Liver tumour and failure Flashcards
Liver cysts
usually simple
bile duct origin
common
usually asymptomatic
Simple liver cysts
thin-walled
homogeneous
usually asymptomatic
treat if large/symptomatic
Complex liver cysts
thickened walls large septations papilae non-homogeneous need to investigate
Hemangioma
disorganized group of blood vessels most common liver tumour endothelial orgin collagen scaffold contrast retention on CT may be multiple usually asymptomatic
Focal nodular hyperplasia
hyperplasia of normal liver cells possibly related to presence of atrial-venous malformation second most common liver tumour rarely symptomatic presence of central scar on CT
Liver cell adenoma
benign neoplasm of hepatocyte origin hormone sensitive - OCP may be symptomatic gross appearance: large, fleshy histological: looks like a well-differentiated HCC risk of rupture may regress with cessation of OCP risk of rupture and of malignant degeneration increases with size, so consider surgical removal if >5cm
HCC
primary malignancy of hepatocytes
associated with cirrhosis (hep B, C, hemochromatosis most high risk)
may be multifocal
HCC diagnosis
tumour marker: alphaFP (can go up with injury as well)
contrast CT - rapid enhancement on arterial phase, wash-out during venous phase
HCC treatment
surgical resection - if the patient has underlying liver disease, cannot take out a large portion of liver
otehr: local ablation, chemoembolization, liver transplant, systemic chemotherapy
cannot do radiotherapy
Cholangiocarcinoma
Malignant neoplasm of the bile duct epithelium
Risk factors: PSC, clonorchis infection, choledochal cysts
usually involve major bile ducts leading to obstructive jaundice
can also arise from intrahepatic ducts
Cholangiocarcinoma treatment
surgical resection
early local extension common and often precludes surgery - difficult
stenting/bypass (Palliative), chemotherapy (poor results)
Liver metastasis
more common than primary tumours in western countries
usually multifocal and systemic
Liver metastasis diagnosis
may be hyper- or hypovascular
occasionally focal
poor blood supply
Liver metastasis treatment
may be responsive to liver resection
ablation
chemotherapy
Gallstone pathophysiology
Bile supersaturated –> precipitation of microscopic crystals, which grows over time
Occlusion of ducts by stones or sludge (gallbladder mucus + crystals)
Cholesterol stones (80%)
- associated with females, European/native Americans
others: calcium, bilirubin, pigment, mixed stones
Gallstone clinical presentation
- Lithogenic - condition favour stone formation
- Asymptomatic - do not require treatment
- episodes of biliary colic during gallbladder wall tension in RUQ - right scapular tip radiation (Collins sign)
- resolves in 30-90 min
- sporadic, unpredictable
- begins postprandially, intense/dull - complicated cholelithiasis
- inflammation
- infection - abscess, necrosis
- progressive fibrosis and loss of function
- GB adenocarcinoma, poor prognosis with invasion
- large stone - cholecystoenteric fistula
Gallstone workup
US
- most sensitive, specific
- EUS also accurate
CT: more expensive, less sensitive
- often used for abdominal pain workup
- superior to US for gallstones in distal common bile duct
MRI
ERCP
Gallstone Tx
Once gallstones become symptomatic, surgical intervention with cholecystectomy indicated
- if uncomplicated, can do medical therapy if not a good surgical candidate
- medical treatments: oral bile salt therapy, contact dissolution, extracorporeal shockwave lithotripsy
Classification of liver tumours
Congenital vs acquired
–> non-neoplastic vs neoplastic
–> cysic vs solid, benign vs malignant
if malignant –> primary vs metastatic
Acute liver failure definition
no previous liver disease Hyperacute: within 2 weeks Acute: 8 weeks Subacute: 24 weeks Fulminant failure: severe enough to produce encephalopathy
Etiology of acute liver failure
often not found Viral: hepatitis A-E Drugs& toxins Metabolic: acute Wilson's disease( rare) Autoimmune (very rare)
Pathogenesis of liver cirrhosis
1) Lipocytes (Ito cells) in space of Disse - vitamin A storage
2) Inflammation activates/transforms Ito cells
3) Ito cells release factors leading to collagen deposition
4) Continued deposition –> fibrosis
Decompensated cirrhosis
Clinical: ascites, bleeding esophageal/ gastric varices, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome
Lab: hypoalbuminemia, coagulopathy, hyperbilirubinemia (jaundice)
