AN APPROACH TO LIVER TUMOURS
* Non-neoplastic versus neoplastic:
Non-neoplastic lesions can mimic neoplasms
– , — , — tumour-like
lesions, — : US, CT, MR + context
diagnostic
* Benign versus malignant neoplasms:
* Primary versus secondary malignancies
* Consider different types of primary neoplasm
Depending on tissue type of origin, e.g. for
malignancies: carcinoma, possibly of different
types, sarcomas of different types, lymphoma etc.
* But focus/highlight commoner entities
Cysts, haemangiomas, regenerative, abscesses
PRIMARY LIVER TUMOURS
Benign
* — (= liver cell adenoma, anabolic — and oral — pill (OCP))
* — adenoma (rare)
* —
Malignant
* Hepatocellular — (=liver cell carcinoma, — , – )
* Intrahepatic — (=intrahepatic bile duct adenocarcinoma)
* — (textbook rarity)
hepatic adenoma
anabolic steroids and oral contraceptive pills
bile duct adenoma
haemagioma
carcinoma
hepatoma , HCC
Intrahepatic cholangiocarcinoma
Haemangiosarcoma
SECONDARY TUMOURS/LIVER
METASTASES
* — ‘liver tumour’ in Europe/N America
* Carcinoma - primary in – , — , –
* Other malignancies can infiltrate liver e.g. – , —
* Metastases may obstruct —
Early: few symptoms/effects, Alk Phos —
Late: rising — , —
* Generally poor —
* Identify primary site of origin for —–
* — for isolated colorectal metastases
commonest
GI tract , lung , breast
lymphoma and leukaemia
bile flow
raised
rising bilirubin , jaundice
poor prognosis
treatment
surgery
— IS USED IN LIVER METASTASIS HISTOLOGY
* CK20, CDX2 : —
* TTF1 : —
* S100, Melan A, HMB, SOX10 : —
immunohistochemsity
large intestine
lung
melanoma
Multiple pale deposits are —
(don’t confuse with cirrhosis, not diffuse change)
metastases
( check slide 8 for pic )
HEPATOCELLULAR CARCINOMA
* Europe/North America relatively uncommon
* East and SE Asia/Africa common
* Associated with — / — (>90%)
* Can occur in non-cirrhotic fibrotic — livers
* — mass or — , may have vascular —
* — not as usual as in some other tumour types
* Presentation:
High incidence areas - co-presents with or precedes — , in relatively — patients
Low incidence areas : — of cirrhosis, 3% HCC/yr, vague/changing symptoms
cirrhosis/chornic hepatitis
hbv
single or multifocal
vascular invasion
metastases
cirrhosis
young
decompression
HEPATOCELLULAR CARCINOMA
Diagnosis:
* Radiology: US, specific contrast-enhanced — and/or — protocols
* Assessment of nodules in cirrhosis, >1cm or enlarging
* Alpha-fetoprotein (AFP): ‘— ’
* — rarely necessary
Screening:
* High risk patients ( — cirrhosis), every —
* US
* AFP blood test – alone not specific/sensitive enough
Prevention
* Treatment of cause of underlying chronic liver disease?
* Prevention of chronic liver disease (HBV — )
CT , MRI
tumour marker
biopsy
compensated cirrhosis
6/12
HBV vaccination
HEPATOCELLULAR CARCINOMA
Treatment
* — if early
* OLT
* Local ablative treatments: — , arterial —
Prognosis– depends on:
* –
* Degree of — impairment
* —
* Typically poor but in selected cases 5 year survival of 50%
Aetiology:
* — (HBV/HCV/HFE > other causes cirrhosis?)
* Chronic — directly oncogenic?
