PATHOPHYSIOLOGY
Gallstones are formed from impaired metabolism of cholesterol, bilirubin, in bile acids. Some gallstones contain cholesterol, unconjugated bilirubin, bilirubin calcium salts, fatty acids, calcium carbonate’s hand phosphates, and mucin glycoproteins. Gallstones are of 3 types depending on chemical composition: (1) cholesterol; (2) pigmented; and (3) mixed. Cholesterol gallstones form in bile that is supersaturated with cholesterol produced by the liver in deficit bile acids and phospholipids. Supersaturation sets the stage for cholesterol crystal formation, with the formation of “microtones.” More crystals then aggregate on the micro stones, which grow deformed macro stones. This process usually occurs in the Gallbladder, which may have decreased motility and biliary stasis. The stones may ride dormant in silent or become lodged in the cystic or common duct, causing pain when the Gallbladder contracts in cholecystitis. The stones can accumulate and fill the entire Gallbladder. Pigmented Brown gallstones formed from calcium bilirubin 8 and fatty acid soaps that bond with calcium, usually in common bile duct. They are associated with biliary stasis, bacterial infections, and Billy Ray parasites. They’re more common in East Asia. Black gallstones are rare and usually form in the Gallbladder. They are seriously dated with chronic liver disease and hemolytic disease is composed of calcium bilirubin 8 with mucin glycoproteins (McCance & Huether, 2019).
It is not known why the hepatocytes secrete bile that is supersaturated with cholesterol. Proposed mechanisms include 1)an enzymatic defect that increases the parasite synthesis of cholesterol; 2) diminished secretion of bile acids, which normally promote cholesterols solubility; 3) decrease your petition of bile salts from the ilium, which decreased the bio acid pool; 4) Gallbladder smooth muscle hypermotility and stasis; 5) increase secretion of Gallbladder museum and biliary calcium; 6) genetic predisposition; and 7) some combination of these mechanisms. In obese individuals, the mechanism appears to involve cholesterol synthesis, whereas, in non-obese individuals, it appears to involve decreased secretion of bile acids (McCance & Huether, 2019).
CLINICAL MANIFESTATIONS
Cholelithiasis can often be asymptomatic. Epigastric and right hypochondrium pain and intolerance to fatty foods are the most common signs of cholelithiasis. Symptoms include heartburn, flatulence, epigastric discomfort, pruritis, jaundice, and food intolerances. Pain typically occurs 30 minutes or up to several hours after eating a fatty meal and is caused by the lodging of one or more gallstones in the cystic or common duct with obstruction and distension. It can be intermittent or steady and usually is located in the right upper quadrant and radiates to the mid-upper back. Jaundice indicates that the stone is located in the common bile duct. Abdominal tenderness and fever indicate cholelithiasis (McCance & Huether, 2019).
EVALUATION & TREATMENT
Diagnosis is based on medical history, physical examination, and imaging evaluation. Imaging techniques include transabdominal ultrasound, endoscopic ultrasound, in magnetic resonance cholangiopancreatography. Oral bile acids may dissolve cholesterol stones, but the stones may recur when the drug is discontinued. Laparoscopic cholecystectomy is the preferred treatment for gallstones that causes obstruction or inflammation. The use of transluminal endoscopic surgery is advancing rapidly. Endoscopic retrograde cholangiopancreatography and sphincterotomy with stone retrieval are used for the treatment of bile duct stones. Large stones, or intrahepatic stones, may be managed with open surgery or lithotripsy (McCance & Huether, 2019).