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Gastrointestinal Pathology > Jaundice and Chronic Liver Disease > Flashcards

Jaundice and Chronic Liver Disease Flashcards

1
Q

Definition of jaundice

A

Yellowish discolouration of the sclera and mucous membrane

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2
Q

When does jaundice manifest?

A

Serum bilirubin > 3mg/dL (51 umol/L)

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3
Q

Types of jaundice

A

Haemolytic / pre hepatic
Hepatocellular
Obstructive / post hepatic

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4
Q

What is unconjugated bilirubin?

A

Bilirubin = plasma proteins

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5
Q

Another name for unconjugated bilirubin

A

Indirect bilirubin

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6
Q

Features of unconjugated bilirubin

A

Water insoluble

High molecular weight

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7
Q

Can unconjugated bilirubin be excreted into urine by the kidneys?

A

No

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8
Q

Where is conjugated bilirubin made?

A

Liver

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9
Q

Features of conjugated bilirubin

A

Low molecular weight

Water soluble

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10
Q

Can conjugated bilirubin be filtered by the kidneys if needed?

A

Yes

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11
Q

Does conjugated bilirubin normally need to be filtered into the urine by the kidneys?

A

No

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12
Q

Where does conjugated bilirubin travel from and to?

A

From bile duct
to bowel
to stomach

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13
Q

What does conjugated bilirubin do to stools?

A

Makes them brown

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14
Q

What particular part of bilirubin makes stools brown?

A

Stercobilin

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15
Q

If excretion of conjugated bilirubin is hindered, what happens?

A

It is excreted in the kidneys making the urine dark

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16
Q

Causes of haemolytic / pre hepatic jaundice

A

Haemolytic anaemia

Post transfusion

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17
Q

In increased RBC destruction, what bilirubin is elevated?

A

Unconjugated

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18
Q

Colour of urine in haemolytic jaundice. Why?

A

Normal

As cannot be filtered

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19
Q

Colour of stool in haemolytic jaundice

A

Normal

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20
Q

LFTS in haemolytic jaundice

A

Serum bilirubin - mainly indirect
ALT and AST - normal
ALP - normal

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21
Q

What does ALP stand for?

A

Alkaline phosphatase

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22
Q

Causes of hepatocellular jaundice

A

Viral hepatitis
Liver cirrhosis and liver cell failure
Drug induced and liver toxins

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23
Q

Two possible pathologies of hepatocellular jaundice

A
  1. Suboptimal function of hepatocytes

2. Degree of intrahepatic biliary obstruction

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24
Q

Pathology of suboptimal function of hepatocytes causing hepatocellular jaundice

A

Suboptimal function of hepatocytes
Bilirubin will be partially conjugated
Increase unconjugated bilirubin due to accumulation, as cannot conjugate the full amount

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25
Q

Pathology of intrahepatic biliary obstruction causing hepatocellular jaundice

A

Inflammation of the hepatocytes so they are swollen / oedematous
So conjugated bilirubin will increase
Urine; dark
Stool colour depends on degree of intrahepatic biliary obstruction
If marked obstruction -> pale stool
If mild obstruction -> may have more normal stool as still have some conjugated bilirubin

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26
Q

LFTs in hepatocellular jaundice

A

Serum bilirubin; direct and indirect
ALT and AST; Markedly increased
ALP; mild increase

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27
Q

What are ALT and AST?

A

Transaminases

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28
Q

What are ALT and AST markers of?

A

Liver cell damage

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29
Q

Where is ALP found?

A

Bile canniculi

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30
Q

What is ALP a marker of?

A

Bile duct obstruction

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31
Q

So if ALP is elevated, what does this indicate?

A

An obstructive process

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32
Q

What is gamma GT elevated in?

A

Obstruction
Alcohol
(therefore less specific)

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33
Q

Where is the first place on the body to present with jaundice and why?

A

Sclera
It has a high affinity for bilirubin
(also last place to get rid of jaundice)

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34
Q

What do you have an increased risk of developing if you have spherocytosis?

