Brief introduction of retrobulbar ulcer

Directory 1 pinyin 2 English reference 3 disease classification 4 disease overview 5 disease description 6 symptoms and signs 7 disease etiology 8 pathophysiology 9 diagnostic examination 10 differential diagnosis 1 treatment scheme 6 5438+02 complications 13 prognosis and prevention 14 epidemiology/kloc.

2 English references Retrobulbar ulcer

Classification of diseases Gastroenterology

4 disease overview duodenal ulcer is a common disease, which is more common than gastric ulcer. Mainly located in the duodenal bulb, followed by retrobulbar ulcer, duodenal ulcer is rare.

Clinical manifestations: most of them are periodic and rhythmic pain in the upper and middle abdomen, accompanied by acid and belching. The pain of penetrating ulcer in the back wall can radiate to the back. When the ulcer has complications, it may have corresponding clinical manifestations, such as coffee-like vomiting, melena, obstruction, perforation and so on.

5 disease description refers to the ulcer below the duodenal bulb, mostly at the proximal end of the duodenum, which is easy to be missed by X-ray and gastroscope. Retrobulbar ulcer mostly has the clinical characteristics of duodenal ulcer, but nocturnal pain and back radiation pain are more common, which have poor response to drug treatment and are more prone to bleeding. Retrobulbar ulcers outside the second segment of the duodenum usually suggest the existence of gastrinoma.

6 Symptoms and Signs Retrobulbar ulcer mostly has the clinical characteristics of duodenal ulcer, but nocturnal pain and back radiation pain are more common, which have poor response to drug treatment and are more prone to bleeding. Retrobulbar ulcers outside the second segment of the duodenum usually suggest the existence of gastrinoma. Complications: In recent ten years, with the continuous emergence of effective drugs for treating peptic ulcer and the extensive development of anti-Hp treatment, the complications of peptic ulcer have been greatly reduced.

First, bleeding? Peptic ulcer is the most common cause from digestion to bleeding, accounting for about 50% of all causes. 15%-25% patients may be complicated with bleeding. The amount of bleeding is related to the size of eroded blood vessels. The rupture of Moses' blood vessels only caused oozing, and the amount of bleeding was very small. If the artery ruptures, the bleeding is urgent and excessive; The light person shows black feces, and the heavy person has new hematemesis. Generally, when bleeding is 50-1000ml, melena will occur; when it exceeds1000 ml, it will cause circulatory disorder, dizziness, sweating, blood pressure drop and heart rate increase; when it exceeds 1500ml, it will cause shock within half an hour. About 40% can recur after the first bleeding, which is easy to be induced by NSAID. Ulcer associated with NSAID can suddenly bleed without symptoms.

General medical conservative treatment is effective, and sometimes emergency gastroscopy and hemostasis are needed. If the bleeding is urgent and large, and medical treatment can't control the condition, emergency surgery should be performed.

Second, perforation? The perforation of peptic ulcer can cause three consequences: ① the ulcer enters the abdominal cavity and causes diffuse peritonitis (free perforation); (2) Ulcer perforation reaches and is blocked by adjacent parenchymal organs, liver, pancreas and spleen (penetrating ulcer); ③ Ulcer perforation enters the cavity control organ to form fistula. About 1%-5% of Du and Gu can carry out free perforation. Du's free perforation mostly occurs in the anterior wall, and the posterior wall ulcer is usually accompanied by bleeding or penetrating into the parenchymal organs, but occasionally it collapses and penetrates into the omental sac, causing localized peritonitis and even abscess. At this point, the back pain is severe. Gu free perforation mostly occurs in the minor curvature, mainly manifested as sudden and severe abdominal pain, which continues and intensifies, first appearing in the upper abdomen and then gradually expanding to fullness. Abdominal wall sclerosis, tenderness and rebound pain, half of them are meteorological, the voiced area of the liver disappears, and some of them are in shock. About 10% was accompanied by perforation bleeding. Posterior wall perforation occurs slowly and adheres to adjacent parenchymal organs (liver and pancreas). This penetrating ulcer has changed the law of abdominal pain, and the stool is stubborn and persistent. If it penetrates the pancreas, abdominal pain will radiate to the back, and serum amylase will increase significantly. It is rare for an ulcer to penetrate into a fistula. Du Can penetrates into the common bile duct, while the valley can penetrate into the duodenum or transverse colon.

