Liver Flashcards
Why does jaundice occur?
Due to increased levels of bilirubin in the blood
What is bilirubin?
A normal breakdown product of RBCs
What are the classifications of jaundice?
pre-hepatic
hepatocellular
post-hepatic
What causes pre-hepatic jaundice? Examples?
excessive RBC breakdown - overwhelms to livers ability to conjugate bilirubin
causes a unconjugated hyperbilirubinaemia
haemolytic anaemia
Gilbert’s syndrome
What causes hepatocellular jaundice? Examples?
dysfunction or injury to hepatic cells - liver loses ability to conjugate bilirubin (unconjugated hyperbilirubinaemia)
alcoholic liver disease viral hepatitis medication PBC, PSC hepatocellular carcinoma
What causes post-hepatic jaundice? Examples?
obstruction to biliary drainage
conjugated hyperbilirubinaemia
gall stones
cholangiocarcinoma, strictures
pancreatic cancer
When does dark urine occur in jaundice?
in conjugated hyperbilirubinaemia - as conjugated bilirubin can be excreted via the urine (unconjugated can’t)
Why might you get pale stools in obstructive jaundice?
decreased stercobilin entering GI tract (colours stool)
What does a raised ALT/AST suggest?
intrahepatic damage
is specific to the liver
What does a raised ALP suggest?
post hepatic obstruction of bile flow
is also raised in bone disease, pregnancy, some cancers - not specific
What is gamma GT used for?
to confirm raised ALP is hepatic in nature
How is hepatitis A spread?
faecal oral spread (ask about foreign travel)
How does hepatitis A usually present?
acute - not associated with chronic liver disease/cirrhosis prodromal phase (flu like illness) jaundice hepatosplenomegaly lymphadenopathy
How is hep A investigated?
LFTs - raised ALT/AST, raised bilirubin
serology - hep A IgM
How is hep A managed?
supportive management
vaccine prophylaxis
How is hep B transmitted?
vertical
UPSI
blood contact
high risk populations: PWID, MSM
How does hep B present?
acute: similar to hep A but ++, extrahepatic features (arthralgia, urticaria), deranged LFTs
chronic: that of chronic liver disease
When is hepatitis B deemed chronic?
When HBsAg has been +ve for more than 6 months
What serology is positive in all ongoing infections of hep B?
HBsAg
What does the presence of anti-HBs in a patient’s blood indicate?
immunity to hep B (either vaccine or infection)
When is Hep B IgM positive?
acute or recent infection (present about 6 months)
How is Hep B managed?
acute: supportive
minimise exposure to high risk groups
vaccination
chronic:
peg interferon
antivirals e.g. tenevir, entecavir
How is Hep C transmitted?
blood
sex
vertical
What is the natural history of hep C?
acute infection - mild, asymptomatic
majority progress to chronic infection
How does hep C present?
acute - as per hep A (usually mild)
chronic - as per chronic liver disease
How is hep C investigated?
patient at risk or signs of chronic disease
test for hep C antibody
if positive: (past or active infection)
- test for Hep C RNA (PCR)
- positive in active infection
How is hep C managed?
peg interferon + ribavirin
When does hep D occur?
only alongside hep B
exacerbates hep B
What is the route of transmission for hep E?
faecal oral
How does hep E present?
similar to hep A
severe disease in pregnant women
What is acute liver disease?
any insult to the liver causing damage - previously normal liver
<6mths
What can cause acute liver disease?
viral hep drugs: NSAIDS, fluclox, coamox alcohol cholangitis malignancy ask about paracetemol
What are clinical features of acute liver disease?
abnormal LFTs itch pain arthralgia anorexia, nausea, malaise, lethargy jaundice
How is acute liver disease managed?
rest - up to 3 to 6 months
no alcohol
itch - sodium bicarb bath, urseodeoxycholic acid
observe for failure
How would acute liver failure present?
prolonged coagulation
encephalopathy
in a patient with a previously healthy liver
How does chronic liver disease present?
stigmata of cirrhosis jaundice deranged LFTs clubbing, palmar erythema, Dupuytren's gynaecomastia spider naevia, caput medusa
What is the pathophysiology of chronic liver disease?
insult/injury
recurrent inflammation and process of fibrosis
cirrhosis (compensated)
cirrhosis (decompensated) - chronic liver failure
What is cirrhosis?
formation of fibrotic bands that seperate nodules of functional liver tissue
common end point for chronic liver disease
What is portal hypertension?
complication of cirrhosis
increased pressure within low pressure portal system
What does portal hypertension cause?
splenomegaly - as splenic vein drains into portal vein
varices - portal vein collaterals form at anastomoses with systemic circulation (oesophagus, umbilical, haemorrhoidal, retroperitoneal)
What are caput medusa?
portal vein collaterals around umbilicus
How is chronic liver disease investigated?
