peptic ulcer
Introduction
Introduction to peptic ulcer Peptic ulcer (pepticulcer) mainly refers to chronic ulcers that occur in the stomach and duodenum. It is a frequently-occurring disease. The formation of ulcers has various factors, and the digestion of mucous membrane by acidic gastric juice is the basic factor of ulcer formation, hence the name. Any part of the contact with acidic gastric juice, such as the lower esophagus, anastomosis after gastrointestinal anastomosis, jejunum and Meckel's diverticulum with ectopic gastric mucosa, most ulcers occur in the duodenum and stomach, so it is also called stomach, ten Duodenal ulcer. Recent experimental and clinical studies have shown that factors such as excessive gastric acid secretion, Helicobacter pylori infection and weakened gastric mucosal protection are the main causes of peptic ulcer. Peptic ulcer belongs to the category of typical psychosomatic diseases. Psycho-social plays an important role in the disease, so optimistic mood, regular life, avoiding excessive stress and fatigue, whether in the attack period or remission period of the disease important. basic knowledge Sickness ratio: 1%-5% Susceptible people: no specific population Mode of infection: non-infectious Complications: upper gastrointestinal bleeding, pyloric obstruction, gastric perforation
Cause
Cause of peptic ulcer
Excessive gastric acid secretion (30%):
Hydrochloric acid is the main component of gastric juice, secreted by parietal cells, regulated by nerves and body fluids. It is known that parietal cells contain three receptors, namely hirstamine receptors, cholinergic receptors and gastrin receptors, which receive histamine, acetylcholine and gastric secretion, respectively. Activation of the prime. When the surface cell surface receptor is bound by the corresponding substance, the second messenger in the cell is activated, thereby affecting gastric acid secretion.
In the pathogenesis of duodenal ulcer, excessive gastric acid secretion plays an important role. The amount of gastric acid basal secretion (BAO) and maximum secretion (MAO) in patients with duodenal ulcer were significantly higher than those in normal people. Duodenal ulcers never occurred in people with little gastric acid secretion or secretion.
After the chyme enters the duodenum from the stomach, under the stimulation of gastric acid and chyme, the pancreas secretes a large amount of pancreatic secretion, trypsin, and cholecystokinin. In addition to secretory mucus, the intestinal mucosa also releases hormones such as intestinal high. Glucagon, gut peptide (GIP), vasoactive intestinal peptide (VIP), which inhibits gastric acid secretion and stimulates secretion of gastrin, so when the function of releasing these hormones in the duodenal mucosa is reduced, It can cause gastrin and gastric acid secretion to increase, which contributes to the formation of duodenal ulcer.
The long-term and repetitive nature of gastric ulcer, the nature of complications, and the tendency of ulcers to heal under conditions of reduced gastric acid suggest that the pathogenesis is similar to that of duodenal ulcer. However, BAO and MAO in patients with gastric ulcer are similar to normal people, even lower than normal. Some gastric mucosal protective drugs (non-antacids) can promote the healing of ulcers, but some damage to gastric mucosa, although they do not reduce the effect of gastric acid. Drugs such as aspirin can cause gastric ulcers, and the fact that experimental animals continue to suck mucus from the stomach cavity can cause gastric ulcers, etc., all suggest that the occurrence of gastric ulcers is caused by the local part of the gastric mucosa. Due to the destruction of the gastric mucosal protective barrier, it is not effective against the erosion and digestion of gastric acid and pepsin, and ulceration occurs.
Helicobacter pylori infection (10%):
HP infection is the main cause of chronic gastritis and an important cause of peptic ulcer. In the HP-adhered epithelial cells, microvilli were reduced, cell-to-cell connections were lost, cells were swollen, the surface was irregular, the intracellular mucus particles were depleted, vacuolated, and the adhesion between the bacteria and the cells formed a sticky pedicle and a shallow cup-like structure.
Gastric mucosal protection (20%):
Under normal circumstances, the physical and chemical factors of various foods and the digestion of acidic gastric juice can not damage the gastric mucosa and cause ulcer formation, because the normal gastric mucosa has protective functions, including mucus secretion, gastric mucosal barrier integrity, and abundant mucosal blood. Flow and regeneration of epithelial cells, etc.
Delayed gastric emptying and bile reflux (10%):
This degenerative change of the gastric antrum and pyloric region during gastric ulcer can invalidate the contraction of the antrum and affect the advancement of the chyme. Delayed gastric emptying may be a factor in the pathogenesis of gastric ulcer disease.
Certain components of the duodenal contents, such as bile acids and lysolecithin, can damage the gastric epithelium. The duodenal contents can flow back into the stomach and cause chronic inflammation of the gastric mucosa. The damaged gastric mucosa is more susceptible to damage by acid and pepsin. In gastric ulcer, the concentration of bile acid conjugate in fasting gastric juice is significantly higher than that in normal controls, suggesting that bile reflux into the stomach may play an important role in the pathogenesis of gastric ulcer.
The role of gastrointestinal peptides (5%):
Many gastrointestinal peptides are known to affect gastric acid secretion, but only studies on the relationship between gastrin and peptic ulcer are more common. The role of gastrin in the pathogenesis of peptic ulcers is unclear.
