What Are Arterial Ulcers?

It mainly refers to chronic ulcers that occur in the stomach and duodenum. There are various factors for the formation of ulcers. The digestive effect of acidic gastric juice on the mucosa is the basic factor for ulcer formation, hence the name. Anywhere the acidic gastric fluid contacts, such as the lower esophagus, the anastomosis after gastrointestinal anastomosis, the jejunum, and Meckel's diverticulum with ectopic gastric mucosa. Most ulcers occur in the duodenum and stomach, so they are also called stomach and duodenal ulcers. After the diagnosis of the disease, comprehensive treatment measures are generally adopted, including basic medical treatment, drug treatment, treatment of complications and surgical treatment. The purpose of treating peptic ulcer is to: relieve clinical symptoms; promote healing of ulcers; prevent recurrence of ulcers; reduce complications. However, the existing various therapies have not yet changed the natural course of peptic ulcer and completely cured the ulcer.

ulcer

[kuì yáng]

An ulcer is a localized defect or ulcer on the surface of the skin or mucous membranes. The surface is often covered with pus, necrotic tissue, or crusts, and scars are left after healing. It can be caused by infection, trauma, nodules, or tumor ulceration. Its size, shape, depth, and development process are also inconsistent. Chronic infections are common and may persist. Such as gastric ulcer, duodenal ulcer, chronic calf ulcer and so on.

Causes of ulcers

It mainly refers to chronic ulcers that occur in the stomach and duodenum. There are various factors for the formation of ulcers. The digestive effect of acidic gastric juice on the mucosa is the basic factor for ulcer formation, hence the name. Anywhere the acidic gastric fluid contacts, such as the lower esophagus, the anastomosis after gastrointestinal anastomosis, the jejunum, and Meckel's diverticulum with ectopic gastric mucosa. Most ulcers occur in the duodenum and stomach, so they are also called stomach and duodenal ulcers. After the diagnosis of the disease, comprehensive treatment measures are generally adopted, including basic medical treatment, drug treatment, treatment of complications and surgical treatment. The purpose of treating peptic ulcer is to: relieve clinical symptoms; promote healing of ulcers; prevent recurrence of ulcers; reduce complications. However, the existing various therapies have not yet changed the natural course of peptic ulcer and completely cured the ulcer.

ulcer

Ulcers are usually limited skin tissue defects caused by trauma, microbial infections, tumors, circulatory and neurological dysfunction, immune dysfunction, or congenital skin defects. Traumatic ulcers are often caused by physical and chemical factors directly acting on tissues. Microbial infectious diseases are mostly caused by bacteria, fungi, Borrelia, viruses and other tissue damage. Nodule or tumor ulceration. Vascular inflammatory ulcers caused by immune abnormalities are formed by arterial or arteritis necrosis of tissue. Circulatory or neurological dysfunction is a nutritional disorder that causes tissue necrosis, such as varicose veins and leprosy ulcers.

(A) bacterial diseases

Bloated, swollen, cellulitis, sweat glanditis, skin tuberculosis, sores, skin anthrax, glanders, skin diphtheria, necrotizing acne, infertile pustular disease, leprosy, tropical ulcer, mycobacterial ulcer, Swimming pool granulomas, oral tuberculosis ulcers.

(B) fungal diseases

Bacillus filariasis, cutaneous cryptococcosis, histoplasmosis, coccidiomycosis, aspergillosis, podomycosis, actinomycosis, nocardiosis, yellow ringworm, psoriasis, mucor skin disease.

(Three) viral diseases

Hand-foot-mouth disease, foot-and-mouth disease.

(Four) parasitic diseases

Skin amoebiasis, skin fly maggot disease.

(V) Sexually transmitted diseases

Genital sores, syphilis, soft sore cleft granuloma, sexually transmitted lymphogranuloma.

(6) Allergic skin diseases

Fixed drug eruption.

(VII) Vasculitis and vascular diseases

Nodular polyarteritis, allergic vasculitis, thromboocclusive vasculitis, papular necrotizing tuberculosis, hard erythema, gangrene

Pyoderma, lethal midline granulomatosis, wegener granulomatosis, occlusive arteriosclerosis, stasis dermatitis, Raynaud's disease.

(Eight) physical diseases

Ray dermatitis, frostbite, bedsores.

(9) Occupational skin diseases

Chromium, nickel, sodium, zinc, cobalt, hydrochloric acid, sulfuric acid, hydrofluoric acid, sodium hydroxide, and sodium carbonate can cause skin ulcers.

(10) Autoimmune Diseases

Behcet's disease.

(11) Tumor

Eczema-like cancer, eczema-like cancer, basal cell carcinoma. Squamous cell carcinoma, malignant melanoma, sebaceous adenocarcinoma, sarcoid granuloma, malignant histiocytosis on kaposi sarcoma, hairy sheath cancer, fibrosarcoma, proliferative erythema, verrucous carcinoma, multiple plasma cell tumor.