LFTs liver screen imaging - fibroscan (transient elastography) - MRCP - USS (ascites, splenomegaly, irregular liver contour) US guided biopsy - gold standard but risky (pain and bleeding)
What is the management of chronic liver disease?
weight loss
no alcohol
ascites: drain, spironolactone, fluid and salt restriction
routine monitoring: OGD, bloods, fibroscan
itch: urseodeoxycholic acid
transplant is only curative management
What are complications of chronic liver disease?
encephalopathy portal hypertension hepatocellular carcinoma decreased synthetic function: coagulopathy, hypoalbuminaemia, hypoglycaemia spontaneous bacterial peritonitis
What bacteria is most commonly found in SBP in patients with chronic liver failure?
E. coli
When should you suspect SBP?
sudden detioration of a patient with ascites
What is SBP?
peritonitis without an obvious source
almost exclusively a patient with portal htn
What is non alcoholic fatty liver disease?
fatty liver
What does NAFLD progress to?
NASH - non alcoholic steatohepatitis (inflammation of liver due to fat deposition)
How are NAFLD/NASH diagnosed? management?
USS +/- biopsy
weight loss and exercise
What are the autoimmune liver disease?
PBC - primary biliary cholangitis/cirrhosis
PSC - primary sclerosis cholangitis
Autoimmune hepatitis
What is PBC?
destruction of interlobar bile ducts
chronic, progressive, granulomatous inflammatory disorder
What does PBC cause?
cholestasis
How does PBC present?
itch fatigue obstructive jaundice ?asymptomatic middle aged women association with other AI conditions
How is PBC investigated?
positive AMA
cholestatic LFTs
liver biopsy
How is PBC managed?
urseodeoxycholic acid (itch)
What is PSC?
autoimmune destruction, fibrosis and stricturing of large and medium bile ducts
What liver disease is associated with UC?
PSC
How does PSC present?
recurrent cholangitis
RUQ pain
fatigue
How is PSC investigated?
cholestatic LFTs
MRCP - multiple biliary strictures (beaded appearence)
positive pANCA
biopsy - onion skinning fibrosis
How is PSC managed?
maintain bile flow
monitor for cholangiocarcinoma, colorectal carcinoma
Who commonly gets autoimmune hepatitis?
young to middle aged women
What are the types of autoimmune hepatits?
type 1 - affects children and adults, ANA, antismooth muscle
type 2 - only children, anti LKM
What is the hallmark of autoimmune hepatitis?
interface hepatitis
piecemeal necrosis
How is AI hep managed?
steroids
azathioprine
transplant
What is Wilson’s disease?
autosomal recessive disorder
failure to adequately excrete copper
Where does copper accumulate in Wilson’s?
liver
CNS - basal ganglia
How does Wilson’s disease present?
neurological signs, psych and behavioural problems
children
cirrhosis or liver failure
on exam - Keyser Fischer rings
How is Wilson’s diagnosed?
24 hour copper increased
serum copper and caeruloplasmin reduced
How is Wilson’s managed?
copper chelation drugs - penicillamine
What is a1-anti-trypsin deficiency?
autosomal recessive
loss of a1 antitrypsin enzyme
What are the clinical features of a1 anti trypsin deficiency?
lung emphysema
liver deposition of mutant protein –> cirrhosis and hepatocellular carcinoma
How is A1AT deficiency diagnosed? managed?
serum A1AT levels
supportive
What is haemachromatosis?
autosomal recessive
defect in iron regulating hormone - increased intestinal absorption
What are the clinical features of haemachromotosis?
‘the bronzed diabetic’
cirrhosis
cardiomyopathy
pancreatic failure
How is haemachromatosis managed?
venesection
What is liver failure?
failure of the liver to maintain synthetic and metabolic functions
end stage liver disease or an acute event on top of chronic liver disease
How does liver failure present?
reduced synthetic function
- coagulopathy
- ascites (reduced albumin and protein)
- variceal bleeds (portal htn)
reduced metabolic function
- encephalopathy (accumulation of toxins produced by gut - ammonia)
- jaundice
What are the signs of liver failure?
ascites jaundice confusion, altered behaviour, slurred speech, drowsy hepatosplenomegaly liver flap stigmata of cirrhosis
How is hepatic encephalopathy managed?
lactulose - promotes excretion of ammonia
How is the synthetic function of the liver best assessed?
prothrombin time
albumin level
What are risk factors for hepatocellular carcinoma?
chronic inflammatory processes - viral hep - haemachromatosis - chronic alcholism - PBC >70 family history
What are clinical features of hepatocellcular carcinoma?
features of cirrhosis
non specific malignancy symptoms
dull ache RUQ
advanced - liver failure
O/E - irregular, enlarged, craggy and tender liver
What are investigations of suspected hepatocellular carcinoma?
deranged LFTs
prolonged clotting, reduced platelets
tumour marker - AFP (alpha fetoprotein)
imaging
- USS (mass + raised AFP virtually diagnostic)
- MRI liver scanning
- biopsy - risks of biopsy and tumour seeding
What are the surgical options for hepatocellular carcinoma?
resection (early disease)
transplant
What are non surgical options for hepatocellular carcinoma?
ablation transarterial chemoembolisation (TACE)
Where metastasises to the liver?
bowel breast pancreas stomach lung
What are clinical features of a liver abscess?
fever
rigors
abdo pain
on exam - hepatomegaly, RUQ tenderness
