Chronic erosive gastritis

Introduction to chronic erosive gastritis Chronic erosive gastritis, also known as verrucous gastritis or pox-like gastritis. Generally only see symptoms of dyspepsia such as fullness, pantothenic acid, hernia, and irregular abdominal pain after meals. Chronic erosive gastritis is a clinically common digestive system disease between chronic superficial gastritis and peptic ulcer, and has a high clinical incidence. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: gastric cancer, erosive gastritis, gastric ulcer, gastric perforation

Causes of chronic erosive gastritis

Trauma factors (30%):

Including serious infections, severe trauma, intracranial hypertension, severe burns, major surgery, shock, excessive stress and fatigue. Severe shock can cause release of serotonin and histamine. The former stimulates the gastric wall cells to release lysosomes and directly damages the gastric mucosa. The latter increases the secretion of pepsin and gastric acid and impairs the gastric mucosal barrier.

Drug factors (35%):

Certain drugs, such as non-steroidal anti-inflammatory drugs, certain antibiotics, alcohol, etc., can damage the mucosal barrier of the stomach, leading to increased mucosal permeability, and hydrogen ions in the gastric juice can be infiltrated into the gastric mucosa, causing gastric mucosal erosion and bleeding. Adrenal corticosteroids can increase the secretion of hydrochloric acid and pepsin, reduce the secretion of gastric mucus, and slow the rate of renewal of gastric epithelial cells to cause this disease.

Hormone factor (30%):

During stress, norepinephrine and adrenocortical hormone secretion increased, visceral vasoconstriction, gastric blood flow decreased, and reverse-dispersed H+ could not be eliminated; hypoxia and norepinephrine reduced prostaglandin synthesis, and mucus secretion was insufficient, HCO3- Secretion is also reduced; gastrointestinal motility is slow during stress, pyloric dysfunction, causing bile reflux, bile salts further damage the ischemic gastric mucosal epithelium, causing damage to the gastric mucosal barrier, eventually leading to erosion and bleeding of the mucosa.

Pathogenesis

The specific pathogenesis is as follows:

1. Drugs:

1 non-steroidal anti-inflammatory drugs, including aspirin, indomethacin (indomethacin) and so on. These drugs can directly damage the gastric mucosa and inhibit cyclooxygenase damage.

2 anti-tumor drugs.

2. Stress: severe trauma, major surgery, extensive burns, intracranial lesions, sepsis, severe organ damage and multiple organ failure can cause this disease.

When stressed:

1 Increased release of adrenaline and norepinephrine, leading to gastric mucosal vasoconstriction and decreased blood flow, mucosal ischemia caused by insufficient secretion of mucus and sodium bicarbonate, decreased local prostaglandin synthesis and regeneration, and decreased gastric mucosal barrier, resulting in mucosa damage.

2 Increased secretion of adrenal glucocorticoids leads to hypersecretion of gastric acid and increased mucosal invasion.

3 gastrointestinal motility and pyloric dysfunction can lead to reflux of bile and pancreatic juice and cause damage to the gastric mucosal barrier.

3. Alcohol: The lipophilic and lipolytic properties of alcohol lead to the destruction of the gastric mucosal barrier, epithelial cell damage, intramucosal hemorrhage and edema can also lead to mucosal damage caused by hypersecretion of gastric acid.

Sudden onset of the disease, the clinical manifestations of the above gastrointestinal bleeding is the main manifestation of the disease, the incidence of which accounts for more than 1/4 of the cause of upper gastrointestinal bleeding, second only to peptic ulcer bleeding. Lighter patients only have fecal occult blood positive, while most patients have hematemesis and melena. Bleeding occurs intermittently with repeated illnesses. Usually the disease is more severe than peptic ulcer bleeding, although after a large number of blood transfusions, hemoglobin is more difficult to raise.

Chronic erosive gastritis prevention

Should avoid drinking strong tea, coffee, alcohol, etc.; eat less prone to flatulence foods, such as potatoes, sweet potatoes, onions, boiled soybeans and so on.

1. Relaxing mood

Mental stress is a contributing factor to chronic gastritis and should be avoided. Emotional uneasiness and impatience can easily cause gastric mucosal disorders and gastric dysfunction. Therefore, emotional stress should be avoided as much as possible to relieve tension. Usually do not anger when you are in trouble, do not worry in the matter, do not worry, keep your mood comfortable, and it is very beneficial to the recovery of gastritis.