* — - fungal contaminants of food stores
- important info in microscopic appearance of HCC:
Tumour cells resemble hepatocytes but show –
resection
radio frequency , arterial chemo-embolisation
stage
liver function
co-morbidity
cirrhosis
HBV
aflatoxin
polymorphism
CHOLANGIOCARCINOMA
* – arising from – epithelium
— or — location
* Commonest site at — of –
— tumour = obstructing bifurcation of CHD
* Intrahepatic cholangiocarcinoma a minority of primary
liver malignancy (10%)
* Associations: —
Rare: chronic fluke infestation, congenital biliary
abnormalities
* Diagnosis – and often – , outcome —
* Selected cases – surgical —
* Typically, — obstruction with — placement
adenocarcinoma
bile duct
intahepatic or extra hepatic
him of liver
klatskin
PSC
difficult , late , poor
surgical resection
palliate , stent
PANCREAS
* — location
* — components, — distinct
* Exocrine 98%: makes — enzymes
* Endocrine: — , —
* Exocrine composed of glandular — grouped into —
* Exocrine secretions drain via — , joining to form—
retroperitoneal
2
embryologically
digestive enzymes
islets of Langerhans, hormones
acini
lobules
ducts
pancreatic duct
histology of normal pancreas:
Small pancreatic duct (centre) surrounded by — pancreatic glandular — .
— collection of cells (left centre) is islet of Langerhans
exocrine
acini
pale
PANCREATIC TUMOURS
Exocrine pancreas:
* Malignant: pancreatic (ductal) —
* Other less common tumours, sometimes —
* May be – or have — behaviour
* Some recognised as precursors to pancreatic —
Endocrine:
* Pancreatic — tumours rare
* Behaviour difficult to —
* Classified by — type produced
* Hormone may cause — symptoms
* Association with — and — in inherited — syndrome
adenocarcinoma
cystic
bengin
intermediate
pancreatic ca
neruoendocrine
predict
hormone
clinical
h parathyroid hyperplasia and pituitary adenomas
MEN type 1
PANCREATIC CARCINOMA
* — , arising from —
* Common: 5th/6th by rank of cancer deaths
* M — F, 80% >60 years
* 60-70% from — , rest from — &—
* Spread:
Direct local: — (vessels, nerves),
duodenum, CBD = ‘ — advanced’
Lymph nodes or to liver (50% — at diagnosis)
* Risk factors (relatively weak)
Smoking, DM, chronic pancreatitis
Family history (5%)
adenocarcinoma
pancreatic duct
m > f
head , body , tail
peritoneum
locally advanced
metastatic
PANCREATIC CARCINOMA
Symptoms
* Typically symptomatic only with — disease
* Easily missed
* — , —
* — obstructive — (tumours in — )
* Vague abdominal pain, may radiate to —
* Rare: palpable mass, thrombotic tendency
Migratory thrombophlebitis = — sign
Diagnosis:
* — serum marker for pancreatico-biliary cancer
Not useful in diagnosis, used for — / — assessment
* Imaging (US, CT, EUS), FNA cytology via EUS
* Avoid unnecessary invasive investigation in majority
advanced
anorexia , weight loss
painless obstructive jaundice
head
back
Trousseau’s
CA 19-9
response/relapse
PANCREATIC CARCINOMA
Prognosis
* 5 year survival <3%, most patients die <1 year
* 10-20% suitable for surgery
* 10-20% 5yr survival in these selected patients
Treatment:
* Pancreatico-duodenectomy ( — procedure)
* Chemotherapy ( — ), modest benefit
* Majority: —
Stenting, analgesia
* Painless extrahepatic cholestasis/obstructive
jaundice a/w weight loss: suspect —
malignancy
Whipple
adjuvant
palliation
pancreatico-biliary
NORMAL GALL BLADDER
* — and – bile (not vital)
* Anatomical variants (— , — )
* Bile contents:
— and — ( — action for digestion of fats)
Excretory: – , — , — , —
* Cholesterol remains in solution by forming — with — – often may be an — solution
stores and concentrates
cystic duct and vessels
bile salt and phospholipid
detergent
bilrubin , cholesterol , calcium salts and copper
micelles
bile salt
unstable
GALLSTONES
* Common, easily identified with —
* Formed from — (+/- — )
Predominantly — >90%, may be mixed
Predominantly — <10%
10% only are — (+ calcium) on plain x ray
* Cholelithiasis = stones in —
* Choledocholithiasis = stones in —-
Typically, pass from — to — via —
Less commonly, form primarily in CBD
* Significant part of workload for general surgeons
ultrasound
bile constituents ( calcium )
cholesterol
bilrubin
radio-opaque
gall bladder
common bile duct
gall bladder to CBD to cystic duct
WHO GETS GALLSTONES?
