Home Pathophysiology Cholelithiasis (Gallstones) Pathophysiology & Schematic Diagram

Cholelithiasis (Gallstones) Pathophysiology & Schematic Diagram


Gallstones or Cholelithiasis is the most common disease of the biliary system affecting nearly 20 million people in the United States alone. Gall stones are solid, pebble like collections that accumulates in the gallbladder.

Bile is composed of various constituents such as water, inorganic ions, bile salts, cholesterol, lecithin and conjugated bilirubin. Bile salts and lecithin combines with cholesterol to form large, water soluble complexes. When there is an excess of cholesterol or a deficiency of bile salts it reaches a level that exceeds the bile’s ability to dissolve it. High cholesterol level irritates the gall bladder mucosa that resulting in surface changes that is predispose to cholesterol precipitation. Furthermore, mucosal irritation stimulates mucus secretion thereby interfering with gallbladder emptying and enhancing precipitation of components out of the bile. This leads to the formation of small crystals in the gallbladder mucosal surface. When the crystals accumulate they form grossly visible stone over 1cm in diameter. Eighty to ninety percent of gallstones are precipitated cholesterol, the rest are mostly calcium bilirubinate and other materials. These types of stones are called pigment stones.

The presence of stones in the gallbladder does not usually present itself with symptoms. Most cases are discovered in abdominal tests unrelated to gallstones. The major complication of cholelithiasis is the obstruction of bile flow when the stones move into the bile duct. When the bile duct muscle contracts the mucosa presses on the stone’s surface producing pain commonly referred to as biliary colic. It is an intense episode of epigastric pain that radiates to the back or shoulder with accompanying nausea and vomiting. Cholestatic jaundice also develops as a consequence of bile flow obstruction. Furthermore, lack of normal bile flow may also contribute to the ascent of bacteria from the intestine to the biliary system leading to the inflammation of the ducts and gallbladder. Irritation of the mucosa by an obstructing stone may also contribute to inflammation. Rupture and peritonitis may result from necrosis of the gallbladder and bile duct walls brought upon by bacterial damage and compression of the vessels. Bile duct obstruction also reduces fat digestion and absorption. Bacteria degrade the unabsorbed fat, forming products that draw water in the lumen resulting in water and electrolyte depletion.

The usual therapy for gallstones is surgical removal. If surgery is not recommended because of old age or reduced clotting mechanism, an alternative is to dissolve the existing cholesterol stones by long-term administration of bile acids. Another alternative is to use ultrasonic energy to fragment the stones for it to easily pass for evacuation.

Signs and Symptoms

  • Anorexia
  • Nausea and Vomiting
  • Weight Loss
  • Diarrhea
  • Fat Intolerance
  • Tea colored urine
  • Clay colored stool
  • Jaundice
  • Biliary colic

Risk Factors

  • Obesity
  • Drugs
  • Rapid Weight Loss
  • Dehydration
  • Increased triglycerides
  • Fatty Diet

Cholelithiasis Pathophysiology & SchematicDiagram

Originally posted 2013-02-05 14:07:55. Republished by Blog Post Promoter