Genetic factors (5%):
It has been agreed that the occurrence of peptic ulcer is genetically pleasing, and that gastric ulcer and duodenal ulcer disease are genetically independent and irrelevant. In the family of patients with gastric ulcer, the incidence of gastric ulcer is three times higher than that of normal people, and in the family of patients with duodenal ulcer, duodenal ulcer is more common than gastric ulcer.
Drug factor
Some antipyretic analgesics, anticancer drugs, etc., such as indomethacin, phenylbutazone, aspirin, adrenocortical hormone, fluorouracil, methotrexate, etc. have been classified as ulcerative factors. Among the above drugs, there are many studies on aspirin, and the results show that people who regularly use aspirin are prone to gastric ulcer disease. It has been pointed out that the prevalence of regular application of aspirin is about three times higher than that of aspirin.
Adrenal corticosteroids are likely associated with ulcer formation and reactivation. A group of 5,331 studies have shown that corticosteroid treatment for more than 30 days or a total of more than 1000 mg of prednisone can cause ulcers. In patients with a history of ulcers, the disease can be aggravated.
Non-steroidal anti-inflammatory drugs, such as indomethacin, phenylbutazone, ibuprofen, naproxen, etc., can also inhibit the synthesis of prostaglandins to varying degrees, which in theory can produce clinical effects similar to aspirin. Lixue et al. have a histamine-like effect, which can increase gastric acid secretion, so it has the potential to cause ulceration.
envirnmental factor
Smoking can stimulate the increase of gastric acid secretion, which is generally 91.5% higher than that of non-smokers. Smoking can cause vasoconstriction and inhibit the secretion of pancreatic juice and bile, which weakens its ability to neutralize gastric acid in the duodenum, leading to duodenum. Sustained acidification, nicotine in tobacco can reduce the pyloric sphincter tension, affecting its closing function and causing bile reflux, destroying the gastric mucosal barrier. The incidence of peptic ulcer was significantly higher in smokers than in the control group. Under the same effective drug treatment conditions, the former rate of ulcer healing was also significantly lower than the latter. Therefore, long-term large-scale smoking is not conducive to the healing of ulcers, but can also cause recurrence.
Food can cause physicochemical properties damage to the gastric mucosa. Overeating or irregular eating may disrupt the rhythm of gastric secretion. According to clinical observations, coffee, tea, spirits, spicy spices, kimchi and other foods, as well as partial eating, too fast, too hot, too cold, overeating and other bad eating habits, may be related to the occurrence of this disease.
Mental factors
According to the modern psycho-social-biomedical model, peptic ulcer is one of the typical psychosomatic diseases. Psychological factors can affect the secretion of gastric juice.
[Pathogenesis]
1. Excessive secretion of gastric acid Hydrochloric acid is the main component of gastric juice. It is secreted by parietal cells and regulated by nerves and body fluids. It is known that parietal cells contain three kinds of receptors, namely hirstamine receptors and cholinergic receptors. (cholinergic receptors) and gastrireceptors, which are activated by histamine, acetylcholine and gastrin, respectively. When the surface cell surface receptors are bound by the corresponding substances, the second messenger in the cells activates, thereby affecting Gastric acid secretion, there are two major second messengers in parietal cells: cAMP and calcium. The receptors in the parietal cell membrane, after binding to histamine, are coupled to an excitatory GTP-binding protein to activate adenosine. Acid cyclase, which catalyzes the conversion of ATP to cAMP, which then activates a protein kinase that phosphorylates an unrecognized intracellular protein, ultimately resulting in a H+K+-ATPase in the parietal cell (also known as a hydrogen ion pump). Or proton pump) activates, promotes acid secretion, and acetylcholine receptor and gastrin receptor bind to GTP-binding protein after binding to acetylcholine and gastrin, respectively, and activate membrane-bound phospholipase C, which catalyzes membrane Phospholipids decompose to produce inositotrisphosphate (IP3) and diacylglycerol. IP3 promotes the release of calcium from the intracellular reservoir, and then activates H+K+-ATPase to promote H+ secretion. Acetylcholine also increases the cell membrane to calcium. Permeability, gastrin and acetylcholine can promote the release of histamine from intestinal chromoblast-like cells (ECL), which can synergize with histamine. There are still somatostatin substances on the surface of parietal cells. Excitatory and inhibitory membrane receptor Gi Binding, inhibiting adenylate cyclase by an inhibitory GTP-binding protein, thereby reducing intracellular cAMP levels, reducing the secretion of H+ by parietal cells, and exciting the receptors of parietal cells, regardless of the stimulus. Finally, through the second messenger - cAMP and Ca2+, affecting the secretory membrane structure at the top of the parietal cells and the proton pump - H +, K + - ATPase, increase or decrease H + secretion.
The proton pump is a hydrogen ion ATPase that relies on ATP to provide energy. It is a counter-transport pump that catalyzes the equivalent exchange of intracellular H+ and extracellular K+. A gradient of 4 million:1 H+ is produced inside and outside the cell, which is much higher than the gradient produced by the proton pump in other parts of the body (eg colon, renal cortical collecting duct).
