prepyloric ulcer
Introduction
Introduction The chronic ulcer located between Tuen Mun and the pylorus is called gastric ulcer (GU) and is a type of peptic ulcer. Peptic ulcer can occur in the stomach, duodenum, or in the lower esophagus, near the gastric-jejunum anastomosis, and in the internal ectopic gastric mucosa of the Meckel. The formation of these ulcers is related to the digestion of gastric acid and pepsin, so it is called peptic ulcer. The vast majority of the disease is located in the stomach and duodenum (98% to 99%). About 10% of people in the population may suffer from this disease during their lifetime, so it is a frequently-occurring disease and a common disease, and it plays an important role in digestive surgery.
Cause
Cause
The cause of ulceration in the pyloric area:
(1) Causes of the disease: Gastric ulcer is a multi-factor disease, and the cause is complicated. It has not been fully understood so far, which is caused by a comprehensive factor.
1. Genetic factors: gastric ulcer sometimes has a family history, especially in children with ulcers, family history can account for 25% to 60%. In addition, people with type A blood are more susceptible to this disease than people with other blood types.
2. Chemical factors: long-term consumption of alcohol or long-term use of aspirin, corticosteroids and other drugs may cause this disease, in addition to long-term smoking and drinking tea seems to have a certain relationship.
3. Living factors: Patients with ulcer disease seem to be more common in some occupations such as drivers and doctors, and may be related to the law of diet. Work too much can also induce the disease.
4. Mental Cause: Mental stress or anxiety, sentimentality, excessive mental work is also a predisposing factor for this disease. May be caused by vagus nerve excitement and excessive gastric acid secretion.
5. Infectious factors: The effect of Helicobacter pylori (HP) on the occurrence of gastric ulcer is still difficult to explain, because only a small number of HP infected people have gastric ulcer. However, almost all patients with gastric ulcers have chronic active gastritis. HP is the leading cause of the onset and spread of gastritis. When the HP is cleared, the gastritis disappears. Quantitative studies of HP infection have shown that gastric ulcers, especially those located in the upper part of the stomach, often involve severe HP infection.
6. Other factors: The incidence of this disease varies from country to country and from region to region. The incidence rate varies from season to season, indicating that the geographical environment and climate are also important factors. In addition, the disease can also occur on the basis of other primary diseases such as burns, severe traumatic brain injury, gastrinoma, hyperparathyroidism, emphysema, cirrhosis, and renal failure, so-called "secondary ulcer" (secondary Ulcer). This may be related to gastrin, hypercalcemia and excessive vagal nerve excitability.
(2) Pathogenesis:
1. Bile reflux and gastric ulcers In 1883, Beaumont first observed that bile flowed back into the stomach under certain unusual conditions, but it failed to attract attention. It was not until 1965 that du Plessis suggested that bile reflux may play an important role in the pathogenesis of gastric ulcer. Studies have shown that bile reflux into the stomach is common in patients with gastric ulcer disease and is not common in normal people. Bile is present in both fasting gastric fluid specimens and postprandial specimens of patients with gastric ulcer disease. After the stomach ulcer heals, reflux can be reduced or stopped.
The dysmotility of the stomach or duodenum is the cause of bile reflux, but the underlying factors that contribute to dysmotility remain unclear. In some patients, taking a straight position and smoking can increase reflux. Bile reflux is not limited to gastric ulcers, but can also be seen in gastritis, such as alcoholic gastritis and atrophic gastritis, as well as some conditions of gastritis, such as duodenal ulcer disease and chronic respiratory disease. It is unclear whether gastritis itself can cause dysfunction and cause reflux.
According to Hollander, the normal stomach has a double barrier: mucus and mucosal epithelium. It not only protects the mucous membrane from ulceration, but also prevents acid from penetrating into the gastric mucosa and allowing acid secretion to remain within the stomach cavity. The normal gastric mucosa prevents the reverse dispersion of acid from being associated with lipoprotein membranes on the surface of epithelial cells. The harmful effect of bile in the stomach is that it destroys the barrier, causing hydrogen ions to penetrate the gastric mucosa and damage the gastric mucosa. Bile can change the nature of gastric mucus. The surface mucus is exfoliated and the epithelial cells are depleted of their mucus content. In addition to its effect on mucus, bile also destroys the mucosal barrier, making it no longer prevent hydrogen ions from penetrating into the mucosa. The reverse dispersion of hydrogen ions causes further damage to the mucosa. Bile acids can also destroy surface epithelial cells and diffuse into the mucosa. Stimulates mast cells to release histamine. An increase in histamine concentration in the gastric intercellular fluid causes vasodilation with increased mucosal blood flow and capillary permeability, resulting in mucosal edema, hemorrhage, inflammation, and even acute erosion. The damaged mucous membrane is prone to ulceration.
