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Digestive System > Hepatobiliary Disorders > Flashcards

Hepatobiliary Disorders Flashcards

Liver Gallbladder

1
Q

What are the main causes of acute liver failure?

A

Hepatitis

Intrahepatic bile duct obstruction

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2
Q

What can cause acute hepatitis?

A

Viral
Drugs
Alcohol

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3
Q

What is the main cause for pre-hepatic jaundice?

A

Excess haemoglobin released from RBC (haemolysis)

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4
Q

What are possible causes of hepatic jaundice?

A

Cholestasis

Intrahepatic bile duct obstruction

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5
Q

What are possible causes of post-hepatic jaundice?

A

Gallbladder disease
Cholelithiasis (gallstones)
Bile duct obstruction (extrahepatic)

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6
Q

Which bile duct disease is associated with increased risk of cholangiocarcinoma?

A

Primary sclerosing cholangitis

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7
Q

What are raised ALP and raised anti-mitochondrial autoantibodies characteristic signs of?

A

Primary biliary cholangitis

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8
Q

What is a histological difference between primary biliary and primary sclerosing cholangitis?

A

Primary biliary has granulomas. Primary sclerosing doesn’t

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9
Q

What is ascending cholangitis normally a consequence of?

A

Obstruction of bile duct by gallstones

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10
Q

What is the pathology behind jaundice?

A

High levels of bilirubin in circulation

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11
Q

What feature of jaundice can indicate a tumour?

A

Jaundice with pain

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12
Q

What can be causes of extrahepatic bile duct obstruction?

A

Gallstones
Tumours (bile duct or compression from outside)
Stricture (benign/malignant)

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13
Q

What are possible causes of intrahepatic bile duct obstruction?

A

Primary biliary cholangitis
Primary sclerosing cholangitis
Tumours in liver (primary/mets)

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14
Q

what is cholestasis, and what can cause it?

A

pooling of bile in canaliculi of liver

can be caused by liver failure, cirrhosis, viral/alcoholic hepatitis, tumour, drugs

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15
Q

what are the main types of gallbladder disease which may cause jaundice?

A

acute inflammation

chronic inflammation

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16
Q

what are some causes of cirrhosis?

A 
alcohol
chronic viral hepatitis
obesity
DM2
drugs
metabolic diseases
autoimmune diseases
cryptogenic (no cause)
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17
Q

what other GI disease is primary sclerosing cholangitis closely associated with?

A

IBD

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18
Q

what are some complications of cirrhosis?

A

impaired liver function
impaired blood flow - portal hypertension
increased risk of hepatocellular carcinoma

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19
Q

what other organ is affected by portal hypertension, other than the liver?

A

spleen

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20
Q

what is ascending cholangitis caused by?

A

caused by obstruction of common bile duct leading to inflammation of bile and bile duct above the obstruction

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21
Q

what are the common liver function tests carried out? (8)

A 
Bilirubin
Aminotransferases (AST/ALT)
Alkaline phosphatase (ALP)
gamma-GT
Albumin
Pro-thrombin time
Creatinine
Platelet count
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22
Q

which liver function test may be raised in pregnant women, and why?

A

ALP

because it’s also found in the placenta

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23
Q

which is the most important liver test for determining extent of liver damage?

A

pro-thrombin time

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24
Q

why does liver disease cause ascites?

A

because the liver synthesises albumin and plasma proteins. if it doesn’t produce them properly, there is a lack of oncotic pressure

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25
Q

which aminotransferase test is the most specific for liver damage?

A

ALT

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26
Q

what are examples of other disorders which can cause a raised AST?

A

muscle damage, heart disease

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27
Q

what liver condition shows a raised gamma-GT?

A

alcohol-induced liver disease

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28
Q

why can ALP and gamma-GT be useful liver tests together?

A

if raised, a gamma-GT can confirm that a raised ALP is caused by liver damage and not something else (eg pregnancy)

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29
Q

what do creatinine levels show as a liver function test?