Predisposing factors:
* — (16% of US women vs 9% US men)
* Increasing age
* Obesity, high fat/low fibre
* High lipids, type —
* Geography and race (Native Americans, Hispanic)
* High does — : pregnancy, ?Pill, ?HRT
* Gall bladder – / — : rapid weight loss (bariatric surgery), fasting, TPN
* Bilirubin (pigment) stones: bile salt — (Crohn’s ileitis, ileal surgery), — , — , —
females
type 2 DM
osterogen
hypo motility/stasis
depletion
cirrhosis , haemolytic , parasite
HOW DO GALLSTONES FORM?
Pathogenesis:
* Altered bile composition (“ — bile”), precise mechanism typically unexplained (cholesterol
supersaturation?)
* Gall bladder —
* Phases of accelerated — and —
(sluggish/static gall bladder) in stone formation
* Stones form in — episodes over — period
* Lithogenic bile may cause – and bile — , as well as or instead of stones
* — not a primary event in pathogenesis of stones
lithogenic bile
hypomotility
nucleation and growth
sequential
long
microlithiasis and bile sludge
infection
SYMPTOMATIC GALLSTONES & BILIARY COLIC
* — most common symptom related to gall stones
– may be difficult to confidently diagnose
Pain will recur in 70%
1-2% with biliary colic get complications of gallstones
* — RUQ/epigastric pain, > — minutes, < — hours
May radiate to – , —
Usually — pattern/persistent
— pain due to distension of GB following transient obstruction of —
No fever/raised WCC/tenderness
Moderately severe pain: differential diagnosis –
dyspepsia, PUD, acute pancreatitis, oesophageal
pain, MI
biliary colic
steady
30
4 hrs
back , right shoulder
crescendo
visceral
cystic duct
ASYMPTOMATIC GALLSTONES
Most gallstones — / —findings
* Only 20% cause symptoms if followed up x 15yrs
* Biliary pain (biliary colic) develops in 1-4% annually
* If asymptomatic, treatment not indicated
* Other symptoms – vague abdominal pain, dyspepsia,
fatty food intolerance – are they due to gallstones?
* Distinction between asymptomatic and symptomatic can be difficult
* Will patients benefit from cholecystectomy?
asymptomatic/incidental
COMPLICATIONS OF GALLSTONES
* Acute cholecystitis and its complications
* Common bile duct —- if stone moves into CBD (or forms there)
Obstructive —- (—– cholestasis)
Ascending cholangitis
Acute pancreatitis
* Gall bladder adenocarcinoma (rare, low overall risk)
* Complications: approx. 1% risk if gallstones, higher if
biliary colic
obstruction
jaundice
extra hepatic
ACUTE CHOLECYSTITIS
* Nearly always (>90%) a/w —
* — obstruction (sustained), causing:
— in gall bladder
— infection
Small % — (i.e. without stone)
* Fever, nausea, vomiting, pain RUQ x days
* RUQ tenderness, Murphy’s sign +ve
* High WCC, US findings characteristic
* No — (exception: rare Mirizzi syndrome)
* Fluid, analgesia, antibiotics
* Cholecystectomy
gallstones
cystic duct
stasis
2ndary infection
small acalculus
no jaundice
COMPLICATIONS OF ACUTE
CHOLECYSTITIS
Occur in 10-20%
* — (chronically obstructed, ongoing active
inflammation)
* — (chronically obstructed, sterile)
* — inflammation with risk of perforation
* Pericholecystic abscess or generalised biliary peritonitis
(very rare, high mortality)
* — to duodenum with cholecysto-duodenal —
* Fistula followed by risk of — (small intestinal obstruction due to stone)
empyema
mucocole
necrotising inflamamtion
adhesion
fistula
gallstone ileus