Experiments have shown that the damage of the duodenal contents to the gastric mucosa is much greater than that of the simple bile or pancreas. Some of the destructive components secreted by bile and pancreas have been identified. Bile acids are known to cause mucosal damage. The lysolecithin produced by mixing bile and pancreatic juice in the duodenum can cause damage to the mucosal barrier. Lecithin in normal bile is converted to lysolecithin by pancreatic secretory phospholipase A; this reaction is activated by both trypsin and bile acids. High concentrations of lysolecithin have been detected in nighttime gastric fluid samples from patients with gastric ulcer disease. In addition, the damage of bile to the gastric mucosa depends not only on the decontamination of bile acids, but also on the acidity of the stomach contents. When the destruction of three different human bile solutions at pH 8, 4 and 2 was observed, it was found that the pH 8 was the least disrupted, while the pH 2 was the most disruptive. This finding suggests that bile, especially with acid, acts as a destructive agent.
Bile also promotes the release of gastrin from the G cells of the sinus, which in turn stimulates the secretion of acid and pepsin. Therefore, on the one hand, bile increases the reverse dispersion of hydrogen ions and on the other hand increases acid secretion. Extraction of gastric contents to determine acidity may not reveal the effect of bile reflux increasing acid secretion, as this method of detection only reflects the final effect of bile reflux on gastric acidity. Long-term bile reflux can further alter the effect of bile reflux on gastric acid secretion by forming atrophic gastritis with parietal cell loss and intestinal metaplasia. It has been suggested that bile reflux can play a role in the pathogenesis of duodenal ulcer disease by the release of gastrin caused by intermittent gastric hypersecretion. However, this hypothesis has yet to be confirmed.
2. Acid and gastric ulcer disease: The role of acid in the pathogenesis of gastric ulcer has been widely noticed. "There is no ulcer without acid." This famous saying also applies to gastric ulcer disease, but because of gastric sore ulcer patients The secretion is reduced or normal, and the amount of acid secretion does not seem to occupy an important position in the pathogenesis of gastric ulcer.
The role of acid in gastric ulcer disease may not determine the location of the ulcer but the location of the ulcer. After observing the gastrectomy specimens of 149 patients with gastric ulcer disease, it was found that all ulcers occurred in the pyloric gland area and were adjacent to the acid secretion zone. This may be due to the fact that the pyloric mucosa in this area is more acidic than any other part. The reduction in acid secretion in many patients with gastric ulcer can be partially explained by Davenport's comments. That is, the patient's gastric mucosa has defects that cause hydrogen ions to diffuse back into the mucosa from the stomach cavity. This defect has been confirmed by Overhoit and Pollard in some patients with gastric ulcer. Another important factor is that patients with gastric ulcer have fewer parietal cell populations and are often accompanied by atrophic gastritis.
3. Gastric emptying and motility during gastric ulcer disease: In the etiology of gastric ulcer disease, gastric emptying delay and retention are considered to be an important factor. This theory can explain the formation of ulcers secondary to vagus nerve severing but without drainage surgery, which is far from being a satisfactory explanation for most naturally occurring gastric ulcers. There is no definitive evidence that dysmotility or retention in gastric ulcer patients is more common than normal.
4. Gastric mucosa at the time of ulcer disease: Gastric ulcer disease often coincides with chronic gastritis. In 1965, duPlessis found that 65 of them had gastric gastritis in 75 stomach ulcers. The gastritis spread from the pylorus to the proximal end. The pyloric gland is often extensively affected and may involve the fundic gland. Chronic gastritis in these cases is more extensive and severe than chronic gastritis in cases of duodenal ulcer. He also found that gastric ulcers are often located within areas with chronic gastritis. In general, the higher the position of the ulcer in the stomach, the wider the range of gastritis damage. In 1966 Lawson proved that mucosa with gastritis is prone to peptic ulcer. These findings support the notion that gastric ulcer disease occurs on the basis of chronic gastritis. The concept that gastritis is the result of gastric ulcer disease may not be correct, because chronic gastritis is not only distributed around the ulcer, but also affects the distal end of the entire stomach. The gastric ulcer itself is unlikely to cause such a wide range of gastritis.
