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GI and General Surgery > Liver > Flashcards

Liver Flashcards

1
Q

Why does jaundice occur?

A

Due to increased levels of bilirubin in the blood

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2
Q

What is bilirubin?

A

A normal breakdown product of RBCs

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3
Q

What are the classifications of jaundice?

A

pre-hepatic
hepatocellular
post-hepatic

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4
Q

What causes pre-hepatic jaundice? Examples?

A

excessive RBC breakdown - overwhelms to livers ability to conjugate bilirubin
causes a unconjugated hyperbilirubinaemia

haemolytic anaemia
Gilbert’s syndrome

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5
Q

What causes hepatocellular jaundice? Examples?

A

dysfunction or injury to hepatic cells - liver loses ability to conjugate bilirubin (unconjugated hyperbilirubinaemia)

alcoholic liver disease 
viral hepatitis 
medication 
PBC, PSC
hepatocellular carcinoma
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6
Q

What causes post-hepatic jaundice? Examples?

A

obstruction to biliary drainage
conjugated hyperbilirubinaemia

gall stones
cholangiocarcinoma, strictures
pancreatic cancer

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7
Q

When does dark urine occur in jaundice?

A

in conjugated hyperbilirubinaemia - as conjugated bilirubin can be excreted via the urine (unconjugated can’t)

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8
Q

Why might you get pale stools in obstructive jaundice?

A

decreased stercobilin entering GI tract (colours stool)

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9
Q

What does a raised ALT/AST suggest?

A

intrahepatic damage

is specific to the liver

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10
Q

What does a raised ALP suggest?

A

post hepatic obstruction of bile flow

is also raised in bone disease, pregnancy, some cancers - not specific

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11
Q

What is gamma GT used for?

A

to confirm raised ALP is hepatic in nature

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12
Q

How is hepatitis A spread?

A

faecal oral spread (ask about foreign travel)

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13
Q

How does hepatitis A usually present?

A 
acute - not associated with chronic liver disease/cirrhosis 
prodromal phase (flu like illness)
jaundice 
hepatosplenomegaly 
lymphadenopathy
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14
Q

How is hep A investigated?

A

LFTs - raised ALT/AST, raised bilirubin

serology - hep A IgM

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15
Q

How is hep A managed?

A

supportive management

vaccine prophylaxis

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16
Q

How is hep B transmitted?

A

vertical
UPSI
blood contact

high risk populations: PWID, MSM

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17
Q

How does hep B present?

A

acute: similar to hep A but ++, extrahepatic features (arthralgia, urticaria), deranged LFTs
chronic: that of chronic liver disease

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18
Q

When is hepatitis B deemed chronic?

A

When HBsAg has been +ve for more than 6 months

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19
Q

What serology is positive in all ongoing infections of hep B?

A

HBsAg

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20
Q

What does the presence of anti-HBs in a patient’s blood indicate?

A

immunity to hep B (either vaccine or infection)

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21
Q

When is Hep B IgM positive?

A

acute or recent infection (present about 6 months)

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22
Q

How is Hep B managed?

A

acute: supportive
minimise exposure to high risk groups
vaccination

chronic:
peg interferon
antivirals e.g. tenevir, entecavir

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23
Q

How is Hep C transmitted?

A

blood
sex
vertical

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24
Q

What is the natural history of hep C?

A

acute infection - mild, asymptomatic

majority progress to chronic infection

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25
Q

How does hep C present?

A

acute - as per hep A (usually mild)

chronic - as per chronic liver disease

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26
Q

How is hep C investigated?

A

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
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27
Q

How is hep C managed?

A

peg interferon + ribavirin

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28
Q

When does hep D occur?

A

only alongside hep B

exacerbates hep B

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29
Q

What is the route of transmission for hep E?

A

faecal oral

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30
Q

How does hep E present?

A

similar to hep A

severe disease in pregnant women

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31
Q

What is acute liver disease?