A

Gallstones

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35
Q

Causes of obstructive / post hepatic jaundice

A 
Common bile duct stones
Common bile duct strictures
- iatrogenic injury during cholecystectomy
- cholangiocarcinoma
Periampullary malignancy 
Carcinoma of head of pancreas
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36
Q

LFTs in post hepatic / obstructive jaundice

A

Serum bilirubin - mainly direct
ALT and AST - mild increase
ALP - markedly increased

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37
Q

What type of gallstones do you get in haemolytic anaemia?

A

Pigmented

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38
Q

Urine and stool colours in haemolytic jaundice

A

Urine - normal

Stool - normal

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39
Q

Urine and stool colours in hepatocellular jaundice

A

Urine; dark

Stools; either pale or normal

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40
Q

Urine and stool colours in obstructive / post hepatic jaundice

A

Urine; dark

Stools; pale

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41
Q

What does CBD stand for?

A

Common bile duct

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42
Q

Medical obstructive jaundice is caused by what?

A

Intrahepatic biliary obstruction i.e. small duct obstruction

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43
Q

Surgical obstructive jaundice is caused by what?

A

Extrahepatic biliary obstruction I.e. large duct obstruction

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44
Q

Surgical jaundice is further classified into what?

A

Calcular obstructive jaundice

Malignant obstructive jaundice

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45
Q

Presentation of calcular obstructive jaundice

A 
Biliary colic
No weight loss
Fluctuating jaundice
- with intermittent fever, pain and rigors - charcots triad
- pale lemon to bright orange 
Biliary dyspepsia
Dark brown urine 
Pale/clay coloured stool 
Itching often present (scratch marks)
Bradycardia
Gallbladder usually NOT distended (courvoisiers sign)
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46
Q

Presentation of malignant obstructive jaundice

A

Painless / pain continuous epigastric and radiating to back
Weight loss
Progressive jaundice
- deep; could be olive green
Urine dark brown
Stool pale / clay coloured
Itching is marked - scratch marks
Melena (if ulceration of periampullary tumour)
May have enlarged nodular liver (liver mets)
Gallbladder usually distended (Courvoisier’s sign)

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47
Q

Which gender gets calcular obstructive jaundice more?

A

F > M (approx. 40 y/o)

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48
Q

Which gender gets malignant obstructive jaundice more?

A

M > F (> 40 usually)

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49
Q

What is charcots triad?

A

RUQ pain
Jaundice
Fever

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50
Q

Why would the patient be bradycardic in calcular obstructive jaundice?

A

Due to inhibitory effect of the bile salts on the SA node

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51
Q

What is the saying of Courvoisier’s sign?

A

In the prescence of a palpable gallbladder, jaundice is unlikely to be caused by gallstones

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52
Q

How Courvoisiers sign works?

A

Palpable gallbladder = malignancy
Gallstones are formed over a long period of time, which results in a shrunken fibrotic gall bladder which does not distend easily
Therefore the gall bladder is more often enlarged in diseases which causes obstruction of the biliary tree over a shorter period of time such as pancreatic malignancy

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53
Q

What % of renal stones can be seen on plain X Ray compared to gallstones? Why is this?

A

Renal stones - 90%
Gallstones - 10%
Not a lot of calcium in gallstones

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54
Q

What may also be present in spherocytosis and how may this affect management?

A

Hypersplenism

So can get a cholestectomy and a splenectomy

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55
Q

Definition of obstructive jaundice

A

Obstruction in the main biliary tree i.e. CHD, CBD, ampulla of water

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56
Q

What are benign biliary strictures almost always caused by?

A

Cholecystectomy

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57
Q

In patients who present with jaundice, what do you always have to ask about?

A

Previous biliary surgery

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58
Q

What will a head of the pancreas tumour compress? Why?

A

Common bile duct

As some of the duct is in the head of the pancreas

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59
Q

What does calcular obstructive jaundice mean?

A

The stone can move so the symptoms can fluctuate

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60
Q

What colour is jaundice urine, and what would general dark urine mean?

