Stomach ulcers are caused by what reasons?

(A) etiology

Gastric ulcer is a multifactorial disease, the cause complex, has so far not entirely clear, due to a combination of factors.

1. Genetic factors, family history of gastric ulcer sometimes, especially children, have a family history of ulcer patients may account for 25% to 60%. Another blood type A blood type than the other people easily this disease.

2. Chemical factors long-term consumption of alcohol or long-term use of aspirin, corticosteroids and other drugs prone to cause disease occurs, in addition to long-term smoking and drinking tea may have a certain relationship.

3. Lifestyle factors, in some ulcer patients and doctors and other professional drivers, such as seems to be more common among people, possibly due to regular diet-related. Work can also be induced Benbingfasheng too tired.

4. Mental stress or anxiety factors, sentimental, excessive mental work is the disease predisposing factors. May be due to stimulation of vagus nerve, caused by excessive gastric acid secretion.

5. Factors of Helicobacter pylori infection (HP) on gastric ulcer is still difficult to explain the role of place, because a lot of HP infected gastric ulcer occurred in only a few. However, the ulcers were almost as chronic active gastritis. The incidence of gastritis and HP is a major cause of the spread. HP is cleared then the gastritis disappeared. The quantitative study showed that HP infection, ulcers, particularly those in the upper half of stomach ulcers, often associated with severe HP infection.

6. Other factors in different countries, different regions of the incidence of the disease varied incidence in different seasons are not the same, that geography and climate are also important factors. Also the disease can also be in other primary disease, such as burns, severe traumatic brain injury, gastrinoma, hyperparathyroidism, emphysema, cirrhosis, renal failure, on the basis of the disease, the so-called "secondary ulcers" (secondary ulcer .) This may be related to gastrin, hypercalcemia, and over-excited about the vagus nerve.

(B) of the pathogenesis

1. Bile reflux and gastric ulcer disease Beaumont in 1883 and first observed in the case of some unusual bile reflux into the stomach, but was unable to arouse people's attention. Until 1965 du Plessis put forth bile reflux in gastric ulcer disease may account for the pathogenesis of an important position. Studies have shown that bile reflux into the stomach, but not common in patients with gastric ulcer disease is common in healthy subjects. Gastric ulcer disease in patients with bile juice fasting and postprandial samples were specimens exist. After ulcer healing, reflux can be reduced or stopped.

Stomach or duodenum motility disorder is the leading cause of bile reflux, but caused by fundamental factors into a dynamic disorder is still unknown. In some patients, take an upright position, smoking can increase reflux. Bile reflux is not limited to gastric ulcer disease, gastritis can be found, such as alcohol gastritis and atrophic gastritis, and gastritis complicated by a number of situations, such as duodenal ulcer disease and chronic respiratory diseases. Gastritis induced into power in itself can cause dysfunction and reflux, is unclear.

According to Hollander, the normal stomach has a double sticky barrier: mucus and mucosa. It can not only protect the mucosa from ulceration to make, and can prevent the infiltration of gastric acid secretion so that the acid retained within the stomach cavity. Normal gastric mucosa against acid back diffusion may be related to epithelial cell surface lipoprotein membrane related. The harmful effects of stomach bile is its sticky barrier damage, which makes hydrogen ions penetrate and damage the gastric mucosa. Bile can change the nature of gastric mucus. Stripping the surface mucus and the epithelial cells in the mucus content of air consumption. Beyond its role in removing mucus, bile can damage mucosal barrier, so that it can no longer prevent the infiltration of mucosal hydrogen ion. Reverse diffusion of hydrogen ions caused further damage to the mucosa. Bile acids can damage the surface of epithelial cells and diffuse into the mucosa. Stimulate mast cells to release histamine. Histamine in gastric fluid cell concentration increased with mucosal blood flow caused by vasodilation and increased capillary permeability and suppressing mucosal edema, hemorrhage, inflammation, and even acute erosion. Easy to form the damaged mucosal ulcers.

Experimental results show that duodenal contents on the gastric mucosal damage than a pure bile or pancreatic secretion on gastric mucosa injury is much greater. Bile and pancreatic secretion of some of the destruction of components have been identified. Known bile acid can cause mucosal injury. Bile and pancreatic juice mixed with each other resulting in the duodenal mucosal barrier lysophosphatidylcholine can cause damage. Lecithin normal bile secretion by pancreatic phospholipase A into lysolecithin; this response was both trypsin and activated by bile acids. High concentrations of lysophosphatidylcholine in patients with peptic ulcer disease was found in samples of gastric juice at night. In addition, the damage of bile on gastric decontamination depends not only on the role of bile acids, but also on the acidity of gastric contents. Observed pH8, 4 and 2 in three different role in the destruction of human bile solution, we found that those who destroy the smallest pH8, and pH2 are the most destructive. The findings suggest that bile and acid in particular, together, serve to undermine the role.

