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Residency Exam > Biochemical Tests for Liver function/Dysfunction (Panopto Video File) > Flashcards

Biochemical Tests for Liver function/Dysfunction (Panopto Video File) Flashcards

1
Q

What is the body’s main serum-binding protein?

A

Albumin

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2
Q

What is albumin?

A

A natural plasma protein which is synthesised almost exclusively produced by the liver

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3
Q

What is the usual rate of albumin production by the liver in a healthy patient?

A

9 to 14 grams a day

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4
Q

What is the median half-life of albumin in the body of a healthy patient?

A

20 days

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5
Q

How is albumin broken down in the body?

A

It is broken down by most organs in the body at a similar rate

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6
Q

What is the reference range for albumin?

A

40 to 60 g/L

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7
Q

What is the primary physiological determinant of colloidal osmotic pressure?

A

Albumin

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8
Q

How may hepatic insufficiency affect serum albumin?

A

Hepatic insufficiency may lead to a decrease in serum albumin

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9
Q

Approximately what percentage of the total body pool of albumin is produced in a day?

A

3%

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10
Q

What are 3 main roles of albumin?

A
  1. Binding of drugs
  2. Transport of hormones
  3. Maintenance of colloidal osmotic pressure
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11
Q

How does nephrotic syndrome affect serum albumin?

A

Nephrotic syndrome leads to a reduction in serum albumin

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12
Q

What is the mechanism by which nephrotic syndrome leads to a reduction in serum albumin?

A

By potentiating albumin loss via the kidneys

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13
Q

Is albumin typically lost through the glomerulus?

A

No

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14
Q

Why is albumin not typically lost through the glomerulus?

A

As it is too large

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15
Q

What are 3 causes of low serum albumin?

A
  1. Hepatic insufficiency
  2. Nephrotic syndrome
  3. Poor nutritional intake
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16
Q

Where is all albumin in the body produced?

A

In the liver

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17
Q

How is albumin distributed throughout the body?

A

It is distributed across both the intravascular fluid (plasma) and interstitial fluid

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18
Q

What is the mean volume of intravascular fluid (plasma) in a healthy adult?

A

3 L

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19
Q

What is the mean volume of interstitial fluid in a healthy adult?

A

10 L

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20
Q

Is the concentration of albumin greater in the intravascular fluid (plasma) or interstitial fluid?

A

Intravascular fluid (plasma)

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21
Q

What is the usual concentration of albumin in the intravascular space (plasma)?

A

40 g/L

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22
Q

What is the concentration of albumin in the interstitial space?

A

18 g/L

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23
Q

What does total protein encompass as a liver function test?

A

Albumin, globulins and fibrinogen

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24
Q

What is the principal protein in the plasma?

A

Albumin

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25
Q

What is the role of fibrinogen?

A

Clotting factors

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26
Q

What are 3 examples of formed elements?

A
  1. red blood cells
  2. white blood cells
  3. platelets
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27
Q

What is a common cause of Hyperglobulinaemia?

A

hypoalbuminemia (a characteristic picture of liver disease)

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28
Q

Why do serum globulins tend to increase when serum albumin decreases?

A

As a compensatory mechanism

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29
Q

What is the role of globulins?

A

They are the basis for antibodies, glycoproteins, lipoproteins and clotting factors

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30
Q

What are the 3 main groups of globulins?

A

alpha, beta and gamma globulins

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31
Q

What is the role of nutrition in total protein concentration?

A

serum albumin and globulins are markers of nutrition

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32
Q

What are 2 examples of patients who will commonly have low total protein levels?

A
  1. Malnourished patients (particularly post surgery)
  2. Patients with burns or other protein-losing syndromes
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33
Q

What are two reasons clotting factors may be reduced in the body?

A

Due to primary liver cell failure or Vitamin K deficiency

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34
Q

What is a good prognostic marker for liver function?

A

Prothrombin time

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35
Q

Why is prothrombin time a good prognostic marker for liver disease?

A

Prolonged prothrombin time indicates severe liver damage

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36
Q

Why is prothrombin time a good prognostic marker for liver disease?

A

Prolonged prothrombin time indicates severe liver damage

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37
Q

What is a common cause of vitamin K deficiency?

A

Malnourishment/malabsorption

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38
Q

what is the relationship between the half life of clotting factors and albumin?

A

Clotting factors typically have a shorter half life and albumin

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39
Q

How does the half life of clotting factors relate to the usefulness of prothrombin time as a prognostic marker in liver disease?

