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Good day everyone, Today we are going to discuss fully on diseases of the stomach;

Learning outcomes

After studying this section, you should be able to:

  • compare the main features of chronic and acute gastritis
  • discuss the pathophysiology of peptic ulcer disease
  • describe the main tumours of the stomach and their consequences
  • define the term congenital pyloric stenosis.
Disease of the stomach
Disease of the stomach


Inflammation of the stomach can be an acute or chronic condition.

Acute gastritis

This is usually a response to irritant drugs or alcohol. The drugs most commonly implicated are non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin, even at low doses, although many others may also be involved. Other causes include the initial response to Helicobacter pylori infection and severe physiological stress, e.g. extensive burns and multiple organ failure.

There are varying degrees of severity. Mild cases can be asymptomatic or may present with nausea and vomiting associated with inflammatory changes of the gastric mucosa. Erosions, which are characterised by tissue loss affecting the superficial layers of the gastric mucosa may also occur. In more serious cases, multiple erosions may result in life threatening haemorrhage causing haematemesis (vomiting of frank blood or black ‘coffee grounds’ when there has been time for digestion of blood to occur) and melaena (passing black tarry faeces), especially in okler adults.

The outcome depends on the extent of the damage. In many cases recovery is uneventful after the cause is removed. Where there has been extensive tissue damage, healing is by fibrosis causing reduced elasticity and peristalsis.

Chronic gastritis

Chronic gastritis is a milder but longer-lasting condition. It is usually associated with Helicobacter pylori but is sometimes due to autoimmune disease or chemical injury. It is more common in later life.

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Helicobacter-associated gastritis.Helicobacter pylori is abacterium that can survive in the gastric mucosa and is commonly associated with gastric conditions, especially chronic gastritis and peptic ulcer disease.

Autoimmune chronic gastritis. This is a progressive disease. Destructive inflammatory changes that begin on the surface of the mucous membrane may extend to affect its whole thickness, including the gastric glands. When this stage is reached, secretion of hydrochloric acid and intrinsic factor are markedly reduced. The antigens are the gastric parietal cells and the intrinsic factor they secrete. When the parietal cells are destroyed as a result of this autoimmune condition, the inflammation subsides. The causes of the autoimmunity are not known but there is a familial predisposition and an association with thyroid disorders. Secondary consequences include:

  • pernicious anaemia due to lack of intrinsic factor
  • increased risk of cancer of the stomach.

Peptic ulcer disease

Ulceration involves the full thickness of the gastrointestinal mucosa and penetrates the muscle layer . It is caused by disruption of the normal balance between the corrosive effect of gastric juice and the protective effect of mucus on the gastric epithelial cells. It may be viewed as an extension of the gastric erosions found in acute gastritis. The most common sites for ulcers are the stomach and the first few centimetres of the duodenum. More rarely they occur in the oesophagus and round the anastomosis of the stomach and small intestine, following gastrectomy. The incidence of peptic ulcers is greater in men than women and increases with age. The underlying causes are not known but there is a strong association with H. pylori infection. It is believed that H. pylori, some drugs, e.g. non-steroidal anti-inflammatory drugs (NSAIDs), and smoking may impair the gastric mucosal defences in some people. However, H. pylori is present in many people who show no signs of peptic ulcer disease.

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If gastric mucosal protection is impaired, the epithelium can be exposed to gastric acid causing the initial cell damage that leads to ulceration. The main protective mechanisms are: a good blood supply, adequate mucus secretion and efficient epithelial cell replacement.

Blood supply. Reduced blood flow and ischaemia may be caused by cigarette smoking and severe stress, either physical or mental. In stressful situations the accompanying sympathetic activity causes constriction of the blood vessels supplying the alimentary tract.

Secretion of mucus. The composition and the amount of mucus may be altered, e.g.:

  • by regular and prolonged use of aspirin and other anti-inflammatory drugs
  • by the reflux of bile acids and salts
  • in chronic gastritis.

Epithelial cell replacement. There is normally a rapid turnover of gastric and intestinal epithelial cells. This may be reduced:

  • by raised levels of steroid hormones, e.g. in response to stress or when they are used as drugs
  • in chronic gastritis
  • by radiotherapy and cytotoxic drugs.

Acute peptic ulcers

These lesions may be single or multiple. They are found in many sites in the stomach and in the first few centimetres of the duodenum. Their development is often associated with acute gastritis, severe stress, e.g. severe illness, shock, burns, severe emotional disturbance and following major surgery. Healing without the formation of fibrous tissue usually occurs when the stressor is removed, although haemorrhage, which may be life-threatening, can be a complication.

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