(12) Other

Continuous acral dermatitis, nodular fat necrosis, lipogranuloma, foot penetrating ulcer, aphthous stomatitis, gangrenous balanitis, acute vulvar ulcer. ^[1]

Signs and symptoms of ulcers

The clinical manifestations of this disease vary, and some patients may be asymptomatic, or complications such as bleeding and perforation may be the first symptoms. Most peptic ulcers have the following characteristics:

Chronic processes are recurrent, with a history of several years or even ten years.

Seizures are periodic and alternate with remission. The length of the period varies from a few weeks or months to a few years. The seizures are seasonal, mostly at the turn of autumn and winter and winter and spring, and can be induced by poor mental or emotional or NSAID service.

The epigastric pain was rhythmic during the attack.

I. Symptoms Upper abdominal pain is the main symptom. It can be dull pain, burning pain, soreness or severe pain, but it can only have hunger-like discomfort. Typical cases are mild or moderate persistent pain under the xiphoid process, which can be relieved by antacids or eating. About two-thirds of the pain is rhythmic: upper abdominal pain begins to appear 1 to 3 hours after breakfast. If you do not take medicine or eat, you must persist until lunch. The pain is 2 to 4 hours after eating, and it is necessary to eat to relieve it. About half of them have midnight pain, and patients often wake up. GU can also cause regular pain, but it appears earlier after a meal, about 1/2 to 1 hour after a meal, and disappears before the next meal. Midnight pain can also occur, but it is not as common as DU. Some cases do not have the typical pain described above, but only show irregular and vague upper abdominal pain and discomfort, accompanied by symptoms of fullness, anorexia, belching, and acid reflux, which are more common in GU cases. As the disease progresses, symptoms can change due to the onset of symptoms. Ulcer pain is a type of visceral pain that has epigastric pain without a well-defined location. If the pain is aggravated and the part is fixed and radiated to the back, it cannot be relieved by antacids, often suggesting chronic perforation of the posterior wall; acute perforation should be considered when sudden and severe upper abdomen extends to the whole abdomen; those with sudden dizziness may indicate that And issued blood.

Second, the signs of ulcer activity under the xiphoid process may have a fixed and limited tenderness point, no obvious signs of relief.

Ulcer pathophysiology

First, a large number of studies on Helicobacter pylori infection have fully proved that Helicobacter pylori (Hp) infection is the main cause of peptic ulcer.

(1) Hp infection rate is high in patients with peptic ulcer. If you can exclude factors such as antibiotics, bismuth or non-steroidal anti-inflammatory drugs (NSAID) before the test, the Hp infection rate in patients with DU is 90% -100%. GU is 80% -90%. The risk of peptic ulcer in patients with H. pylori infection is also significantly increased. Prospective studies have shown that peptic ulcers can develop in approximately 15% to 20% of people with Hp infection.

(2) According to the treatment points that Hp can promote ulcer healing and significantly reduce the recurrence rate of ulcers without eradicating Hp without inhibiting gastric acid secretion, it can effectively heal ulcers; conventional inhibition is used to treat so-called refractory ulcers with unsatisfactory effects of scattered secretion drugs After effective eradication of Hp treatment, healed; treated with high-efficiency Hp regimen for 1 week, then no longer given anti-ulcer treatment, and re-examined 4 weeks after the end of treatment, the healing rate of ulcer was higher than or equal to continuous treatment with conventional drugs that inhibit gastric acid secretion 4-6 weeks healing rate. These results demonstrate from different perspectives that eradication of Hp can promote ulcer healing. Frequent recurrences have been one of the main features of the natural history of peptic ulcer. The ulcers that heal after treatment with conventional drugs that inhibit gastric acid secretion have an annual recurrence rate of 50% -70%. Eradication of Hp can reduce the annual recurrence rate of DU and GU to less than 5%, which can completely cure most ulcer patients. In addition, eradication of Hp can significantly reduce the incidence of complications such as peptic ulcer bleeding.