A

Tea coloured

Dark urine just means concentrated

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61
Q

What is biliary dyspepsia?

A

Dyspepsia due to fatty foods

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62
Q

Presentation of pancreatic tail cancer

A

Deep seated pain
Then infiltrates nerve and get back pain
Very vague presentation and so dont see them early

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63
Q

If someone aged 40 - 60 presents with vague upper abdominal pain > 6 weeks which is not getting better with PPIs, send for a what?

A

CT scan

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64
Q

What part of the pancreas if it has a tumour would present the earliest?

A

Even a tiny tumour in the ampulla of vater

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65
Q

What is the key investigation for obstructive jaundice?

A

USS

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66
Q

On USS if there is a dilated biliary tree, what possible investigations could be done next?

A

CT
ERCP
PTC
MRCP

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67
Q

On USS if there is a non dilated biliary tree, what investigation should be done next?

A

Liver biopsy

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68
Q

What % of stones can be visualised in the gallbladder on AUS?

A

98%

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69
Q

What % of stones can be visualised in the common bile duct on AUS?

A

50%

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70
Q

What can AUSS pick up?

A 
Dilated biliary tree
Biliary stones
Pancreatic tumours
Enlarged abdominal lymph nodes
Changes in liver texture e.g. cirrhosis, liver mets
Dilated portal vein
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71
Q

What key investigation is done to look for a dilated biliary tree?

A

USS

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72
Q

What investigations are done to look for tumours/solid masses in pancreas and liver?

A

CT and MRI

73
Q

What can ERCP detect diagnostically?

A

Filling defects
Biliary stricture
Dilated biliary tree
Cytology and biopsy

74
Q

Where does ERCP travel from and to?

A

Scope from oesophagus to 2nd part of duodenum

75
Q

What are the therapeutic reasons for ERCP?

A

Endoscopic sphincterectomy

Biliary stent

76
Q

What is endoscopic sphincterectomy?

A

Cut to get the stone out

77
Q

How does the stent work?

A

To drain the CBD
Metal - used for malignant
Plastic - used for benign

78
Q

If there is multiple filling defects, what does this indicate?

A

Gallstones are not the cause

79
Q

Complications of ERCP

A

Cholangitis
Pancreatitis
Bleeding
Perforation (bile duct / duodenum)

80
Q

Where is the stricture located that is typical of post cholecystectomy?

A

Where the cystic duct goes in to the common bile duct

81
Q

What % get post ERCP pancreatitis? Is it serious?

A

3%

Can be fatal

82
Q

What type of therapy is ERCP reserved for at the moment?

A

Therapeutic

83
Q

What does PTC stand for?

A

Percutaneous transhepatic cholangiography

84
Q

How does PTC work?

A

AUSS to find dilated bile duct
Inject die
Then can see swelling and blockage

85
Q

Diagnostic indications for PTC

A

Allows visualisation of the proximal biliary tree

86
Q

Therapeutic indications for PTC

A

Transhepatic placement of biliary stents

87
Q

Complications of PTC

A

Bleeding (liver)
Biliary peritonitis
Cholangitis

88
Q

Contraindications to PTC

A

Bleeding tendency

89
Q

Why does biliary peritonitis occur?

A

Low resistance track for a high pressure system

90
Q

ERCP vs PTC in what they can visualise

A

ERCP - anatomy DISTAL to obstruction

PTC - anatomy PROXIMAL to obstruction

91
Q

What does MRCP stand for?

A

Magnetic resonance cholangiopancreaticography

92
Q

What is MRCP?

A

A non invasive assessment of CBD

93
Q

What can MRCP visualise?