Third, pyloric obstruction? About 2%-4% of cases are mainly caused by ulcer or pyloric canal cavity ulcer. Acute ulcer attack can cause temporary obstruction due to inflammation, edema and pyloric spasm, which can be relieved with the improvement of inflammation. Chronic obstruction is persistent, mainly due to scar contraction. Pyloric obstruction causes delayed emptying, abdominal distension and discomfort, aggravated pain after meals, often accompanied by peristalsis waves and nausea and vomiting. Symptoms can be temporarily relieved after a lot of vomiting, and the vomit contains fermented acidic food. Severe vomiting can lead to dehydration and low chlorine and low potash poisoning. Malnutrition and weight loss often occur. If there is a shock sound in the stomach on an empty stomach in the morning, and the amount of liquid pumped out by inserting a gastric tube is more than 200ml, the existence of this disease should be considered and further X-ray or gastroscopy should be done.

Fourth, cancer? Several aunts will become cancerous, but Du won't. The canceration of the valley occurred at the edge of the ulcer, and the estimated canceration rate was below 1%. We should be alert to those with long history of chronic GU, under 45 years old and intractable ulcer. Multi-point biopsy under gastroscope for pathological examination, reexamining gastroscope after active treatment until the ulcer is completely healed, and regular follow-up if necessary.

7 Etiology of the disease The gastroduodenal mucosa is not only frequently exposed to high-concentration gastric acid, but also attacked by pepsin, microorganisms, bile salts, ethanol, drugs and other harmful substances. However, under normal circumstances, gastroduodenal mucosa can resist the damage of these invasive factors and maintain the integrity of mucosa. This is because gastroduodenal mucosa has a series of defense repair and repair mechanisms, including mucus/bicarbonate barrier, mucosal barrier, mucosal blood flow, cell renewal, prostaglandin and epidermal growth factor. The occurrence of peptic ulcer is due to the imbalance between the invasive factors that damage gastroduodenal mucosa and the self-defense and repair factors of mucosa. This balance may be due to the enhancement of invasion factors, the weakening of defense-repair factors, or both. There are differences in pathogenesis between Gu and Du. The former is mainly the weakening of defense and repair factors, while the latter is mainly the strengthening of invasion factors. Peptic ulcer is a disease caused by many reasons, that is, the etiology and pathogenesis of patients may be different, but the clinical manifestations are similar.

8 pathophysiological pathogenesis:

1. Helicobacter pylori infection? A large number of studies in recent ten years have fully proved that Helicobacter pylori (Hp) infection is the main cause of peptic ulcer.

(1) Is Hp infection rate high in patients with peptic ulcer? If antibiotics, bismuth or non-steroidal anti-inflammatory drugs (NSAID) can be excluded, the infection rate of Hp in DU patients is 90%- 100%, and that in GU patients is 80%-90%. The risk of peptic ulcer in Hp infected people is also significantly increased. Prospective studies show that about 15%-20% people infected with Hp can develop peptic ulcer.

(2) According to HP, it can promote ulcer healing and significantly reduce ulcer recurrence rate? The treatment of eradicating Hp without inhibiting gastric acid secretion can effectively cure ulcers; The so-called refractory ulcer with unsatisfactory curative effect is treated with conventional drugs that inhibit the secretion of Wei San, and Hp is effectively eradicated and cured after treatment. Hp regimen with high curative effect was used 1 week, and no anti-ulcer treatment was given afterwards. After 4 weeks of treatment, the ulcer healing rate was higher than or equal to that of conventional gastric acid secretion inhibitors for 4-6 weeks. These results prove that eradicating Hp can promote ulcer healing from different angles.

Frequent recurrence of ulcer is one of the main characteristics of the natural course of peptic ulcer. The annual recurrence rate of ulcers healed after treatment with conventional drugs that inhibit gastric acid secretion is 50%-70%. Eradication of Hp can reduce the annual recurrence rate of Du and Gu to below 5%, and make most ulcer patients completely cured. In addition, the eradication of Helicobacter pylori can significantly reduce the incidence of complications such as peptic ulcer bleeding.