In static parietal cells, the proton pump is present in the lumen vesicles of the cytoplasm. After the wall cells are excited, the tube containing the proton pump moves toward the top of the cell, and the vesicle membrane fuses with the apical membrane. The apical membrane area increases, and the apical membrane retracts to form a secretory canaliculus, which merges into the glandular lumen. The movement of the vesicle is promoted by cAMP and Ca2+, and the fusion of the membrane is accompanied by H+, K+-ATPase. Activation, on the one hand, increases the permeability of the membrane to Cl- and K+. It is not known whether the transport of Cl- and K+ on the membrane is achieved by K+, Cl- co-operation through the respective channels or through the KCl channel. Which mechanism, because K+ and Cl- are simultaneously transported extracellularly, H+ and K+ are exchanged under the action of H+, K+-ATPase, and finally HCl secretion is caused, and the concentration of hydrochloric acid secreted by parietal cells is constant, which is 160 mmol/ L, pH 0.9, but the pH in the gastric juice is actually 1.3 to 1.8, because there are alkaline mucus and reflux intestinal fluid in the gastric juice.
In the pathogenesis of duodenal ulcer, excessive gastric acid secretion plays an important role. The argument that no acid is no ulcer is consistent with duodenal ulcer, and the amount of gastric acid basal secretion in patients with duodenal ulcer ( Both BAO) and maximal secretion (MAO) were significantly higher than normal, and duodenal ulcers never occurred in people without gastric acid secretion or secretion.
After the chyme enters the duodenum from the stomach, under the stimulation of gastric acid and chyme, the pancreas secretes a large amount of pancreatic secretion, trypsin, and promotes cholecystokinin. In addition to secretory mucus, the intestinal mucosa also releases hormones such as intestinal high. Glucagon, gut peptide (GIP), vasoactive intestinal peptide (VIP), which has the effect of inhibiting gastric acid secretion and stimulating secretion of gastrin, so when the function of releasing these hormones in the duodenal mucosa is reduced, It can cause gastrin, increased gastric acid secretion, and promote the formation of duodenal ulcer.
The long-term, repeated nature of the gastric ulcer, the nature of the complications, and the tendency of the ulcer to heal under conditions of reduced gastric acid suggest that the pathogenesis is similar to that of duodenal ulcer, but the patient with gastric ulcer Both BAO and MAO are similar to normal people, even lower than normal. Some gastric mucosal protective drugs (non-antacids) can promote the healing of ulcers without reducing the effect of gastric acid. Some drugs that damage the gastric mucosa such as aspirin can cause Gastric ulcers, as well as the fact that experimental animals continue to suck mucus from the stomach cavity, can lead to gastric ulcers, etc., all suggest that the occurrence of gastric ulcers is caused by the local part of the gastric mucosa, which cannot effectively fight stomach acid and pepsin due to the destruction of the gastric mucosal protective barrier. Erosion and digestion, and ulceration occurs.
2. Helicobacter pylori infection HP infection is the main cause of chronic gastritis, and it is an important cause of peptic ulcer. In the HP-adhered epithelial cells, microvilli are reduced, cell-to-cell connections are lost, cells are swollen, and the surface is irregular. The mucous particles are depleted, vacuolated, and a sticky pedicle and a shallow cup-like structure are formed between the bacteria and the cells.
3, gastric mucosal protection Under normal circumstances, the physical and chemical factors of various foods and the digestion of acidic gastric juice can not damage the gastric mucosa and lead to ulcer formation, because the normal gastric mucosa has protective functions, including mucus secretion, gastric mucosal barrier integrity Sexual, abundant mucosal blood flow and regeneration of epithelial cells.
There is a mucus layer of about 0.25-0.5 mm on the surface of the gastric mucosa. This thickness is about 10-20 times of the thickness of the surface epithelial cells, which is about 1/2 to 1/4 of the depth of the gastric gland. The mucus forms a non-cell surface. In the unstirred zone, mucus contains mucin, its concentration is about 30 ~ 50mg / ml, most of the water contained in the mucus is filled between the molecules of mucin, which helps to prevent the reverse dispersion of hydrogen ions, stomach Surface epithelial cells can also secrete bicarbonate, which is about 5% to 10% of the maximum gastric acid excretion. The process of gastric secretion of HCO3- depends on metabolic energy. The action of intracellular CO2 and H2O in carbonic anhydrase Next, HCO3- is produced, which passes through the endometrium of the lumen, exchanges with Cl-, and is secreted into the gastric cavity. Na+K+-ATPase is present in the basal membrane of the cell. Under the action of the enzyme, the extracellular Na+ is maintained. At a high concentration, Na+ is dispersed into the cells, and in exchange, the H+ produced during the formation of HCO3- is excreted outside the cell.
No matter whether it is mucus or bicarbonate, it can not prevent the gastric epithelium from being harmed by gastric acid and pepsin alone. The combination of the two forms an effective barrier. The mucus acts as a non-flowing layer to buffer. In the mucus layer, heavy carbon The acid salt slowly moves to the stomach cavity, neutralizing the acid that slowly moves to the surface of the epithelium, resulting in an H+ gradient across the mucus layer. With a pH of 2.0 in the stomach, the pH in the mucus layer on the epithelial surface can be maintained at 7.0. The formation of this gradient depends on the rate of alkali secretion and its thickness through the mucus layer, which in turn depends on the rate at which mucus is freshened and lost from the epithelial cell surface into the gastric cavity, any one or more of the above factors. When the interference is disturbed, the pH gradient will be reduced and the protective barrier will be destroyed.
