What types of diseases are included in GERD? There are three types of GERD: non-erosive GERD (endoscopic negative GERD, NERD), reflux esophagitis (erosive esophagitis, RE or EE), and Barrett’s esophagus (BE). What is the pathogenesis of GERD? Gastroesophageal reflux disease is currently considered to be a dysmotic disease of the GI tract caused by multiple factors. The main pathogenesis is the result of a weakened anti-reflux defense mechanism and the attack of reflux on the esophageal mucosa: 1. Weakened anti-reflux defense mechanism of the esophagus, including: anti-reflux barrier, esophageal clearance of reflux and mucosal resistance to reflux action. 2. Attack of reflux on the esophageal mucosa. On the basis of the decreased anti-reflux defense mechanism of the esophagus, reflux stimulates and damages the esophageal mucosa, and the degree of damage is related to the quality and quantity of reflux, as well as to the contact time and site of reflux with the mucosa. What is the lower esophageal sphincter (LES) and how is it related to GERD? For many years, the structure and anatomical location of the lower esophageal sphincter have been debated. Most experts and scholars now believe that the lower esophageal sphincter is a 3-4 cm long circular muscle bundle at the end of the esophagus, which is made up of thickened circular fibers of smooth muscle in the lower esophagus. When the function of the LES is abnormal or the structure is damaged, the LES pressure may drop, causing the onset of gastroesophageal reflux. Why does GERD cause chest pain? The exact mechanism of chest pain caused by GERD is still unclear, but it is considered to be related to several factors, such as the presence of chemical, mechanical and temperature receptors on the esophageal wall, which can produce pain when the esophageal wall is stimulated by mechanical tension, acid and alkali, temperature, etc.; pain can also occur when the esophageal wall is ischemic; in recent years, it has been found that esophageal hypersensitivity may be one of the important mechanisms of chest pain caused by GERD. Why does GERD cause asthma, pneumonia and other pulmonary symptoms? The possible pathogenesis of pulmonary manifestations caused by GERD is the aspiration of gastric contents into the lung tissue, or not being aspirated into the lungs, the reflux activates the vagal arc from the esophagus to the lungs, resulting in tracheospasm, asthma attacks and or lung infections. It is well documented that gastroesophageal reflux disease is present in 34-89% of asthma, and 40% of asthma has reflux esophagitis. Patients may present with choking cough, waking up in the middle of the night, asthma-like attacks, asphyxia, aspiration pneumonia, interstitial fibrosis, pulmonary maculopathy, chronic obstructive pulmonary disease, etc. Gastroesophageal reflux should be considered for unexplained long-term chronic cough, choking cough, recurrent laryngospasm attacks, unexplained asthma, recurrent aspiration pneumonia, which is closely related to diet, especially in elderly patients who are bedridden for a long time and develop the above diseases possible. What are the complications of GERD? GERD can cause damage to the esophageal mucosa, resulting in esophageal strictures, bleeding esophageal ulcers, and complications of Barrett’s esophagus. Gastroesophageal reflux to the oropharynx, ears, eyes and lungs can lead to ear, nose and throat, oral cavity, both eyes and respiratory complications accordingly, such as deafness, rhinitis, chronic pharyngitis, asthma, pneumonia, etc. What are the tests required to diagnose GERD? Gastroscopy can directly observe esophagitis and its esophageal complications, and evaluate the efficacy and prognosis. 2. Dynamic 24h esophageal pH monitoring, pH monitoring can be used to evaluate the correlation between symptoms and reflux. 3. Dynamic 24h bile reflux monitoring, simultaneous monitoring of acid and bile reflux is more meaningful for GERD diagnosis. 4. Esophageal manometry, which does not directly reflect reflux, but can be used to diagnose GERD. directly respond to the reflux situation, but can show the dynamic situation of LES and esophageal body. 5.PPI test, PPI test can be used for patients with heartburn, acid reflux and other reflux symptoms and suspected GERD. This method is suitable for those who have no alarm symptoms. 6.Barium meal test, dual gas-barium imaging has a high specificity for the diagnosis of RE. Others such as excitation test, nuclear gastroesophageal reflux determination, gastric emptying test, etc. Can GERD be excluded if the gastroscopy is normal? No. GERD includes three types: non-erosive GERD (NERD), reflux esophagitis (RE) and Barrett’s esophagus (BE). Gastroscopy is a very important diagnostic method to confirm the diagnosis of GERD, to detect and assess esophagitis damage and to grade it; endoscopic biopsy is mandatory to diagnose BE. However, more than half of GERD patients have no RE manifestation under endoscopy, such as NERD is caused by GERD with typical symptoms present, including heartburn, acid reflux, chest pain and extraesophageal manifestations (cough, foreign body sensation in the pharynx, asthma, etc.), while no esophageal mucosal breakage exists on gastroscopy. Therefore, for the diagnosis of GERD, the importance of symptoms should still be emphasized. Heartburn, acid reflux or reflux of gastric contents all have moderate sensitivity and high specificity for diagnosis. In contrast, gastroscopy has a limited role in the diagnosis of GERD. Since most GERD patients have normal gastroscopic findings, gastroscopy is less sensitive in the diagnosis, but has good specificity once mucosal rupture is detected. Therefore, gastroscopy can confirm the diagnosis of RE and BE, but cannot exclude NERD. How is Barrett’s esophagus diagnosed? The diagnosis of Barrett’s esophagus is usually made by endoscopy, when orange-red gastric columnar epithelium appears in the pale pink squamous epithelium of the lower esophagus. However, the greatest difficulty in the diagnosis of BE is that the endoscopic position of the junction of squamous and columnar epithelium at the gastroesophageal junction and the lower and middle esophagus does not coincide, so it may sometimes be difficult to determine whether the orange mucosa is from the normal fundic cardia mucosa or whether the squamous epithelium of the esophagus has been columnarized? If it is the latter, it is BE, and if it is the former, it is normal. Thus, we should neither miss nor arbitrarily expand the diagnosis during endoscopy. Usually if fenestrated vessels are found at the lesion, it suggests that the site is the submucosal segment of the esophagus, and the diagnosis of BE can be made endoscopically. Staining method endoscopy and magnified endoscopic observation also help in the diagnosis of BE, but its gold standard is still the presence or absence of cupped cells within the columnar epithelium by mucosal biopsy. About whether columnar epithelium must have intestinal chemosis to diagnose BE?There is no definite conclusion, some western views think that chemosis of columnar epithelium is BE, but Barret himself only described squamous epithelium was replaced by columnar epithelium, and Japan thinks that as long as there is columnar epithelium, it can be diagnosed as BE with or without intestinal chemosis, and domestic consensus opinion adopts this criterion. Because intestinalization is a pathological diagnosis and only endoscopic observation is the first-line diagnosis, determining the presence of columnar epithelium in the lower esophagus is a decisive indicator for the diagnosis of BE. Relationship between esophageal hiatal hernia and gastroesophageal reflux disease? In normal subjects, there is a normal anti-reflux anatomical relationship between the stomach and esophageal junction area, with the main structure being the lower esophageal sphincter, in addition to the diaphragmatic esophageal hiatus, the diaphragmatic esophageal membrane, and the esophagogastric angle. When a hiatal hernia occurs, the normal anatomical relationship of the above-mentioned gastroesophageal junction is disrupted, resulting in displacement of the lower esophageal sphincter and weakening of the “spring clamp” and external pressure of the diaphragmatic esophageal membrane and esophagogastric horn on the LES, leading to relaxation of the LES and gastroesophageal reflux. Therefore, esophageal hiatus hernia is an important factor in the formation of GERD.