Hepatobiliary III Flashcards
Bile duct obstruction common causes
- 3 locations + 1 example
Intramural - Stones, Parasites
Mural - strictures of wall from inflammation
Extramural - LN enlargement, neoplasm, @HOP also
Malformation, Atresia
- Neonatal cholestasis top cause is Extrahepatic biliary atresia
Cholestasis sequelae
Ascending Cholangitis, abscess, sepsis
Chronic: Biliary Cirrhosis (Primary Biliary Cholangitis), - bile duct autoimmune, then cholestasis then, bile is toxic to liver
Primary Hepatolithiasis sequelae and predisposition to what
Hepatolithiasis is the presence of gallstones in the BILIARY DUCTS of the liver
Ascending cholangitis (commonly bacteria infection; AKA acute cholangitis),
Predispose to Biliary Intraepithelial Neoplasia and CC AKA Cholangiocarcinoma
Name autoimmune cholangiopathies
Primary Sclerosing Cholangitis
Primary Biliary Cholangitis
Name cystic congenital malformations of bile duct [2]
Think intrahepatic and extrahepatic
- Choledochal cyst - CD means bile duct
- Fibropolycystic disease - superset of Polycystic liver disease (PLD)
— FPC also sees Fibrosis of Liver parenchymal + Intrahepatic Bile Duct dilations (cysts)
Name 3 cell types in Liver and corresponding neoplasm and their properties
- minus HCC and CC properties
Endothelial Cells “connective tissue” - Cavernous Hemangioma
- Dilated vascular channels, thin fibrous tissues; congenital, vascular tumor
- Cx: rupture, hemorrhage, thrombosis, DIVC
Hepatocytes - Hepatocellular Adenoma, HCC
- HA: HORMONE-INFLUENCED, OCP, increase oestrogen - most px are Wahmen taking OCP
- Note liver is a gland for bile
-HCC:
Bile Duct - Cholangiocarcinoma
Name non-neoplastic mass of liver [1] and its properties
Very impt!
Focal Nodular Hyperplasia
- Due to congenital arteriovenous malformation, and hyperplastic response; thought to be the result of increased hepatocyte number caused by hypoperfusion or hyperperfusion from anomalous arteries within the hepatic lobule.
- Central stellate scar!
- radiating fibrous septa w misshaped arteries
HCC
genetic triggers,
risk factor,
investigation,
histology of cancer!!!
Genes:
- beta catenin - oncogene hence activation
- p53 inactivation
Risk factor:
- Chronic liver disease - due to repeated cell cycles from death, inflammation, also IL6 triggers hepatocyte regeneration
Investigation
- alpha-fetoprotein (insensitive test)
- imaging
Histology
- thickened cords, trabeculae, (more than 4 hepatocytes) HCA is less than 4
- if well differentiated - BILE PRODUCING
- compact growth patterns - pseudoacinar around ducts;
CC risk factors, location probability
Risk factors
- Chronic inflammation, Cholestasis
Hilar > Extra Hepatic > Intrahepatic
- extra hepatic presents earlier
Liver mets possibilities and presentation
Breast, Colon, Pancreas, Lungs
- note background non-cirrhotic, liver function retained
Cholelithiasis Cx [3]
Acute cholecystitis (gallbladder inflammation), empyema CBD obstruction - Pancreatitis -- Cystic Duct joins Common Hepatic Duct to form Common Bile duct which then joins Pancreatic Duct to open at Ampulla of Vater at duodenum Perforation, fistula
CC risk
Acute Cholecystitis causes [2 major]
1st: Cholelithiasis
- obstruction, chemical irritation + inflammation
- protective GP mucosal layer disrupted, bile salts work on mucosal epithelium, PG released, inflammation
- - Distension and increased intramural pressure compromise blood flow to mucosa
2nd: others LOL
- Immunocompromised, DM, alot
- Ischemia - cystic artery end artery from Hepatic Artery
Cholecystitis Gross [3] and Cx [5]
- Ulcers, Fibrinopurulent exudate
- May have stones
- Fibrosis and thickening if chronic
Cx:
- Ascending Cholangitis, Liver Abscess
- Gangrene, Empyema
- Sepsis
Gall Bladder Carcinoma AKA Extrahepatic Cholangiocarcinoma AKA Adenocarcinoma
- microscopy [1]
GLANDS
Pathogenesis of cholecystitis to gangrene
- -Protective GP mucosal layer disrupted, bile salts work on mucosal epithelium, PG released, inflammation
- Distension and increased intramural pressure compromise blood flow to mucosa
- -It is the result of marked distension of the gallbladder causing increased tension in the gallbladder wall. Associated inflammation leads to ischemic necrosis of the wall, with or without associated cystic artery thrombosis.
alpha-fetoprotein elevated in which cancers
fyi AFP in fetus produced in liver
HCC
Non-SGCT
Yolk Sac Tumor
beta-catenin and e-cadherin cancers
beta-catenin is oncogene; overexpression leads to cancers including HCC, breast, Colon cancer from FAP APC loss of function control;
e-cadherin: DUCTAL; lobular is absence
Whats the Cx of Cavernous Hemangioma [4]
- think both in anatomy and materials involved
rupture, hemorrhage, thrombosis, DIVC
Whats the deal w Hepatocellular Adenoma [2]
Wahmen, OCP, oestrogen caused
Hepatocytes are on a regular reticulin scaffold and less or equal to three cell thick (vs HCC w 4 cells thick or more)
Sheets of Hepatocytes
Gimme bile flow anatomy
Liver ductules join to form bile ducts that eventually right or left hepatic bile duct. The two ducts join to form the common hepatic duct, which in turn joins the cystic duct from the gall bladder, to give the common bile duct.
This duct then enters the duodenum at the ampulla of Vater.
