Bile, Gallbladder and Gallstones

• What are the main components of the biliary system?

  • Liver (produces bile)
  • Gallbladder (stores and concentrates bile)
  • Bile ducts:
  • Right and Left hepatic ducts → form the common hepatic duct
  • Cystic duct (from gallbladder) joins common hepatic duct → forms common bile duct
  • Common bile duct joins pancreatic duct near the duodenum
  • Ends at the ampulla of Vater, regulated by the sphincter of Oddi
• What is the function of the gallbladder?

  • Stores and concentrates bile produced by the liver
  • Releases bile into the cystic duct → common bile duct during digestion (especially fatty meals)
  • Contraction triggered by cholecystokinin (CCK) released from the small intestine
• Describe the anatomical path of bile from the liver to the duodenum

  1. Bile produced in liver → Right/Left hepatic ducts
  2. Hepatic ducts merge → Common hepatic duct
  3. Bile can go:

  • Into cystic duct → gallbladder (for storage)
  • Or directly continue into common bile duct

  1. When needed, bile flows from gallbladder → cystic duct → common bile duct
  2. Joins pancreatic duct → forms hepatopancreatic ampulla (ampulla of Vater)
  3. Empties into duodenum (2nd part) via major duodenal papilla, regulated by sphincter of Oddi
• Where is the sphincter of Oddi located, and what is its function?

  • Located at the end of the common bile duct and pancreatic duct, at the major duodenal papilla
  • Controls the flow of:
  • Bile from common bile duct
  • Pancreatic juice from pancreatic duct
  • Prevents reflux of duodenal contents into the ducts
• What is the anatomical relationship between the bile duct and pancreatic duct?

  • Both ducts usually merge at the ampulla of Vater (hepatopancreatic ampulla)
  • Then open into the second part of the duodenum at the major duodenal papilla
  • Flow is regulated by the sphincter of Oddi
• What are gallstones (cholelithiasis), and how do they form?

  • Solid deposits (usually cholesterol or bilirubin) that form in the gallbladder
  • Causes:
  • Bile stasis
  • High cholesterol
  • Low bile salts
  • Risk factors: "4 Fs" – Female, Fat, Forty, Fertile
• How can gallstones affect the biliary system?

  • May block:
  • Cystic duct → causes biliary colic or cholecystitis
  • Common bile duct → choledocholithiasis, bile flow obstruction
  • At ampulla of Vater → blocks both bile and pancreatic ducts→ causes jaundice and possibly pancreatitis
• Why does blockage at the ampulla of Vater cause pancreatitis?

  • Gallstones can obstruct the common channel where bile and pancreatic ducts merge
  • This prevents pancreatic enzymes from draining
  • Causes enzyme buildup and autodigestion of pancreatic tissue → acute pancreatitis
• What are the major constituents of bile involved in digestion?

  • Bile salts (bile acids + sodium/potassium)
  • Phospholipids (mainly lecithin)
  • Cholesterol
• What is the primary digestive role of bile salts?

  They emulsify dietary fats, increasing surface area for lipase action.
• How do bile salts assist in fat absorption?

  They form micelles that transport monoglycerides and fatty acids to the intestinal epithelium for absorption.
• What is the role of phospholipids in bile (e.g. lecithin)?

  They stabilise bile salt micelles and aid fat emulsification and absorption.
• Why is cholesterol included in bile if it’s not directly digestive?

  It’s excreted via bile; helps maintain micelle structure but has no direct digestive role.
• What happens if cholesterol concentration in bile becomes too high?

  Cholesterol may precipitate, leading to gallstone formation.
• How do imbalances in bile components lead to gallstones?

  Excess cholesterol or reduced bile salts/phospholipids disrupt micelle formation → cholesterol crystallises → gallstones.
• What are gallstones made of?

  Mainly cholesterol; can also contain bilirubin and calcium salts.
• How can gallstones affect digestion?

  They can block bile flow, reducing fat emulsification and absorption → steatorrhea, fat-soluble vitamin deficiency.
• What is steatorrhea and how is it linked to bile dysfunction?

  Fatty stools caused by impaired fat digestion due to insufficient bile salt delivery (e.g., gallstone obstruction).
• What stimulates gallbladder contraction?

  Cholecystokinin (CCK), released from the duodenum in response to fats, stimulates gallbladder contraction.
• How does CCK affect the sphincter of Oddi?

  CCK causes relaxation of the sphincter of Oddi, allowing bile and pancreatic juices to enter the duodenum.
• How do gallbladder motility and the sphincter of Oddi interact?