(3) Does 3)Hp infection change the balance between mucosal invasion factors and defense factors? Hp colonizes gastric mucosa (stomach and duodenum with gastric metaplasia) by virtue of its virulence factor, which induces local inflammation and immune response and destroys local mucosal defense/repair mechanism; On the other hand, Hp infection can increase the secretion of gastrin and gastric acid, and enhance the invasion factor. The synergistic effect of these two factors leads to gastroduodenal mucosal injury and ulcer formation.

The virulence factors of Helicobacter pylori include factors that make Helicobacter pylori colonize gastric mucosa and factors that induce tissue damage, and some factors have both. The colonization site of Hp is on the epithelial surface of gastric mucosa and the bottom of mucosa. Generally, there are more Hp in the antrum, less HP in the body and bottom of the stomach, and it can also inhabit the metaplastic mucosa of duodenum and stomach. The colonization of Hp in the stomach should not only resist the killing effect of gastric acid, but also rely on its movement through the mucus layer. Hp bacteria are spiral with flagella at one end, which provides power for its application. Urease produced by Hp hydrolyzes urea into ammonia and carbon dioxide, and ammonia forms an "ammonia cloud" around Hp to neutralize the surrounding gastric acid, thus protecting Hp. Hp attaches specifically to gastric epithelium, making its toxin easy to act on epithelial cells. The adhesion specificity of Hp reflects that it has adhesion factors, while gastric epithelial cells have specific receptors for adhesion factors.

Hp toxin, toxic enzyme and mucosal inflammatory reaction caused by Hp can all cause gastroduodenal mucosal barrier damage. Vacuotoxin (VacA) protein and cytotoxin related gene (CagA) protein are the main signs of Hp virulence. VacA protein can make cultured cells produce vacuoles; The exact function of CagA protein is not clear. Ammonia produced by urease decomposition of urea can not only protect Hp itself, but also directly and indirectly cause mucosal barrier damage. Hp mucinase degrades mucus and promotes the reverse dispersion of H+; Hp lipopolysaccharide has the characteristics of endotoxin, which can release cytokines and interfere with the interaction between gastric epithelial cells and laminin, thus making the mucosa lose its integrity. Esterase and phosphatase A of Hp degrade lipids and phospholipids and destroy the integrity of cell membrane. Some low molecular weight proteins produced by Hp can chemotactic and activate inflammatory cells, which release various cytokines and produce toxic oxygen free radicals. Some antigens of Hp are similar to some cellular components of gastric mucosa, that is, antigen mimics. Antibodies produced by Hp can cross-react with the cellular components of the host gastric mucosa, resulting in gastric mucosal cell damage.

Hp infection can cause hypergastrinemia, and its mechanisms include: ① Inflammation and tissue damage caused by HP infection reduce the number of D cells in gastric antrum mucosa, affect the production of somatostatin, and weaken the inhibitory effect of somatostatin on the release of gastrin from G cells. ② Ammonia produced by urease hydrolysis of urea by Helicobacter pylori increased the local mucosal pH, which destroyed the feedback inhibition of gastric acid on gastrin release from G cells.

There are different reports about the influence of Helicobacter pylori infection on gastric acid. Most reports show that the gastric acid secretion of Hp-positive DU patients is higher than that of Hp-positive healthy volunteers in basic gastric acid, meal and gastrin, and the gastric acid secretion of Hp-positive healthy volunteers is also higher than that of Hp-negative control group, but the increase is smaller than that of HP-positive DU patients. Hypergastrinemia caused by Hp infection is one of the causes of hypergastric acid secretion.

There are many hypotheses about the mechanism of peptic ulcer caused by Helicobacter pylori infection. The "roof leakage" hypothesis compares the gastric mucosal barrier to the "roof", which protects the mucosal tissue under it from the damage of gastric acid ("rain"). When the mucosa is first destroyed by Hp (forming a "leaky roof"), it will cause "muddy water" (H+ anti-dispersion), resulting in mucosal damage and ulcer. This hypothesis emphasizes that the defensive factors caused by Hp infection are weakened, which can explain the occurrence of Hp-related GU. The six-factor hypothesis integrates six factors, such as gastric acid-pepsin, gastric metaplasia, duodenitis, Hp infection, hypergastrinemia and sodium salt secretion, to explain the role of Hp in the pathogenesis of DU. Gastric antrum Hp infection and genetic factors lead to excessive gastric acid secretion, which directly damages epithelium or causes secondary inflammation, which makes duodenal mucosa metaplasia and creates conditions for Hp to colonize duodenal mucosa. Hp infection in duodenum aggravates local inflammation (duodenum), and then promotes gastric metaplasia. This vicious circle keeps the duodenal mucosa in a state of inflammation and injury, and the local bicarbonate secretion decreases, weakening the defense factors of the duodenal mucosa. Hypergastrinemia and gastric acid secretion caused by Hp infection increase invasive factors. The enhancement of invasive factors and the weakening of defensive factors lead to the formation of ulcers.

