Which pathophysiological alteration leads to the development of esophageal varices in patients with cirrhosis?
Group of answer choices
A Blocked blood flow to and from liver.
B Impairment of venous drainage from thorax to the liver.
C Increased vascular volume due to hepatic failure.
D Increased pressure in esophagus due to prolonged vomiting.
The correct answer and explanation is:
The correct answer is A: Blocked blood flow to and from liver.
Esophageal varices are enlarged, swollen veins in the lower part of the esophagus, and they are a common complication in patients with cirrhosis. The development of these varices is primarily due to increased pressure in the portal venous system, which is known as portal hypertension. Cirrhosis of the liver causes scarring (fibrosis) of the liver tissue, which obstructs normal blood flow through the liver. This leads to increased pressure in the portal vein, the blood vessel that carries blood from the digestive organs to the liver.
As the portal hypertension worsens, blood is diverted through smaller veins that bypass the liver. Some of these veins are located in the esophagus, and the blood flow through them increases dramatically. These veins, which are normally small, become engorged and can eventually form varices. Because the veins in the esophagus are fragile, they are at high risk of rupture, which can lead to life-threatening bleeding.
This pathophysiological process does not involve impairment of venous drainage from the thorax to the liver (choice B) or increased vascular volume due to hepatic failure (choice C). Prolonged vomiting (choice D) may contribute to the risk of variceal rupture, but it does not directly cause the formation of esophageal varices. The main mechanism is the obstructed blood flow due to cirrhosis-induced liver damage, leading to portal hypertension and the formation of varices as a result of blood shunting away from the liver.