Gastroesophageal reflux disease (GERD)
Gastroesophageal reflux disease (GERD for short) is a condition in which the stomach? GERD is a clinical syndrome characterized by heartburn and acid reflux caused by the reflux of duodenal contents into the esophagus. GERD is a clinical syndrome characterized by heartburn and acid reflux. There are two types of GERD: physiological and pathological. Pathological reflux is caused by the dysfunction of the lower esophageal sphincter and/or abnormalities in the tissue structure related to its function, resulting in low pressure of the lower esophageal sphincter and causing a series of clinical symptoms and complications.
Gastroesophageal reflux disease can be divided into two types according to the endoscopic findings: non-erosive gastroesophageal reflux disease (NERD) if there is no obvious lesion in the esophageal mucosa; non-erosive gastroesophageal reflux disease (NERD) if there is obvious erosion? If inflammatory lesions such as ulcers are evident, the disease is called reflux esophagitis (RE).
Causes
1.Anti-reflux jaundice
Jaundice is a symptom and sign of yellowing of the skin, mucous membranes and sclera due to elevated bilirubin in the serum. Certain liver diseases, gallbladder disease and blood disorders often cause jaundice. If the bilirubin concentration in the blood exceeds 2 mg/dL (34 μmol/L), a yellow color will appear that is discernible to the naked eye.
As the red blood cells in the blood age and die, the hemoglobin from the hemoglobin in the red blood cells pools in the Kuffer’s cells of the liver and spleen to be converted into bilirubin. After being processed by the liver, bilirubin is secreted into the duodenum with bile, partially reabsorbed through the intestine, and the rest is excreted with feces. Abnormalities in the links affecting the formation, metabolism and excretion of bilirubin may lead to jaundice.
Jaundice is divided into three main categories.
1, hemolytic jaundice: hemolytic jaundice caused by increased destruction of red blood cells and excessive bilirubin production.
2, hepatocellular jaundice: jaundice that occurs when the liver itself is diseased and unable to process bilirubin properly.
3, obstructive jaundice/: a jaundice condition that occurs when the liver is unable to properly eliminate bilirubin. Mechanical obstruction of the intrahepatic or extrahepatic biliary system occurs, affecting the excretion of bilirubin and resulting in obstructive (obstructive) jaundice.
In addition, congenital non-hemolytic jaundice occurs if there is some congenital defect in the hepatocytes that prevents the normal metabolism of bilirubin. Physiological jaundice can occur in newborns shortly after birth due to massive destruction of red blood cells and impaired uptake of bilirubin by hepatocytes. Low flow barrier function ①Lower esophageal sphincter pressure: Under physiological conditions, when there is a swallowing action, the lower esophageal sphincter reflexively relaxes and the pressure drops, pushing the food into the stomach through normal esophageal peristalsis, and then returns to normal levels, and there is a reactive pressure increase to prevent food reflux; when the intragastric pressure and intra-abdominal pressure rise, the lower esophageal sphincter will actively contract to make its pressure exceed the increased When intragastric and intra-abdominal pressures rise, the lower esophageal sphincter actively contracts so that its pressure exceeds the increased intragastric pressure, acting as an anti-reflux agent. If this function is disturbed by some factors, it can cause regurgitation of gastric contents into the esophagus. (2) Weakness of the tissue around the lower esophageal sphincter, such as: lack of abdominal segment of the esophagus, resulting in increased intra-abdominal pressure can not conduct intra-abdominal pressure to the lower esophageal sphincter contraction to achieve the anti-reflux effect; septal esophageal ligament and lower esophageal mucosa defense anatomical structure of organic or functional lesions, etc., can destroy its normal anti-reflux function.
2, esophageal contouring ability to reduce under normal circumstances, relying on the pushing peristalsis of the esophagus, the neutralization of saliva, the gravity of the esophagus pill and the bicarbonate secreted under the esophageal mucosa and other factors to play a role in the removal of reflux to shorten the contact time of reflux and esophageal mucosa; when the amplitude of esophageal peristalsis is weakened, or disappears, or when pathological peristalsis occurs, the ability of the esophagus to remove the opposite matter through peristalsis is reduced, and at the same time It prolongs the residence time of the harmful substances in the esophagus and increases the damage to the mucous membrane.