A

CBD stones

Biliary strictures

94
Q

3 possible outcomes when carried out an USS for obstructed jaundice

A
  1. Dilated CBD with gallstones in gallbladder
  2. Dilated CBD with no gallstones
  3. Non dilated CBD with gallstones
95
Q

Next steps once see a dilated CBD with gallstones in gallbladder on USS

A

Do MRCP
If shows a stone in the bile duct, then ERCP
If no clear stone, then do not do ERCP

96
Q

Next steps once see a dilated CBD with no gallstones on USS

A

Think tumour
Do CT
Then ERCP

97
Q

Next steps once see a non dilated CBD with gallstones present on USS

A

Gallstones very small that spontaneously passes
LFTs take 2- 3 weeks to get back to normal
Do MRCP
If negative, then do EUS

98
Q

Indications for a pancreatico-biliary endoscopic ultrasound (EUS)

A

Small (< 3cm) pancreatic tumours and ampullary neoplasms
Small ( < 4 mm) bile duct stones
To define vascular invasion in pancreatic and peri ampullary neoplasms
EUS FNA

99
Q

What does OTC stand for?

A

On table cholangiogram

100
Q

Indications for OTC

A

Suspected CBD stones

Verification of the biliary anatomy during cholecystectomy

101
Q

Points to establish during OTC

A

Complete visualisation of the billiard tree (proximal and distal)
No filling defects
No strictures
Free flow of contrast into the duodenum

102
Q

Risk factors for operative management

A

Bleeding tendency
Infections
Renal failure
Hepatic failure

103
Q

Definition of choledocholithiasis

A

Common bile duct stones

104
Q

Why do people with obstructive jaundice have a higher risk of bleeding in surgery?

A

If no bile -> cannot absorb fat soluble vitamins (e.g. vitamin K)

105
Q

What are the vitamin K dependent factors and what is a way to remember this?

A

2, 7, 9, 10

1972

106
Q

How must vit K be given in obstructive jaundice?

A

IV

107
Q

How long does vit K take to work?

A

6 - 8 hours

108
Q

What is obstructive jaundice extremely sensitive to?

A

Dehydration

109
Q

How long would it take to have hepatic failure after obstruction?

A

< 4 weeks

110
Q

What % of bile duct stones can CT pick up?

A

50%

111
Q

Treatment options for choledocholithiasis

A
  1. ERCP, endoscopic sphincterotomy (ES) and CBD stone extraction, followed by laparoscopic cholecystectomy
  2. Cholecystectomy, CBD exploration, stone extraction and T tube insertion (laparoscopic / open)
112
Q

Cause of traumatic bile duct strictures

A

Previous cholecystectomy

113
Q

Presentation of traumatic bile duct strictures

A

Complete - post op jaundice

Partial - intermittent cholangitis and jaundice

114
Q

Treatment of traumatic bile duct strictures

A

Biliary stent

Roux-en-Y hepatico-jejunostomy

115
Q

Cause of malignant bile duct strictures

A

Cholangiocarcinoma

116
Q

Presentation of malignant bile duct obstruction

A

Obstructive jaundice

117
Q

Treatment of malignant bile duct obstruction

A

If operable
- resection and biliary reconstruction
If inoperable
- CBD stent

118
Q

What is a klatskin tumour?

A

Hilar cholangiocarcinoma at the bifurcation of the common hepatic duct

119
Q

Treatment of pancreatic head tumour

A

Pancreatioduodenectomy (Whipples procedure)

Reconstruction

120
Q

What is a whipples procedure?

A 
Pancreaticoduodenectomy
Involves removing
- CBD
- Gallbladder
- Duodenum 
- Head of pancreas
121
Q

Treatment of inoperable pancreatic carcinomas

A

Internal biliary stent placed by ERCP or PTC to relief jaundice
Duodenal stent or laparoscopic gasrojejunosomty for relief of gastric outlet obstruction

122
Q

Functions of liver

A 
Synthetic function 
- clotting factors
- bile acids
- carbohydrates
- proteins - albumin
- lipids (cholesterol, lipoprotein, TG)
- hormones (angiotensin, insulin like growth factor)
Detoxification 
- bilirubin metabolism 
- urea production from ammonia
- detoxification of drugs
- breakdown of insulin and hormones 
Immune function 
Storage function
- glycogen 
- vit A, D, B12 and k 
- copper
- iron
123
Q

Differential diagnosis of jaundice

A

Carotenemia

124
Q

Where is ALP also present?