2, taking antibiotics

Helicobacter pylori can cause gastritis and other digestive tract problems, and taking two weeks of antibiotics can defeat these bacteria. Helicobacter pylori can be measured by testing blood and saliva.

3. Use antacids

For the treatment of mild gastritis commonly used antacids, it is best to take the medicine after eating about 1-2 hours, this is the highest peak of gastric acid, just play an anti-acid effect, such as before going to bed at 9-10 o'clock in the evening It is better to take it once.

4, prudent medication

Avoid taking aspirin, acetaminophen, phenylbutazone, steroids, tetracycline, erythromycin, prednisone and other drugs, especially during the active period of chronic gastritis.

5. Appropriate exercise

Appropriate exercise is a good way to increase gastrointestinal motility, can effectively promote gastric emptying, enhance gastrointestinal secretion function, improve digestion, and help the recovery of gastritis.

6, quit smoking

Smoking can promote the onset of stomach pain. After smoking, nicotine (ie nicotine) can stimulate the gastric mucosa to cause an increase in gastric acid secretion, which has a harmful stimulating effect on the gastric mucosa. Excessive smoking leads to pyloric sphincter dysfunction, causing bile reflux, damage to the gastric mucosa, and affecting the blood of the gastric mucosa. Supply and repair and regeneration of gastric mucosal cells, so stop smoking.

7, ringing

Alcohol can directly destroy the gastric mucosal barrier, invading the gastric mucosa causing mucosal congestion, edema, erosion.

Chronic erosive gastritis complications Complications Gastric cancer erosive gastritis gastric ulcer gastric perforation

1. Inducing other diseases: If the erosive gastritis is not treated in time or treated, it is likely to induce the occurrence of atrophic gastritis, and weaken the patient's self-healing ability, resulting in aggravation of the patient's condition.

2, gastric cancer: erosive gastritis if not treated in time, will lead to more bacteria breeding, there may be changes in gastric cancer, to bring greater harm to patients, while the treatment will be more difficult.

3, gastric ulcer: erosive gastritis if not actively treated, its erosion position will appear worse, resulting in the emergence of gastric ulcer, resulting in further enlargement of erosion area, the condition worsened.

4, gastric perforation: erosive gastritis, if there is deep erosion, it may have gastric perforation, and even threaten the patient's life and health.

Chronic erosive gastritis symptoms Common symptoms Nausea left upper abdominal pain Upper abdominal discomfort Loss of appetite Stomach sputum Fullness upper gastrointestinal bleeding Diarrhea Left upper abdominal mass accompanied by...

symptom

1. Chronic erosive gastritis is mostly non-specific, mainly including nausea, vomiting and upper abdominal discomfort.

2. Most patients often have asymptomatic or varying degrees of dyspepsia such as abdominal pain, acid reflux, postprandial fullness, loss of appetite and so on. When the disease develops into chronic atrophic gastritis, the patient may have symptoms such as anemia, diarrhea, glossitis and water thinness. Individual patients with mucosal erosion have obvious upper abdominal pain and may have bleeding.

3. In the course of the primary disease, sudden upper gastrointestinal bleeding will occur, manifested as hematemesis and black feces, and black feces alone are rare. Bleeding is often intermittent. A large amount of bleeding can cause syncope or shock, accompanied by anemia. In the bleeding, the upper abdomen is painful or uncomfortable.

4. Patients with erosive gastritis secondary atrophy may have anemia, water thinness, glossitis, diarrhea and so on. Individual patients with mucosal erosion have more obvious upper abdominal pain and may have bleeding.

Sign

The first point: bloating. Mainly due to retention of the stomach, delayed emptying, indigestion, in addition, there may be loss of appetite, acid reflux, nausea and vomiting, fatigue, constipation or diarrhea.

The second point: pain in the upper abdomen. This is the most common symptom of chronic superficial gastritis. Generally manifested as diffuse upper abdominal burning, pain, pain and so on. If you eat too cold, too hot, too hard, spicy or other irritating foods will aggravate the condition.

The third point: suffocating. The patient showed an increase in gas in the stomach and was discharged through the esophagus to relieve the symptoms of upper abdominal fullness.

