sometimes accompanied by mucosal erosions. Multiple small erosions, often with an oedematous mucosa, are described as acute erosive gastritis.Acute gastric ulceration occurs in the same setting as erosions, but are larger and less superficial. Gastritis can be commonly produced by drugs such as aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) (Information box 4.2), and occasionally by infections, e.g. cytomegalovirus and herpes simplex, particularly in the imrnunocornprornised. Aspirin and other NSAIDs deplete mucosal prostaglandins which leads to mucosal damage. Alcohol in high concentrations damages the gastric mucosal barrier and is associated with acute gastric mucosal lesions and upper gastrointestinal bleeding.Acute ulcers are also seen after severe stress (stress ulcer) and secondary to burns (Curling’s ulcer), trauma, shock, renal or liver disease. The underlying mechanism for these ulcers is unknown but may be related to analteration in mucosal flow.
The correlation between the pathological changes and symptoms is poor, but some patients with acute gastritis may suffer from indigestion and vomiting, usually shortlived. Gastrointestinal haemorrhage can occur.
In many patients symptoms settle without diagnosis, but endoscopy is necessary in patients with a gastrointestinal haemorrhage to confirm the presence of acute ulcers or erosions.
No specific therapy is required apart from removal of the offending cause, if possible.