A

Bone
Placenta
Intestines

125
Q

What is gamma GT?

A

Non specific liver enzyme

126
Q

What is albumin levels an important test for?

A

Synthetic function of the liver

127
Q

What produces albumin?

A

Liver

128
Q

Causes of hypoalbumineria

A

Liver problems
Kidney disorders
Malnutrition

129
Q

What does prothrombin time tell you about the liver?

A

Degree of liver dysfunction

130
Q

What does platelet count have to do with the liver?

A

Liver important source of thrombopoietin

Thrombopoietin drives bone marrow to produce platelets

131
Q

What are low platelets an indirect marker for? Why?

A

Portal hypertension

As cirrhosis results in splenomegaly, which chews up all the platelets and decreases their count

132
Q

4 symptoms of liver failure

A

Jaundice
Ascites
Variceal bleeding
Hepatic encephalopathy

133
Q

What is ascites?

A

Accumulation of fluid in the belly

134
Q

What is variceal bleeding?

A

Bleeding from engorged veins

135
Q

What is hepatic encephalopathy?

A

Build up of toxins in the brain due to a failed liver that results in deteriorated brain function

136
Q

Definition of chronic liver disease

A

Liver disease that persists over 6 months

137
Q

Examples of chronic liver diseases

A 
Chronic hepatitis
Chronic cholestasis
Fibrosis and cirrhosis
Steatosis
Liver tumours
138
Q

Causes of liver cirrhosis

A 
Alcohol 90% 
Autoimmune 
- autoimmune hepatitis
- PBC
- PSC
Hemochromatosis
Chronic viral hepatitis B and C
NAFLD
Drugs - MTX, amiodarone
CF
a-1 antitrypsin deficiency 
Wilsons disease
Portal HTN +/- liver disease
Cryptogenic 
Sarcoidosis
Amyloid
Schistosomiasis
139
Q

Possible types of presentation of cirrhosis

A 
Compensated chronic liver disease
- screening tests
- abnormality of LFTs
Decompensated chronic liver disease
- ascites
- variceal bleeding 
- hepatic encephalopathy
Hepatocellular carcinoma
140
Q

Clinical features of ascites

A

Dullness in flanks
Shifting dullness (approx. 1500cc)
USS can detect up to 100cc

141
Q

Supporting features of decompensated liver failure

A 
Ascites
Hepatic encephalopathy 
Variceal bleeding 
Spider naevi 
Palmar erythema 
Abdominal veins 
Fetor hepaticus 
Umbilical nodule
JVP elevation 
Flank haematoma
142
Q

What does the liver convert oestrogen to?

A

Testosterone

143
Q

A disproportionate amount of oestrogen due to liver failure can lead to what?

A

Palmar erythema
Spider naevi
Gynaecomastia

144
Q

Investigations of acites

A

New onset ascites - paracentesis
Protein and albumin concentration
Cell count and differential
SAAG - serum ascites albumin gradient

145
Q

Levels of SAAG and what they are suggestive of?

A 
High = liver disease
Low = not liver disease
146
Q

If levels of SAAG > 1.1g/dl, what could be causing the ascites?

A 
Portal HTN
CHF
Constrictive pericarditis 
Budd Chiarri 
Myxoedema 
Massive liver metastases
147
Q

What is budd chiarri?

A

VERY RARE

Occlusion of hepatic veins that drain the liver

148
Q

If levels of SAAG < 1.1g/dl, what could be causing the ascites?

A 
SLOW - suggestive of an infiltrative condition e.g. malignancy
Malignancy 
TB
Chylous ascites
Pancreatic 
Biliary ascites
Nephrotic syndrome
Serositis
149
Q

What is chylous ascites?

A

Milky chyle in peritoneal cavity

150
Q

Treatment of ascites

A 
Diuretics
Large volume paracentesis 
TIPS
Aquaretics
Liver transplant if all else fails
151
Q

What Is TIPS?