4, gastric emptying delay and bile reflux gastric ulcer disease in the gastric antrum and pyloric region of this degenerative changes can cause gastric sinus contraction, thereby affecting the advancement of the chyme, gastric emptying may be gastric ulcer disease A factor in the pathogenesis.
Certain components in the contents of the duodenum, such as bile acids and lysolecithin, can damage the gastric epithelium. The contents of the duodenum can flow back into the stomach and cause chronic inflammation of the gastric mucosa. The damaged gastric mucosa is more susceptible to acid and stomach. The destruction of proteases, the concentration of bile acid conjugates in the gastric juice in gastric ulcer is significantly higher than that in normal controls, suggesting that bile reflux into the stomach may play an important role in the pathogenesis of gastric ulcer.
5, the role of gastrointestinal peptides It is known that many gastrointestinal peptides can affect gastric acid secretion, but only the relationship between gastrin and peptic ulcer is more, about the role of gastrin in the pathogenesis of ordinary peptic ulcer ,still not clear.
6, genetic factors have now agreed that the occurrence of peptic ulcer has a genetic quality, and that the gastric ulcer and duodenal ulcer disease are genetically independent, irrelevant, the family of gastric ulcer patients, the incidence of gastric ulcer is normal The person is 3 times higher, and in the family of patients with duodenal ulcer, duodenal ulcer rather than gastric ulcer occurs more frequently.
7, drug factors, some antipyretic analgesics, anticancer drugs, such as indomethacin, phenylbutazone, aspirin, adrenocortical hormone, fluorouracil, methotrexate, etc. have been classified as ulcerative factors, in the above drugs, on aspirin There are many studies, and the results show that people who regularly use aspirin are prone to gastric ulcer disease. It is pointed out that the prevalence of regular application of aspirin is about three times higher than that of aspirin.
Adrenal corticosteroids are likely associated with ulcer formation and reactivation, and a group of 5,331 studies have shown that corticosteroid treatment for more than 30 days or a total of more than 1000 mg of prednisone can cause ulcers in patients with a history of ulcers. Make the disease worse.
Non-steroidal anti-inflammatory drugs, such as indomethacin, phenylbutazone, ibuprofen, naproxen, etc., can also inhibit the synthesis of prostaglandins to varying degrees, which in theory can produce clinical effects similar to aspirin, equal to blood equality The drug has a histamine-like effect, which can increase gastric acid secretion, so it has the potential to cause ulceration.
8. Environmental factors Smoking can stimulate the increase of gastric acid secretion, which is generally 91.5% higher than that of non-smokers. Smoking can cause vasoconstriction and inhibit the secretion of pancreatic juice and bile, which weakens its ability to neutralize gastric acid in the duodenum, resulting in The duodenum is continuously acidified. Nicotine in tobacco can reduce the pyloric sphincter tension, affecting its closing function and causing bile reflux, destroying the gastric mucosal barrier. The incidence of peptic ulcer is significantly higher in smokers than in the control group. Under the effective drug treatment conditions, the former rate of ulcer healing is also significantly lower than the latter. Therefore, long-term large-scale smoking is not conducive to the healing of ulcers, and can also cause recurrence.
Food on the gastric mucosa can cause physical and chemical damage, overeating or irregular eating may destroy the rhythm of gastric secretion, according to clinical observation, coffee, tea, spirits, spicy spices, kimchi and other foods, as well as partial eclipse, diet Fast, too hot, too cold, overeating and other bad eating habits may be related factors in the occurrence of this disease.
9. Mental factors According to the modern psycho-society-biomedical model, peptic ulcer is one of the typical psychosomatic diseases, and psychological factors can affect gastric juice secretion.
Prevention
Peptic ulcer prevention
It is very important to remove and avoid the factors that induce the onset of peptic ulcer, such as mental stimulation, overwork, irregular life, irregular diet, smoking and alcohol abuse. Peptic ulcers can be relieved after drug treatment and ulcers heal. Continue to give a maintenance amount of drug treatment for 1 to 2 years, which is positive for preventing ulcer recurrence. HP-related gastroduodenal ulcer is effective in antibacterial drugs while reducing gastric acid drugs. Eradication of HP infection is also preventing ulcers. An important part of recurrence, in addition, gastrinoma or multiple endocrine neoplasia, hyperparathyroidism, Meckel diverticulum, Barrett's esophagus and other diseases can often be associated with peptic ulcer, should be treated in time.
Complication
Peptic ulcer complications Complications upper gastrointestinal bleeding pyloric obstruction gastric perforation
1, a lot of bleeding
Is the most common complication of this disease, the incidence of which accounts for about 20% to 25% of patients with this disease, is also the most common cause of upper gastrointestinal bleeding, complicated by duodenal ulcer more common in gastric ulcer, and concurrent with the ball Post-ulcer patients are more common, and blood is emitted. The history of peptic ulcer is mostly within one year, but after a single bleeding, it is prone to second or more bleeding, and 10% to 15% of patients can A large amount of bleeding is the first symptom of peptic ulcer.