Bile also encourage the release of gastrin in antrum G cells, which in turn stimulate the secretion of acid and pepsin. Therefore, an increase of bile on the one hand the reverse diffusion of hydrogen ions, and partly to increased acid secretion. Determination of acidity of stomach contents taken may be able to detect the secretion of bile acid reflux increases the effect, because such examination can only reflect the degree of bile reflux, the final effect on gastric acid. Long-term bile reflux also through the formation of atrophic gastritis with intestinal metaplasia of parietal cell loss and further changes in bile reflux on gastric acid secretion in effect. It was suggested that bile reflux can cause the release of gastrin by means of intermittent excessive gastric secretion in the pathogenesis of duodenal ulcer disease played a role, but this hypothesis has yet to be confirmed.

2. Acid and gastric ulcer disease on the acid in gastric ulcer disease the role of the attention has been extensive, "no acid no ulcer will be" famous words also apply to gastric ulcer disease, but because of gastric acid secretion in the body of ulcer patients reduced or normal, the amount of acid secretion in gastric ulcer disease does not appear to occupy a prominent position on.

Acid in the role of gastric ulcer disease may not be the decision but the decision ulcer ulcer site. Other observed 149 patients with gastric ulcer disease specimens, found that all the ulcers occurred in the pyloric gland area, and the area close to acid secretion. This may be the parts of the pyloric mucosa than any other part of the reason has more contact with acid.

Acid secretion in gastric ulcer disease in many patients can be partially reduced by: Davenport's opinion to explain. The gastric mucosa of patients with this defect, making the hydrogen ion diffusion from the stomach back into the mucosa. This shortcoming has been Overhoit and Pollard ulcer disease in some patients to be confirmed. Another important factor is the gastric parietal cells in the patient group of patients less, and often associated with atrophic gastritis.

3. Ulcer disease and gastric emptying during exercise-induced etiology in gastric ulcer disease, gastric emptying delay and retention is considered to be an important factor. This doctrine can be explained by vagotomy but not only do drainage operations to cause the patient into the gastric retention secondary to ulcer formation, but the vast majority of naturally occurring gastric ulcers it is far from a satisfactory explanation. Now there is no evidence that the power must decline or remain in the gastric ulcer disease is more common than normal patients.

4. Ulcer disease, gastric ulcer disease when the regular and chronic gastritis exist. 1965, duPlessis removed at 75 due to stomach ulcers and found 65 with chronic gastritis, and its extension to the proximal gastritis from Helicobacter pylori, pyloric gland region often extensive involvement, and involving the fundic gland area. These cases were compared with duodenal ulcer disease, chronic gastritis and chronic gastritis cases more extensive and severe. He also found that gastric ulcers are often located within the area suffering from chronic gastritis. In general, the higher the position in the stomach ulcer, gastritis and the more extensive the scope of the damage. Lawson 1966, through animal experiments show that the mucosa prone to suffering from gastritis and peptic ulcer. These findings all support the notion that in chronic gastritis, gastric ulcer disease of the basis. Past that gastritis is the result of the concept of peptic ulcer disease may not be correct, because the distribution of chronic gastritis not only around the ulcer, but also involving the entire distal stomach, gastric ulcer itself is unlikely to cause such widespread gastritis.

5.Hp and gastric ulcer disease present sufficient evidence that the pathogenesis of duodenal ulcer Hp not only occupy a prominent position, and in the pathogenesis of gastric ulcer also occupy a certain position.

6. Pathological type gastric ulcer is a chronic disease. According to different parts of ulcers, the ulcers were divided into 4 types (Figure 1):




Ⅰ: the lesser curvature ulcer, gastric notch located near the lesser curvature, especially prevalent in the gastric mucosa and gastric mucosa at the junction of the body. Often low gastric acid secretion, accounting for about 80% of gastric ulcer;

Ⅱ: gastroduodenal ulcer compound. Often the first occurrence of duodenal ulcer, gastric ulcer secondary. High gastric acid secretion, easy to hemorrhage, intractable disease. 5% ~ 10%;

Ⅲ: prepyloric and pyloric ulcers. Usually high gastric acid secretion, medical treatment is easy to recur;

Ⅳ: high gastric ulcer, located in the upper stomach, 1 / 3, 4cm from the esophagogastric junction, less than 2cm were in the "near cardia ulcers." Low gastric acid secretion, easy to send blood and perforation.

Lesser curvature of gastric ulcers can be seen in the most common, especially the antrum lesser curvature. Some of the larger ulcers can occur even in the lesser curvature of the upper part of cardiac region. In the fundus and greater curvature is very rare.

7. Pathologic ulcers are usually single, round or oval diameter of 0.5 ~ 2cm, rarely more than 3cm. Ulcer edges neat, like a knife, usually through the bottom of the submucosa, deep muscle or muscle pulp. Submucosa to the muscular layer is eroded completely destroyed and replaced by granulation tissue and scar tissue. Active ulcer at the bottom of the deep from the surface to turn can be divided into four layers: ① oozing layer; ② necrotic; ③ layer of granulation tissue; ④ layer of scar tissue. 2% ~ 5% of gastric ulcers can occur suddenly evil.