A

creatinine levels show whether liver damage is affecting the kidneys –> poorer prognosis

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30
Q

what is the purpose of platelet count as liver function test and why?

A

it shows whether the spleen is enlarged, because low platelet count = overactive (enlarged) spleen. can indicate portal hypertension

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31
Q

how can pre-hepatic and post-hepatic or hepatic jaundice be differentiated by their signs and why?

A

pre-hepatic - unconjugated, not water soluble. normal urine/faeces
hepatic/post-hepatic - conjugated, water soluble, dark urine and faeces

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32
Q

what happens to bilirubin when taken up by the hepatocytes in the liver?

A

bilirubin is conjugated with glucuronic acid, which makes it water soluble so it can be excreted

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33
Q

what is bilirubin conjugated with in the hepatocytes to make it water soluble?

A

glucuronic acid

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34
Q

of what nutrient is the liver the only storage place in the body?

A

vitamin A

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35
Q

why is ALT a more specific liver function test than AST?

A

becaust ALT is specific to hepatocyte damage. AST can be elevated in other things (eg heart damage, muscle damage)

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36
Q

where is alkaline phosphatase (ALP) found?

A

in bile ducts
in placenta
in bone

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37
Q

what are the features of urine and stool in the different kinds of jaundice?

A

pre-hepatic: normal stools and normal urine
hepatic: normal stools but dark urine
post-hepatic: pale stools and dark urine

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38
Q

what are the main investigations to be done when suspecting liver disease?

A
  • liver screen
  • ultrasound of liver
  • MRCP/CT scan
  • ERCP for therapeutic procedures
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39
Q

what tests are included in a liver screen?

A 
ferritin and transferrin saturation
ceruloplasmin and copper test
autoantibody profile
hepatitis B and C serology
fasting lipid and glucose profile
alpha 1 antitrypsin
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40
Q

what are the disadvantages of an ERCP?

A 
radiation/contrast
sedation
complications
failure
only shows bile ducts
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41
Q

what are the disadvantages of MRCP?

A

expensive
claustrophobic
timeconsuming

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42
Q

what are some indications for therapeutic ERCP?

A

gallstones (bile duct obstruction, acute pancreatitis)
stenting of obstructed bile duct
tumor/gallstone removal
post-operative complications

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43
Q

what is choledocholithiasis?

A

gallstones in common bile duct

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44
Q

what are some possible complications of ERCP?

A
  • cardio-respiratory problems due to sedation
  • inflammation (cholangitis, pancreatitis)
  • bleeding, perforation due to sphincterotomy
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45
Q

what is the purpose of a sphincterotomy during gallbladder removal?

A

widening the opening of the Sphincter of Oddi to allow more space for removing gallstones

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46
Q

what are less commonly used techniques for gallstone removal and bile duct imaging?

A

PTC (percutaneous transhepatic cholangiography)

EUS (endoscopic ultrasound)

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47
Q

what is an advantage of using EUS in GI imaging?

A

useful in identifying pancreatic masses
can be used to biopsy or aspirate material
useful in staging tumours

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48
Q

what are some of the more common causes of chronic liver disease?

A 
alcohol liver disease
Viral hepatitis (B, C)
autoimmune diseases of liver/bile duct
non-alcoholic steatohepatitis (NASH)
liver tumours
haemochromatosis
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49
Q

what do most chronic liver diseases eventually lead to in the liver?

A

fibrosis –> cirrhosis

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50
Q

when is a liver disease defined as chronic?

A

when it’s lasted longer than 6 months

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51
Q

what are two pathological changes in liver parenchyma during cirrhosis?

A
  • Kuppfer cells in sinusoids enlarged –> increased resistance to blood flow –> portal hypertension
  • hepatic stellate cells enlarged and proliferate in ECM
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52
Q

what are some of the presenting symptoms of chronic liver disease?