The clinical manifestations of peptic ulcer bleeding depend on the location, speed and amount of bleeding, such as the duodenal posterior wall ulcer, which often breaks through the adjacent pancreaticoduodenal artery and causes an extremely rapid massive hemorrhage. Because there is no large artery adjacent to the anterior wall, a large amount of bleeding is less likely to occur. The oozing of the granulation tissue of the base of the ulcer or the erosive bleeding of the mucous membrane around the ulcer generally only causes a small amount of temporary bleeding, and the bleeding of the peptic ulcer is fast. If the amount is more, it will be characterized by hematemesis and black feces. If the amount of bleeding is small and the bleeding rate is slow and long-lasting, it may be characterized by gradual hypopigmentation of small red blood cell anemia and fecal occult blood positive, duodenal ulcer bleeding, black. Feces are more common than hematemesis, and gastric ulcers are bleeding. The chances of both are similar. A large amount of bleeding in a short period of time can cause dizziness, vertigo, weakness, thirst, palpitations, tachycardia, blood pressure due to a sharp decrease in blood volume. Decreased, fainting, even shock, before peptic ulcer and blood, often caused by aggravation of local congestion of the ulcer, resulting in increased abdominal pain, bleeding can be reduced by congestion, and alkaline blood Acid neutralization and dilution, will ease the pain.
According to the history of peptic ulcer disease and the clinical manifestations of hemorrhage, the diagnosis is generally not difficult to establish. Those with atypical clinical manifestations and difficult diagnosis should strive for emergency endoscopy within 24 to 48 hours after hemorrhage, and the diagnosis rate can reach 90%. Above, so that patients get timely diagnosis and treatment.
2. Perforation
Ulcer penetrates the serosa layer and reaches the free abdominal cavity to cause acute perforation. For example, ulcer penetration and adjacent organs, tissue adhesion, it is called penetrating ulcer or chronic perforation of ulcer, and the posterior wall perforation or perforation is small and only causes limitation. In the case of peritonitis, it is called subacute perforation.
In acute perforation, due to the duodenum or stomach contents flowing into the abdominal cavity, resulting in acute diffuse peritonitis, clinically sudden severe abdominal pain, abdominal pain often starts in the right upper abdomen or the middle upper abdomen, and continues to spread to the umbilical cord. Even the whole abdomen, because the gastrointestinal leakage stimulates the diaphragm, so the pain can be radiated to one side of the shoulder (mostly the right side). If the leakage of the contents flows into the lower right pelvic cavity along the mesenteric root, it can cause pain in the right lower quadrant and resemble acute appendicitis. Perforation, abdominal pain can be exacerbated by turning over, coughing, etc., so patients often stay in bed, legs are curled and not willing to move, abdominal pain often accompanied by nausea and vomiting, patients are irritated, pale, cold limbs, tachycardia, such as perforation Occurred after a full meal, the stomach contents leak more, the abdominal muscles are highly strong, and there is full abdominal tenderness and rebound tenderness. If the leakage is small, the abdominal muscles are stiff, tenderness and rebound pain can be limited to the upper abdomen. Nearby, the bowel sounds are reduced or disappeared, and the liver dullness is reduced or disappeared, indicating that there is pneumoperitoneum. For example, if the gastrointestinal contents are up to the pelvic cavity, the rectal examination can detect the tenderness of the right rectum. The total number of white blood cells and neutrophils increased. Abdominal fluoroscopy showed that there was free gas under the armpits, which confirmed the presence of gastrointestinal perforation, but there was no free gas under the septum and the perforation could not be discharged. Severe perforation cases or ulcer wear Serum amylase may also increase when the pancreas is involved, but generally does not exceed 5 times the normal value.
Symptoms caused by subacute or chronic perforation are not as severe as acute perforation, which can only cause localized peritonitis, intestinal adhesions or signs of intestinal obstruction, and can be improved in a short period of time.
3, pyloric obstruction
Mostly caused by duodenal ulcer, but can also occur in the pyloric and pyloric canal ulcers, the cause of which is usually due to the active period of the ulcer, inflammatory hyperemia of the tissue surrounding the ulcer, edema or reflexive pyloric spasm, such Pyloric obstruction is temporary, can disappear with the ulcer to improve, medical treatment is effective, it is called functional or internal pyloric obstruction, and conversely, ulcer healing, scar formation and scar tissue contraction or adhesion to surrounding tissues to block the pyloric passage The result is permanent, non-surgical and can not be automatically relieved, called organic and surgical pyloric obstruction, due to gastric retention, the patient can feel abdominal fullness discomfort, and often accompanied by loss of appetite, belching, anti Acid and other gastrointestinal symptoms, especially after meals, vomiting is the main symptom of pyloric obstruction, more than 30 to 60 minutes after the meal, the number of vomiting is not much, about once every 1-2 days, a vomiting can be More than 1L, containing fermented food, patients can be significantly reduced in weight due to long-term, repeated vomiting and eating, but not necessarily abdominal pain, such as abdominal pain occurs more in the early morning And no rhythm, due to repeated large vomiting, H+ and K+ loss, can cause metabolic alkalosis, and shortness of breath, limb weakness, irritability, and even hand and foot snoring, upper abdominal fullness and reversal on an empty stomach The peristaltic stomach type and the sound of the upper abdomen are the characteristic signs of pyloric obstruction.
