Gall Bladder and Bile ducts

CONGENITAL ANOMALIES (Robbins pp 893/851)

Gall bladder: Congenital anomalies include: absence, two gall bladders with independent or joined cystic ducts, a septum dividing the gall bladder into two lobes, variable anatomical locations of it, and folded fundus≫Phrygian cap (Fig 19-46 pp 893).

Bile ducts: Parts of the biliary tree (intrahepatic / extrahepatic) may not develop at all ≫ agenesis. Both intrahepatic and extrahepatic bile ducts can close off (inappropriate fibrosis from inflammation) during development producing a blind ended tube ≫ called atresia. Atresia occurs in extrahepatic biliary tree in 90% of cases (10% - intrahepatic) and this is called ≫ neonatal cholestasis (meaning: stoppage of bile flow in neonates). Morphology of biliary atresia: Back up of bile leads to build up of bile pigment in liver parenchyma ≫enlarged green liver. The canaliculi are distended, and Kuffer cells phagocytose excess bile (bile spillage). The back pressure causes bile ductal proliferation, further delaying biliary movement ≫ forms bile concrements. Neutrophils settle around ducts (periductal inflammation), and liver is damaged ≫ neonatal hepatitis ≫ biliary cirrhosis.

ACQUIRED DISEASES (Robbins pp 893)

Cholelithiasis (Gallstones):

• This is the presence of stones in the gall bladder.
  
• There are four major types of stones:
  
• 1) mixed composition: inner core of organic material (sometimes contain bacteria) surrounded by cholesterol + bile pigment (calcium bilirubinate),
  
• 2) pure cholesterol (most common in Western),
  
• 3) pure calcium carbonate,
  
• 4) pure bile pigment (most common in Asia).
• Epidemiology/At risk individuals: Gall stones are extremely common in Western populations compared to Asian populations. Remember the saying: “A fair, fat, female, in her forties, carrying a foetus” is a high risk individual.
• Pathogenesis:
  
• 1) supersaturation*(cholesterol stones): Bile salts and lecithins solublise cholesterol by acting as detergents. When cholesterol concentrations rise so much that there is not enough detergent left to solubilise it, it tends to form solid cholesterol monohydrate crystals (also aided by gallbladder hypomotility),
  
• 2) infection (pigment stones): E coli, Ascaris lumbricoides, Opisthorchis sinensis,
  
• 3) stasis: bile stasis may occur because there is obstruction at neck of gall bladder, or hypomotility of gall bladder from infection (see above). Clinical features/
• Sequalae: 70-80% of patients are asymptomatic. Symptomatic patients have biliary pain (stone is impacted to wall of gall bladder) or biliary colic (stone not impacted) ≫ chemical inflammation (acute cholecystitis) ≫hypersecretion of mucus (mucocele) ≫ infection (empyema of gall bladder) ≫ pus drags more water, more swelling of gall bladder ≫ swelling obstructs blood supply ≫necrosis, rupture of gall bladder (peritonitis) / or eventually form diverticula that connect to intestines (gall stone ileus). There is increased risk of carcinoma of gallbladder (discussed later). A small stone may break off to obstruct the ampulla of Vater ≫ acute pancreatitis. Other sequelae include: ascending cholangitis, chronic cholecystitis.

Choledocholelithiasis: = presence of stones in extrahepatic biliary tree. Note that the epidemiology/at risk individuals, pathogenesis, clinical features are all the same. Sequelae: Obstruction causes back up of bilirubin ≫ eventually goes into plasma ≫ post-hepatic jaundice ≫ infection settles in biliary tree (cholangitis) ≫ bile backs up (2^nd biliary cirrhosis) ≫ small stone can break off to obstruct ampulla of Vater (pancreatitis).

Category: Pathology Notes