A
  • jaundice
  • ascites
  • varices (caput medusae, oesophageal varices)
  • hepatic encephalopathy
  • splenomegaly
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53
Q

what is the difference between compensated and decompensated chronic liver disease?

A
  • compensated: liver disease with little/no symptoms

- decompensated: liver disease with symptomatic evidence

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54
Q

how is compensated chronic liver disease picked up?

A
  • through screening tests

- high LFT’s

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55
Q

what are the three main complications of chronic liver disease?

A

ascites
varices (+/- bleeding)
hepatic encephalopathy

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56
Q

how is ascites picked up on examination?

A

shifting dullness
fluid thrill
ultrasound

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57
Q

how is ascites investigated?

A

Diagnostic paracentesis:

  • protein and albumin concentration
  • cell count
  • Serum Ascitic Albumin Gradient (SAAG) analysis
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58
Q

how are differentials derived from investigation of ascitic fluid?

A

through SAAG:

less or more than 1.1g/dL

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59
Q

what are common lab analyses carried out on ascitic fluid?

A 
albumin
protein
cell count
glucose
amylase
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60
Q

what are possible causes for a SAAG concentration higher than 1.1g/dL?

A 
chronic heart failure
portal hypertension
myxedema
Budd-Chiari Syndrome
large liver metastases
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61
Q

what are possible causes for a SAAG concentration lower than 1.1g/dL?

A 
TB infection
chyloedema
pancreatic disease
malignancy
chylous ascites
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62
Q

what is the rule of thumb for classification of ascites based on SAAG?

A 
>1.1g/dL = portal hypertension related
<1.1g/dL = not related to portal hypertension
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63
Q

what are treatment options for ascites?

A

diuretics/aquaretics
large volume paracentesis
TIPPS

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64
Q

what are the treatment options for bleeding varices?

A 
resuscitation
IV access
fluid replacement
endoscopic band ligation
TIPPS if bleeding occurs again
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65
Q

what is the pathology behind hepatic encephalopathy?

A

liver’s inability to turn ammonia into urea - ammonia in circulation crosses BB - causes confusion

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66
Q

what are some of the signs often associated with hepatic encephalopathy?

A

fetor hepaticus

asterixis (flapping tremor)

67
Q

how is hepatic encephalopathy treated?

A
  • by treating underlying cause

- laxatives

68
Q

what should be considered in cases of recurrent hepatic encephalopathy?

A

liver transplant

69
Q

how does hepatocellular carcinoma present?

A
  • with decompensated liver failure
  • abdominal pain
  • weight loss
  • abdominal mass
  • bleeding from tumour
70
Q

what are the imaging investigations appropriate for hepatocellular carcinoma?

A
  • ultrasound
  • CT scan
  • MRI scan
71
Q

what are the treatment options for hepatocellular carcinoma?

A
  • systemic treatment (chemotherapy, tyrosine kinase inhibitor)
  • radiofrequency ablation
  • alcohol injection
72
Q

what is the main biomarker used to test for hepatocellular carcinoma in the blood?

A

Alpha-feto protein (AFP)

73
Q

what pathology connects gynaecomastia and spider naevi in liver disease, and why?

A

liver fails to break down oestrogen:

  • angiogenic hormone (causes spider naevi to form and burst)
  • causes gynaecomastia
74
Q

what other liver disease is associated with hepatocellular carcinoma?

A

hepatitis B and C

75
Q

why is the anatomy of the biliary tree important for a surgeon?

A

because of the anatomical/vascular variation between patients

76
Q

what is cholesterosis?

A

“strawberry gallbladder” - degenerative change in gallbladder structure due to excess cholesterol in the gallbladder wall

77
Q

are gallstones always symptomatic?

A

no

78
Q

what are the types of gallstone composition?

A
  • mixed cholesterol + pigment
  • only cholesterol
  • only pigment
79
Q

where in the world are pigment gallstones seen more commonly?

A

east asia

80
Q

what are the risk factors for developing gallstones in general?