4, cancer
Gastric cancer cancer is still a controversial issue. It is generally estimated that the incidence of gastric ulceration is only 2% to 3%, but duodenal ulcer does not cause cancer.
Symptom
Peptic ulcer symptoms Common symptoms Ulcer pain Gastrointestinal symptoms Abdominal pain Radioactive pain Heartburn Digestive tract perforation Nausea qi refractory ulcer Upper abdominal pain
(1) Characteristics of peptic ulcer pain
1. Long-term: It can heal itself after ulceration, but it will recur after healing. Therefore, it often has the characteristics of long-term recurrent episodes of upper abdominal pain. The whole course is 6 to 7 years, and some can be as long as one or twenty. Year, even longer.
2, periodicity: repeated episodes of pain in the upper abdomen, is one of the characteristics of this type of ulcer, especially duodenal ulcer is more prominent, the upper abdominal pain can last for several days, weeks or longer After a long period of relief, it can occur throughout the year, but it is more common in spring and autumn.
3, rhythm: the relationship between ulcer pain and diet has obvious correlation and rhythm, in the day, from 3 am to breakfast for a period of time, gastric acid secretion is the lowest, so there is little pain during this time, The pain of duodenal ulcers occurs well between meals, and continues until the next meal or after taking acid-based drugs. Some patients with duodenal ulcers have higher stomach acid at night, especially before going to bed. For diners, mid-night pain can occur, and the occurrence of gastric ulcer pain is irregular. It usually occurs within 1 hour after a meal, and gradually relieves after 1 to 2 hours, until the above rhythm occurs again after eating.
4. Pain area: The pain of duodenal ulcer occurs in the middle and upper abdomen, or above the umbilicus, or on the right side of the umbilicus. The location of gastric ulcer pain is also in the upper abdomen, but slightly higher, Or under the xiphoid process and the left side of the xiphoid process, the pain range is about a few centimeters in diameter. Because the pain of the visceral cavity is not very accurate on the body surface, the painful part does not necessarily accurately reflect the ulcer. Anatomical position.
5, the nature of pain: more dull pain, burning or hunger-like pain, generally light and tolerable, persistent severe pain suggesting ulcer penetration or perforation.
6. Influencing factors: Pain is often induced or aggravated by factors such as mental stimulation, excessive fatigue, inadvertent diet, drug influence, climate change, etc., due to rest, eating, taking acid medicine, hand pressing pain parts, vomiting, etc. Reduce or alleviate.
(B) other symptoms and signs of peptic ulcer
1, other symptoms: in addition to the upper abdominal pain, this disease can also have increased salivary secretion, heartburn, nausea, niacin, hernia, nausea, vomiting and other gastrointestinal symptoms, appetite and more normal, but even due to food After the onset of pain and fear of eating, so that weight loss, systemic symptoms may have manifestations of neurosis such as insomnia, or symptoms of autonomic nervous system imbalance such as slow pulse, sweating.
2, signs: ulcers, mid-upper abdomen can have localized tenderness, the degree is not heavy, and its tenderness is more consistent with the location of the ulcer.
(three) special types of peptic ulcer
1. Asymptomatic ulcer: refers to patients with peptic ulcer without obvious symptoms. It is accidentally found when other diseases are examined by gastroscopy or X-ray barium meal, or when complications such as bleeding or perforation occur, even when the autopsy is performed. It has been found that such peptic ulcers can be seen at any age, but are more common in the elderly.
2, childhood peptic ulcer: the incidence of peptic ulcer in childhood is lower than adults, can be divided into 4 different types.
(1) Infant type: Infant type ulcer is an acute ulcer that occurs in newborns and infants under two years of age. The cause of the disease is unknown. In the neonatal period, duodenal ulcer is more common than gastric ulcer, and the ulcer is rapid. Healing, or perforation or bleeding, and rapid death, after the neonatal period to infants within two years of age, the performance of ulcers and newborns are not much different, mainly for bleeding, obstruction or perforation.
(2) secondary hair: the occurrence of this type of ulcer is related to some serious systemic diseases, such as sepsis, central nervous system diseases, severe burns and the application of corticosteroids, it can also occur in congenital pyloric stenosis, liver disease After cardiac surgery, this type of ulcer occurs equally in the stomach and duodenum and can be seen in children of any age and gender.
(3) Chronic type: This type of ulcer mainly occurs in school-age children. As the age increases, the ulcer performance is similar to that of adults. However, in young children, the pain is more diffuse, mostly in the umbilical cord, and has nothing to do with eating, often vomiting. This may be due to the small duodenum, which is prone to obstruction due to edema and spasm. Only adolescents present a typical rhythmic pain confined to the upper abdomen. Duodenal ulcers are more common than gastric ulcers. There are many girls, and the onset of this type of ulcer is the same as the basic cause of ulcer disease in adults.
