superficial gastritis
Introduction
Introduction to superficial gastritis Superficial gastritis is a superficial inflammation of chronic gastric mucosa, which is the most common type of chronic gastritis, accounting for about 50% to 85% of all chronic gastritis in gastroscopy. The basic pathology of superficial gastritis is epithelial cell degeneration, epithelial hyperplasia and intrinsic inflammatory cell infiltration. Sometimes intestinal epithelial metaplasia of surface epithelium and pituitary epithelium can be seen without the reduction of intrinsic glands. The lesion site is often marked by gastric antrum, mostly diffuse, gastroscopy for gastric mucosal congestion, edema and punctiform hemorrhage and erosion or accompanied by yellow-white mucinous exudate. The most common symptom is upper abdominal pain, which accounts for about 85%. The upper abdominal pain of patients with superficial gastritis is mostly irregular, and has nothing to do with diet (some patients are comfortable on an empty stomach and uncomfortable after a meal), generally suffering from chronic upper abdominal burning, dull pain, and pain. Symptoms are often aggravated by cold foods, hard foods, spicy or other irritating foods, and a few are related to climate change. This kind of upper abdominal pain is not easy to relieve with antispasmodic agents and antacids. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: stomach cancer
Cause
The cause of superficial gastritis
Chronic infection (20%):
Chronic infections of the nasal cavity, mouth, pharynx, etc., such as alveolar pus, tonsillitis, sinusitis and other long-term ingestion of bacteria or toxins, can repeatedly stimulate the gastric mucosa and cause superficial gastritis. Chronic inflammatory changes were found in the stomach of 90% of patients with chronic tonsillitis.
Excessive gastric acid (15%):
Gastric acid is an acidic secretion in gastric juice. Normal gastric acid can digest food together with pepsin and kill the Helicobacter pylori in the stomach. When the gastric acid is excessively secreted, the stomach acid retains more while neutralizing the digested food. It will corrode the gastric mucosa and erode the stomach wall, causing ulceration or inflammation of the mucosal layer.
Smoking (20%):
The main harmful component in tobacco is nicotine. Long-term heavy smoking can relax the pyloric sphincter, duodenal fluid reflux, and gastric vasoconstriction, and the gastric acid secretion increases, thereby destroying the gastric mucosal barrier and causing chronic inflammatory lesions. According to Eward, 40% of people who smoke more than 20 cigarettes a day can develop inflammation of the gastric mucosa.
Bacterial factors (25%):
More common in acute gastritis, gastric mucosal lesions have prolonged unhealed or repeated episodes, gradually evolved into superficial gastritis.
Drug factors (10%):
Certain drugs such as salicylic acid preparations, corticosteroids, digitalis, indomethacin, phenylbutazone, etc., can cause chronic gastric mucosal damage.
Irritating food (5%):
Long-term consumption of spirits, strong tea, coffee, spicy and rough foods, as well as irregular eating patterns such as hunger or satiety can destroy the gastric mucosal protective barrier and produce gastritis.
Pathogenesis
(1) Circulatory and metabolic dysfunction: The structural and functional integrity of the gastric mucosa and its ability to defend against various damaging factors are closely related to adequate mucosal blood flow. In patients with congestive heart failure or portal hypertension, the stomach is in a state of blood stasis and hypoxia for a long time, resulting in a weakening of the gastric mucosal barrier function, a decrease in gastric acid secretion, and a large number of bacteria, which may easily cause inflammatory damage of the gastric mucosa. In chronic renal failure, urea is excreted from the gastrointestinal tract, and ammonium carbonate and ammonia are produced by bacteria or intestinal hydrolase, causing irritative damage to the gastric mucosa, resulting in congestion and edema of the gastric mucosa, and even erosion.
(2) Bile or duodenal reflux: The discovery or confirmation of bile reflux by fiberoptic endoscopy is an important cause of chronic gastritis. Due to dysfunction of the pyloric sphincter or duodenal juice or bile after gastric surgery, it can reflux into the stomach and destroy the gastric mucosal barrier, which promotes the reverse diffusion of H?+ and pepsin into the mucosa, causing a series of pathological reactions, leading to chronic gastritis. .