(3) Hp infection changes the balance between invasive and defensive factors of mucosa. Hp relies on its virulence factors to colonize gastric mucosa (stomach and duodenum with gastric metaplasia) and induce local inflammation and immunity. Reaction, damage the local mucosal German defense / repair mechanism; on the other hand, H. pylori infection can increase the secretion of gastrin and gastric acid and enhance the invasion factors. The synergy of the two analyses resulted in gastroduodenal mucosal damage and ulcer formation. The virulence factors of Hp include the factors that enable Hp to colonize gastric mucosa and the factors that induce tissue damage, and some factors have both functions. The colonization site of Hp is on the epithelial surface of the gastric mucosa and the bottom of the mucus. Generally, there are more Hp in the gastric antrum, less body and bottom of the stomach, and it can also live in the duodenal metaplasia. Hp colonization in the stomach, in addition to resist the killing effect of gastric acid, but also rely on its movement through the mucus layer. Hp bacteria have a spiral shape with flagella at one end, which provides power for its use. The urease produced by Hp hydrolyzes urea into ammonia and carbon dioxide. Ammonia forms an "ammonia cloud" around Hp, which neutralizes the surrounding stomach 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, while gastric epithelial cells have specific receptors for adhesion factors. Hp toxins, toxic enzymes, and Hp-induced mucosal inflammation can cause damage to the gastroduodenal mucosal barrier. The vacuolar toxin protein and cytotoxin-related gene protein are the main signs of Hp virulence. VacA protein can produce vacuoles in cultured cells; the exact function of CagA protein is unknown. In addition to the protective effect of Hp on ammonia produced by urease, urea can directly and indirectly cause damage to the mucosal barrier. Hp's mucus enzymes degrade mucus and promote H + anti-diffusion; Hp lipopolysaccharide has the characteristics of endotoxin, which can stimulate the release of cytokines, interfere with the interaction between gastric epithelial cells and laminin and cause the mucosa to lose integrity. Hp's esterase and phosphoesterase A degrade lipids and phospholipids, destroying cell membrane integrity. Some low molecular proteins produced by Hp can chemotactic and activate inflammatory cells, which release a variety of cytokines and produce toxic oxygen free radicals. The antigens of some components of Hp are similar to certain cellular components of the gastric mucosa, so-called antigenic mimicry. Hp stimulates antibodies produced by the body, which can cross-react with host gastric mucosal cell components, resulting in gastric mucosal cell damage. Hp infection can cause hypergastrinemia, and its mechanisms include:

Inflammation and tissue damage caused by Hp infection reduce the number of D cells in the gastric antral mucosa, affect the production of somatostatin, and weaken the latter's inhibitory effect on the release of gastrin by G cells.

Hp urease hydrolyzes the ammonia produced by urea to increase the local mucosal pH, which destroys the feedback inhibition of gastric acid on the release of gastrin by G cells. The effects of H. pylori infection on gastric acid are not consistent. Most reports show that the basal, meal, and gastrin-stimulated gastric acid secretion in patients with Hp-positive DU is higher than that in Hp-positive healthy volunteers. Less than Hp-positive DU patients. Hypergastrinemia caused by Hp infection is one of the causes of high gastric acid secretion. There are many hypotheses about the mechanism of Hp infection in peptic ulcer. The "leaking roof" hypothesis compares the gastric mucosal barrier to a roof, protecting the mucosal tissue below it from damage from gastric acid. When the mucous membrane is first damaged by Hp (formation of "leaking roof"), it will cause muddy water (H + anti-diffusion), causing mucosal damage and ulcer formation. This hypothesis emphasizes the weakening of defense factors caused by Hp infection and may explain the occurrence of Hp-related GU. The six-factor hypothesis combines the six factors of gastric acid-pepsin, gastric metaplasia, duodenitis, Hp infection, hypergastrinemia, and tannin secretion to explain the role of Hp in the pathogenesis of DU. Hp infection and genetic factors in the gastric antrum cause high gastric acid secretion, which directly damages the epithelium or causes secondary inflammation to cause gastric metaplasia in the duodenal mucosa, creating conditions for Hp colonization in the duodenal mucosa. Duodenal Hp infection exacerbates local inflammation (duodenum), which in turn promotes gastric metaplasia. This vicious circle keeps the duodenal mucosa in an inflamed and injured state, and reduces the local bicarbonate secretion, weakening the defense factors of the duodenal mucosa. The hypergastrinemia caused by Hp infection stimulates gastric acid secretion and enhances invasion factors. Increased invasive factors and weakened defensive factors lead to ulcers.

Second, the final formation of peptic ulcers caused by gastric acid and pepsin is due to pepsin-pepsin self-digestion. This concept has not changed in the "Hp era". Pepsin is a pepsinogen secreted by the main cells that is transformed by the activation of hydrochloric acid. It can degrade protein molecules, so it has an invasion effect on the mucosa. The biological activity of pepsin depends on the pH of gastric juice. This is because not only hydrochloric acid is required for pepsinogen activation, but also pepsin activity is pH-dependent. When the pH of gastric juice rises above 4, pepsin loses its activity. Since the activity of pepsin is restricted by gastric acid, the role of gastric acid is mainly considered when discussing the pathogenesis and treatment of peptic ulcer. In the absence of acid, ulcers rarely occur, inhibiting gastric acid secretion and drugs to promote ulcer healing, so the presence of gastric acid is the determinant of ulcers. Patients without DU had a mean basal acid output (BAO) and pentapeptide gastrin, and the maximum acid output (MAO) after stimulation was often greater than that of a normal person, and those with MAO below 10 mmol / h rarely had DU. However, the range of MAO variation in patients with DU is large, and there is a significant overlap with normal people, which is only 20% -50% higher than normal. The basal and stimulated gastric acid excretion in patients with GU is mostly normal or even lower than normal. Gastric acid excretion in patients with GU who developed in the prepyloric area or with DU may be higher than normal, and the amount of scattered secretion in GU does not seem to be significantly changed compared to DU. Increased gastric acid secretion in DU patients is mainly related to the following factors:

The total number of parietal cells increases : the gastric acid secretion is parallel to the total number of parietal cells. The average PCM of DU patients can reach 1.5-2 times that of normal people. The increase in parietal cell numbers may be affected by genetic factors and / or the result of long-term stimulation of hypergastrinemia (such as in gastrinoma, Hp infection).

Increased sensitivity of parietal cells to stimuli : DU patients have more gastric acid secretion response to things or pentagastrins than those of normal people. This may be the increase of the affinity of gastrin receptors on the parietal cells of patients or the promotion of stimulants in vivo. Gastrin stimulates gastric acid secretion and inhibits substances such as reduced somatostatin (such as Hp infection).

Defects in the normal feedback inhibition mechanism of gastric acid secretion : The function of gastrin secretion by G cells in the normal gastric antrum is regulated by negative feedback of gastric pH. When the pH of the gastric antrum falls below 2.5, the function of gastrin secretion by G cells Is suppressed. In addition, when chyme enters the duodenum, gastric acid and chyme stimulate the duodenum and small intestinal mucosa to release secretin, cholecystokinin, gastrointestinal peptide (GIP) and vasoactive intestinal peptide (VIP), etc. Hormones have the effect of inhibiting gastric acid secretion. Therefore, under normal circumstances, gastric acid secretion has a self-regulating effect. This feedback mechanism of some DU patients is defective, and heredity and Hp infection are possible factors.

Increased vagus nerve tension : The vagus nerve releases acetylcholine, which has the effects of directly stimulating parietal cells to secrete hydrochloric acid and stimulating G cells to secrete gastrin.

Third, non-steroidal anti-inflammatory drugs Some drugs have damage to the gastroduodenal mucosa, of which NSAID is the most significant. Long-term intake of NSAID can induce peptic ulcers, prevent ulcer healing, increase the recurrence rate of ulcers and the incidence of complications such as bleeding and perforation. Since NSAID intake lasts longer than the duodenum, it is more closely related to GU. Among those taking NSAID for a long period of time, about 50% of patients have endoscopic gastroduodenal erosions and / or bleeding points, and 5% -30% of patients have peptic ulcers. The risk of ulcers is related to the type of NSAID, the size of the dose, and the length of the treatment. It may also be related to factors such as patient age, Hp infection, smoking, and concurrent use of glucocorticoids. In addition to the direct effects of drugs, NSAID causes damage to the gastroduodenal mucosa by inhibiting prostaglandin synthesis and weakening the latter's protective effect on the gastroduodenal mucosa. Approximately 5% of DU and 25% of GU in the United States are associated with long-term NSAID use.

4. Genetic factors With the recognition of the important role of Hp in the pathogenesis of peptic ulcer, the importance of genetic factors has been challenged.

First , does the family clustering of peptic ulcer play a major role in heritage or environmental factors? Epidemiological investigations show that Hp infection has a "family aggregation" phenomenon. Most members of the family have isolated Hp from the same strain, suggesting that Hp is transmitted from person to person within the family. Therefore, the family clustering phenomenon of peptic ulcer may be mainly due to the transmission of Hp infection in the family.

Second , the subclinical markers of peptic ulcer that were thought to be genetically related, namely hyperpepsinogenemia I and familial hypergastrinemia, can mostly return to normal after eradication of Hp, suggesting Hp infection rather than heredity Play a major role.

Third , people with blood type O are at a higher risk of developing DU than those with other blood types, and were once considered indirect "genetic markers." In recent years, it has been found that the specific colonization of Hp in gastric epithelium is due to the specific binding of its adhesion investment with gastric receptor cells. The Lewisb blood group antigen is a specific receptor. There are more adhesion receptors on the surface of type O blood cells, suggesting that O The prevalence of DU in people with blood type is still related to Hp infection. But the role of genetic factors cannot be neglected. Observations of twins show that the consistentity of ulcers among siblings of twins is higher than that of twins; in some rare genetic syndromes, such as polyendocrine adenoma type I, systemic mastocytosis, etc., digestion Sexual ulcers are part of their clinical manifestations.