(4) Ulcers complicated by endocrine neoplasia: This type of ulcer occurs in gastrinoma and multiple endocrine neoplasia type I, namely Wermer syndrome.
3, the elderly peptic ulcer: gastric ulcer is more common, duodenal ulcer can also occur, the diameter of gastric ulcer can often exceed 2,5cm, and more often occur in the posterior wall of the high corpus or small main sputum, the elderly digestion Ulcers often manifest as irregular mid-abdominal pain, hematemesis and/or black feces, weight loss, rarely rhythmic pain, nocturnal pain and acid reflux, and easily complicated by massive bleeding, often difficult to control.
4, pyloric tube ulcer: relatively rare, often accompanied by gastric acid secretion is too high, its main manifestations are: 1 immediately after the occurrence of mid-abdominal pain, the degree is more intense and rhythmic, and can make patients fear of food, antacids Can relieve abdominal pain. 2 vomiting, vomiting pain immediately relieved, abdominal pain, vomiting and diet can lead to weight loss, such peptic ulcer medical treatment is less effective.
5, post-ball ulcer: about 5% of peptic ulcer, ulcers are mostly located in the proximal end of the duodenal papilla, nighttime abdominal pain and post-radiation pain more common in the post-ball ulcer, and a large number of bleeding are also common. Medical treatment is less effective.
6, complex ulcers: refers to the presence of ulcers in the stomach and duodenum, most of which occurs in the duodenum, after gastric ulcer, the disease accounts for about 7% of peptic ulcer, more common in men, its clinical Symptoms are not specific, but the incidence of pyloric stenosis is higher, the incidence of bleeding is as high as 30% to 50%, and the bleeding is mostly from gastric ulcer. The disease is more stubborn and the incidence of complications is high.
7, giant ulcers: giant gastric ulcer refers to X-ray gastric sputum meal examination to measure the diameter of ulcers more than 2,5cm, not all are malignant, pain is often atypical, often can not be completely relieved by antacids, vomiting and weight loss is obvious, Fatal bleeding can occur, sometimes in the abdomen to touch the lumps of fibrous tissue, long-term giant gastric ulcer often requires surgical treatment.
Giant duodenal ulcer refers to a diameter of more than 2cm, most of which are located in the ball, or after the ball. There are often inflammatory masses around the posterior wall of the ball, and it can invade the pancreas. The pain is severe and stubborn. Radiation to the back or right upper abdomen, vomiting and weight loss are obvious, bleeding, perforation and obstruction are common, bleeding and perforation can also occur simultaneously, and the giant duodenal ulcer with complications is mainly treated with surgery.
8, esophageal ulcer: its occurrence is also the result of contact with acidic gastric juice, ulcers occur in the lower part of the esophagus, mostly single, about 10% of multiple, ulcer size from a few millimeters to quite large, the disease occurs mostly in reflux Esophagitis and sliding esophageal hiatus hernia with squamous esophageal reflux, ulcers can occur in the squamous epithelium, can also occur in the columnar epithelium (Barrett epithelium), esophageal ulcer can also occur in esophagogastric anastomosis or esophageal lumen After anastomosis, it is the result of reflux of bile and pancreatic secretions.
Examine
Peptic ulcer examination
(a) endoscopy
Regardless of whether fiberoptic or electronic gastroscope is used, it is the main method for the diagnosis of peptic ulcer. Under endoscopic direct vision, peptic ulcer is usually round, elliptical or linear, with sharp edges and basic smoothness. It is grayish white or grayish yellow. Covered by the membrane, the surrounding mucosa is congested, edema, slightly elevated.
Japanese scholars divide the gastroscopic performance of the life cycle of peptic ulcer into three phases:
The active period (A period) is divided into two phases, A1 and A2.
A1: Round or oval, covered with white moss at the center, often with small bleeding, flushing around, inflammatory edema.
A2: The ulcer surface is covered with yellow or white moss, no bleeding, and the surrounding inflammation and edema are alleviated.
The healing period (H period) is divided into two phases, H1 and H2.
H1: The swelling around the ulcer disappears, and the mucosa is red with new capillaries.
H2: The ulcer becomes shallower and smaller, and the surrounding mucosa is wrinkled.
The scar stage (S period) is also divided into two phases, S1 and S2.
S1: The ulcerated white moss disappears and the new red mucous membrane appears (red scar stage).
S2: The red gradient is white (white scar period).
(2) X-ray barium meal inspection
The main X-ray of peptic ulcer is the sputum or shadow, which is caused by the sputum suspension filling the depressed part of the ulcer. In the front view, the shadow is round or oval, and the edge is neat, due to the inflammation around the ulcer. Edema forms an annular translucent area.
The shadow of gastric ulcer is more common in the small curvature of the stomach, and often see the sacral gastric incision on the opposite side of the ulcer. The shadow of duodenal ulcer is common in the ball, usually smaller than the shadow of the stomach, and the shadow is ulcer. Direct signs of existence, due to inflammation and local spasm around the ulcer, local tenderness and irritation can be found on X-ray barium meal examination, ulcer healing and scar contraction, local deformation, especially in duodenal bulb Ulcer, the latter may be clover-shaped, petal-like deformation.
