Gallbladder and Bile Duct Anatomy and Physiology

connects the gallbladder with the common bile duct
usually 2 to 4 cm long
contains the spiral valves of Heister, which allow easy entry of bile into the gallbladder but resist its outflow

point of union of the cystic duct with the common hepatic duct is extremely variable
the cystic duct may enter the hepatic duct high or low, it may be adherent to the common hepatic duct, it may be very short or absent, it may join the right hepatic duct, or it may course underneath the common hepatic duct and enter it posteriorly or on its left side
accessory ducts from the liver may enter the cystic duct or common hepatic duct
small ducts (of Luschka) may drain directly from the liver into the gallbladder
knowledge of these common variations is important in order to avoid iatrogenic injury during cholecystectomy

the cystic artery originates from the right hepatic artery (90%) and has an anterior and posterior branch
venous drainage is into the portal vein
lymphatic drainage is into the cystic duct node
hepatic branch of the vagus nerve supplies parasympathetic fibers
pain of biliary colic is mediated by sympathetic afferent fibers

in 20% of cases, the right hepatic artery comes off the SMA
in 5% of the cases, there are 2 right hepatic arteries
since the right hepatic artery is variable in location, the cystic artery can also be in variable locations
rarely, the cystic artery may arise from a different artery than the right hepatic

extrahepatic bile ducts are located within the hepatoduodenal ligament
right hepatic duct is formed by the union of the right anterior and posterior segmental ducts; left hepatic duct is formed by the union of the left lateral and left medial segmental ducts
the left hepatic duct is longer than the right and a greater portion of it is extrahepatic since it follows a more transverse course to the liver
common hepatic duct is formed by the union of the left and right hepatic ducts
length of the common hepatic duct is variable since this is dependent on where the cystic duct joins it

formed by the union of the cystic duct and common hepatic ducts
located to the right of the hepatic artery and anterior to the portal vein in the hepatoduodenal ligament
blood supply is via two axial vessels, the 3 o’clock and 9 o’clock arteries
travels through the pancreas and the wall of the duodenum to form the papilla of Vater
its distal end is surrounded by the sphincter of Oddi, which regulates the flow of bile into the duodenum
pancreatic duct may share a common orifice on the papilla of Vater with the common bile duct, it may join the common duct proximal to its entrance into the duodenum, or the two ducts may open separately on the papilla

~1000 ml/day of bile is produced by the hepatocytes
rate of secretion is under neurogenic, humoral, and chemical control
vagal stimulation increases bile flow; sympathetic splanchnic stimulation decreases bile flow by decreasing hepatic blood flow
gastrointestinal hormones such as secretin, cholecystokinin, gastrin, and glucagon all increase bile flow, primarily by increasing water and electrolyte secretion from duct cells
most important factor in regulating the volume of bile secretion is the rate of bile salt secretion, which in turn is regulated by the return of bile salts to the liver from the enterohepatic circulation

water constitutes 85% of the volume of bile
the major organic solutes of bile are bile salts, bilirubin, phospholipids, and cholesterol

steroid molecules synthesized from cholesterol in the liver
amphipathic compounds, containing both a hydrophobic and a hydrophilic portion
2 primary bile salts, cholic and chenodeoxycholic acid
the primary bile salts are conjugated with either taurine or glycine
primary bile salts may then undergo chemical alteration in the intestine to form secondary bile salts (deoxycholate and lithocholate)
purpose of bile salts is to solubilize lipids and facilitate their absorption

breakdown product of hemoglobin excreted almost entirely in bile
conjugated in the liver with glucuronide
in the intestine, bilirubin is converted into urobilinogen and excreted in the stool

cholesterol is highly nonpolar and thus insoluble in water (and bile)
micelles, a bile salt-phospholipid-cholesterol complex, are the keys to maintaining cholesterol in solution
in aqueous solutions, bile salts are oriented with their hydrophilic portion outwards
phospholipids are incorporated into the micellar structure, allowing cholesterol to be added to the hydrophobic central portion of the micelle
in this way, cholesterol can be maintained in an aqueous environment
however, cholesterol solubility depends on the relative concentrations of cholesterol, bile salts, and lecithin - any changes in these relative concentrations can alter the ability of the micelle to keep cholesterol in solution

main function is to store and concentrate hepatic bile during the fasting state, allowing for a coordinated response to a meal

gallbladder mucosa has the greatest absorptive capacity per unit area of any structure in the body
bile is usually concentrated 5-fold to 10-fold by the active transport of sodium and the passive transport of water
this absorptive ability of the gallbladder allows the small capacity gallbladder (30 to 50 ml) to store the large output (1000ml/day) of bile from the liver

glands of the gallbladder neck and cystic duct secrete mucus glycoproteins
mucus layer protects the gallbladder epithelium from the strong detergent effect of the highly concentrated bile salts
responsible for the ‘white bile’ present in hydrops of the gallbladder

gallbladder filling occurs because the resting pressure in the common bile duct is greater than in the gallbladder (tonic contraction of the sphincter of Oddi)
passage of bile into the duodenum involves the coordinated contraction of the gallbladder and relaxation of the sphincter of Oddi, which is largely mediated by the release of CCK from the duodenum after the ingestion of food
emptying of the gallbladder takes place 30 minutes after ingestion of a fatty meal
between meals, the gallbladder empties ~ 10% to 15% of its volume with each passage through the duodenum of the MMC (this process is mediated in part by motilin)
defects in gallbladder motility, which increase the length of time of bile in the gallbladder, play a role in the pathogenesis of gallstones

80% of conjugated bile salts are absorbed in the terminal ileum
majority of the rest are deconjugated by bacterial activity and absorbed by the colon
ultimately, 95% of the bile salts are reabsorbed and returned to the liver via the portal vein
5% of the bile salt pool is lost each day in the stool and must be resynthesized by the liver
in cases of ileal resection or biliary fistula, bile salt production by the liver is increased to maintain a normal bile salt pool