and peptic ulcer disease

Chapter 47 Gastritis and peptic ulcer disease

What is peptic ulceration and what are its main causes?

How may it present clinically and what are its complications?

Peptic ulceration is defined as a breach in the mucosa (i.e. full-thickness loss) of the gastrointestinal tract caused by the action of acidic gastric juice. Peptic ulcers can be acute or chronic, although sometimes the term peptic ulcer is confined to the chronic variety (Fig. 3.47.1). Some types of inflammation of the stomach (gastritis) are especially associated with peptic ulcer formation, and these are discussed in this chapter.

Fig. 3.47.1 Cross-section through a chronic peptic ulcer.

Gastritis

Acute gastritis

The principal causes of acute gastritis are:

NSAIDs: cause reduced prostaglandin synthesis in the gastric mucosa, leading to exfoliation of surface epithelial cells and inhibition of mucus secretion, thus reducing mucosal defences against acid attack

alcohol (ethanol): direct irritant of the lining of the stomach

stress (e.g. severe burns, major trauma): associated with gastric inflammation, erosion and ulceration, possibly as a result of mucosal ischaemia

bile reflux: reflux of bile through the pylorus from the duodenum.

Acute gastritis is often associated with partial-thickness defects in the mucosa. Such defects are sometimes called erosions (as opposed to an ulcer, which is a full-thickness breach). These erosions often bleed and may present as gastric haemorrhage. In severe cases, the erosions deepen to become true ulcers.

Chronic gastritis

Chronic gastritis can be generated by any of the causes of acute gastritis if they act for long enough. In addition, chronic gastritis can occur de novo through autoimmune mechanisms. For example, pernicious anaemia is an autoimmune condition in which damage to parietal cells causes l0ss of intrinsic factor and hence failure of vitamin B₁₂ absorption. It is associated with inflammation and subsequent atrophy of the mucosa in the gastric body and fundus. However, the most common cause of chronic gastritis is infection with Helicobacter pylori.

Although H. pylori does not invade the tissues, it lives in the surface mucus of gastric mucosa (Fig. 3.47.2) where it secretes a number of toxins that damage surface epithelial cells and break down the mucus barrier. When first acquired, this organism produces a transient acute gastritis, but this is self-limiting and often produces no symptoms. Some individuals mount an effective defence and eliminate the organism. Many individuals do not clear the organism, however, and a chronic carrier state develops. This carrier state is associated with chronic inflammation of the mucosa driven by a Th1 immune response, the severity of the inflammation depending on the strain of the infecting organism. As a result, patients may either have abdominal symptoms or be asymptomatic. The most common serious sequela of H. pylori infection is peptic ulceration.