A
  • age
  • gender
  • oral contraceptive pill
  • parity
81
Q

what are some of the risk factors for developing cholesterol gallstones?

A
  • obesity
  • DM
  • cirrhosis
  • cystic fibrosis
  • heart transplant
  • delayed gallbladder emptying
  • total parenteral nutrition (TPN)
  • prolonged low-fat diet
82
Q

what are some of the risk factors for developing pigment gallstones?

A
  • bile infection (e. coli, bacterioides)

- haemolytic anaemia

83
Q

what are the possible symptoms of gallstones in the gallbladder?

A
  • asymptomatic
  • painful jaundice (Mirrizi’s syndrome)
  • dyspepsia
  • dyspeptic flatulence
  • biliary colic
  • empyema
  • perforation
  • gallstone ileus
  • acute cholecystitis
84
Q

what are the common investigations for detecting gallstones?

A 
Bloods: LFT's, amylase, lipase
USS
EUS
CT scan
MRCP/ERCP
PTC
85
Q

what are some symptoms associated with choledocholithiasis?

A
  • painful obstructive jaundice
  • itching
  • dark urine, pale stool
  • acute pancreatitis
  • ascending cholangitis
86
Q

what is Charcot’s triad?

A
  • jaundice
  • pain
  • rigors
87
Q

what are treatment options for gallstones?

A
  • laparoscopic cholecystectomy
  • lithotripsy (only if not fit for surgery)
  • open cholecystectomy
  • cholecystostomy while waiting for cholecystectomy
88
Q

what are the risks of lithotripsy for dissolving gallstones?

A

risk that smaller fragments move further down and block the Sphincter of Oddi, causing acute pancreatitis

89
Q

what does a cholecystostomy involve?

A

inserting a stoma in the gallbladder for drainage until the patient is fit for a cholecystectomy

90
Q

how are common bile duct stones managed?

A

common bile duct exploration (laparoscopic)
ERCP to remove stones
transepatic removal of stones

91
Q

what are some congenital biliary tree abnormalities?

A
  • biliary atresia

- biliary cysts

92
Q

what are some benign causes of biliary abnormalities?

A
  • congenital: atresia, cysts
  • benign strictures: iatrogenic, Mirrizi’s syndrome (compression from gallstone outside bile duct)
  • Inflammation: PSC, pancreatitis
93
Q

which type of cholangiocarcinoma is most common?

A

Extrahepatic hilar

94
Q

what are the classifications of intrahepatic cholangiocarcinoma?

A

intraductal
periductal
mass forming

95
Q

what are the treatment options for cholangiocarcinoma?

A

surgery only for treatment

palliative otherwise

96
Q

what are the main symptoms of cholangiocarcinoma?

A

painless jaundice

itching

97
Q

what investigations should be done for cholangiocarcinoma?

A 
blood test
USS
EUS
PTC
CT scan
MRA
98
Q

what is the association between gallstones and gallbladder cancer?

A

the majority of gallbladder cancers occur in gallbladders that contain stones

99
Q

what are the complications of alcohol on the liver?

A
  • fatty liver
  • alcoholic hepatitis
  • hepatic
100
Q

what is the method used to assess whether someone has an alcohol problem?

A

FAST/AUDIT

101
Q

what are some of the chemical changes that occur in the liver as a result of alcohol abuse?

A
  • reduced gluconeogenesis –> hypoglycaemia

- increased lipid production –> steatosis

102
Q

what are possible presentations of alcoholism?

A

often none unless late stage liver disease

  • hepatic encephalopathy
  • withdrawal symptoms (asterixis, delirium tremens)
  • jaundice if severe
  • muscle wasting
103
Q

what investigations should be done if alcoholic liver disease is suspected?

A
  • bloods, LFTs, glucose

- USS to show fatty liver

104
Q

what investigations should be done to diagnose hepatic encephalopathy?

A
  • LFT’s

- ammonia levels

105
Q

what are possible causes of hepatic encephalopathy?

