Pyloric ulcer

Introduction The pyloric tube ulcer, pathophysiology is similar to duodenal ulcer (DU), and gastric acid is generally increased. The pyloric canal ulcer often lacks the periodic and rhythmic pain of typical ulcers. The upper abdominal pain is more common after meals, the reaction against acid is poor, vomiting or pyloric obstruction is easy to occur, and complications such as perforation or bleeding are also more. The disease has a recurrent tendency, which is related to the systolic dysfunction of the pyloric tube smooth muscle and the difficulty in healing the ulcer surface. The pyloric tube is located at the distal end of the stomach and borders the duodenum and is about 2 cm long. The pyloric tube ulcer is similar to duodenal ulcer (DU) and has a higher gastric acid secretion. The rhythm of upper abdominal pain in pyloric tube ulcer is not obvious, the response to drug treatment is poor, vomiting is more common, and complications such as pyloric obstruction, hemorrhage and perforation are more likely to occur.

Cause

Since the bile reflux first flows through here, the bile salt component in the bile can damage the gastric mucosal barrier, and the chyme stays here for a longer period of time, the local pressure increases, and the blood circulation is relatively poor. In the past, this disease was rare. With the popularity of endoscopy and the attention of endoscopists, the incidence of this disease was not low.

Because ulcers occur at the junction of the end of the stomach and the duodenum, and its pathophysiology is similar to duodenal ulcer, gastric acid generally increases, and abdominal pain of some pyloric canal ulcers is similar to DU; however, the abdominal pain of several patients is stubborn and relieves after eating. Not obvious, even taking antacids is not as significant as DU; another part of the patient has abdominal pain immediately after a meal, which may cause frequent stagnation of the stomach pylorus due to eating, which is caused by the direct stimulation of the ulcer on the narrow channel. Therefore, the abdominal pain of the pyloric tube ulcer has no periodicity and regularity of typical ulcers. At the same time, the disease has a recurrent tendency, which is related to the systolic dysfunction of the pyloric tube smooth muscle and the difficulty in healing the ulcer surface.

In addition to frequent exposure to high concentrations of gastric acid, the gastroduodenal mucosa is also attacked by pepsin, microorganisms, bile salts, ethanol, drugs and other harmful substances. However, under normal circumstances, the gastroduodenal mucosa can resist the damage of these invasive factors and maintain the integrity of the mucosa. This is because the gastroduodenal mucosa has a range of defense repair and repair mechanisms, including mucus bicarbonate barrier, mucosal barrier, mucosal blood flow, cell renewal, prostaglandins and epidermal growth factor. The occurrence of peptic ulcer is the result of a loss of balance between the invasive factors that damage the gastric mucosa mucosa and the mucosal defense-repair factors. This balance may be due to increased invasive factors, or may be a reduction in defense-repair factors, or both. There are differences in the pathogenesis between GU and DU. The former is mainly due to the weakening of defense and repair factors, while the latter is mainly due to the enhancement of invasive factors. Peptic ulcer is a disease caused by a variety of causes, that is, the etiology and pathogenesis of patients may not be the same, but the clinical manifestations are similar.

Pathogenesis:

1. A large number of studies on Helicobacter pylori infection in the past decade or so have fully proved that Helicobacter pylori (Hp) infection is the main cause of peptic ulcer.

(1) Hp infection rate in patients with peptic ulcer is high. If the patient has taken antibiotics, expectorants or non-steroidal anti-inflammatory drugs (NSAIDs) before the test, the Hp infection rate of DU patients is 90%-100%. GU is 80%-90%. The risk of developing peptic ulcer in Hp-infected patients is also significantly increased. Prospective studies have shown that approximately 15%-20% of people with Hp infection develop peptic ulcer.

(2) According to Hp, it can promote the healing of ulcers and significantly reduce the recurrence rate of ulcers, and eliminate the Hp without inhibiting the secretion of gastric acid. It can effectively heal ulcers; the conventional inhibition is a so-called refractory ulcer with unsatisfactory curative effect. After effective eradication of Hp treatment, healed; treated with high-efficiency Hp regimen for 1 week, then no anti-ulcer treatment, 4 weeks after the end of treatment, ulcer healing rate is higher than or equal to the application of conventional inhibition of gastric acid secretion drug continuous treatment 4-6 weeks of healing rate. These results demonstrate from different perspectives that eradication of Hp promotes ulcer healing.

Frequent recurrence of ulcers has been one of the main features of the natural history of peptic ulcer. The ulcers healed after conventional treatment of gastric acid-secreting drugs have an annual recurrence rate of 50%-70% after withdrawal. Eradication of Hp can reduce the annual recurrence rate of DU and GU to less than 5%, so that most ulcer patients are completely cured. In addition, eradication of Hp can significantly reduce the incidence of complications such as peptic ulcer bleeding.

(3) Hp infection changes the balance between mucosal invasion factors and defensive factors. Hp colonizes the gastric mucosa (stomach and stomach metaplasia of the duodenum) by its virulence factors, inducing local inflammation and immunity. The reaction impairs the local mucosal defense repair mechanism; on the other hand, Hp infection can increase the secretion of gastrin and gastric acid, and enhance the invasive factors. The synergistic effect of these two factors causes mucosal duodenal mucosal damage and ulceration.

