Bile is manufactured in and secreted from hepatocytes and transported to the gallbladder for storage via the canaliculi, ductiles, and bile ducts. The bile ducts become progressively larger and eventually coalesce to form the right and left hepatic ducts, which unite to form the common hepatic duct. The common hepatic duct joins with the cystic duct from the gallbladder to form the common bile duct, which empties into the duodenum through the ampulla of Vater. The pancreatic duct often merges with the common bile duct immediately prior to entering the duodenum. The wall of the gallbladder is innervated with sympathetic and parasympathetic nerves from the celiac plexus.5
Bile is composed primarily of water (80 percent), bile acids (10 percent), lecithin and other phospholipids (4 to 5 percent), cholesterol (1 percent), conjugated bilirubin, electrolytes, mucus, and various proteins. The major stimulus for release of bile is the gastrointestinal hormone cholecystokinin, which is secreted from the small intestinal mucosal cells when fats and amino acids enter the duodenum. Cholecystokinin causes forceful contraction of the gallbladder, relaxation of the sphincter of Oddi, increased hepatic bile production, and ultimately release of bile into the duodenum for digestion of a meal. Approximately 95 percent of bile is conserved via enterohepatic circulation.
Gallstones, crystalline structures formed from both normal and abnormal bile components, are divided into three major types: cholesterol (70 percent), pigment (20 percent), and mixed (10 percent). Cholesterol stones, the most commonly encountered gallstones, contain more than 70 percent cholesterol monohydrate. The formation of such stones is complex, involving cholesterol supersaturation of the bile; the formation of monohydrate crystals, with aggregation into successively larger structures; and delayed gallbladder emptying, with bile stasis. Pigment stones are subdivided into black and brown varieties. Black stones are noted in patients with advanced liver disease and hemolytic disorders, while brown stones are found commonly in patients of Asian descent, usually resulting from bacterial or parasitic infection. Both subtypes of pigment stones result from abnormal solubilization of unconjugated bilirubin coupled with the precipitation of calcium salts. The calcium content of cholesterol stones is much lower than that of pigment stones, making cholesterol stones most frequently radiolucent and pigment stones radiopaque. Anatomically, cholesterol gallstones are found in the gallbladder, cystic duct, intrahepatic ducts, and common bile duct. Brown pigment stones have a distribution similar to that of cholesterol gallstones, while black stones occur exclusively in the gallbladder.
The pathogenesis of symptomatic cholelithiasis involves stone migration from the gallbladder into the biliary tract and eventual obstruction. The stone, once lodged in either the cystic or common bile duct, produces increased intraluminal pressure and distention of the hollow viscus, resulting in pain, nausea, and vomiting. Forceful, repetitive contractions of the entire biliary system may relieve the obstruction. If obstruction persists, particularly in either the cystic duct or the infundibulum of the gallbladder, acute cholecystitis may develop. The inflammatory response in acute cholecystitis results from a combination of three factors: mechanical, chemical, and infectious. The mechanical factor produces the rise in intraluminal pressure and distention of the viscus, which culminates in visceral ischemia. Chemical inflammation occurs with the release of various mediators (lysolecithin, phospholipase A, and prostaglandins), resulting in direct mucosal injury. The contribution to the inflammatory response by bacterial agents is variable, occurring in 50 to 80 percent of patients with acute cholecystitis. Bacterial pathogens include enterobacteriaceae (70 percent, particularly Escherichia coli and Klebsiella species), enterococci (15 percent), bacteroides (10 percent), Clostridium species (10 percent), group D Streptococcus, and Staphylococcus species. The inflammatory process may progress to gangrene of the gallbladder wall with or without perforation.
Gallstone pancreatitis is similarly multifactorial, since it is experimentally produced by injecting bile, bacteria, and trypsin under pressure. 6
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One of the main home remedies that you need to follow to prevent gallstones is a healthy lifestyle. You need to maintain a healthy body weight to prevent gallstones. The following are the best home remedies that will help you to treat and prevent gallstones.