A
  • infection
  • drugs
  • constipation
  • GI bleed
106
Q

what should be excluded as a cause for hepatic encephalopathy?

A
  • intracranial bleed
  • infection
  • hypoglycaemia
107
Q

how can hepatic encephalopathy be treated?

A
  • bowel clearance/enema/lactulose
  • antibiotics
  • supportive (ITU)
108
Q

how can spontaneous bacterial peritonitis present?

A
  • ascites
  • abdominal pain
  • rigors
  • vomiting
  • hepatic encephalopathy
109
Q

what should be the first investigation to diagnose spontaneous bacterial peritonitis?

A

paracentesis of ascitic fluid

110
Q

how should spontaneous bacterial peritonitis be managed?

A
  • IV antibiotics
  • IV albumin infusion
  • ascitic drainage
111
Q

what are possible symptoms of alcoholic hepatitis?

A
  • jaundice
  • hepatic encephalopathy
  • signs of decompensated liver failure
  • infection
112
Q

what tests confirm alcoholic hepatitis?

A
  • raised LFT’s (bilirubin, ALP, gammaGT, ALT)
113
Q

what is the management of alcoholic hepatitis?

A
  • supportive (ITU)
  • treat infection
  • treat encephalopathy
  • steroids if severe (Glasgow Alcoholic Hepatitis Score or Maddrey’s)
  • nutrition (frequent high energy meals)
114
Q

what are the two normally used scales to decide the severity of alcoholic hepatitis?

A

Glasgow Alcoholic Hepatitis Score

Maddrey’s Score

115
Q

what are non-alcohol causes of fatty liver (NASH)?

A
  • obesity
  • diabetes
  • hypercholesterolaemia
116
Q

what are the symptoms of steatohepatitis?

A

normally asymptomatic, picked up on USS (fatty liver)

117
Q

what is the management of steatohepatitis?

A

weight loss and exercise

118
Q

what LFT test is often raised in steatohepatitis?

A

ALT

119
Q

what is a likely complication of steatohepatitis?

A

fibrosis and cirrhosis

120
Q

which viral forms of hepatitis are enteral?

A

Hep A and E

121
Q

which viral forms of hepatitis are parenteral?

A

Hep B, C and D

122
Q

which viral forms of hepatitis are acute and self-limiting?

A

Hep A and E

123
Q

which viral forms of hepatitis are chronic?

A

Hep B, C and D

124
Q

when is Hepatitis A likely to occur?

A

in childhood and early years

125
Q

how is Hepatitis A diagnosed?

A

through blood test serology:

  • raised ALT
  • raised CRP
  • raised IgM (sign of acute infection)
126
Q

how does Hepatitis B evade the immune system?

A

by secreting Hepatitis B surface Antigen (HBsAg) to fool the immune system

127
Q

on serology testing, which antigens show what activity of the Hepatitis B?

A

HBsAg (surface antigen) - only shows presence of virus
HBeAg (e antigen) - shows active replication
HBV DNA - shows active replication

128
Q

which Hepatitis B antigen shows that the virus is replicating, but can’t be picked up in the blood? why is it not picked up?

A

Hepatitis B core antigen

not picked up as it’s not secreted in the blood

129
Q

which antibodies signal that a Hepatitis B infection is inactive?

A

Anti HBe antibodies

130
Q

which antibodies signal an acute infection of Hepatitis B?

A

IgM anti-HBc (core)

131
Q

which antibodies signal a chronic infection of Hepatitis B?

A

IgG anti-HBc (core)

132
Q

what are the different prognoses for Hepatitis B infection when infected in childhood and adulthood?

A

childhood infection: 90% likely to become chronic, 10% will clear infection
adulthood infection: 90% chance to clear infection, 10% to become chronic

133
Q

what are the complications of Hepatitis B infection?

A
  • chronic infection
  • fibrosis and cirrhosis
  • hepatocellular carcinoma
  • end stage liver disease
134
Q

what are treatment options for Hepatitis B?