A

Because clotting factors have a shorter half life than albumin, this can help a clinician to assess both acute and chronic liver disease

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40
Q

What is the relationship between prothrombin time and INR?

A

INR is a standardised form of prothrombin time

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41
Q

What are 4 markers of synthethic liver function?

A
  1. INR
  2. Prothrombin time
  3. Albumin
  4. Globulins
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42
Q

What are 4 markers of synthethic liver function?

A
  1. INR
  2. Prothrombin time
  3. Albumin
  4. Globulins
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43
Q

For drug induced liver injury, is it more common to look at markers of liver damage, or synthetic function of the liver?

A

Markers of liver injury

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44
Q

What is a hepatocellular disorder characterised by?

A

Damage to hepatocytes

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45
Q

What is cholestasis (or an obstructive liver disorder)?

A

A clinical and biochemical syndrome that results when bile flow is impaired

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46
Q

How can hepatocellular damage lead to cholestasis?

A

The inflammation caused by hepatocellular damage can block bile flow

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47
Q

How can cholestasis lead to hepatocellular damage?

A

If blockage has been present for long enough, eventually there will be damage to the hepatocytes as a result.

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48
Q

Which three LFTs are most present in the hepatocytes?

A

ALT, AST and LDH

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49
Q

Which two LFTs are most commonly found in the bile canaliculi?

A

GGT and ALP

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50
Q

What is the mechanism by which bile flow obstruction leads to LFTs derrangement?

A

When bio flow is obstructed, ALP and GGT leak into the blood sinusoid, increasing their concentration in the blood.

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51
Q

What is the mechanism by which hepatocellular damage leaves to LFT derangement?

A

When hepatocytes rupture, they release their intracellular enzymes (ALT, AST and LDH) into the bloodstream

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52
Q

where is alkaline phosphatase found in the body?

A

In the liver bones and gut

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53
Q

What is the specific application for LFTs in pregnancy?

A

The placenta produces large amounts of alkaline phosphatase in the third trimester

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54
Q

what is the role of alkaline phosphatase in the body?

A

It’s exact metabolic function is unclear but it does play an important role in the calcification of bone

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55
Q

What is the disorder other than liver disorder which can lead to an increase in alkaline phosphatase?

A

Disorders involving bone, such as Paget’s disease, fractures, hyperparathyroidism, and tumours

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56
Q

If alkaline phosphatase is elevated in isolation, what is the usual cause?

A

A bone disorder

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57
Q

What is a useful way to determine if alkaline phosphatase elevation is the result of cholestasis?

A

Look at other markers of cholestasis such as GGT and bilirubin

58
Q

What are three causes of cholestasis?

A

Gallstones, tumours and alcoholic hepatitis

59
Q

describe the sensitivity of alkaline phosphatase as a marker of hepatic obstruction

A

It is very sensitive indicator of both intra-hepatic and extrahepatic obstruction

60
Q

When biliary obstruction is incomplete, what is the usual range of ALP?

A

2 to 3 times the upper limit of normal

61
Q

When biliary obstruction is incomplete, what is the usual range of ALP?

A

2 to 3 times the upper limit of normal

62
Q

When biliary obstruction is complete, what is the usual range of ALP?

A

3 to 8 times the upper limit of normal

63
Q

GGT is a catalyst for what reaction in the body?

A

The transfer of a glutamyl group from one peptide to another

64
Q

Where is GGT stored in the body?

A

In the liver, kidneys and pancreas

65
Q

What is a common cause of an isolated elevation of GGT?

A

Induction (without liver damage)

66
Q

What are 5 drugs which can raise GGT without causing liver damage (through induction)?

A
  1. ethanol
  2. phenytoin
  3. phenobarbitone
  4. carbamazepine
  5. rifampicin
67
Q

Describe the magnitude of GGT elevation caused by induction due to chronic ethanol intake?

A

This may give elevations up to 200 to 400U/L

68
Q

How can LFTs denote that ethanol is causing hepatocellular damage?

A

The ALT begins to rise (usually when GGT > 250 to 400U/L)

69
Q

Describe the presentation of GGT elevation in cholestatic liver disease

A

There is a parallel increase in GGT and ALP in both intrahepatic and extrahepatic cholestasis

70
Q

Where is ALT produced?

A

Within hepatocytes

71
Q

Describe the sensitivity of ALT for liver tissue

A

Is it very specific for hepatic tissue

72
Q

How does ALT typically rise in hepatocellular damage?

A

They tend to rise faster and higher than AST

73
Q

When do ALT levels tend to rise?