V. The gastric emptying of DU patients with abnormal gastroduodenal motility is faster than that of normal people, especially the liquid emptying. Accelerating gastric fluid emptying increases the acid load in the duodenal bulb and the mucosa is vulnerable to damage. A small number of people with this abnormality have a family history, and some patients with GU have gastric dyskinesias, manifested by delayed gastric emptying and duodenal-gastric reflux. Containers increase the tension of the gastric antrum, stimulate G cells in the gastric antral mucosa to secrete gastrin, and thereby increase gastric acid secretion; the latter is mainly caused by gastric antrum-duodenal motor agreement and pyloric sphincter dysfunction. Bile, pancreatic juice, and lysophosphatidylcholine (lecithin) in reflux fluid can damage gastric mucosa. Gastric dyskinesia itself is unlikely to be the primary cause of GU, but it can aggravate the damage of gastric mucosa by Hp infection or ingestion of NSAID.

6. Stress and psychological factors Acute stress can cause stress ulcers. However, in patients with chronic ulcers, the pathogenic effects of emotional stress and psychological conflict have been debated. Clinical observations show that people with long-term mental stress, fluctuating rates, or mood swings are prone to peptic ulcers; when DU is healed and suffers mental stress, ulcers are prone to recurrence or complications; during the war, the incidence of this disease increased. The above facts suggest that psychological factors have a significant effect on the occurrence of peptic ulcer, especially DU. However, psychological analysis could not find any special personality in patients with peptic ulcer. Stress and psychological factors can affect the regulation of gastroduodenal secretion, movement, and mucosal blood flow through the vagus nerve mechanism.

Seven other risk factors

(1) The incidence of peptic ulcer is higher in smokers than in non-smokers. Smoking affects healing of ulcers, promotes recurrence of ulcers, and increases the incidence of ulcer complications. The exact mechanism by which smoking affects ulcer formation and healing is unknown, and may be related to factors such as increased gastric acid and pepsin secretion, inhibited bicarbonate secretion from the pancreas, decreased pyloric sphincter tension, and affected gastric mucosa prostaglandin synthesis.

(B) the relationship between diet and peptic ulcer is not very clear. Alcohol, strong tea, coffee, and some beverages can stimulate gastric acid secretion, which is prone to indigestion symptoms after ingestion, but there is no sufficient evidence that long-term drinking will increase the risk of loss. It is said that increased intake of essential fatty acids is associated with a reduction in the incidence of peptic ulcers, which promotes prostaglandin synthesis by increasing prostaglandin prerequisites in the gastroduodenal mucosa. High-salt diets are thought to increase the risk of GU, which is related to the damage of gastric mucosa by high salt concentrations.

(3) Viral infections. Herpes simplex virus type I can be detected in gastric sinus ulcers or in the anterior pyloric ulcers in some patients with ulcers, but negative in tissues far from the ulcers. These patients have no systemic HSV-1 infection or Evidence of immunodeficiency suggests that local infection with HSV-1 may be related to the formation of "peptic ulcer". Cytomegalovirus infection may also occur in patients with kidney transplantation or immunodeficiency.

Pathology: DU mostly occurs in the bulb, the anterior wall is more common; GU is mostly in the histology of the gastric angle and gastric antrum, and most of GU occurs at the junction of the pyloric gland area (gastric antrum) and the acid secretion area (gastric body). Side of the pyloric gland area. The mucosa of the pyloric gland area can expand with age (pseudopyloric gland metaplasia and / or intestinal metaplasia), so that the boundary between it and the mucosa of the acid secretion area shifts, so the GU in elderly patients is higher. Ulcers are usually single or multiple, and are round or oval. DU diameter is less than 10mm, GU is slightly larger than DU. Huge ulcers larger than 2 cm in diameter were also seen. The edge of the ulcer is smooth, the bottom is clean, and it is composed of granulation tissue, and the upper side is covered with gray or gray-yellow fiber exudate. Mucosa around active ulcers often has inflammatory edema. The superficial ulcers involve the mucosal muscle layer, the deeper ones reach the muscle layer and even the serosa layer, causing bleeding when the blood vessels are ruptured, and causing perforation when the serosa layer is penetrated. When the ulcer heals, the surrounding mucosa inflammation and edema subsides, and the marginal epithelial cell proliferation covers the ulcer surface (reconstruction of the mucosa). The granulation tissue underneath becomes fibrosis, and the shrinkage of the scar causes the surrounding mucosa to fold.