Second, gastric acid and pepsin? The final formation of peptic ulcer is caused by gastric acid-pepsin self-digestion, and this concept has not changed in the "HP era". Pepsin is a pepsinogen secreted by main cells and activated by hydrochloric acid. It can degrade protein molecules, so it has invasive effect on mucosa.

9 Diagnostic examination 1. X-ray barium meal examination? Air-barium double contrast radiography can better display mucosal images. There are direct and indirect X-ray signs of ulcer: niche shadow is a direct sign, which has certain value for the diagnosis of ulcer. Benign ulcer protrudes out of the outline of barium in stomach and duodenum, with smooth ring around it and radial mucosal folds around it. Indirect signs include local tenderness, incision spasm of greater curvature of stomach, duodenal bulb irritation and bulbar deformity. Indirect signs only indicate ulcers.

Second, gastroscopy and mucosal biopsy? Gastroscopy can not only directly observe and photograph gastroduodenal mucosa, but also take biopsy under direct vision for pathological and Hp detection. Its preparation for the diagnosis of peptic ulcer and the differential diagnosis of benign and malignant ulcer is higher than that of X-ray barium meal examination. When the ulcer is too small or superficial, barium meal examination is difficult to find; Duodenal bulbar malformation found by barium meal examination can be explained in many ways, and it is difficult to diagnose. Active upper gastrointestinal bleeding is a contraindication of barium meal examination, and endoscopic examination can determine its source and nature. About 5% of ulcers that look benign by barium meal examination or endoscopy are actually malignant, while a few ulcers that look malignant are proved to be benign, so it is difficult to distinguish them without biopsy. In addition, endoscopic examination can also find gastritis and duodenitis with ulcer. Endoscopically, peptic ulcer is mostly round or oval, occasionally linear, with smooth edges, and the bottom is filled with grayish yellow or white exudate. The surrounding mucosa may be hyperemia and edema, and sometimes the folds are concentrated in the ulcer. Endoscopic ulcer can be divided into three stages: active stage (a), healing stage (h) and scar stage (s), and each stage can be divided into two stages: 1 and 2.

10 differential diagnosis: the main clinical manifestation of this disease is epigastric pain, so it needs to be differentiated from other diseases with epigastric pain symptoms. In addition, it should be differentiated from gastrinoma with gastric and duodenal ulcer.

First, functional dyspepsia? Refers to those with dyspeptic symptoms but no ulcer and other organic diseases (such as hepatobiliary and pancreatic diseases), which can be completely normal or only mild gastritis. Autoimmune diseases are common, especially among young women. It is characterized by fullness, belching, acid regurgitation, nausea and loss of appetite in the upper abdomen after meals, and sometimes the symptoms are similar to peptic ulcer. The differentiation from peptic ulcer depends on X-ray and gastroscopy.

Second, chronic cholecystitis and cholelithiasis? Pain is related to eating greasy food. The pain is located in the right upper abdomen and radiates to the back. Typical cases of fever and jaundice are not difficult to distinguish from peptic ulcer. For atypical patients, B-ultrasound or endoscopic retrograde cholangiography is needed for differential diagnosis.

Third, stomach cancer? Gu and gastric cancer are difficult to distinguish from symptoms, and they must rely on barium meal examination and endoscopy, especially the latter can take tissues for pathological examination under direct vision. Endoscopic and X-ray findings of type ⅲ (ulcer type) early gastric cancer are easily confused with benign gastric ulcer, and biopsy is helpful to clarify it. If it is advanced gastric cancer, barium meal and endoscopy are generally easy to distinguish from benign ulcer. X-ray barium meal examination of malignant ulcer showed that the niche was located in the gastric cavity with uneven edge, and the gastric wall around the niche was stiff and nodular, and the folds gathered in the direction of ulcer were interrupted. Endoscopically, the malignant ulcer has irregular shape, uneven bottom, dirty moss and nodular protuberance on the edge. It should be emphasized that: ① For patients with 1 100 million malignant ulcer with negative biopsy, gastroscopy must be performed again in a short time. ② After treatment with drugs that strongly inhibit gastric acid secretion, ulcer shrinkage or partial healing is not a reliable basis for judging benign and malignant ulcers, and the follow-up of patients with GU should be strengthened.