A

Shunts that puncture the intrajugular vein and go into the liver and through the IVC and the shunt into the liver takes care of the blockage. Portal pressure comes down and ascites will get better

152
Q

What is aquaresis?

A

Excretion of water without electrolyte loss

153
Q

Causes of varices

A

Portal HTN

154
Q

Where do varices occur?

A

At porto-systemic anastomoses

  • skin (caput medusae)
  • oesophageal
  • gastric
  • rectal
  • posterior abdominal wall
  • stomal
155
Q

Treatment of variceal haemorrhage

A 
Resuscitate patient 
Blood transfusion as required 
Endoscopic band ligation 
Terlopressin for control 
Sengstaken blaken tube for uncontrolled bleeding
TIPSS for rebleeding after banding
156
Q

Precipitants of hepatic encephalopathy

A 
GI bleed
Infection 
Constipation 
Dehydration 
Medication
157
Q

Treatment of hepatic encephalopathy

A

Treat the cause;

  • Laxatives - phosphase enemas and lactulose
  • broad spec abtibiotics
158
Q

What is an indicator for liver transplant?

A

Repeated admissions with hepatic encephalopathy

159
Q

What is the commonest cause of liver cancer?

A

Hepatocellular carcinoma

160
Q

What does hepatocellular carcinoma occur in the background of?

A

Cirrhosis

161
Q

What does hepatocellular carcinoma occur in association with?

A

Chronic hepatitis B and C

162
Q

Presentation of hepatocellular carcinoma

A 
Decompensation (deterioration) of liver disease
Abdominal mass
Abdominal pain 
Weight loss
Bleeding from tumour
163
Q

Investigations for hepatocellular carcinoma

A

Tumour markers; AFP
USS
CT
MRI

164
Q

What is done to everyone with liver cirrhosis?

A

Get put on surveillance programme, every 6 months will come in and get investigations checking for hepatic cancer

165
Q

Treatment of hepatocellular carcinoma

A 
Hepatic resection 
Liver transplantation 
Chemotherapy 
Locally ablative treatments
- alcohol injection 
- radiofrequency ablation 
Sorafenib (tyrokinase inhibitor)
Hormonal therapy; tamoxifen 
Palliative options
166
Q

What are all of the investigations that can be done of the liver?

A 
Hep B and C serology 
Autoantibody profile
Serum immunoglobulins 
Caeruloplasmin and copper 
Ferritin and transferrin saturation 
Alpha 1 anti trypsin 
Fasting glucose
Lipid profile
167
Q

What is the first test to be done with anyone with jaundice?

A

USS

168
Q

Clues in the history/examination which would point to pre hepatic jaundice

A 
Fatigue 
Dyspnoea
Chest pain 
Alcohol 
Pallor
Splenomegaly
169
Q

Clues in the history which would point to hepatic jaundice

A 
IVDU 
Drug intake
Ascites
Variceal bleeding
Encephalopathy 
Spider naeivi 
Gynaecomastia
Asterixis
170
Q

Clues in the history which would point to post hepatic jaundice

A 
Abdominal pain 
Pruritus 
Pale stools
Dark coloured urine
Possible Courvoisier's sign
171
Q

Definition of asterixis

A

Flapping tremor due to liver failure

172
Q

Inheritance of gilberts syndrome

A

Autosomal recessive

173
Q

What is gilberts syndrome?

A

An autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase

174
Q

Presentation of gilberts syndrome

A 
Unconjugated hyperbilirubinaemia 
Jaundice may only be seen during
- exercise
- fasting
- intercurrent illness
175
Q

Investigations of gilbert syndrome

A

Rise in bilirubin after a prolonged fast or IV nicotinic acid

176
Q

Treatment of gilbert syndrome

A

No management required

177
Q

What two vessels are connected in TIPS?

A

Hepatic vein and portal vein

178
Q

Treatment of patients with ascites secondary to liver cirrhosis

A

Spironolactone

Gastrointestinal Pathology (26 decks)

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