Ulcer diagnosis test

I. The diagnosis of H. pylori infection by Helicobacter pylori has become a routine detection item for peptic ulcers. The methods can be divided into two types, invasive and non-invasive. The former requires gastroscopy and gastric mucosal biopsy. Gastroduodenal disease, which only provides information on the presence or absence of H. pylori infection. Currently commonly used invasive tests include rapid urease test, histological examination, mucosal smear staining microscopy, microaerobic culture and polymerase chain reaction (PCS), etc .; 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 an invasive test, with simple operation and low cost. The combinatorial examination can directly observe Hp. Compared with conventional HE staining, special staining such as Warthin-Starry can improve the detection rate. Staining and microscopic examination after gastric mucosal smear is simple, but it is easy to miss diagnosis when the number of bacteria is small. The technical requirements and costs of Hp culture and PCR detection are relatively high, which are mainly used for scientific research. 13C-UBT or 14C-UBT has high sensitivity and specificity in detecting H. pylori infection in non-invasive tests, and it can be used as the preferred method for review after eradication treatment. A serological test for the qualitative detection of anti-Hp antibody IgG should not be used as the preferred method for review after treatment. A serological test for the qualitative detection of anti-Hp antibody IgG should not be used as a confirmation test for the eradication of Hp after treatment.

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2. Gastric fluid analysis Gastric acid secretion in patients with GU is normal or lower than normal, and some patients with DU increase, but there is a large overlap with normal people. Therefore, gastric fluid 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, and the ratio of BAO / MAO> 60%, it is suggested that gastrinoma is possible.

Third, the determination of serum gastrin. Peptic ulcer serum gastrin is slightly higher than normal people, but the diagnostic significance is not significant, so it should not be classified as routine. However, if a gastrinoma is suspected, this determination should be made. Serum gastrin value is generally inversely proportional to gastric acid secretion. Gastric acid is low and gastrin is high. Gastric acid is high and gastrin is low. In the case of gastrinoma, both are increased.

Diagnosis: Medical history analysis is important. Typical periodic and rhythmic epigastric pain is the main clue to the diagnosis of peptic ulcer. However, it must be pointed out that those with ulcer symptoms do not necessarily have peptic ulcers, and quite a few patients with peptic ulcers often have atypical upper abdominal pain, and some patients may have no pain symptoms. Therefore, it is difficult to make a reliable diagnosis based on medical history alone. Confirmation depends on X-ray barium meal examination and / or endoscopy, the latter is of particular diagnostic value.

First, X-ray barium meal examination of gas-barium double contrast angiography can better display mucosa. There are two types of direct and indirect X-ray signs of ulcer: shadow is a direct sign, which has a diagnostic value for the diagnosis of ulcer. Benign ulcers protrude beyond the contours of the barium of the stomach and duodenum. A smooth loop is often found around it, and its peripheral radial mucosal folds are common. Indirect signs include local tenderness, spasmodic incisions on the greater curvature of the stomach, duodenal irritation, and bulbous deformities. The indirect signs only indicate ulcers.

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2. Gastroscopy and mucosal biopsy Gastroscopy can not only directly observe and photograph the gastroduodenal mucosa, but also take biopsy for pathological and Hp tests under direct vision. Its readiness for the diagnosis of peptic ulcer and differential diagnosis of benign and malignant ulcers is higher than that of X-ray barium meal examination. Barium meal examination is difficult to find when the ulcer is too small or superficial; there are many explanations for duodenal bulbar abnormalities found in barium meal examination. Difficult diagnosis cannot be confirmed; active upper gastrointestinal bleeding is a contraindication for barium meal examination. Determine its source and nature. About 5% of GUs that appear to be benign under barium meal examination or endoscopy are actually malignant. On the other hand, a small number of seemingly benign ulcers have proved to be benign and difficult to distinguish without biopsy. In addition, endoscopy can reveal gastritis and duodenitis with ulcers. Endoscopic peptic ulcers are mostly round or oval, occasionally linear, and the edges are smooth. The bottom is filled with gray-yellow or white exudates. The surrounding mucosa may be congested and edema. Sometimes wrinkles are concentrated in the ulcer. Endoscopic ulcers can be divided into three disease phases: active phase (A), healing phase (H) and scarring phase (S). Each of these phases can be divided into two phases: 1 and 2.

Ulcer treatment plan

The purpose of treatment is to eliminate the cause, relieve symptoms, heal ulcers, prevent recurrence and avoid complications. The cause of peptic ulcer varies in different patients, and the pathogenesis is also different. Therefore, the possible pathogenic factors and pathophysiology should be analyzed for each case and given appropriate treatment.

First, the general treatment of life should be regular, work should be combined with work and rest, to avoid overwork and mental stress, if anxiety, should be enlightened, if necessary, sedative medicine. In principle, it is important to emphasize that meals should be taken regularly to avoid spicy, oversalty foods and strong teas, coffee and other beverages. Although cow's milk and soybean paste can dilute gastric acid for a while, the calcium and protein contained in it can stimulate gastric acid secretion, so it should not be drunk. If you have a tobacco and alcohol addiction that is confirmed to be related to the onset of ulcers, you should give up immediately. People taking NSAID should stop taking it as much as possible; even if patients do not take such drugs, they should be cautioned in the future.