Fourth, gastrinoma? Zolinger-Ellison syndrome, also known as Zolinger-Ellison syndrome, is caused by pancreatic non-β-cell tumors that secrete a large amount of gastrin. Tumors are often very small (< 1 cm), with slow growth and half of them are malignant. A large amount of gastrin can make parietal cells proliferate and secrete a large amount of gastric acid, which often makes the upper digestive tract in a high acid environment, leading to multiple ulcers in the bulbous and atypical parts of the stomach and duodenum (descending and transverse segments of the duodenum, and even the proximal end of the intestine). The main point of differentiation from common peptic ulcer is that the ulcer occurs in atypical parts and has refractory characteristics, such as high gastric acid secretion and gastrin in abdominal control serum > 200 pg/ml (often > 500 pg/ml).

1 1 The purpose of the treatment plan is to eliminate the cause, relieve the symptoms, heal the ulcer, prevent recurrence and avoid complications. The etiology and pathogenesis of peptic ulcer vary from patient to patient. We should analyze the possible pathogenic factors and pathophysiology of each case and give corresponding treatment.

First, general treatment? Life should be regular, work and rest should be combined to avoid overwork and mental stress. If you are anxious, you should enlighten them and give them sedatives if necessary. In principle, we should emphasize the timing of eating and avoid spicy and salty food and strong tea, coffee and other drinks. Although milk and soybean paste can temporarily dilute gastric acid, they contain calcium and protein, which can secrete gastric acid and should not be drunk too much. If you have a hobby of smoking and drinking, which is proved to be related to the onset of ulcers, you should quit smoking immediately. Those who take NSAID should stop taking them as much as possible; Even if patients have not taken such drugs, they should be reminded to use them with caution in the future.

Second, drug treatment? Before 1970s, the treatment of this disease mainly depended on antacids and anticholinergic drugs, and the appearance of H2RA caused the first change of treatment methods. The eradication of Hp advocated in recent years is a major milestone in treatment.

(1) The treatment to eradicate Hp? Eradication of Hp can make most patients with Hp-related ulcer completely achieve the therapeutic purpose. The international community has reached a consensus on the treatment of Hp-related ulcers, that is, whether the ulcer is primary or recurrent, whether it is active or quiescent, whether there is a history of complications or not, it should be treated for Hp.

1, the treatment plan to eradicate Hp? Hp infection is not easy to eradicate because the activity of most antibacterial drugs decreases in the low pH environment of the intestine and cannot penetrate the mucus layer to reach bacteria. Up to now, there is no single drug that can effectively eradicate Hp, so a treatment scheme of combining gastric acid secretion inhibitor, antibacterial drugs or synergistic colloidal bismuth has been developed. Therapeutic schemes for eradicating Helicobacter pylori can be roughly divided into two categories: proton pump inhibitors (PPI) and colloidal bismuth. PPI or colloidal bismuth plus clarithromycin (erythromycin), tetracycline and metronidazole (or tinidazole) constitute triple therapy.

The resistance rate of Hp strains to metronidazole increased rapidly. Furazolidone has a strong anti-Hp effect, and Hp is not easy to produce drug resistance. Furazolidone can be used instead of metronidazole, with a dose of 200mg/d, taken twice. H2RA can be used instead of PPI to reduce the cost, but the curative effect is also reduced. The first failure can be treated with PPI and colloidal bismuth combined with two antibacterial drugs.

2. Is it necessary to continue anti-ulcer treatment after 2.Hp eradication treatment? This has not been unified. Under the condition of high curative effect and small ulcer area, a single anti-Hp treatment 1-2 weeks can effectively heal the active ulcer. If the curative effect of Hp eradication program is slightly low, the ulcer area is large, the patient's symptoms are not relieved at the end of anti-Hp treatment or there is a recent history of complications such as bleeding, it should be considered to continue to treat with gastric acid secretion inhibitors for 2-4 weeks after anti-Hp treatment.