(3) Helicobacter pylori (HP) infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the gastric mucosal layer and epithelial cells of patients with chronic gastritis. Since then, many scholars have carried out a large number of experimental studies on patients with chronic gastritis, HP is cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis, and then it is found that the degree of HP infection is positively correlated with the degree of inflammation of the gastric mucosa. Therefore, in 1986, the eighth session of the World Gastroenterology Society proposed that HP infection is one of the important causes of chronic gastritis. The pathogenesis of HP may be mainly caused by destroying the gastric mucosal barrier and causing H+ to diffuse in the opposite direction, eventually causing inflammation of the gastric mucosa.
(4) Psychosomatic factors: Because mental health is unhealthy, long-term mental stress, anxiety or depression can cause imbalance of systemic sympathetic and parasympathetic functions. In particular, the sympathetic nerves are in an excitatory state for a long time, which may also lead to vasomotor dysfunction of the gastric mucosa, resulting in a decrease in blood flow of the gastric mucosa, destroying the barrier function of the gastric mucosa, and forming a chronic inflammatory reaction of the gastric mucosa over time.
In addition, in summer, the body's resistance is reduced, it is easy to get sick, and drug stimulation is also a cause of high incidence of chronic superficial gastritis in summer. Dean Wen reminded the majority of patients with stomach diseases to take antipyretic and analgesic drugs after taking a cold in summer. These drugs have a greater stimulating effect on the gastric mucosa, leading to contraction and ischemia of the gastric mucosa, induction of chronic superficial gastritis, or aggravation of chronic shallowness. Epigastric gastritis. If you must take these drugs, it is recommended that patients take them after meals to reduce the stimulating effect of the drugs on the stomach.
Prevention
Superficial gastritis prevention
Chronic superficial gastritis is a common disease, frequently-occurring disease, and the course of the disease is lingering, easy to recurrent, and deeply suffered by patients. In addition, some superficial gastritis loses treatment or does not pay attention to life adjustment, and it is easy to progress to chronic atrophic gastritis and cause gastric cancer, with serious consequences. Therefore, the prevention of superficial gastritis should be paid attention to.
The prevention of superficial gastritis should mainly pay attention to life and diet, and actively avoid and eliminate various pathogenic factors. details as follows:
1. Avoid eating a variety of irritating foods such as spirits, espresso, raw garlic mustard and other foods that are harmful to the gastric mucosa, while avoiding foods that are too hard, too acidic, too hot, too cold, too hot and too rough. You can use easy-to-digest foods and pay attention to cooking methods such as frying and frying. Food should be light and soft.
2. Increase nutrition, pay attention to choose protein foods with high nutritional value and soft foods rich in vitamins, such as milk, tofu, carrots and some fermented foods, food should be chewed slowly.
3. Diet should be regular, regular quantitative, not overeating, develop good eating habits, reduce the burden on the stomach. Pay attention to food mix, it is best to have dry and thin, protein food and a small amount of staple food.
4. Diet should be light, rich in nutrition, regular and regular, regular quantitative, avoid hunger and overeating, overeating. At the same time, avoid intensive tea, coffee, spices, rough and hard food intake, quit smoking and alcohol, to prevent damage to the gastric mucosa.
5. Avoid mental stress, depression and excessive fatigue. It is advisable to have a life, a combination of work and rest, and an emotional optimism. At the same time, physical exercise should be strengthened to enhance physical fitness and strengthen gastrointestinal function.
6. Active treatment of systemic diseases that can lead to chronic gastritis, such as liver, gallbladder, pancreas, heart, kidney disease and endocrine diseases.
Complication
Superficial gastritis complications Complications
Long-term chronic stomach symptoms, digestive and dysfunction, leading to gastric disease and nutrient metabolism, autonomic regulation, endocrine hormone release, growth and development, and overall immune function, becoming an important potential for secondary diseases Factors; the physique of the patient group is weakened, the quality of life is declining, and even an important factor that causes people's psychosocial abnormalities.
Psychosomatic factors, due to unhealthy mental health, long-term mental stress, anxiety or depression, can cause imbalance of systemic sympathetic and parasympathetic functions. In particular, the sympathetic nerves are in an excitatory state for a long time, which may also lead to vasomotor dysfunction of the gastric mucosa, resulting in a decrease in blood flow of the gastric mucosa, destroying the barrier function of the gastric mucosa, and forming a chronic inflammatory reaction of the gastric mucosa over time.