  When CCK is released:

  • The gallbladder contracts, pushing bile out.
  • The sphincter of Oddi relaxes, allowing bile to flow into the duodenum. This coordination ensures efficient bile delivery during digestion.
• What can go wrong with this system to cause gallstones?

  Gallstones can form if bile becomes concentrated with cholesterol or pigments. Poor gallbladder motility or sphincter dysfunction can cause bile stasis, promoting stone formation.
• How can dysfunction of the sphincter of Oddi contribute to gallstone problems?

  If the sphincter doesn't relax properly, bile can't drain effectively. This can lead to bile stasis in the gallbladder, increasing the risk of gallstone formation.
• How can impaired gallbladder motility lead to gallstones?

  If the gallbladder doesn't contract well (hypomotility), bile is retained longer and becomes more concentrated, which promotes gallstone formation.
• What stimulates the release of CCK (cholecystokinin) from the small intestine?

  The presence of fatty acids and amino acids in the duodenum stimulates I cells in the small intestine to release CCK (cholecystokinin).
• What is the role of CCK in gallbladder motility?

  • CCK binds to CCK-A (CCK1) receptors on gallbladder smooth muscle, causing contraction.
  • This releases bile into the cystic duct → common bile duct → duodenum to aid fat digestion.
• How does CCK affect the sphincter of Oddi?

  CCK causes relaxation of the sphincter of Oddi, allowing bile to flow into the duodenum.
• What is the role of the vagus nerve in gallbladder motility?

  • The vagus nerve (parasympathetic) stimulates gallbladder contraction via acetylcholine release, especially during the cephalic and gastric phases of digestion (before food reaches the small intestine).
  • It also indirectly enhances CCK release.
• What is the combined effect of vagus nerve stimulation and CCK on gallbladder motility?

  • Vagus nerve primes the gallbladder and supports contraction via ACh.
  • CCK provides the primary stimulus for contraction in response to fat.
  • Together, they ensure coordinated gallbladder emptying and bile delivery into the intestine.
• What happens to gallbladder motility when the vagus nerve is damaged?

  • Impaired vagal stimulation may reduce initial gallbladder contraction, delaying bile release.
  • However, CCK can still trigger contraction, though less efficiently.
• What causes gallstones in relation to gallbladder motility?

  • Reduced gallbladder motility (e.g. due to insufficient CCK or vagal tone) → bile stasis → cholesterol crystallisation → gallstone formation.
• How does CCK deficiency contribute to gallstone formation?

  • Without adequate CCK, the gallbladder does not contract effectively.
  • This leads to bile retention and promotes gallstone formation, especially cholesterol stones.
• During which digestive phase is vagus nerve stimulation of the gallbladder most active?

  • During the cephalic and gastric phases (before and while food is in the stomach).
  • This primes the gallbladder in anticipation of fat digestion.
• What is the main difference in bile acid concentration between hepatic and gallbladder bile?

  Gallbladder bile contains much higher concentrations of bile acids than hepatic bile due to water reabsorption and concentration during storage.

  • Hepatic bile: ~12 mmol/L bile acids
  • Gallbladder bile: ~200–300 mmol/L bile acids
• Compare cholesterol levels in hepatic vs gallbladder bile.

  Cholesterol concentration increases in gallbladder bile due to water removal during storage.

  • Hepatic bile: low cholesterol
  • Gallbladder bile: concentrated cholesterol (risk factor for gallstones if oversaturated)
• What is the effect of gallbladder concentration on bile composition?

  Gallbladder stores and concentrates bile by reabsorbing water, increasing the concentration of:

  • Bile acids
  • Bilirubin
  • Cholesterol
  • But decreasing: Bicarbonate (reabsorbed)
• How does the bile composition contribute to gallstone formation?

  Gallstones form when bile becomes supersaturated with cholesterol, often due to:

  • High cholesterol
  • Low bile acids or phospholipids (less solubilisation)
  • Gallbladder stasis → bile concentration ↑This leads to precipitation of cholesterol or pigment (bilirubin) stones.
• What are the ideal bile acid to cholesterol ratios to prevent gallstones?

  • A high bile acid to cholesterol ratio is essential to keep cholesterol dissolved.
  • When this ratio drops (e.g., ↑cholesterol or ↓bile acids), cholesterol may crystallise → gallstones.
• Why does cholesterol precipitate from bile to form gallstones?

  When bile becomes supersaturated with cholesterol, it exceeds the solubilising capacity of bile salts and phospholipids, leading to crystallisation.
• What are the main components of bile involved in gallstone prevention?

  1. Bile salts – solubilise cholesterol.
  2. Phospholipids (e.g., lecithin) – help emulsify cholesterol.
  3. Cholesterol – normally kept in solution by the above two.