2. Drug treatment Before the 1970s, the treatment of this disease relied mainly on antacids and anticholinergics. The advent of H2RA caused the first change in treatment; eradication of Hp was a major milestone in treatment.

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(1) H. pylori eradication The eradication of H. pylori can make most patients with H. pylori-associated ulcer completely achieve the purpose of treatment. Internationally, consensus has been reached on the management of Hp-related ulcers, that is, anti-Hp treatment should be performed regardless of the onset or recurrence of the ulcer, whether active or stationary, and whether there is a history of complications.

1. Treatment schemes for Hp eradication Because most antibacterial drugs have reduced activity in the intestinal low pH environment and cannot penetrate the mucus layer to reach bacteria, Hp infection is not easy to eradicate. To date, no single drug has been effective in eradicating Hp. Therefore, a combination of a drug that inhibits gastric acid secretion, an antibacterial drug or a colloidal bismuth agent has been developed. The treatment options for H. pylori eradication can be broadly divided into two categories: proton pump inhibitor (PPI) -based and colloidal bismuth-based. A PPI or a colloidal bismuth agent plus two of the three antibacterial drugs clarithromycin (methotomycin), amoxicillin (or tetracycline), and metronidazole (or tinidazole) constitute a triple therapy . Hp strains are rapidly increasing in resistance to metronidazole. Furazolidone has a strong anti-Hp effect, and Hp is not prone to drug resistance. Furazolidone can be used to replace metronidazole at a dose of 200 mg / d in two divided doses. H2RA can be used to replace PPI to reduce costs, but the efficacy is also reduced. For those who fail the first treatment, a quadruple therapy with PPI and colloidal bismuth combined with two antibacterial drugs can be used.

2. Whether anti-ulcer treatment should be continued after H. pylori eradication is not unified. When the treatment scheme is highly effective and the ulcer area is not large, a single anti-Hp treatment can effectively heal active ulcers within 1-2 weeks. If the efficacy of Hp eradication is slightly lower, the ulcer area is larger, the patient's symptoms are not relieved at the end of anti-Hp therapy, or there is a recent history of complications such as bleeding, consideration should be given to continuing treatment with gastric acid secretion inhibitors for 2-4 weeks after the end of anti-Hp .

3. Review of anti-Hp treatment After anti-Hp treatment, a test to determine whether Hp eradication should be performed at least 4 weeks after the completion of treatment. Most patients with DU who are treated with a highly effective anti-Hp regimen (90% eradication rate) do not need a trial to confirm H. pylori eradication. For refractory ulcers or DUs with a history of complications, it should be established whether Hp is eradicated. Due to the risk of potential malignant transformation of GU, in principle, a gastroscopy and Hp review should be performed at an appropriate time after treatment. In patients with persistent dyspepsia after appropriate treatment, it should also be established whether Hp eradication.

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(2) The healing of ulcers treated by drugs that inhibit gastric acid secretion, especially the healing of DU is directly proportional to the intensity and time of antacid therapy. Alkaline antacids (such as aluminum hydroxide, magnesium hydroxide, and their preparations) neutralize gastric acid (with a certain cytoprotective effect), which has a better effect on relieving pain-like symptoms, but large doses are required to promote ulcer healing Take multiple doses to be effective. The inconvenience of taking the medicine several times and the adverse reactions caused by taking large doses of antacids for a long time limit its application. At present, antacids are rarely used alone to treat ulcers, and can be used as an adjuvant treatment to strengthen analgesia. The anticholinergic drugs pirenzepine (piperzepine) and the gastrin receptor antagonist propylglutamine are not very effective in treating ulcers and have been rarely used in the treatment of ulcers. H2RA and PPI are two commonly used drugs to inhibit gastric acid secretion. When PPI acts on H + -K + -ATPase, a key enzyme in the final step of gastric acid secretion of parietal cells, parietal cells restore acid secretion. Therefore, PPI has a stronger inhibitory effect on gastric acid secretion than H2RA, and its effect is long-lasting. At least four PPIs are currently in clinical use, namely omeprazole, lansoprazole, pantoprazole, and rabeprazole. The general dose is 20 mg of omeprazole, 30 mg of lansoprazole, 40 mg of pantoprazole and 10 mg of rabeprazole, orally once a day; the dose needs to be doubled for the eradication of Hp.