The virulence factors of Hp include two factors that enable Hp to colonize gastric mucosa and factors that induce tissue damage. Some factors play a two-fold role. The colonization site of Hp is on the surface of gastric mucosa epithelium and the mucus bottom layer; generally, the number of gastric antrum Hp is large, the stomach and stomach are less, and it can also inhabit the duodenal gastric mucosa. Hp is colonized in the stomach, and it must resist the action of gastric acid killing, and it must rely on its movement through the mucus layer. Hp cells are spiral and have flagella at one end, providing power for their use. The urease produced by Hp hydrolyzes urea into ammonia and carbon dioxide, and ammonia forms an ammonia cloud around Hp, neutralizing the surrounding gastric acid, thereby protecting Hp. Hp specifically adheres to the gastric epithelium, making it easy for toxins to act on epithelial cells. The adhesion specificity of Hp reflects its presence of adhesion factors, whereas gastric epithelial cells have specific receptors for adhesion factors.

Hp toxin, toxic enzymes and Hp-induced mucosal inflammation can cause damage to the gastroduodenal mucosal barrier. The vacuolating toxin (VacA) protein and the cytotoxin associated gene (CagA) protein are major markers of Hp virulence. VacA protein can produce vacuoles in cultured cells; the exact function of the CagA protein is unclear. In addition to the protective effect of Hp itself, ammonia produced by urease decomposing urea can directly and indirectly cause mucosal barrier damage. Hp mucinase degrades mucus and promotes H+ anti-dispersion; Hp lipopolysaccharide has endotoxin properties, can stimulate the release of cytokines, interfere with the interaction of gastric epithelial cells and laminin and lose the integrity of mucosa. Hp esterase and phosphatase A degrade lipids and phospholipids, destroying cell membrane integrity. Some low molecular proteins produced by Hp can chemotaxis and activate inflammatory cells, which release a variety of cytokines and produce toxic oxygen free radicals. Certain component antigens of Hp are similar to certain cellular components of the gastric mucosa, so-called antigen simulation, and Hp-excited antibodies produced by the body can cross-react with host gastric mucosal cell components, resulting in damage of gastric mucosal cells.

Hp infection can cause high gastrin blood test, the mechanism includes: inflammation and tissue damage caused by 1Hp infection reduce the number of D cells in gastric mucosa, affecting the production of somatostatin, and the latter inhibits the release of gastrin from G cells. The effect is weakened. The 2Hp urease hydrolyzes the ammonia produced by urea to raise the pH of the local mucosa, which destroys the feedback inhibition of gastrin release by gastric acid.

Reports of the effects of Hp infection on gastric acid are not consistent. Most reports showed that the basal gastric acid and stimulating gastric acid secretion of Hp-positive DU patients was higher than that of Hp-positive healthy volunteers. The basal gastric acid and stimulating gastric acid secretion were also higher than Hp-negative controls, but the increase was Less than Hp positive DU patients. Hypergastrinemia caused by Hp infection is one of the causes of high gastric acid secretion.

There are various hypotheses about the mechanism by which Hp infection causes peptic ulcers. The leaky roof hypothesis compares the gastric mucosal barrier to the roof and protects the underlying mucosal tissue from gastric acid (rain) damage. When the mucosa first damages Hp (formation of a leaky roof), it will cause muddy water (H+ anti-dispersion), leading to mucosal damage and ulceration. This hypothesis emphasizes that the defensive factors caused by Hp infection are weakened, which may explain the occurrence of Hp-related GU. The six-factor hypothesis combines six factors of gastric acid-pepsin, gastric metaplasia, duodenitis, Hp infection, hypergastrinemia, and talk about hydrogen secretion, explaining the role of Hp in the pathogenesis of DU. Hp infection and genetic factors in the antrum of the stomach cause high gastric acid secretion. High acid directly damages the epithelium or causes secondary inflammation to cause gastric metaplasia of the duodenal mucosa, which creates conditions for Hp colonization in the duodenal mucosa. Duodenal Hp infection aggravates local inflammation (duodenum), which in turn promotes gastric metaplasia. This vicious cycle keeps the duodenal mucosa in a state of inflammation and damage, and the local bicarbonate secretion is reduced, which weakens the defense factor of the duodenal mucosa. The high gastrinemia caused by Hp infection stimulates gastric acid secretion and enhances the invasive factors. The enhancement of invasive factors and the weakening of defensive factors lead to ulcer formation.

