Synonyms in a broader sense
Medical: Gastroduodenal ulcer, ventriculitis, duodenal ulcer, peptic ulcer, duodenal ulcer, ulcer disease, gastritis
Definition Stomach Ulcer
Frequency (Epidemiology)
Occurrence in the populationApproximately 10% of the population have had a stomach or duodenal ulcer at least once in their lives. The duodenal ulcer is about five times more common than the gastric ulcer (ulcus ventriculi). Men are three times more frequently affected by a duodenal ulcer than women.
In the case of the ulcer ventriculi, the sex ratio is 1:1. The peak age of onset of the disease is between 50 and 70 years of age. Anatomy stomach
- Esophagus (esophagus)
- Cardia
- Corpus
- Small Curvature
- Fundus
- Large Curvature
- Duodenum (duodenum)
- Pylorus
- Antrum
Ulcer forms classification
A distinction is first made between an acute (sudden) and a chronic recurrent (recurrent) stomach ulcer (ulcer). The acute “stress ulcer” occurs as a result of a superficially damaging (erosive) inflammation of the mucous membrane of the stomach (gastritis). The cause of this ulcer development is strong physical stress factors, which lead to the sudden collapse of the protective mucous membrane barrier.
Such stress situations include burns, major operations and many other diseases requiring intensive care. The chronic recurrent ulcers occur more frequently and can have various causes (see below). Furthermore, ulcers are divided according to their localization into gastric ulcers and duodenal ulcers.
The peptic ulcer is most frequently located in the area of the small gastric curvature (Curvatura minor). The duodenal ulcer lies almost exclusively at the beginning of the duodenum, the bulbus duodeni. If ulcers are found in more distant sections of the intestine than described (e.g. jejunum section of the small intestine), this may be an indication of a rare Zöllinger-Ellison syndrome.
The balance between the mucous membrane aggressive and mucous membrane protecting (defensive) factors plays an essential role in the development of a gastrointestinal ulcer. If the aggressive factors predominate or the defensive factors fail, an ulcer may occur. A distinction is made between the causes, those that originate from the body itself (endogenous cause) and those that are caused from outside (exogenous cause).
Endogenous causes, i.e. causes caused by the body itself, are possible:
- Gastric acid
- Gastrointestinal motility (peristalsis)
- Zöllinger-Ellison syndrome
- Hyperparathyroidism
- Rare causes
a) Gastric acidA very important factor in the development of an ulcer is gastric acid. This finding can be derived from the fact that patients with an autoimmune inflammation of the mucous membrane of the stomach (gastritis), who can no longer produce gastric acid, do not develop ulcers. However, it should be noted that the production of gastric acid is rarely increased in the case of a gastric ulcer.
In the case of a peptic ulcer, therefore, gastric acid is not the triggering factor but an accompanying factor (permissive factor) for the continued existence of the peptic ulcer. In the case of a duodenal ulcer, however, the excessive secretion of gastric juice plays an important role. Here, the still largely unexplained increased formation of gastric acid and pepsin (aggressive protein enzyme of the digestive chain) during the night should be mentioned in particular.
It is also assumed that the insufficient binding of gastric acid by the basic bicarbonate, which is formed in the duodenum, is a partial cause of the development of duodenal ulcers (lack of acid neutralization). b) Gastrointestinal motility (peristalsis)More and more often, a disturbed coordination of the movement between the gastric cavity (antrum) and the duodenum is discussed. In some patients with peptic ulcer, in addition to a longer gastric passage for food, a return flow of bile acid (bile reflux) into the stomach is observed.
Bile acids are among the factors that are aggressive to the mucous membrane. c) Zöllinger-Ellison-SyndromeThis term refers to a rare tumor that is most frequently located in the pancreas and produces the hormone gastrin. The benign tumor is also called gastrinoma.
The excessive production of gastrin by the tumor leads to an overstimulation of the acid-forming stomach cells (tumor cells). This means that too much gastric acid is produced.This excess of gastric acid leads to the predominance of aggressive factors in the gastrointestinal tract and the development of many simultaneously occurring (multiple) gastric ulcers. A Zöllinger-Ellison syndrome often leads to multiple ulcers in the duodenum and even in the further course of the intestine (jejunum).
These ulcers prove to be particularly persistent. Treatment is long and difficult. This syndrome causes only 1% of all gastro-duodenal ulcer diseases.
d) HyperparathyroidismHyperparathyroidism describes an overactive parathyroid gland (parathyroidea). An overfunction of the hormone-producing cells (epithelial bodies) of the parathyroid gland leads to an excess of calcium (hypercalcaemia) in the body. This in turn leads to stimulation of the G-cells in the stomach and duodenum, which produce the hormone gastrin described above.
This in turn leads to an overstimulation of acid-forming stomach cells. e) Rare causesVery rare causes are viral infections, e.g. with the Cytomegalovirus (CMV) or the Herpes Simplex Virus (HSV), and chronic intestinal diseases, such as Crohn’s disease. Exogenous causes of a peptic ulcer are understood to be causes that enter the stomach from outside.
These are particularly relevant here:
- Helicobacter pylori (H. p.)
- Non steroidal anti-inflammatory drugs (NSAIDs)
a) Helicobacter pylori Since its discovery in the early 1990s, the bacterium Helicobacter pylori (H. p.) has emerged as one of the most important causes of gastroduodenal ulcer disease (chronic ulcer). The risk of developing a gastrointestinal ulcer increases 3-4 times in the presence of Helicobacter-induced gastritis. This does not mean that every person whose stomach mucosa is colonized by the bacterium necessarily develops a gastritis or ulcer.
The Helikobacter bacterium can be detected in almost all patients with a duodenal ulcer. About 75% of patients with a stomach ulcer are infected with the Helicobacter bacterium. Helicobacter pylori is also a permissive factor in the development of ulcers, which means that infection with the bacterium alone is not sufficient for the development of a peptic ulcer.
Other aggressive factors (see above) must also be present at the same time. b) Non-steroidal anti-inflammatoryNSAIDs, such as acetylsalicylic acid (ASA), are also frequently used as painkillers for joint diseases and other painful conditions. These drugs have a stomach mucus-destroying effect.
The machanism behind this is related to the inhibition of the so-called prostaglandin formation. Prostaglandins have a vasodilating effect on the stomach mucosa and also promote the formation of the protective stomach mucus. By reducing the formation of prostaglandin, the stomach lining loses important protective factors.
The risk of developing a gastric ulcer increases. The risk of developing an ulcer multiplies with NSAID medication and simultaneous Helicobacter pylori infestation. The symptoms of peptic ulcer disease are often very unspecific.
Statistics show that 20% of ulcer patients are completely free of symptoms (asymptomatic) and again 20% of patients with symptoms similar to those of an ulcer disease did not have an ulcer in gastroscopy (endoscopy). Typically, the NSAIDs are those that cause no or very uncharacteristic signs (symptoms) of disease. The symptoms include: There may also be pain, which often radiates into the chest (thorax), back or lower abdomen.
This pain is often described as “hungry” and “gnawing”. In some patients, a certain rhythm can be observed in the pain symptoms, which occasionally indicates the location of the ulcer. Nocturnal pain and relief of pain after meals seem to be typical for duodenal ulcers.
Deterioration after eating is more likely to occur in the case of a gastric ulcer (ulcus ventriculi). However, the diagnosis can only be really confirmed by a gastrointestinal endoscopy.
- Upper abdominal complaints
- Nausea
- Feeling of fullness
- Food intolerances.