The barrier function of esophageal mucosa is destroyed. The barrier function is composed of mucus layer, intracellular buffer, cell metabolism and blood supply. Certain substances in the reflux (gastric acid, pepsin, bile salts and pancreatic enzymes from duodenal reflux into the stomach) impair the barrier function of the esophageal mucosa, weaken the mucosal resistance and cause inflammation of the esophageal mucosa.
4, gastric and duodenal malfunction ① low gastric emptying function increases gastric contents and pressure, which can induce opening of the lower esophageal sphincter when it exceeds the pressure of the lower esophageal sphincter; increased gastric volume also leads to gastric dilatation, resulting in shortening of the pancreatic esophageal segment, which reduces the anti-reflux barrier function. ②In duodenal lesions, incomplete closure of the cardia sphincter leads to duodenal gastric reflux.
Clinical manifestations
The esophagus is located behind the sternum, which is behind the bone in the midline position of the chest cavity. Typical symptoms are heartburn? acid reflux and regurgitation. Heartburn is the most prominent symptom, manifested as a burning sensation behind the sternum or under the glabella, often extending upward from the lower part of the sternum, mostly occurring one hour after a meal, and can be aggravated when lying down, bending over or increasing abdominal pressure? Sometimes the heartburn sensation is especially like being scalded by boiling water. Regurgitation refers to the influx of stomach contents into the mouth without nausea or exertion, of which acidic reflux is called acid reflux.
Other symptoms are chest pain, epigastric pain and nausea; as acid reflux enters the esophagus and can even reach the throat, it can also cause symptoms including the mouth, throat and lungs, such as cough, throat discomfort, asthma, etc.? There are also repeated diagnoses of angina pectoris? The difference between gastroesophageal reflux and angina pectoris is that the former has a chronic course with recurrent episodes, often related to the position of the disease, especially in the prone position, and can be relieved by sitting or activity, or by the use of acid suppressants? Angina pectoris, on the other hand, often radiates to the left shoulder and the inner side of the left arm, and the pain is mostly triggered, often during excitement and activity, and lasts for a short time.
Treatment
1. General treatment
Lifestyle changes should be used as the basic measure of treatment. Elevating the head of the bed by 15-20 cm is a simple but effective way to enhance acid clearance during sleep using gravity and reduce nocturnal reflux. Foods such as fat, chocolate, tea and coffee can reduce lower esophageal sphincter pressure and appropriate control is advisable. Smoking and alcohol can weaken the acid scavenging ability of the esophagus, reduce the lower esophageal sphincter pressure and weaken the protective function of the esophageal epithelium, and patients should quit smoking and alcohol. Avoiding a full stomach 3 hours before bedtime can also reduce nocturnal reflux. 25% of patients can have their symptoms improved after changing the above habits.
2. Drug treatment
If the symptoms of reflux cannot be improved by changing the lifestyle, systematic medication should be started. The purpose of treatment is to reduce reflux, relieve symptoms, reduce mucosal damage from reflux material, and enhance the anti-reflux defense function of esophageal mucosa to cure esophagitis, prevent recurrence, and prevent and treat important complications.
2. 1 H2 receptor blockers
Such as cimetidine, ranitidine, famotidine and nizatidine, etc., are less commonly used at present.
2.2 Proton pump inhibitors
These drugs are commonly used in clinical practice, such as omeprazole, lansoprazole, pantoprazole and esomeprazole.
2.3 Prokinetic drugs
GERD is a power disorder disease, there are often abnormal esophageal and gastric motility, H2 receptor blockers and proton pump inhibitors when treatment is ineffective, can be applied domperidone, cisapride or mosapride and other prokinetic drugs.
2,4 Mucosal protective agents
Aluminum thioglycollate, as a local action agent, can provide a physical barrier against refluxed gastric contents by adhering to the esophageal mucosal surface, and has a mild buffering effect on gastric acid, but does not affect the secretion of gastric acid or pepsin. Magnesium aluminum carbonate can bind the refluxed bile acid and reduce its damage to the mucosa, and can adhere to the mucosal surface as a physical barrier.
2.5 Surgical treatment
Anyone who is ineffective in long-term medication or needs lifelong medication, or who cannot tolerate dilation, or who needs repeated dilation can be considered for surgical operation. The advent of laparoscopic anti-reflux surgery has provided clinicians with a new surgical treatment method.