Disease etiology: Gastroesophageal reflux disease is a dysmotic disease of the digestive tract caused by a variety of factors, the presence of acid or other harmful substances such as monoacid, pancreatic enzymes and other esophageal reflux Under normal circumstances, the esophagus has a defense against the attack of gastric acid and duodenal contents, including the anti-reflux barrier, esophageal contouring function and resistance of esophageal mucosal tissue. The development of GERD is the result of a decrease in anti-reflux defense mechanisms and the effect of reflux on esophageal mucosal attack. Esophagogastric reflux barrier: It refers to a complex anatomical area at the junction of the esophagus and stomach, including the lower esophageal sphincter (LES), diaphragmatic foot, diaphragmatic esophageal ligament, and the acute angle between the esophagus and gastric fundus (His angle), etc. Structural and functional defects in each of these parts can cause gastroesophageal reflux, the most important of which is the functional state of the LES. (i) LES and LES pressure LES is a circular muscle bundle about 3-4 cm long at the end of the esophagus. The LES pressure is 10-30 mmHg in normal people at rest, which is a high pressure band to prevent reflux of gastric contents into the esophagus, and the LES pressure can be reduced when the structure of the LES is first destroyed, e.g., pancreatic dystrophy is easily complicated by reflux esophagitis after surgery. Some factors can affect the decrease of LES pressure, such as certain hormones (e.g. cholecystokinin, pancreatic glucagon, vasoactive intestinal peptide, etc.), food (e.g. high fat, chocolate, etc.), drugs (e.g. calcium channel blockers, diazepam), etc. Increased intra-abdominal pressure (e.g. pregnancy, ascites, vomiting, weight-bearing labor, etc.) and increased internal pressure (e.g. gastric dilatation, delayed gastric emptying, etc.) can affect the corresponding decrease in LES pressure and lead to gastric test tube reflux. （TLESR is different from the LES relaxation caused by swallowing, because it is not stimulated by the current swallowing action and esophageal peristalsis, and the relaxation time is longer, and the rate of decrease of LES pressure is faster and the minimum pressure of LES is lower. Although TLESR is also present in normal subjects, it is less frequent, while TLESR is more frequent in patients with GERD. TLESR is now considered to be the main cause of GERD. (iii) Columnar hernia May aggravate reflux and reduce acid clearance by the esophagus, which can lead to gastroesophageal reflux. Esophageal acid clearance: Under normal conditions, part of the esophageal contents are discharged into the stomach by gravity, and most of them are discharged into the stomach by spontaneous and secondary propulsive peristalsis of the esophageal body; this is volume clearance, which is the way of esophageal contouring. Swallowing action induces autonomic peristalsis, reflux back into the esophagus causing dilatation and stimulating secondary peristalsis. Volume clearance reduces the volume of acid in the esophagus and the remaining acid is neutralized by swallowed saliva. Esophageal mucosal defense: In GERD, esophageal inflammation occurs in only 48%-79% of patients, and another part of patients have reflux symptoms but no obvious esophageal mucosal damage, suggesting that the esophageal mucosa has a defense against reflux items, and this defense is called esophageal mucosal tissue resistance. It includes the structural and functional defenses of esophageal epithelial surface mucus, immobile water layer and surface HCO3, complex squamous epithelium and the protective effect of mucosal blood supply. Delayed gastric emptying: Gastroesophageal reflux occurs more frequently after meals, and its reflux frequency is related to the content and composition of gastric contents and gastric emptying. Gastroesophageal reflux can be promoted in those with delayed gastric emptying. Pathology:In patients with GERD with reflux esophagitis, the pathological histological changes may include: ① hyperplasia of the complex squamous epithelial cell layer; ② prolongation of the papillae towards the deep luminal surface; ③ infiltration of inflammatory cells, mainly neutrophils, in the lamina propria; ④ ballooning of the squamous epithelium; ⑤ erosion and ulceration. Barrett’s esophagus is a condition in which the squamous epithelium is replaced by columnar epithelium 2 cm above the dentate line at the junction of the esophagus and stomach. The histological manifestation is a special type of columnar epithelium, cardia-type epithelium or fundic-type epithelium. The typical endoscopic presentation is a pinkish reddish-white esophageal mucosa presenting as an orange-red color of the gastric mucosa, and the distribution may be circumferential, lingual or insular. Diagnostic tests Endoscopy: Endoscopy is the most accurate way to diagnose reflux esophagitis and to determine the severity of reflux esophagus and the presence of complications. Combined with biopsy, it can be differentiated from other causes of esophagitis and other esophageal lesions (e.g. esophageal cancer). Endoscopic sighting of reflux esophagitis can establish the diagnosis of GERD, but the absence of reflux esophagitis cannot exclude GERD. Grading of GERD according to the degree of damage to the esophageal mucosa seen endoscopically is helpful in judging the condition and guiding treatment. The long-standing Savary-Miller grading method classifies reflux esophagitis into 4 grades: grade I as a single or several non-fused lesions showing erythema or superficial erosions; grade II as a fused lesion, but not diffuse or circumferential; grade III as a diffuse circumferential lesion with erosions but no strictures; and grade IV as a chronic lesion showing ulceration, stenosis, esophageal constriction, and Barrett’s disease. stenosis, esophageal constriction and Barrett’s esophagus. 24-hour esophageal pH monitoring: 24-hour continuous monitoring of esophageal pH with a portable pH recorder under physiological conditions can provide objective evidence of excessive W acid reflux in the esophagus, and is now recognized as an important diagnostic method for the diagnosis of GERD, especially when the patient has atypical symptoms, no reflux esophagitis, and when treatment is ineffective despite typical symptoms.