3. Review after anti-Hp treatment? After anti-Helicobacter pylori treatment, the test to determine whether Helicobacter pylori has been eradicated should be carried out at least 4 weeks after the treatment is completed. Most DU patients who receive highly effective anti-Hp regimen (eradication rate ≥ 90%) do not need to carry out experiments to confirm Hp eradication. DU with a history of refractory ulcers or complications should determine whether Hp has been eradicated. Because of the potential risk of malignant transformation, gastroscopy and Hp reexamination should be done at an appropriate time after treatment in principle. For patients with persistent dyspepsia after appropriate treatment, it should also be established whether Hp has been eradicated.

(2) Drug therapy to inhibit gastric acid secretion? The healing of ulcers, especially DU, is directly proportional to the intensity and time of acid-resistant treatment. Alkaline antacids (such as aluminum hydroxide, magnesium hydroxide and their compound preparations) neutralize gastric acid (which also has a certain cytoprotective effect), which has a good effect on relieving pain-like symptoms, but it takes a lot of time to promote ulcer healing. The inconvenience of taking drugs for many times and the possible adverse reactions caused by taking large doses of antacids for a long time limit its application. At present, antacids are rarely used to treat ulcers, which can be used as adjuvant therapy to strengthen analgesia. Pirenzepine, an anticholinergic drug, and proglumide, a gastrin receptor antagonist, are not effective in treating ulcers, so they are rarely used to treat ulcers.

At present, there are two drugs commonly used in clinic to inhibit gastric acid secretion: H2RA and PPI. Only when PPI acts on H+-K+-ATPase, the key enzyme in the last step of gastric acid secretion, can parietal cells recover their acid secretion function. Therefore, PPI has a stronger and more lasting inhibitory effect on gastric acid secretion than H2RA. At present, at least four PPI have been used in clinic, namely omeprazole, lansoprazole, pantoprazole and Labeira. The general dosage is omeprazole 20mg, lansoprazole 30mg, pantoprazole 40mg, Labeira 10mg, daily 1 time; After Hp is eradicated, the dose should be doubled.

(3) Protection of gastric mucosa? There are three kinds of gastric mucosal protective agents, namely sucralfate, bismuth potassium citrate and prostaglandin misoprostol. The ulcer healing rate of these drugs after 4-8 weeks is similar to that of H2RA. The anti-ulcer mechanism of sucralfate is mainly related to its adhesion and covering on the ulcer surface, preventing the attack of Wei San and pepsin on the ulcer surface, and promoting the synthesis of endogenous prostaglandin and the secretion of epidermal growth factor. There are few adverse reactions of sucralfate, and constipation is the main adverse reaction. Potassium bismuth citrate not only has a similar mechanism to sucralfate, but also has a strong anti-Hp effect. Short-term use of bismuth potassium citrate has almost no adverse reactions except black tongue coating; In order to avoid excessive accumulation of bismuth in the body, it is not suitable to take it continuously for a long time. Misoprostol can inhibit gastric acid secretion, increase mucus/bicarbonate secretion of gastroduodenal mucosa and increase mucosal blood flow. The main adverse reaction is diarrhea, because it can cause uterine contraction, so pregnant women should not take it.

Treatment and prevention of NSAID ulcer? For NSAID-related ulcers, the dosage of NSAID should be stopped or reduced as much as possible, and Hp infection should be detected and eradicated. With PPI treatment, the healing of GU or DU may not be affected by NSAID, so PPI should be used when NSAID treatment is not stopped. Those who have a history of peptic ulcer in the past or can't bear the ulcer and its complications due to serious illness, old age and other factors can take preventive anti-peptic ulcer drugs at the same time. Misoprostol can prevent GU and DU caused by NSAID. PPI can also play a preventive role, but the standard dose of H2RA does not.

(5) Prevent ulcer recurrence? Hp infection, taking NSAID, smoking, etc. It is a removable risk factor affecting ulcer recurrence and should be removed as much as possible. When ulcers recur frequently, don't forget to rule out gastrinoma. Because most peptic ulcers are Hp-related ulcers, and the recurrence rate of ulcers can be significantly reduced after the eradication of Hp, it is very important to determine whether there is Hp infection. It should be pointed out that Hp infection may still be positive after it is "eradicated", or if it is negative for the first time. This happens mostly because the interference factors were not eliminated during the detection, Hp was temporarily suppressed, and it could not be detected, or the detection was not reliable enough. After the eradication of Hp, the adult reinfection rate is very low, about 1%-3% per year. In the treatment of eradicating Helicobacter pylori, due to the adverse drug reactions of drug-resistant strains and poor patient compliance, some patients still failed to eradicate Helicobacter pylori after one or even two courses of treatment. Ulcers with complications and refractory ulcers are easy to recur, and the elderly or the seriously ill can't bear ulcers and their complications, which is the key object to prevent recurrence.

