Session 5 Pancreas and Liver

• Components of potal triad?

  • Portal vein
  • Hepatic artery
  • Bile duct
• Bile acids = precursors of bile salts.

  Bile acids synthesized from cholesterol
• 1 o bile acids = cholic acid and chenodeoxycholic acid {Hepatic}

  2 o bile acids = deoxycholic acid and lithocholic acid {intestinal bacteria}
• 1 o bile acids may be conjugated with either glycine or taurine to form bile salts prior to secretion in bile.
• Cholagogue – substance which promotes gall bladder contraction.
• Bilirubin is metabolized in the large intestine which results in, urobilinogen (excreted in urine) and stercobilin and urobilin (gives color and is excreted through faeces).
• Types of jaundice?

  • Haemolytic
  • Hepatic
  • Obstructive
• Exocrine pancreas produces enzymes (acinar cells) and alkaline fluid (ductular epithelial cells)
• The sphincter of Oddi controls the entry of contents into the duodenum.
• Functional anatomy of the exocrine pancreas?

  • It consists of lobules of acinar cells that secrete enzymes/fluid into microscopic ducts – intercalated ducts.
  • Intercalated ducts drain into -> intralobular ducts -> interlobular ducts -> main pancreatic duct.
  • The main pancreatic generally fuses with the bile duct before draining into the duodenum
  • a smaller pancreatic duct (duct of Santorini) that empties directly into the duodenum.
• Bile salts are amphipathic.
• Enterohepatic circulation –actively reabsorbs bile salts from the distal ileum and returned via the portal system back to the hepatocytes
• Bilirubin = potentially toxic metabolite of haem.
• Role of bile in excretion?

  • Haem is converted to biliverdin -> bilirubin in spleen
  • Bilirubin then binds to albumin and is transported to liver into the hepatocytes
  • It is then conjugated with glucuronic acid (via UDP glucuronyl transferase) and secreted into bile.
  • Subsequent large intestine microbial metabolism results in - Urobilinogen (water soluble and clourless), Stercobilin and urobilin (give faeces their colour).
• Jaundice appears with hyperbilirubinaemia.
• Types of jaundice?

  • Haemolytic jaundice – excessive haemolysis
  • Hepatic jaundice – inability to remove or conjugate bilirubin (cirrhosis)
  • Obstructive jaundice – inability of bile to flow to intestine (gallstones, white stools).
• Dual blood supply of liver?

  Hepatic artery proper and Hepatic portal vein.
• Venous drainage of liver?

  hepatic veins → inferior vena cava.
• Liver function tests?

  • Hepatocellular damage - Aminotransferases (ALT/AST), γ-Glutamyl transpeptidase (γ-GT/GGT)
  • Cholestasis (bile ducts) Bilirubin, Alkaline phosphatase (ALP)
  • Synthetic function - Albumin, Prothrombin time (clotting), Glucose
• Causes of pre-hepatic jaundice?

  • Haemoglobinopathies
  • Sickle cell anaemia
  • Hereditary spherocytosis.
  • red cell membrane defects
  • Drugs
  • Burns
  • Infection
• Hepatocellular jaundice - causes?

  • Cirrhosis (formation of scar tissue that impairs liver function)
  • Inflammation
  • Gilbert’s syndrome
  • Autoimmune hepatitis
  • Alcohol
  • Drugs
  • Congenital bilirubinaemias
• Post-hepatic jaundice - causes?

  • Extrahepatic (obstruction distal to bile canaliculi)
  • Intrahepatic (hepatocyte swelling) - Hepatitis, Drugs, Cirrhosis, Primary biliary cirrhosis.
  • Carcinoma
  • Gall stones
  • Pancreatitis
• 'in the presence of a non-tender palpable gallbladder, painless jaundice is unlikely to be caused by gallstones' - Courvoisier’s law
• Liver cirrhosis?

  • Liver cell necrosis →nodular regeneration and fibrosis
  • increased resistance to blood flow
  • deranged liver function
• Portal venous pressure >12 mmHg due to intrahepatic or • extrahepatic portal venous compression or occlusion. - portal hypertension
• Causes of portal hypertension?

  • Obstruction of portal vein
  • Obstruction of flow within liver
  • Cirrhosis
• Complications of Gallstone?

  • Biliary colic
  • Cholecystitis
  • Ascending cholangitis – inflammation/infection of the common bile duct
  • Obstructive jaundice
  • Acute pancreatitis
• Triangle of Calot?

  • Lateral: Cystic Duct
  • Medial: Common Hepatic Duct
  • Superior: Liver
  • Contents: Right Hepatic artery, Cystic artery, Any aberrant/accessory ducts
• Acute pancreatitis - grey turner's sign and cullen's sign
• Pathogenesis of acute pancreatitis?

  • Duct obstruction - Juice & bile reflux
  • Acinar damage - From reflux or drugs
  • Protease - Tissue destruction
  • Lipase - Fat necrosis
  • Elastase - Blood vessel destruction
• Why does cystic fibrosis cause steatorrhea?

  Malabsorption of fat due to deficiency of pancreatic enzymes.