5. Hp and gastric ulcer disease: There is sufficient evidence that Hp not only plays an important role in the pathogenesis of duodenal ulcer, but also occupies a certain position in the pathogenesis of gastric ulcer.
6. Pathological classification: Gastric ulcer is a chronic disease. According to the location of the ulcer, the ulcer is divided into 4 types:
Type I: small curved ulcer, located near the small curved side of the gastric incision, especially found at the junction of the gastric antrum mucosa and the gastric mucosa. Often low gastric acid secretion, accounting for about 80% of gastric ulcer;
Type II: Gastric duodenal complex ulcer. Duodenal ulcers often occur first, followed by gastric ulcers. For high gastric acid secretion, easy to merge with bleeding, the condition is stubborn. 5% to 10%;
Type III: pre-pyloric and pyloric tube ulcers. Usually high gastric acid secretion, medical treatment is easy to relapse; Type IV: high gastric ulcer, located in the upper third of the stomach, within 4cm from the esophagogastric junction, within 2cm is called "near cardia ulcer". Low gastric acid secretion, easy to send out blood and perforation.
It can be seen that gastric ulcer is the most common with small curved ulcers, especially the small antrum of the stomach. Some large ulcers can occur in the upper part of the small bend and in the Tuen Mun area. It is very rare on the fundus and the large curved side.
7. Pathological morphology: The ulcer is usually single-shot, round or oval, with a diameter of 0.5 to 2 cm and rarely more than 3 cm. The edge of the ulcer is neat, shaped like a knife, and the bottom usually passes through the submucosa, deep into the muscle layer or even the muscle layer. The submucosa to the muscular layer are completely destroyed by erosion and replaced by granulation tissue and scar tissue. During the active period, the bottom of the ulcer can be divided into four layers from the surface layer to the deep layer: 1 exudation layer; 2 necrotic layer; 3 granulation tissue layer; 4 scar tissue layer. A gastric ulcer can occur in 2% to 5% of the ulcer.
Examine
an examination
Related inspection
Immunological detection of Helicobacter pylori by Helicobacter pylori
Examination and diagnosis of pyloric area ulcers:
The clinical manifestations of gastric ulcers are somewhat similar to those of duodenal ulcers, but they have their own specificities.
1. Clinical features: The clinical manifestations of gastric ulcer have three characteristics: 1 chronic process. From a few years to more than 10 years or more. 2 periodicity. The onset of the attack and the remission period often occur in the course of the disease. 3 rhythm: Pain manifests as postprandial pain, pain starts half an hour after a meal, disappears until the next meal, and begins again and again. Symptoms of gastric ulcer are mainly abdominal pain; with or without vomiting, nausea, acid reflux, belching and other symptoms. However, many patients have the first symptoms of various complications of gastric ulcer such as perforation, hemorrhage, and pyloric obstruction.
2. Clinical symptoms and signs: (1) Pain in the upper abdomen: The pain of gastric ulcer is a kind of pain of visceral nature. The location of the body surface is not exact. At the same time, the pain is not severe and can be tolerated. It is characterized by burning pain and painful discomfort. Wait. The active period is rhythmic, manifested as postprandial pain, with periodic and seasonal characteristics as the pathology develops. Ulcers near the cardia can also manifest as a burning sensation in the back of the chest and pain in the left chest. When the ulcer penetrates, it manifests as aggravation of pain, radiation to the back or back pain, and nighttime pain. When the nature of the pain changes and the rhythm changes, you should be alert to the possibility of malignant transformation.
(2) nausea and vomiting: vomiting without pyloric obstruction indicates that the ulcer is in active phase and vomiting is intermittent. Frequent vomiting prompts pyloric obstruction.
(3) acid reflux, hernia, diarrhea: acid reflux also suggests that the ulcer may be in active phase.
(4) bleeding, perforation: bleeding, perforation have their special clinical manifestations, see the complications section.
(5) Signs: There is generally no positive signs during the remission period. During the active period, only the upper abdomen is tender and tender. However, it should be noted that the anal examination and examination of Weierxiao lymph nodes with or without swelling, in order to distinguish from gastric cancer.