Superficial gastritis affects the abdominal distension of the respiratory tract, the sputum rises, the chest cavity becomes smaller, and the respiratory function of the lung is limited, which may cause difficulty in breathing. Abdominal flatulence, squatting, compression of the chest, heart contraction and diastolic function are affected. Intestinal flatulence, increased intestinal pressure, affecting blood circulation in the intestinal wall. The intra-abdominal pressure is increased, the inferior vena cava is blocked, and the amount of heart is reduced, which affects the ejection of the heart.
Symptom
Superficial gastritis symptoms Common symptoms Scapular tenderness Upper abdominal pain Nausea and vomiting Loss of appetite Repeated bleeding Weight loss Abdominal distension Qi
1, the most common symptom is upper abdominal pain, accounting for about 85%. The upper abdominal pain of patients with superficial gastritis is mostly irregular, and has nothing to do with diet (some patients are comfortable on an empty stomach and uncomfortable after a meal), generally suffering from chronic upper abdominal burning, dull pain, and pain. Symptoms are often aggravated by cold foods, hard foods, spicy or other irritating foods, and a few are related to climate change. This kind of upper abdominal pain is not easy to relieve with antispasmodic agents and antacids.
2, bloating, accounting for 70%. Often due to retention in the stomach, delayed emptying, indigestion.
3, hernia, about 50% of patients with this symptom, the patient's stomach gas increased, discharged through the esophagus, so that the upper abdominal fullness temporarily relieved.
4, repeated bleeding is also a common manifestation of superficial gastritis, the cause of bleeding is a chronic superficial gastritis based on an acute inflammation of the gastric mucosa.
5, nausea and vomiting: inflammatory gastric mucosa acceptance, biological factors, as well as gastric motility disorders, stomach reverse peristalsis, nausea, vomiting.
6. Constipation and diarrhea: Most patients have constipation symptoms and relatively few diarrhea.
7, other, loss of appetite, acid reflux, nausea and vomiting, fatigue, constipation or diarrhea.
8, superficial gastritis lacks typical positive signs, physical examination can have upper abdominal tenderness, a small number of patients may have weight loss and anemia.
Examine
Superficial gastritis examination
1 gastroscopy : combined with direct biopsy is the main method for the diagnosis of chronic gastritis.
2 Helicobacter pylori antibody test : the positive rate of Helicobacter pylori infection in chronic gastritis is as high as 70-90%. The gastric mucosa tissue can be taken by gastroscopy, and the antibody of Helicobacter pylori in the blood can also be checked. In addition, it can be examined before and after treatment of chronic gastritis against Helicobacter pylori as one of the traceable indicators.
3X line barium meal : no abnormalities in most chronic superficial gastritis. Atrophic gastritis can show gastric mucosal atrophy by double contrast of gas sputum, and the gastric wrinkle wall is relatively flat and reduced. Chronic atrophic gastritis has low gastric acid secretion.
4 Determination of gastric acid content : The use of pentagastrin gastrin stimulation, determination of basic basal acid secretion (BAO), maximum acid secretion (MAO), peak acid secretion (PAO), help to diagnose atrophic gastritis.
5 serum wall cell antibody test and serum gastrin test : can be used as a reference for the diagnosis of atrophic gastritis and typing.
Diagnosis
Diagnosis and diagnosis of superficial gastritis
Diagnostic criteria
The history of chronic gastritis is often atypical, with no specific symptoms and fewer signs. Mainly based on the patient's symptoms such as fullness, pain, etc. after a meal, can be suspected of chronic gastritis. X-ray examinations generally only help to rule out other stomach conditions. The diagnosis relies mainly on gastroscopy and gastric mucosal biopsy. Supplemented with gastric secretion examination. The disease needs to be differentiated from peptic ulcer, gastrointestinal neurosis, chronic biliary disease, and the like. Domestically, the inflammatory cells infiltrate the depth of the mucosa to divide the disease into light, medium and heavy. Those who infiltrated the superficial layer of the mucosa were mild, and those involved in the middle third were moderate, and those who exceeded 2/3 of the mucosa were severe.
Differential diagnosis
The disease needs to be differentiated from peptic ulcer, gastrointestinal neurosis, chronic biliary disease.
