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Cirrhosis is a primary factor in the development of esophageal varices due to its impact on the liver's structure and function. In cirrhosis, the liver becomes severely scarred from long-term damage, which can be caused by various factors including chronic alcohol abuse and viral hepatitis. This scarring leads to increased resistance to blood flow within the liver, resulting in elevated pressure in the portal vein, a condition known as portal hypertension.

As the pressure rises, blood is diverted to smaller veins to bypass the liver, one of which is located in the esophagus. These veins are not designed to handle such increased volume and pressure, causing them to stretch, become engorged, and ultimately develop into varices. If these varices rupture, they can lead to life-threatening complications, which is why identifying and managing the underlying causes of cirrhosis is critical in preventing esophageal varices.

In contrast, conditions such as Mallory-Weiss syndrome, reactive gastritis, and peptic ulcers typically do not result in significant portal hypertension and therefore are not direct root causes of esophageal varices. They may cause gastrointestinal bleeding, but the mechanisms and pathologies involved are different from those seen in portal hypertension due to cirrhos