1. Clinical features: deep abdominal pain 2 hours after a meal, usually no abnormal signs.
2. Auxiliary examination: the diagnosis of gastric ulcer mainly depends on the history of symptoms, gastroscope plus biopsy, barium meal examination. In addition, gastric acid determination, serum gastrin determination, serum calcium determination also have certain diagnostic and differential diagnostic significance. In recent years, with the application of electronic gastroscope, the diagnostic coincidence rate of gastric ulcer is extremely high.
Diagnosis
Differential diagnosis
Symptoms of pyloric ulcer in the pyloric area:
Differential diagnosis of pyloric area ulcer: 1, ulcer type gastric cancer: gastric cancer is one of the common malignant tumors in China, and its incidence rate ranks first in all kinds of tumors in China. Among the malignant tumors of the stomach, adenocarcinoma accounts for 95%, which is also the most common malignant tumor of the digestive tract, and even ranks among the top of all human malignant tumors. Early gastric cancer is mostly asymptomatic or only mild. When the clinical symptoms are obvious, the lesion is already advanced. Therefore, we must be very alert to the early symptoms of gastric cancer, so as not to delay the diagnosis and treatment.
2, duodenal ulcer: is a common disease of the digestive tract, it is generally believed that because the cerebral cortex receives external external stimuli, causing sputum in the blood vessels and muscles of the stomach and duodenum, causing dystrophic dysfunction of the gastrointestinal wall cells And the resistance of the gastrointestinal mucosa is reduced, causing the gastrointestinal mucosa to be easily digested by gastric juice to form ulcers. It is currently believed to be caused by Campylobacter pneumoniae infection. The ulcer is often single, but there are also multiple ulcers, stomach and duodenum. Ball ulcers, when present, are called complex ulcers.
The clinical manifestations of gastric ulcers are somewhat similar to those of duodenal ulcers, but they have their own specificities.
1. Clinical features: The clinical manifestations of gastric ulcer have three characteristics: 1 chronic process. From a few years to more than 10 years or more. 2 periodicity. The onset of the attack and the remission period often occur in the course of the disease. 3 rhythm: Pain manifests as postprandial pain, pain starts half an hour after a meal, disappears until the next meal, and begins again and again. Symptoms of gastric ulcer are mainly abdominal pain; with or without vomiting, nausea, acid reflux, belching and other symptoms. However, many patients have the first symptoms of various complications of gastric ulcer such as perforation, hemorrhage, and pyloric obstruction.
2. Clinical symptoms and signs:
(1) Upper abdominal pain and discomfort: The pain of gastric ulcer is a pain of visceral nature. The body surface is not accurate, and the pain is not severe, and it can be tolerated. It is characterized by burning pain, pain and discomfort. The active period is rhythmic, manifested as postprandial pain, with periodic and seasonal characteristics as the pathology develops. Ulcers near the cardia can also manifest as a burning sensation in the back of the chest and pain in the left chest. When the ulcer penetrates, it manifests as aggravation of pain, radiation to the back or back pain, and nighttime pain. When the nature of the pain changes and the rhythm changes, you should be alert to the possibility of malignant transformation.
(2) nausea and vomiting: vomiting without pyloric obstruction indicates that the ulcer is in active phase and vomiting is intermittent. Frequent vomiting prompts pyloric obstruction.
(3) acid reflux, hernia, diarrhea: acid reflux also suggests that the ulcer may be in active phase.
(4) bleeding, perforation: bleeding, perforation have their special clinical manifestations, see the complications section.
(5) Signs: There is generally no positive signs during the remission period. During the active period, only the upper abdomen is tender and tender. However, it should be noted that the anal examination and examination of Weierxiao lymph nodes with or without swelling, in order to distinguish from gastric cancer.
1. Clinical features: deep abdominal pain 2 hours after a meal, usually no abnormal signs.
2. Auxiliary examination: the diagnosis of gastric ulcer mainly depends on the history of symptoms, gastroscope plus biopsy, barium meal examination. In addition, gastric acid determination, serum gastrin determination, serum calcium determination also have certain diagnostic and differential diagnostic significance. In recent years, with the application of electronic gastroscope, the diagnostic coincidence rate of gastric ulcer is extremely high. Breakline
