Gastric duodenal ulcer

xiaoxiao2021-03-06  130

Stomach, duodenal ulcer digestive ulcerative ulceration is a clear limitative tissue, involving mucous membranes, mucosa under the submuscular layer, which forms a digestive effect of gastric acid and gastric protease, so that digestive ulcers. Since the ulcers are mainly in the stomach and duodenity, it is also known as the stomach and dodipicone ulcer.

This disease is a common disease, multiple incidence. It has been estimated that approximately 5 to 10% in a normal population, suffering from the stomach or duodenal ulcer. At present, this disease is generally considered to have a typical physical and mental illness. It has also achieved many results in recent years. Studies have shown that this disease is not a single disease, but a group of diseases closely related to external factors, and is a scope of genetic heterogeneous diseases.

This disease can occur in any age, but there are many young ages. In terms of gender, men are more than women, the ratio is 2 ~ 4: 1. In the clinical duodenal ulcer, the appetite ulcer is more common. Ulcer diseases, such as improper prevention, can cause serious complications, such as large bleeding, gastric perforations or pyloric obstruction. Therefore, it is important to actively prevent this disease.

1. Etiology

The etiology of digestive ulcers is more complicated. In summary, the formation of ulcer is caused by the relationship between the stomach and duodenal mucosa and the relationship between damage factors. When the damage factor is increased and / or the protective factors are weak, ulcers can occur. The incidence of gastric ulcer is mainly attenuated by protective factors, while the incidence of ulcers is mainly due to the role of damage factors. Other factors reflect the influence of genetic and other diseases, and each factor is mostly a series of sections in the incidence of pathogenesis or synthesis.

(1) Damaged factors

1 Effect of gastric acid - gastric protease: In damaged factors, gastric acid-gastric proteases, especially gastric acid, accounts for main positions. Due to high acid secretion, the mucosa is impaired to form an ulcer factor.

2 nervous system and endocrine dysfunction: under the influence of neuristic factors such as continuous and excessive spiritual tensions, emotional excitement, the cerebral cortex function is obstacted, so that gastric acid is too high; it can secrete too much adrenal hormones, excitement of gastric acid, The stomach protease secretion makes ulcers are easily formed.

3 gastrin and gastric sinus retention: deputy-handed neuro-excited, gastric sinus mucosa Contact protein decomposition or gastric sinus retention, expansion, can stimulate gastrointestinal cells secretion of gastrin, causing gastric ulcers.

4 Diet is not or off: food or beverage can physically physically or chemically damage to the mucosa; some of them stimulate gastric acid secretion; irregular meal time can destroy the rhythm of gastric secretion, and the incidence and recurrence of peptic ulcer related.

5 adverse effects of drugs: a variety of drugs such as aspirin, Baitan Song, anti-inflammatory pain, adrenal hormone, etc., can cause digestive ulcers by various mechanisms.

(2) Protecting the mucosa

1 Destruction of the gastric mucosa barrier: some other compounds that can dissolve fat, such as aspirin, wine, other drugs and duodenal intestinal liquid components such as gallcharide and pancreatic and pancreatic, which can impair the lipoprotein of gastric mucosal epithelial cells. The layer has caused the gastric mucosa barrier to be destroyed.

2 mucosa blood circulation and epithelial cell renewal obstacles: good blood circulation and epithelial cell renewal of the stomach and duodenal mucosa, and the effective and appropriate amount of perfusion of the microcirculation system, the complete and mucosal epithelial cells stable basic requirement. If the blood circulation occurs, mucous ischemic necrosis, and the recycled update of the cells can not form ulcers under the action of gastric acid-gastric protease.

3 prostaglandin lack: endogenic prostaglandin in the stomach and duodenal mucosa has the secretion of gastric mucosal epithelial cell secretion and HCO3-, enhanced mucosa blood circulation and protein, inhibit gastrin and gastric acid secretion, protect the stomach Mucosal barrier and other functions. Internal birth prostate synthesis, may be one of the mechanism of ulceration formation.

4 The effects of stomach and duodenal intestinal inflammation: stomach, duodenal ulcer with inflammation, inflammation can weake the mucosa to resist gastric acid, provide the basis for the formation of ulcers. The stomach, duodenal intestinal inflammation may be related to bile, pancreatic fluid refractive flow, and ratio may also be related to Helicobacter pylori (HP) infection. HP often detects in the stomach and duodenal ulcers. Although this bacterium has no direct evidence of ulcers, it may be indirectly involved in the occurrence of ulceration through its mucosa. In August 1990, a comprehensive report of the Ninth World Gastroology Conference held in Sydney, it is believed that HP is contemplated that gastric acid has a negative feedback effect on gastrointestinal secretion, causing long-term gastrins and slogan and wall cell hyperplasia. . Therefore, it is believed that the increase in the increase of the increase in duodenal ulcers, but the consequences of HP infection, and it is considered that HP can prevent ulcers from recurring, so the new concept of "root" ulcer disease is proposed. 5 Smoking: Smoking can cause blood vessel contraction, inhibit the secretion of cholestees and pancreatic and reduce its ability to neutralize with gastric acid in duodenity, while causing a cholesum of anti-current to destroy the gastric mucosal barrier.

(3) Other factors

The occurrence of peptic ulcer has a certain relationship with the genetic relationship, the 12th lyophilic ulcer or Helicobacter's top region of the "O" blood group is higher than other blood type. In addition, digestive ulcer has a certain connection with some diseases, such as rheumatoid arthritis, chronic pancreatitis, perimeter cirrhosis, high calciummia and emphysema, etc. The incidence of duodenal ulcer is high. In general people.

2. Clinical manifestation

1 Symptoms: Abdominal pain can be summarized as limitations, slowly and rhythm, mostly limited to upper abdomen. The pain of gastric ulcer is mostly in the sword, and the duodenal ulcer is located in the upper abdomen or later. The disease is slow, the course of the disease is reached as many years or decades. The pain of gastric ulcer is more than 1/2 to 2 hours after meal. After 1 to 2 hours, the gastric emptying is relieved, and its law is eating → pain → relieve. The duodenal ulcer is painful in an empty stomach. It usually occurs 3 to 4 hours after meals. After eating, the law is eating → relieving → pain, can also have pain before going to bed in the evening, saying night pain. Such as the gastric ulcer is close to the door, and the pain rhythm can be the same as the duodenal ulcer. When the ulcer is deeper, especially the penetrant, the pain can involve the back. This disease is cyclical, related to the season, the late autumn, the early winter, spring, summer is rare. It is also related to diet, mental emotions, and treatment, etc. Pain properties are often painful, burning pain, blunt pain, hunger pain or pain, can be alleviated by alkaline drugs. Special types of ulcers such as pylorial ulcers, ulcers, ulcers, gust of ulcers, giant ulcers, multiple ulcers, complex hypoders, or complicity, pain may not be typically.

In addition to pain symptoms, this disease often has other gastrointestinal symptoms, such as 嗳 嗳, anti-acid, burning, nausea, vomiting. Vomiting and nausea are more reflecting ulcers with a high degree of activity, a large number of vomiting, suggesting Helicobs.

2 intrinsic: There is no obvious syllable, such as no complications, can be compromised in the upper abdominal pain area, generally lighter. The rear wall penetrate ulcers often have a tenderness in the back 11 to 12.

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