how infection and stasis cause gallbladder stone

Infection and stasis can contribute to the formation of gallbladder stones through several mechanisms:

1. Stasis: Stasis refers to the slowing down or interruption of the normal flow of bile in the gallbladder. When there is inadequate emptying of the gallbladder, bile becomes concentrated, leading to the precipitation of cholesterol and other substances that form the stones. Stasis can be caused by various factors such as decreased gallbladder motility, a blockage in the bile ducts, or problems with the sphincter of Oddi.

2. Bacterial infection: Bacterial infection can occur in the gallbladder due to factors such as gallstone obstruction that causes bile stasis and promotes the growth of bacteria. These bacteria can then lead to the formation of gallbladder stones by altering the composition of bile and causing inflammation in the gallbladder wall. Besides, certain bacteria produce an enzyme called β-glucuronidase that can increase the production of calcium bilirubinate, a component of gallstones.

3. Inflammatory response: Infections and inflammation can trigger an immune response in the body. Chronic inflammation in the gallbladder can lead to the release of cytokines (immune system molecules) and the recruitment of immune cells. This immune response can contribute to the production of excess cholesterol, which can accumulate and form gallstones.

4. Bile composition changes: Infection and stasis can alter the composition of bile, promoting the formation of gallstones. For example, bacterial infection can increase the production of calcium bilirubinate, a component of pigment stones. Additionally, bile stasis can cause the concentration of cholesterol and bile salts to increase, favoring the formation of cholesterol stones.

Overall, infection and stasis play significant roles in the formation of gallbladder stones by promoting conditions that lead to the precipitation and accumulation of cholesterol, calcium bilirubinate, and other substances in the gallbladder.