Fourth point: repeated bleeding. Bleeding is due to chronic superficial gastritis combined with an acute inflammatory change in the gastric mucosa.

There are multiple warts, swollen folds or papule-like bulges in the gastric mucosa, with a diameter of 5-10 mm. Mucosal defects or umbilical sag can be seen at the top, and there is erosion in the center. There is no blush around the ridge, but it is often accompanied by erythema of similar size. The antrum is more common and can be divided into continuous type and disappeared type. It is a special type of gastritis in the Sydney system classification of chronic gastritis, and the endoscopic classification is bulging erosive gastritis and flat erosive gastritis. Chronic gastritis lacks specific symptoms, and the severity of symptoms is not consistent with the degree of lesions in the gastric mucosa.

Endoscopic often manifest as multiple punctate or aphthous ulcers. Chronic non-erosive gastritis can be idiopathic, but also drugs (especially aspirin and non-steroidal anti-inflammatory drugs, see the treatment of peptic ulcer) Caused by Crohn's disease or viral infection. Helicobacter pylori may not play an important role here.

Symptoms are mostly non-specific and can include nausea, vomiting, and upper abdominal discomfort. Endoscopically, the edge of the thickened folds is a bit smashed, with white spots or depressions in the center. The histology varies.

Examination of chronic erosive gastritis

Laboratory examination: When the patient presented with vomiting and/or tar-like stools and some patients with acute massive hemorrhage, the total amount of hemoglobin decreased, and the stool and vomit occult blood tests were positive.

Other auxiliary inspections:

1. X-ray examination: gastrointestinal barium meal examination often can not find erosive lesions, and is not suitable for patients with acute active bleeding, because tincture can be applied to the mucosal surface, so that no endoscopic or angiographic examination can be performed in the near future; Superselective angiography of the superior mesenteric artery during acute hemorrhage can make a localized diagnosis of bleeding, which is often negative during intermittent bleeding.

2. Emergency endoscopy: emergency endoscopic examination within 24 to 48 hours after hemorrhage, acute gastric mucosal lesions characterized by multiple erosions and hemorrhagic foci can be seen.

Endoscopic observation

There are multiple warts, swollen folds or papule-like bulges in the gastric mucosa, with a diameter of 5-10 mm. Mucosal defects or umbilical sag can be seen at the top, and there is erosion in the center. There is no blush around the ridge, but it is often accompanied by erythema of similar size. The antrum is more common and can be divided into continuous type and disappeared type. It is a special type of gastritis in the Sydney system classification of chronic gastritis, and the endoscopic classification is bulging erosive gastritis and flat erosive gastritis. Chronic gastritis lacks specific symptoms, and the severity of symptoms is not consistent with the degree of lesions in the gastric mucosa. Most patients often have asymptomatic or varying degrees of dyspepsia such as abdominal pain, loss of appetite, postprandial fullness, and acid reflux. Patients with atrophic gastritis may have anemia, weight loss, glossitis, diarrhea, etc. Individual patients with mucosal erosion have obvious upper abdominal pain and may have bleeding.

Endoscopic often manifest as multiple punctate or aphthous ulcers. Chronic non-erosive gastritis can be idiopathic, but also drugs (especially aspirin and non-steroidal anti-inflammatory drugs, see the treatment of peptic ulcer) Caused by Crohn's disease or viral infection. Helicobacter pylori may not play an important role here.

Symptoms are mostly non-specific and can include nausea, vomiting, and upper abdominal discomfort. Endoscopically, the edge of the thickened fold is slightly erosive, with white spots or depressions in the center. Histological changes.

Diagnosis and diagnosis of chronic erosive gastritis

1, medication situation

In addition to medical history, such as injury, surgery, serious infections, etc., you can also ask if some drugs are applied.

2, clinical manifestations

Can occur at any age and gender. The onset is often more urgent and heavier, there is bleeding in the upper digestive tract, hematemesis, melena, shock, and often relapse after bleeding stops.

3, fiber endoscopy

Strive to carry out within 12-24 hours, has important reference value for the diagnosis of this disease, microscopically visible gastric mucosal congestion and edema, spotted smashed, multiple ulcers of varying sizes, ulcers can have fresh bleeding.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.