A

any insult to the liver causing damage - previously normal liver
<6mths

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32
Q

What can cause acute liver disease?

A 
viral hep 
drugs: NSAIDS, fluclox, coamox
alcohol
cholangitis 
malignancy 
ask about paracetemol
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33
Q

What are clinical features of acute liver disease?

A 
abnormal LFTs 
itch 
pain 
arthralgia 
anorexia, nausea, malaise, lethargy 
jaundice
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34
Q

How is acute liver disease managed?

A

rest - up to 3 to 6 months
no alcohol
itch - sodium bicarb bath, urseodeoxycholic acid
observe for failure

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35
Q

How would acute liver failure present?

A

prolonged coagulation
encephalopathy

in a patient with a previously healthy liver

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36
Q

How does chronic liver disease present?

A 
stigmata of cirrhosis 
jaundice 
deranged LFTs
clubbing, palmar erythema, Dupuytren's 
gynaecomastia 
spider naevia, caput medusa
37
Q

What is the pathophysiology of chronic liver disease?

A

insult/injury
recurrent inflammation and process of fibrosis
cirrhosis (compensated)
cirrhosis (decompensated) - chronic liver failure

38
Q

What is cirrhosis?

A

formation of fibrotic bands that seperate nodules of functional liver tissue
common end point for chronic liver disease

39
Q

What is portal hypertension?

A

complication of cirrhosis

increased pressure within low pressure portal system

40
Q

What does portal hypertension cause?

A

splenomegaly - as splenic vein drains into portal vein
varices - portal vein collaterals form at anastomoses with systemic circulation (oesophagus, umbilical, haemorrhoidal, retroperitoneal)

41
Q

What are caput medusa?

A

portal vein collaterals around umbilicus

42
Q

How is chronic liver disease investigated?

A 
LFTs 
liver screen 
imaging 
- fibroscan (transient elastography)
- MRCP 
- USS (ascites, splenomegaly, irregular liver contour)
US guided biopsy 
- gold standard but risky (pain and bleeding)
43
Q

What is the management of chronic liver disease?

A

weight loss
no alcohol
ascites: drain, spironolactone, fluid and salt restriction
routine monitoring: OGD, bloods, fibroscan
itch: urseodeoxycholic acid

transplant is only curative management

44
Q

What are complications of chronic liver disease?

A 
encephalopathy 
portal hypertension 
hepatocellular carcinoma 
decreased synthetic function: coagulopathy, hypoalbuminaemia, hypoglycaemia 
spontaneous bacterial peritonitis
45
Q

What bacteria is most commonly found in SBP in patients with chronic liver failure?

A

E. coli

46
Q

When should you suspect SBP?

A

sudden detioration of a patient with ascites

47
Q

What is SBP?

A

peritonitis without an obvious source

almost exclusively a patient with portal htn

48
Q

What is non alcoholic fatty liver disease?

A

fatty liver

49
Q

What does NAFLD progress to?

A

NASH - non alcoholic steatohepatitis (inflammation of liver due to fat deposition)

50
Q

How are NAFLD/NASH diagnosed? management?

A

USS +/- biopsy

weight loss and exercise

51
Q

What are the autoimmune liver disease?

A

PBC - primary biliary cholangitis/cirrhosis
PSC - primary sclerosis cholangitis
Autoimmune hepatitis

52
Q

What is PBC?

A

destruction of interlobar bile ducts

chronic, progressive, granulomatous inflammatory disorder

53
Q

What does PBC cause?

A

cholestasis

54
Q

How does PBC present?

A 
itch 
fatigue 
obstructive jaundice 
?asymptomatic 
middle aged women 
association with other AI conditions
55
Q

How is PBC investigated?

A

positive AMA
cholestatic LFTs
liver biopsy

56
Q

How is PBC managed?

A

urseodeoxycholic acid (itch)

57
Q

What is PSC?