A
  • PEGylated interferon injections

- oral antiviral drugs (eg lamivudine)

135
Q

what kind of nucleic acid does Hepatitis B produce?

A

DNA

136
Q

which hepatitis viruses produce RNA?

A

A, C, D and E

137
Q

why Hepatitis C difficult to create a vaccine against?

A

because its RNA uses reverse transcriptase, which makes mistakes creating genetic modifications - hard to pin down to make a vaccine against

138
Q

what is raised in the blood at the early stages of a Hepatitis C infection?

A

viral RNA in the blood

139
Q

why is Hepatitis C difficult to clear?

A

because the antibody against it isn’t very effective

140
Q

what are possible drug treatments for Hepatitis C?

A
  • PEG-Interferon Alpha

- rivabarin

141
Q

what makes Hepatitis D a unique virus compared to the other hepatitis viruses?

A
  • it’s a parasite of another hepatitis virus

- can only infect a host if it’s infected with Hep B already

142
Q

why is Hepatitis E relevant in Scotland?

A

it’s the most common cause of acute hepatitis in Grampian

143
Q

how is Hepatitis E treated?

A

no specific treatment or vaccine currently available

144
Q

what do Epstein-Barr Virus and Cytomegalovirus have in common in terms of hepatitis infections?

A

cause raised LFT’s in immunocompromised patients

145
Q

which autoimmune hepatobiliary diseases occur predominantly in females?

A
  • autoimmune hepatitis

- primary biliary cholangitis

146
Q

what is the most common cause of liver transplant in women apart from alcohol?

A

primary biliary cholangitis

147
Q

what is the serology of autoimmune hepatitis?

A

raised IgG

148
Q

what is the serology of primary biliary cholangitis?

A

raised IgM

149
Q

which gender is worse affected by primary sclerosing cholangitis?

A

males

150
Q

which scores are used to determine the need for a liver transplant?

A

MELD (Mayo End Stage Liver Disease)
UKELD (UK End Stave Liver Disease)
Child-Pugh score

151
Q

what values do the MELD and UKELD scores use to determine the need of a liver transplant?

A
  • bilirubin
  • creatinine
  • INR
  • sodium (UKELD)
152
Q

what is the main imaging technique for primary sclerosing cholangitis?

A

MRCP

153
Q

name the treatment for primary biliary cholangitis

A

UDCA

154
Q

how is autoimmune hepatitis treated?

A

steroids and immunosuppression (azathioprine)

155
Q

what are the metabolic effects of alcohol?

A

hypoglycaemia
acidosis
ketosis
lipid excess

156
Q

what investigations are done for alcoholic liver disease?

A

LFT’s (ALT, AST, gamma-GT, low platelets)

liver ultrasound

157
Q

name some differential causes for hepatic encelopathy

A

constipation
infection
GI bleed
electrolyte imbalance

158
Q

what are some liver diseases associated with alcohol abuse?

A
  • hepatic encelopathy
  • spontaneous bacterial peritonitis
  • alcoholic hepatitis
159
Q

why is prothrombin time important as a liver function test?

A

because it can quantify the level of insufficiency of liver

160
Q

what is the purpose of creatinine testing as part of liver function tests?

A

it acts as a prognostic marker, as it shows how badly the kidneys have been affected by the liver disease

161
Q

what are the two main reasons why platelet count is low in liver disease?

A
  • thrombopoietin production from liver is impaired - less platelets
  • portal hypertension causing a damming of blood in spleen causes spleen to digest blood products (including platelets)
162
Q

what is the first line imaging test for liver disease? what is done after that?

A
  • abdominal ultrasound
  • CT scan
  • MRCP
  • ERCP for treatment
163
Q

name two cells in the liver which contribute to liver disease pathophysiology

A
  • kuppfer cells: macrophages, swell up and block sinusoids

- hepatic stellate cells: proliferate and cause fibrosis and extracellular matrix production

Digestive System (6 decks)

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