Chronic acalculous cholecystitis without biliary sludge static electricity in the body

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Chronic acalculous cholecystitis is an inflammatory disease of gallbladder, associated with chronic inflammation of gallbladder wall and motor dysfunction of the biliary tract, accompanied with biliary pain (1). electricity facts ks2 The cause of the gallbladder motility disorders can be an increased basal cystic duct resistance or cystic duct spasm, the muscle hypertrophy, and the chronic aseptic inflammation in the gallbladder wall.

High degree of COX-2 expression in the smooth muscle cells of the gallbladder wall causes the decrease in the evacuation function of the gallbladder and “active” passage of the hepatic bile into the gallbladder ( fig. 15). electricity outage sacramento High COX-2 expression in the epithelial cells of the gallbladder mucosa causes decrease of the absorption function of the gallbladder (decrease of water and biliary cholesterol absorption) and “passive” passage of the hepatic bile into the gallbladder ( fig. 15).

This is accompanied by the decrease in concentration of total bile acids in the gallbladder bile and increase of concentration of biliary cholesterol in gallbladder bile, and causes disturbance in colloidal stability of the gallbladder bile and precipitation of cholesterol monohydrate crystals and calcium bilirubinate granules, i.e. formation of “lithogenic” gallbladder bile ( fig. 16).

The decrease in the gallbladder-dependent output of biliary cholesterol and in the concentration of total bile acids in the gallbladder bile results in formation of the “lithogenic” gallbladder bile and precipitation of the cholesterol monohydrate crystals in the gallbladder lumen in 40% of patients with chronic acalculous cholecystitis without biliary sludge ( fig. 20).

Surplus COX-2 expression in the epithelial cells of the gallbladder mucosa causes hypersecretion of glycoprotein biliary mucin into the gallbladder bile. eon gas card top up Increase in concentration of glycoprotein biliary mucin in gallbladder bile over 2 mg/ml causes its polymerization and formation of sites of the excessive viscosity. c gastritis im antrum Precipitation of cholesterol monohydrate crystals and calcium bilirubinate granules in the sites of the excessive viscosity of polymerized glycoprotein biliary mucin contributes in formation of biliary sludge and transformation of chronic acalculous cholecystitis without biliary sludge into chronic acalculous cholecystitis with biliary sludge.

Celecoxib is a selective inhibitor of COX-2. gas meter car Inhibiting COX-2 activity in the smooth muscle cells of the gallbladder wall and cystic duct results it brings relief of the biliary pain within 3-5 days, restoration of the evacuation function of the gallbladder and the gallbladder-dependent output of biliary cholesterol, “active” and “passive” passage of the hepatic bile into the gallbladder, and decrease in the gallbladder-independent enterohepatic circulation of bile acids, biliary cholesterol and biliary bilirubin.

Celecoxib, a selective inhibitor of COX-2, inhibiting COX-2 activity in the epithelial cells of the gallbladder mucosa causes inhibition of glycoprotein mucin hypersecretion into the gallbladder lumen, decrease of concentration of glycoprotein biliary mucin in the gallbladder bile and gallbladder bile viscosity, which prevents formation of biliary sludge.

Ursodeoxycholic acid, is a hydrophilic hepatoprotective bile acid. electricity 101 It helps in dissolving the cholesterol monohydrate crystals in the gallbladder, decrease in lithogenicity of gallbladder and hepatic bile, disappearance of the chronic “bland” intrahepatic cholestasis (i.e. results in restoration of the accumulation and excretion functions of the liver).

Celecoxib is a selective inhibitor of COX-2, inhibiting COX-2 activity in the epithelial cells of the biliary tract mucosa causes decrease in secretion of glycoprotein mucin into the biliary tract lumen, concentration of the glycoprotein biliary mucin in the hepatic bile and viscosity of hepatic bile, which prevents formation of biliary sludge and gallstones in the common hepatic duct and common bile duct. Low COX-2 activity in the epithelial cells and the smooth muscle cells of the biliary tract helps in lowering the risk of choledocholithiasis development.

Ursodeoxycholic acid (UDCA) is a hydrophilic hepatoprotective bile acid. It helps in dissolving the cholesterol monohydrate crystals in the biliary tract, decrease in lithogenicity of hepatic bile, disappearance of the chronic “bland” intrahepatic cholestasis (i.e. results in the restoration of the accumulation and excretion functions of liver), and in some patients helps in dissolving the biliary sludge in the biliary tract.

Ursodeoxycholic acid (UDCA) is a hydrophilic hepatoprotective bile acid, decreasing aggressive properties of bile, prevents development of chronic atrophic antral gastritis (duodenogastric reflux and bile reflux gastritis) and duodeno-gastroesophageal reflux (incompetence of Oddi’s sphincter), chronic biliary pancreatitis (biliopancreatic reflux) or chronic spastic aseptic pancreatitis (pancreatic type III of sphincter of Oddi dysfunction).

• Kano M, Shoda J, Irimura T, Ueda T, Iwasaki R, Urasaki T, Kawauchi Y, Asano T, Matsuzaki Y, Tanaka N. Effects of long-term ursodeoxycholate administration on expression levels of secretory low-molecular-weight phospholipases A2 and mucin genes in gallbladders and biliary composition in patients with multiple cholesterol stones. gas kinetic energy formula Hepatology. 1998; 28(2): 302-13.

• Tazuma S, Nishioka T, Ochi H, Hyogo H, Sunami Y, Nakai K, Tsuboi K, Asamoto Y, Sakomoto M, Numata Y, Kanno K, Yamaguchi A, Kobuke T, Komichi D, Nonaka Y, Chayama K. Impaired gallbladder mucosal function in aged gallstone patients suppresses gallstone recurrence after successful extracorporeal shockwave lithotripsy. J Gastroenterol Hepatol. 2003; 18(2): 157-61.