(C) detection of HP infection
The detection methods for HP infection are roughly divided into four categories:
1. Inspect HP directly from gastric mucosal tissue, including bacterial culture, tissue smear or section staining for microscopic examination of bacteria.
2. Determination of urease activity in the stomach by urease test, breath test, gastric urea nitrogen test.
3. Serological examination of anti-HP antibodies.
4. Determination of HP-DNA by polymerase chain reaction (PCR) technique. Bacterial culture is the most reliable method for diagnosing HP infection.
(four) analysis of gastric juice
The average basal acid excretion (BAO) of normal males and females was 2.5 and 1.3 mmol/h, respectively (0-6 mmol/h), and the average BAO of male and female duodenal ulcer patients was 5.0 and 3.0 mmol/h, respectively. When BAO>10mmol/h, it is often suggested that gastrinoma is possible. After injection of pentagastrin at 6g/kg, the maximum acid output (MAO) and duodenal ulcer often exceed 40mmol/h. The gastric juice analysis results of various stomach diseases, the gastric acid amplitude overlaps with normal people, and the diagnosis of ulcer disease is only for reference.
Diagnosis
Diagnosis and diagnosis of peptic ulcer
diagnosis
Can be diagnosed based on clinical performance and laboratory tests.
Differential diagnosis
1, stomach cancer
The identification of benign gastric ulcers and malignant ulcers is important. The identification points are shown in Table 18-10. The identification of the two is sometimes difficult. The following situations should be given special attention:
1 middle-aged and elderly people have mid-upper abdominal pain, bleeding or anemia in the near future.
2 The clinical manifestations of patients with gastric ulcer have changed significantly or the anti-ulcer drug treatment is ineffective.
3 gastric ulcer biopsy pathology of intestinal metaplasia or dysplasia, clinically, patients with gastric ulcer should be actively treated under internal medicine, regular endoscopy follow-up, close observation until ulcer healing.
Table - Identification of benign gastric ulcers and malignant ulcers:
Benign ulcer, malignant ulcer
Age: Most middle-aged and middle-aged, more common in middle age.
Medical history: periodic intermittent episodes, progressive and continuous development.
Course of disease: longer, more in years, shorter, more in months.
Whole body performance: light more obvious, significant weight loss.
Oxidizing agent: can relieve abdominal pain, the effect is not good.
Check: ulcer shape, round or oval, the rules are irregular.
Ulcer edge: drilled, sharp and smooth, congested and uneven, tumor-like protrusions, hard and brittle, can smash bleeding.
Base moss color: smooth, clean, gray or gray-yellow moss uneven, dirty moss, bleeding, island-like residual.
Peripheral mucosa: soft, wrinkled walls often concentrated in ulcers. Cancerous infiltration, thickening, common nodular bulge, broken wall.
Gastric wall peristalsis: normal, weakened or disappeared.
Check: Diaphragm diameter, more <2.5cm more>2.5cm.
Shadow shape: often round or oval, often triangular or irregular.
Ulcer edge: smooth and irregular.
Shadow position: outside the stomach cavity, inside the stomach cavity.
Peripheral mucosa: the thickness of the mucosa is uniform, soft, and there is a lower density of the transparent band caused by inflammatory edema around the shadow. The mouth of the ulcer often shows a translucent shadow of 1 to 2 mm, that is, the Hampton line is infiltrated by gastric cancer and bulges into a nodular shape. Or polypoid, mucous membrane thickening irregular, stiff, wrinkled wall interruption, broken ends, sharp, sharp edges, no shadow areas, no Hampton line.
Gastric wall peristalsis: normal, weakened or disappeared.
Check: fecal hemorrhage, active period can be positive, turned negative after treatment, and more persistent positive.
Gastric juice analysis: normal or low gastric acid, no true lack of acid and acid deficiency.
2, chronic gastritis
The disease also has chronic upper abdominal discomfort or pain, and its symptoms can be similar to peptic ulcer, but the periodicity and rhythm of the attack are generally atypical, and gastroscopy is the main method of identification.
3. Gastric neurosis
The disease may have upper abdominal discomfort, nausea and vomiting, or resemble peptic ulcer, but often accompanied by obvious systemic neurological symptoms, mood swings are closely related to the onset, no obvious abnormalities were found by endoscopy and X-ray examination.
4, cholecystitis cholelithiasis
More common in middle-aged women, often interstitial, paroxysmal right upper abdominal pain, often radiated to the right scapular area, may have biliary colic, fever, jaundice, Murphy sign, eating greasy food can often be induced, B-ultrasound can make a diagnosis.
5, gastrin tumor
This disease is also known as Zollinger-Ellison syndrome, with refractory multiple ulcers, or atopic ulcers, easy to relapse after subtotal gastrectomy, more often accompanied by diarrhea and significant weight loss, patients with pancreatic non-beta cell tumor or stomach Sinus G cell hyperplasia, serum gastrin levels increased, gastric juice and gastric acid secretion increased significantly.
