Under normal condition, the blood flow of human abdominal viscera first returns to the hepatic portal vein, then flows to the hepatic venous capillary network after passing through the hepatic portal vein system vessels and the intrahepatic portal capillary network, and finally converges to the hepatic vein and flows into the inferior vena cava. Blood return flow is like a water channel, any link with blockage or narrowing will lead to poor water flow, and the stagnant water will find other channels to flow away after reaching a certain level. In other words, in the above-mentioned return of blood to the abdominal organs of the human body, whether it is the portal system vessels, the intrahepatic capillary network, or the hepatic veins, any blockage or stenosis at any point may cause stasis and increased pressure in the portal vein, leading to the opening and formation of collateral circulation in the body vessels. Esophagogastric fundic varices are one of the vessels that form the collateral circulation of blood vessels in the body. Normal human abdominal visceral blood flow through the portal vein – liver – hepatic vein is smooth, is not occurring esophagogastric fundic varices, only poor blood flow, the formation of portal hypertension may occur. The factors that cause portal hypertension are generally classified into three kinds: prehepatic, hepatic and posthepatic according to the site of occurrence. The prehepatic is mainly due to portal vein cancer embolism and thrombosis, the posthepatic is mainly due to hepatic vein stenosis, and the hepatic lesion is mainly due to cirrhosis, which is also the main cause of portal hypertension. The main cause of portal hypertension in cirrhosis is the massive necrosis of hepatocytes, replaced by fibrosis of liver tissue and the formation of regenerative nodules and pseudobullets, distortion and deformation of intrahepatic vessels, reduction of capillary network, and obstruction of blood flow through the liver, resulting in blood stasis in the portal vein, and as the degree of blood stasis increases, the pressure in the portal vein gradually increases, eventually leading to the formation and The result is the formation and expansion of collateral circulation vessels, including the esophagogastric fundic veins. The causes of cirrhosis are multiple, including hereditary and immune factors, but at present, cirrhosis caused by hepatitis virus and alcohol is the most common in clinical practice. Therefore, patients who have hepatitis B or C should be actively treated under the guidance of professional doctors to prevent the evolution of cirrhosis as much as possible. For those who have a taste for alcohol, it is important to drink as little or no alcohol as possible. For patients with cirrhosis, in addition to other routine examinations, regular gastroscopy should be performed to find out whether there are esophagogastric fundic varices and the degree of varices so that necessary preventive and therapeutic measures can be taken.