Maintenance treatment was once the main measure to prevent ulcer recurrence. However, compared with Hp eradication therapy, maintenance therapy requires precipitation medication, and the ulcer will still recur after drug withdrawal, and the curative effect is not as good as the former. Therefore, the status of maintenance treatment needs to be re-evaluated. Due to the existence of Hp negative ulcers, a small number of ulcers will recur after Hp eradication. At present, the curative effect of eradication treatment scheme is still difficult to reach 100%, and there is still a certain reinfection rate after Hp eradication, so maintenance treatment still has a certain position. In fact, Hp eradication therapy and maintenance therapy complement each other, which can most effectively reduce ulcer recurrence and complications. H2RA antagonists are commonly used in maintenance treatment, and the common scheme is to take half a dose of standard dose before going to bed, or take omeprazole 10mg/d or 20mg orally for maintenance treatment 2-3 times a week. The length of maintenance treatment depends on the specific situation, ranging from 3-6 months to 1-2 years for the elderly, or even longer.

Third, the treatment strategy of peptic ulcer? For DU or GU diagnosed by gastroscopy or X-ray examination, Hp positive or negative should be distinguished first. If it is positive, anti-Hp treatment should be given first, and then gastric acid secretion inhibition treatment should be given for 2-4 weeks after anti-Hp treatment if necessary. Hp-negative ulcers, including NSAID-related ulcers, can be treated as usual, that is, taking any H2RA or PPI, with a course of 4-6 weeks for DU and 6-8 weeks for GU. Mucosal protectants can also be used to treat GU, rather than drugs that inhibit gastric acid secretion. As for whether to carry out maintenance treatment, it should be decided after comprehensive consideration according to the presence or absence of risk factors such as dowry, patient's age, taking NSAID, smoking, other serious diseases and history of ulcer complications. As for surgical treatment, due to the progress of medical treatment, it is currently limited to a few patients with complications. The indications for operation are: ① when massive hemorrhage is ineffective after medical emergency treatment; ② Acute perforation; ③ Scary pyloric obstruction; (4) Refractory ulcer with ineffective medical treatment; ⑤ Gastric ulcer is suspected of canceration.

12 complications 1. Bleeding? Peptic ulcer is the most common cause from digestion to bleeding, accounting for about 50% of all causes. 15%-25% patients may be complicated with bleeding. The amount of bleeding is related to the size of eroded blood vessels. The rupture of Moses' blood vessels only caused oozing, and the amount of bleeding was very small. If the artery ruptures, the bleeding is urgent and excessive; The light person shows black feces, and the heavy person has new hematemesis. Generally, when bleeding is 50-1000ml, melena will occur; when it exceeds1000 ml, it will cause circulatory disorder, dizziness, sweating, blood pressure drop and heart rate increase; when it exceeds 1500ml, it will cause shock within half an hour. About 40% can recur after the first bleeding, which is easy to be induced by NSAID. Ulcer associated with NSAID can suddenly bleed without symptoms.

General medical conservative treatment is effective, and sometimes emergency gastroscopy and hemostasis are needed. If the bleeding is urgent and large, and medical treatment can't control the condition, emergency surgery should be performed.