2. The final formation of gastric acid and pepsin peptic ulcer is due to the digestion of gastric acid-pepsin itself, and the concept has not changed in the Hp era. Pepsin is a pepsinogen secreted by the main cell transformed by the activation of hydrochloric acid, which can degrade protein molecules, so it has an invasive effect on mucous membranes. Breakline

an examination

Related inspection

Carbon 13 urea breath test stomach ultrasound examination of gastrointestinal diseases ultrasound examination gastrointestinal CT examination gastroparesis angiography

an examination:

1. The diagnosis of Hp infection by Helicobacter pylori has become a routine test for peptic ulcer. The method can be divided into two categories: invasive and non-invasive. The former requires gastroscopy and gastric mucosal biopsy, and can be determined simultaneously. Gastroduodenal disease, the latter only provides information on the presence or absence of Hp infection. Currently used invasive tests include rapid urease test, histological examination, mucosal smear microscopy, microaerobic culture and polymerase chain reaction (PCS); non-invasive tests mainly include 13C- or 14C-urea Gas test (13C-UBT or 14C-UBT) and serological tests. The rapid urease test is the preferred method for diagnosing Hp infection in invasive trials, and is simple and inexpensive. Combinatorial examination can directly observe Hp, and special staining such as Warthin-Starry can improve the detection rate compared with conventional HE staining. Staining microscopy after gastric mucosal smear is simple, but when the number of bacteria is small, it is easy to miss diagnosis. The technical requirements and costs of Hp culture and PCR detection are relatively high, mainly for scientific research. The sensitivity and specificity of 13C-UBT or 14C-UBT for detecting Hp infection in non-invasive trials can be used as the first choice for post-treatment treatment. Serological tests for the qualitative detection of anti-Hp antibody IgG should not be the preferred method for post-treatment review. Serological tests for qualitative detection of anti-Hp antibody IgG are not suitable as a confirmation test for whether Hp is eradicated after treatment.

2, gastric juice analysis GU patients with normal or lower than normal gastric acid secretion, some DU patients increased, but there is a great overlap with normal people, so gastric juice analysis is of little value in the diagnosis and differential diagnosis of peptic ulcer. At present, it is mainly used for the auxiliary diagnosis of gastrinoma. If BAO>15mmol/h, MAO>60mmol, BAO/MAO ratio>60%, it suggests the possibility of gastrinoma.

3, serum gastrin determination of peptic ulcer serum lutein is slightly higher than normal people, but the diagnosis is not significant, it should not be classified as routine. However, if a gastrinoma is suspected, this test should be performed. Serum gastrin value is generally inversely proportional to gastric acid secretion, low gastric acid, high gastrin; high gastric acid, low gastrin; and gastric augmentation.

Differential diagnosis

Differential diagnosis:

1. Duodenal ulcer: Duodenal ulcer is a common disease of the digestive tract. It is generally believed that the cerebral cortex is exposed to external irritations, causing paralysis of the blood vessels and muscles in the stomach and duodenum. The wall cell dystrophies and the resistance of the gastrointestinal mucosa are reduced, causing the gastrointestinal mucosa to be easily digested by gastric juice to form ulcers. At present, some people think that it is caused by Campylobacter pneumoniae infection. The ulcer is often single, but there are also multiple ulcers, stomach. And duodenal bulb ulcers, when present, are called complex ulcers.

2, gastric ulcer: gastric ulcer is a common disease of the digestive system, which is typically characterized by hunger discomfort, fullness of hernia, pantothenic acid or chronic mid-abdominal pain after meal. In severe cases, there may be melena and hematemesis. More obvious diseases are caused by Helicobacter pylori infection, taking non-steroidal anti-inflammatory drugs (NSAID) and excessive gastric acid secretion; in addition, it can be caused by genetic factors and mood fluctuations, overwork, eating disorders, smoking, alcohol abuse and other factors. Due to the long-term condition of the stomach ulcer, the condition is complicated, and it is related to mental emotions. If the condition is aggravated or the treatment is not timely, it will lead to bad consequences such as bleeding, perforation, pyloric obstruction and cancer, which seriously endanger people's health, so it should be highly valued.

diagnosis:

1. Prone to vomiting: vomiting occurs in approximately 40% of patients with pyloric canal ulcers. Mainly because of ulceration caused by pyloric congestion, edema, recurrent episodes of sputum, scar formation, resulting in pyloric tube deformation, leading to slow or difficult gastric contents to the duodenum, resulting in vomiting of gastric contents retention.

2. Easily and bloody: It has been reported that about 1/2 of the patients have blood, which is characterized by hematemesis or melena, and repeated bleeding is not easy to stop. Analysis of the cause, the pyloric sphincter of the pyloric sphincter frequently and strongly contracted, so that the blood stasis formed by the bleeding is easy to fall off and easy to re-spray blood.

3. There is no obvious characteristic of pain: it can be expressed as hunger pain or postprandial pain, and the pain after meals is obvious.

4. Easy to miss diagnosis: X-ray barium meal examination of pyloric tube ulcer is easy to miss diagnosis, so take a gastroscopy. Under the gastroscope, the size and shape of the ulcer and the pyloric obstruction and edema can be directly observed.

5. The effect of drug treatment is not very satisfactory: the general ulcer disease taking the drug for 1 to 2 weeks can be relieved, and the ulcer can be cured in 4 to 6 weeks, but the pyloric tube ulcer is slightly less effective against the bird-killing drug, so it should be extended clinically. Treatment time. Most fools can be cured through strict and reasonable medical treatment. A small number of patients with medical treatment, or repeated recurrence, or those who lead to fatigue pyloric stenosis advocate surgery.

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