GIS22 Pathology Of Liver Tumours And Gallstones Flashcards
1
Q
Primary liver tumour
A
Epithelial - Benign (Rare) —> Hepatocyte 1. Liver cell adenoma —> Bile duct 1. Bile duct adenoma 2. Bile duct cystadenoma
- Malignant —> Hepatocyte 1. ***Hepatocellular carcinoma 2. Hepatoblastoma —> Bile duct 1. ***Cholangiocarcinoma 2. Bile duct cystadenocarcinoma
Non-epithelial
—> Endothelial cell
1. Hemangioma
2. Hemangiosarcoma
2
Q
Relative incidence of primary liver tumours
A
- Hepatocellular carcinoma (80%)
- Cholangiocarcinoma (10%)
- Benign tumours (6%)
3
Q
Etiology of hepatocellular carcinoma
A
- ***Chronic HBV infection (80%)
- HBsAg +ve / HBV DNA +ve - Chronic HCV infection
- Alcoholic steatohepatitis (via cirrhosis)
- Non-alcoholic steatohepatitis (NASH)
- ***Cirrhosis (irrespective of causes)
- Aflatoxin
- produced by common fungus, Aspergillus flatus, in foodstuff/rotten food
- highly carcinogenic
- cause cancer in animals in exceptionally small doses after a long period
- low aflatoxin levels in foodstuffs in HK - Metabolic disorders
- about 60-80% of HCC cases associated with cirrhosis
4
Q
***Clinical aspects of HCC
A
- male:female = 4-6:1
- insidious onset
- ***rapidly fatal course
- ***hepatomegaly, RUQ pain (advanced, since only capsule has pain fibre)
- median survival with symptomatic / inoperable HCC in weeks
- gross appearance:
- **Massive / **Nodular (if in both lobes —> inoperable) / ***Diffuse (inoperable)
-
**Soft, High vascularity and minimal supportive stroma
—> blunt trauma
—> prone to **haemorrhage, frequent necrosis, rupture, peritoneal bleeding (hemoperitoneum) - ***Bile production in other sites (bones): metastatic HCC
5
Q
***HCC clinical presentation
A
- Hypoglycaemia
- tumour replaces liver —> **diminished glycogen storage in the remaining part of liver without tumour
- clear cell HCC with **excessive glycogen storage
- secretion of ***Insulin-like peptide - Venous invasion
- HCC mainly ***spread by vein
- tumour thrombus
- Portal vein branches —> intrahepatic metastasis
- Hepatic vein branches —> lung, bone metastasis
6
Q
Intrahepatic cholangiocarcinoma
A
- Carcinoma of intrahepatic bile ducts (vs extrahepatic bile ducts e.g. common bile duct)
- Risk factors: (x rmb)
1. Chronic inflammatory biliary diseases - ***liver flukes (Clonorchis sinensis)
- ***hepatolithiasis (liver stone —> inflammation + fibrosis)
-
**primary sclerosing cholangitis (PSC)
—> progressive periductal fibrosis with luminal stenosis / obliteration + dilatation
—> radiological **beaded appearance of bile ducts (esp. extrahepatic BD)
- Biliary malformation and developmental disorders
- Chronic advanced, non-biliary, liver diseases (small ductular iCCA subtype) (chronic hepatitis / cirrhosis relating to HBV and HCV)
- others
7
Q
***Cholangiocarcinoma
A
- Central / hilar
- R + L hepatic ducts and their junction (Klatskin tumour)
- causes **jaundice
- present early
- 1. **Mass-forming 2. **Periductal infiltrating 3. **Intraductal growing - Peripheral
- often asymptomatic and presents late
8
Q
***Gross appearance of CC
A
- Whitish
- ***Firm (Fibrous tissue within tumour)
9
Q
***HCC vs CC
A
- M:F ratio
HCC: 6:1
CC: 2:1 - Peak age
HCC: 45-55
CC: 55-65 - Gross appearance
HCC: tan/variegated, **soft with necrosis and haemorrhage
CC: greyish-white, **firm - Architecture
HCC: **trabecular with sinusoids
CC: **glandular with fibrous stroma - Bile production
HCC: fairly common
CC: never - Common mode of spread
HCC: **blood stream (hepatic vein —> lung, bones, portal vein —> intrahepatic)
CC: **lymphatic (LN, peritoneal) - Associated cirrhosis
HCC: ***60-80%
CC: low incidence - Associated HBsAg
HCC: ***60-80%
CC: 10% - Clonorchiasis (liver fluke)
HCC: infrequent
CC: frequent (65%) - Raised serum alpha-fetoprotein (AFP)
HCC: ***common (tumour marker for HCC)
CC: not increased
10
Q
Gallstones (Cholelithiasis)
A
- Prevalence varies (caucasians 10%, asians 3-4%)
- 4”F”s: female, fat, forty, fertile (記: 肥媽)
- constituents:
1. **Cholesterol
2. **Calcium bilirubinate
3. ***Calcium carbonate - types:
1. Pure stones (10%)
2. ***Mixed stones (80%)
3. Combination stones (10%) (one constituent form the core and another the shell)
11
Q
Pathogenesis of gallstones
A
- Abnormalities of bile composition (↑ concentration / ↓ solubility)
-
**Cholesterol stone (↑ cholesterol synthesis in liver)
—> **↑ secretion (obesity, hyperlipidaemia)
—> ***↓ bile acid pool (↓ bile acid reabsorbed at terminal ileum / ileal bypass —> lower concentrations of bile acids or phospholipids in bile reduce cholesterol solubility and lead to microcrystal formation —> bile acid / vit B12 supplement) -
**Pigment stone
—> **Haemolysis (black pigment stone)
- Inflammation / infection
- Bacterial infection of bile ducts (**recurrent pyogenic cholangitis / RPC)
—> **Brown pigment stones in ***intrahepatic bile ducts - Stasis (minor)
- pregnancy (↑ resorption of water + accumulation of mucoproteins)
12
Q
Recurrent pyogenic cholangitis (RPC, HK disease: oriental cholangitis, oriental cholangiohepatitis, intrahepatic pigmented calculus disease)
A
- mainly in ***Left lobe of liver
-
**Intrahepatic bile duct stone (brown pigment stone)
—> obstruction
—> dilatation of bile ducts
—> inflammation
—> **abscess formation (infection), **fibrosis of bile ducts and portal tract, end-stage
—> secondary biliary **cirrhosis
13
Q
Gallstone clinical presentation
A
Gallbladder:
1. Asymptomatic (stone in gall bladder)
- Gallbladder:
- **Cholecystitis (gallbladder inflammation)
- **Obstruction of cystic duct —> infection —> Empyema (pure pus)
Bile ducts:
- Bile ducts within the liver
- ***Cholangitis (infection with pain, fever) - Obstruction of common bile duct
- **Jaundice
- Cholangitis
- **Pancreatitis
14
Q
Cholecystitis (Gallbladder inflammation)
A
- stones causing obstruction and progressive concentration of bile
- Acute cholecystitis: RUQ pain when gallstone in gallbladder or bile ducts —> inflammation (紅腫痛熱)
- Chronic cholecystitis: Fibrosis
