A is an
Ulcer of one of those areas of the
Gastrointestinal Tract that are usually acidic. A more general term, '''peptic ulcer disease''' (PUD), is also in use.
Most ulcers are now known to be associated with ''
Helicobacter Pylori '', a spiral-shaped bacterium that lives in the acidic environment of the stomach. Ulcers can also be caused or worsened by drugs such as
Aspirin and other
NSAID s. About 4 % of gastric ulcers are caused by a malignant tumour, which is one reason to be vigilant in their detection. Duodenal ulcers are generally non-malignant.
Symptoms of a peptic ulcer can be:
- Abdominal Pain , classically epigastric and its severity relating to mealtimes;
- Hematemesis (vomiting of blood);
- Melena (tarry, foul-smelling feces due to Oxidised iron from Hemoglobin );
- Weight loss;
- Rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.
A history of
Heartburn ,
Gastroesophageal Reflux Disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include
NSAID (non-steroid anti-inflammatory drugs) that inhibit
Cyclooxygenase , and most
Glucocorticoid s (e.g.
Dexamethasone and
Prednisolone ).
In patients over 45 with more than 2 weeks of the above symptoms the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).
The timing of the symptoms in relation to the meal may differentiate between ''gastric'' and ''duodenal ulcers'': A gastric ulcer would give
Epigastric Pain ''during'' the meal, as
Gastric Acid is secreted, or ''after'' the meal, as the alkaline duodenal contents reflux into the
Stomach . Symptoms of duodenal ulcers would manifest mostly ''before'' the meal — when acid (production stimulated by hunger) is passed into the
Duodenum .
In patients in whom ''peptic ulcer'' is suspected, the correct test is
Esophagogastroduodenoscopy (EGD), a form of
Endoscopy , sometimes known as just
Gastroscopy . By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
The diagnosis of ''
Helicobacter Pylori '' can be by:
- Biopsy during EGD;
- Breath testing (does not require EGD);
- Direct culture from an EGD biopsy specimen;
- Direct detection of Urease activity in a biopsy specimen;
- Measurement of Antibody levels in Blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy.
The possibility of other causes of ulcers, notably
Malignancy (
Gastric Cancer ) needs to be kept in mind. This is especially true in ulcers of the ''greater (large) curvature'' of the
Stomach ; most are also a consequence of chronic ''H. pylori'' infection.
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.
Classical causes of ulcers (
Tobacco Smoking ,
Blood Group s,
Spice s and a large array of strange things) are of relatively minor importance in the development of peptic ulcers.
A major causative factor (75% of gastric and 90% of duodenal ulcers) is chronic
Inflammation due to ''
Helicobacter Pylori '', a
Spirochaete that inhabits the antral mucosa and increases
Gastrin production.
Gastrin , in turn, stimulates the production of
Gastric Acid by parietal cells.
Another major cause is the use of
NSAID s (see above). The gastric mucosa protects itself from
Gastric Acid with a layer of mucous, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of
Cyclooxygenase 1 (''cox-1''), which is essential for the production of these prostaglandins. Newer NSAIDs (
Celecoxib ,
Rofecoxib ) only inhibit ''cox-2'', which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.
Glucocorticoid s lead to atrophy of all
Epithelial tissues. Their role in ulcerogenesis is relatively small.
''Stress'' in the psychological sense has not been proven to influence the development of peptic ulcers.
Burns and
Head Trauma , however, can lead to "stress ulcers", and it is reported in many patients who are on
Mechanical Ventilation .
Smoking leads to
Atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through
Ischemia .
A
Family History is often present in duodenal ulcers, especially when
Blood Group O is also present. Inheritance appears to be unimportant in gastric ulcers.
Macroscopically: Gastric ulcer is most often localized on the lesser curvature of the stomach. It is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irreguliar as in gastric cancer - ulcerative form. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
Microscopically: Gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.
1
In Western countries the
Prevalence of ''
Helicobacter Pylori ''
Infection s roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in
Third World countries. Transmission is by food and human contact, sharing food utensils etc.
A minority of cases of ''Helicobacter'' infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort,
Abdominal Pain or
Gastritis .
Younger patients with ulcer-like symptoms are often treated with
Antacid s or
H2 Antagonist s before EGD is undertaken.
Bismuth compounds may actually reduce or even clear organisms.
When ''H. pylori'' infection is present, the most effective treatments are combinations of 2 antibiotics (e.g.
Erythromycin ,
Ampicillin ,
Amoxicillin ,
Tetracycline ,
Metronidazole ) and 1
Proton Pump Inhibitor (PPI). An effective combination would be
Amoxicillin +
Metronidazole +
Pantoprazole (a PPI). In the absence of ''H. pylori'', long-term higher dose PPIs are often used.
Treatment of ''Helicobacter'' usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. However, there is mounting evidence of the fact that H. pylori may be protective against certain diseases of the esophagus and cardia, including GERD, Barrett's esophagus, and esophageal adenocarcinoma (a particularly deadly form of cancer). Therefore, a more cautious approach to its eradication may be necessary.
