Hepatobiliary III

Question 1

Bile duct obstruction common causes

- 3 locations + 1 example

Answer 1

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

Question 2

Cholestasis sequelae

Answer 2

Ascending Cholangitis, abscess, sepsis

Chronic: 
Biliary Cirrhosis (Primary Biliary Cholangitis),
- bile duct autoimmune, then cholestasis then, bile is toxic to liver

Question 3

Primary Hepatolithiasis sequelae and predisposition to what

Answer 3

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

Question 4

Name autoimmune cholangiopathies

Answer 4

Primary Sclerosing Cholangitis

Primary Biliary Cholangitis

Question 5

Name cystic congenital malformations of bile duct [2]

Answer 5

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)

Question 6

Name 3 cell types in Liver and corresponding neoplasm and their properties
- minus HCC and CC properties

Answer 6

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

Question 7

Name non-neoplastic mass of liver [1] and its properties

Very impt!

Answer 7

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

Question 8

HCC

genetic triggers,
risk factor,
investigation,
histology of cancer!!!

Answer 8

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;

Question 9

CC risk factors, location probability

Answer 9

Risk factors
- Chronic inflammation, Cholestasis

Hilar > Extra Hepatic > Intrahepatic
- extra hepatic presents earlier

Question 10

Liver mets possibilities and presentation

Answer 10

Breast, Colon, Pancreas, Lungs

- note background non-cirrhotic, liver function retained

Question 11

Cholelithiasis Cx [3]

Answer 11

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

Question 12

Acute Cholecystitis causes [2 major]

Answer 12

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

Question 13

Cholecystitis Gross [3] and Cx [5]

Answer 13

• Ulcers, Fibrinopurulent exudate
• May have stones
• Fibrosis and thickening if chronic

Cx:

• Ascending Cholangitis, Liver Abscess
• Gangrene, Empyema
• Sepsis

Question 14

Gall Bladder Carcinoma AKA Extrahepatic Cholangiocarcinoma AKA Adenocarcinoma
- microscopy [1]

Answer 14

GLANDS

Question 15

Pathogenesis of cholecystitis to gangrene

Answer 15

• -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.

Question 16

alpha-fetoprotein elevated in which cancers

Answer 16

fyi AFP in fetus produced in liver

HCC
Non-SGCT
Yolk Sac Tumor

Question 17

beta-catenin and e-cadherin cancers

Answer 17

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

Question 18

Whats the Cx of Cavernous Hemangioma [4]

• think both in anatomy and materials involved

Answer 18

rupture, hemorrhage, thrombosis, DIVC

Question 19

Whats the deal w Hepatocellular Adenoma [2]

Answer 19

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

Question 20

Gimme bile flow anatomy

Answer 20

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.