A

autoimmune destruction, fibrosis and stricturing of large and medium bile ducts

58
Q

What liver disease is associated with UC?

A

PSC

59
Q

How does PSC present?

A

recurrent cholangitis
RUQ pain
fatigue

60
Q

How is PSC investigated?

A

cholestatic LFTs
MRCP - multiple biliary strictures (beaded appearence)
positive pANCA
biopsy - onion skinning fibrosis

61
Q

How is PSC managed?

A

maintain bile flow

monitor for cholangiocarcinoma, colorectal carcinoma

62
Q

Who commonly gets autoimmune hepatitis?

A

young to middle aged women

63
Q

What are the types of autoimmune hepatits?

A

type 1 - affects children and adults, ANA, antismooth muscle
type 2 - only children, anti LKM

64
Q

What is the hallmark of autoimmune hepatitis?

A

interface hepatitis

piecemeal necrosis

65
Q

How is AI hep managed?

A

steroids
azathioprine
transplant

66
Q

What is Wilson’s disease?

A

autosomal recessive disorder

failure to adequately excrete copper

67
Q

Where does copper accumulate in Wilson’s?

A

liver

CNS - basal ganglia

68
Q

How does Wilson’s disease present?

A

neurological signs, psych and behavioural problems
children
cirrhosis or liver failure

on exam - Keyser Fischer rings

69
Q

How is Wilson’s diagnosed?

A

24 hour copper increased

serum copper and caeruloplasmin reduced

70
Q

How is Wilson’s managed?

A

copper chelation drugs - penicillamine

71
Q

What is a1-anti-trypsin deficiency?

A

autosomal recessive

loss of a1 antitrypsin enzyme

72
Q

What are the clinical features of a1 anti trypsin deficiency?

A

lung emphysema

liver deposition of mutant protein –> cirrhosis and hepatocellular carcinoma

73
Q

How is A1AT deficiency diagnosed? managed?

A

serum A1AT levels

supportive

74
Q

What is haemachromatosis?

A

autosomal recessive

defect in iron regulating hormone - increased intestinal absorption

75
Q

What are the clinical features of haemachromotosis?

A

‘the bronzed diabetic’
cirrhosis
cardiomyopathy
pancreatic failure

76
Q

How is haemachromatosis managed?

A

venesection

77
Q

What is liver failure?

A

failure of the liver to maintain synthetic and metabolic functions
end stage liver disease or an acute event on top of chronic liver disease

78
Q

How does liver failure present?

A

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
79
Q

What are the signs of liver failure?

A 
ascites 
jaundice 
confusion, altered behaviour, slurred speech, drowsy 
hepatosplenomegaly 
liver flap 
stigmata of cirrhosis
80
Q

How is hepatic encephalopathy managed?

A

lactulose - promotes excretion of ammonia

81
Q

How is the synthetic function of the liver best assessed?

A

prothrombin time

albumin level

82
Q

What are risk factors for hepatocellular carcinoma?

A 
chronic inflammatory processes 
- viral hep 
- haemachromatosis 
- chronic alcholism 
- PBC 
>70
family history
83
Q

What are clinical features of hepatocellcular carcinoma?

A

features of cirrhosis
non specific malignancy symptoms
dull ache RUQ
advanced - liver failure

O/E - irregular, enlarged, craggy and tender liver

84
Q

What are investigations of suspected hepatocellular carcinoma?

A

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

85
Q

What are the surgical options for hepatocellular carcinoma?

A

resection (early disease)

transplant

86
Q

What are non surgical options for hepatocellular carcinoma?

A 
ablation 
transarterial chemoembolisation (TACE)
87
Q

Where metastasises to the liver?

A 
bowel 
breast 
pancreas
stomach 
lung
88
Q

What are clinical features of a liver abscess?

A

fever
rigors
abdo pain
on exam - hepatomegaly, RUQ tenderness

GI and General Surgery (10 decks)

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