Second, perforation? The perforation of peptic ulcer can cause three consequences: ① the ulcer enters the abdominal cavity and causes diffuse peritonitis (free perforation); (2) Ulcer perforation reaches and is blocked by adjacent parenchymal organs, liver, pancreas and spleen (penetrating ulcer); ③ Ulcer perforation enters the cavity control organ to form fistula. About 1%-5% of Du and Gu can carry out free perforation. Du's free perforation mostly occurs in the anterior wall, and the posterior wall ulcer is usually accompanied by bleeding or penetrating into the parenchymal organs, but occasionally it collapses and penetrates into the omental sac, causing localized peritonitis and even abscess. At this point, the back pain is severe. Gu free perforation mostly occurs in the minor curvature, mainly manifested as sudden and severe abdominal pain, which continues and intensifies, first appearing in the upper abdomen and then gradually expanding to fullness. Abdominal wall sclerosis, tenderness and rebound pain, half of them are meteorological, the voiced area of the liver disappears, and some of them are in shock. About 10% was accompanied by perforation bleeding. Posterior wall perforation occurs slowly and adheres to adjacent parenchymal organs (liver and pancreas). This penetrating ulcer has changed the law of abdominal pain, and the stool is stubborn and persistent. If it penetrates the pancreas, abdominal pain will radiate to the back, and serum amylase will increase significantly. It is rare for an ulcer to penetrate into a fistula. Du Can penetrates into the common bile duct, while the valley can penetrate into the duodenum or transverse colon.

Third, pyloric obstruction? About 2%-4% of cases are mainly caused by ulcer or pyloric canal cavity ulcer. Acute ulcer attack can cause temporary obstruction due to inflammation, edema and pyloric spasm, which can be relieved with the improvement of inflammation. Chronic obstruction is persistent, mainly due to scar contraction. Pyloric obstruction causes delayed emptying, abdominal distension and discomfort, aggravated pain after meals, often accompanied by peristalsis waves and nausea and vomiting. Symptoms can be temporarily relieved after a lot of vomiting, and the vomit contains fermented acidic food. Severe vomiting can lead to dehydration and low chlorine and low potash poisoning. Malnutrition and weight loss often occur. If there is a shock sound in the stomach on an empty stomach in the morning, and the amount of liquid pumped out by inserting a gastric tube is more than 200ml, the existence of this disease should be considered and further X-ray or gastroscopy should be done.

Fourth, cancer? Several aunts will become cancerous, but Du won't. The canceration of the valley occurred at the edge of the ulcer, and the estimated canceration rate was below 1%. We should be alert to those with long history of chronic GU, under 45 years old and intractable ulcer. Multi-point biopsy under gastroscope for pathological examination, reexamining gastroscope after active treatment until the ulcer is completely healed, and regular follow-up if necessary.

13 prognosis and preventive prognosis: With the development of effective medical methods, the prognosis is much better than in the past, and the mortality rate of peptic ulcer has been significantly reduced to below 1%. The mortality rate of patients under the age of 30 is almost zero; The death of the elderly is mainly due to complications, especially massive bleeding and acute perforation.

Epidemiological data of 14 are temporarily lacking.

15 special tips 1. In terms of living habits, smoking, drinking and unhealthy lifestyle will reduce gastric mucosal secretion and hyperacidity.

2, spicy things contain capsaicin, which will secrete gastric acid and cannot eat more; And foods that are too sour and too sweet should be avoided.

3. Pay attention to the principle of eating less and more meals, and eat more foods containing cellulose, which can reduce the incidence and recurrence rate of peptic ulcer.

4. Retrobulbar ulcer is easy to be missed, and conventional X-ray and endoscopy may not find ulcer. If the symptoms are typical, a duodenoscopy should be performed. This kind of ulcer can be treated surgically if its healing is delayed after drug treatment. If it is complicated with bleeding, it should be operated as soon as possible, because the bleeding of this ulcer is often not easily controlled by drug treatment.

Chinese patent medicine oral ulcer powder for treating retrobulbar ulcer Appendix 4)? Functions and indications: anti-ulcer, analgesic. Used for recurrent oral ulcer and herpetic oral ulcer. Usage and dosage: Immerse the sterilized cotton ball in the medicine and rub the patient. ...

Gastric ulcer tablets, etc. The main functions of gastric ulcer tablets are: relieving pain, making acid and diminishing inflammation. Used for gastric ulcer and duodenal ulcer. Usage and dosage of gastric ulcer tablets: 4 ~ 6 tablets each time. ...

Tin has a dispersing effect. Usage and dosage: Blow the affected area with a little medicine. Clinical application: 1. Oral ulcer: Wang Moumou, male, 38 years old. First diagnosis in June 1972, 17, ...

Zuojin Pill has a high inhibitory effect on Helicobacter pylori, which is the basis of treating gastritis and gastric ulcer. At the same time, it can inhibit gastric acid secretion, protect gastric mucosa and have anti-inflammatory effect. ...

Lizhong pill