(III) Protective treatment of gastric mucosa There are three main types of gastric mucosal protective agents, namely sucralfate, bismuth potassium citrate, and prostaglandin drug misoprostol. The ulcer healing rate of these drugs for 4-8 weeks is similar to H2RA. The mechanism of sucralfate's anti-ulcer effect is mainly related to its adherence and covering as an ulcer surface, preventing the powder and pepsin from invading the ulcer surface, promoting endogenous prostaglandin synthesis, and stimulating epidermal growth factor secretion. Sucralfate has few adverse reactions, and constipation is its main adverse reaction. In addition to the similar mechanism of sucralfate, potassium bismuth citrate also has a strong anti-Hp effect. Short-term administration of bismuth potassium citrate, except for the darkening of the tongue coating, rarely causes adverse reactions. To avoid excessive accumulation of bismuth in the body, it should not be taken continuously for a long time. Misoprostol has the effect of inhibiting gastric acid secretion, increasing gastric duodenal mucosal mucus / bicarbonate secretion, and increasing mucosal blood flow. Diarrhea is the main adverse reaction, and pregnant women should avoid taking it because it can cause uterine contractions.

(D) Treatment and prevention of NSAID ulcers For NSAID-related ulcers, the dose of NSAID should be suspended or reduced as much as possible, Hp infection should be detected and eradication treatment should be performed. With PPI treatment, the healing of GU or DU may not be affected or less affected by continued NSAID. Therefore, PPI should be used when NSAID treatment cannot be discontinued. People with a previous history of peptic ulcer or severe illness, advanced age and other factors can not take ulcers and their concurrent patients, can take anti-peptic ulcer drugs at the same time preventively. Misoprostol prevents NSAID-induced GU and DU. PPI also plays a preventive role, but not the standard dose of H2RA.

(5) Prevention of ulcer recurrence Hp infection, taking NSAID, smoking, etc. are removable risk factors affecting ulcer recurrence and should be removed as much as possible; when ulcer recurrence is frequent, do not forget to exclude gastrin. Since the vast majority of peptic ulcers are Hp-related ulcers, and the rate of recurrence of ulcers can be significantly reduced after Hp eradication, it is important to determine the presence of Hp infection. It should be pointed out that after the eradication of H. pylori infection, or the first negative test, there is still the possibility of positive. This happens mostly because the interference was not eliminated at the time of the test, Hp was temporarily suppressed and failed to detect, or because the detection was not reliable enough. The reinfection rate of adults after H. pylori eradication is very low, about 1% to 3% per year. In the treatment of Hp eradication, due to adverse drug reactions of drug-resistant strains and poor patient compliance, Hp was still not eradicated in some patients after one or even two courses of treatment. Complicated ulcers and refractory ulcers are prone to recurrence. Older people or those with severe diseases cannot tolerate ulcers and their complications. These are the key targets for preventing recurrence. Maintenance treatment has been the main measure to prevent the recurrence of ulcers. However, compared with H. pylori eradication therapy, maintenance treatment requires precipitating medication. The ulcer will still recur after discontinuation of treatment and the 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, the curative effect of current eradication treatment schemes is still difficult to reach 100%, and there is still a certain reinfection rate after Hp eradication, etc., maintenance therapy still has a certain status. In fact, Hp eradication therapy is complementary to maintenance therapy in order to most effectively reduce ulcer recurrence and complications. H2RA antagonists are generally used for maintenance therapy. The usual protocol is a half-dose before bedtime at a standard dose. Omeprazole 10mg / d or 20mg can be used orally 2-3 times a week for maintenance therapy. The length of maintenance treatment needs to be determined according to the specific situation. The shorter is 3-6 months, the older is 1-2 years, or even longer.

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Third, the strategy for the treatment of peptic ulcer For gastroscopy or X-ray diagnosis of DU or GU with a clear diagnosis, we must first distinguish between Hp positive or negative. If positive, anti-Hp therapy should be given first, and if necessary, 2-4 weeks after the end of anti-Hp therapy, gastric acid secretion therapy should be given. Hp-negative ulcers, including NSAID-related ulcers, can be treated as usual in the past, that is, any type of H2RA or PPI, with a duration of DU of 4-6 weeks and a GU of 6-8 weeks. Mucosal protective agents can also be used instead of drugs that inhibit gastric acid secretion to treat GU. As for whether to carry out maintenance treatment, a decision should be made after comprehensive consideration based on the presence of risk factors such as the ulcer recurrence gift, the age of the patient, taking NSAID, smoking, combined with other serious diseases, and history of ulcer complications. As for surgical treatment, due to advances in medical treatment, it is limited to a few patients with complications. The surgical indications are: when a large amount of bleeding is ineffective in emergency medical treatment; acute perforation; scarring pyloric obstruction; refractory ulcers ineffective in medical treatment; gastric cancer is suspected.

Differential diagnosis of ulcer

Mainly needs to identify malignant diseases such as gastric cancer and gastrinoma.

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Prognosis and prevention of ulcers

Prognosis: The development of effective medical treatment has a far better prognosis than the past, and has significantly reduced the mortality of peptic ulcer to less than 1%. The mortality rate for patients under 30 is almost equal to zero; older deaths are mainly due to complications, especially major bleeding and acute perforation.