A

ALT concentrations rarely increase except for in parenchymal liver disease

74
Q

What is the role of aspartate aminotrasnfebase in the body?

A

It is responsible for the transfer of amino groups in gluconeogenesis

75
Q

Where are concentrations of AST highest?

A

In the heart and the liver

76
Q

When do AST levels rise?

A

AST levels rise in all forms of liver disease reflecting either hepatocellular or cholestatic changes

77
Q

What is usually suspected if AST is elevated in isolation?

A

Myocardial infarction

78
Q

In alcoholic liver disease, what is the usual AST:ALT ratio range?

A

Typically > 2

79
Q

Why is the AST:ALT ratio typically > 2 in alcoholic liver disease?

A

Due to a reduction in ALT activity which may be attributed to vitamin B6 deficiency or mitochondrial damage, leading to increased release of AST

80
Q

What is the usual range of AST in alcoholic liver disease?

A

100-200 U/L

81
Q

Is ALT always elevated in alcoholic liver disease?

A

No

82
Q

Why is ALT not always elevated in alcoholic liver disease?

A

Due to the prior death of functional liver cells i.e. there is no ALT left to release

83
Q

If AST is > 500 or ALT is > 200, what may this suggest?

A

A magnitude this great is usually not attributable to alcoholic hepatitis alone, and thus there is usually another cause

84
Q

What is the role of LDH in the body?

A

It catalyses the conversion of pyruvate to lactate to generate ATP

85
Q

Where is LDH found?

A

In cardiac and skeletal muscle, liver, kidneys, lungs and red blood cells

86
Q

How many isoenzymes does LDH have?

A

5

87
Q

Where are LDH1 and LDH2 typically found?

A

In the heart and red blood cells

88
Q

Where are LDH1 and LDH2 typically found?

A

In the heart and red blood cells

89
Q

Where are LDH1 and LDH2 typically found?

A

In the heart and red blood cells

90
Q

Where are LDH4 and LDH5 typically found?

A

In the skeletal muscle and liver

91
Q

What does LDH stand for?

A

Lactate Dehydrogenase

92
Q

What is the important point to note when interpreting LDH as a liver function test?

A

It is not specific

93
Q

What may an isolated elevation of LDH be reflective of?

A

Red blood cell haemolysis

94
Q

Which two LFTs are typically elevated in a myocardial infarct?

A

LDH and AST

95
Q

When is LDH elevated in hepatic conditions?

A

In hepatocellular disorders, primary and secondary liver malignancies and in infectious mononucleosis

96
Q

When is LDH elevated in non-hepatic conditions?

A

It is also elevated in rhabdomyolysis and myocardial infarction

97
Q

When is LDH elevated in non-hepatic conditions?

A

It is also elevated in rhabdomyolysis and myocardial infarction

98
Q

When are ALT, AST and LD elevated?

A

They are relaased in to the blood whenever hepatocellular damage occurs

99
Q

What are 3 examples of causes of hepatocellulalr damage

A
  1. Viral hepatits
  2. toxin-induced damage (i.e. alcohol, drugs, etc)
  3. hypoxic hepatitis (CCF, severe repiartory disease, hypotension)
100
Q

Which LFT is always elevated in a hepatocellular disorder?

A

ALT

101
Q

Which 2 LFTs are elevated in cholestasis or obstructive disorder?

A

ALP and GGT

102
Q

What is the relationship between bilirubin and red blood cells?

A

Bilirubin is a major breakdown product of haemoglobin

103
Q

What enzymes are responsible for the breakdown of senescent red blood cells?

A

Phagocytes

104
Q

What are the three main breakdown products of red blood cells?

A

Globin, Heme, and iron

105
Q

What is the primary breakdown product of heme?

A

Bilirubin

106
Q

What occurs to bilirubin after it is formed by the breakdown of heme?

A

It is bound to albumin and transferred to the liver

107
Q

How is free biliruin made more water soluble so it can be excreted into the bile?

A

It is conjugated with glucuronic acid

108
Q

What is the name for bilirubin which has been conjugated with glucuronic acid?

A

Conjugated bilirubin

109
Q

Which form of bilirubin is excreted into the bile?

A

Conjugated bilirubin

110
Q

Where is the site of bilirubin conjugation to glucuronic acid?

A

The liver

111
Q

Which organ is the site of red blood cell haemolysis to form bilirubin, heme, etc?

A

The spleen

112
Q

Is unconjugated bilirubin soluble or insoluble?

A

Insoluble

113
Q

What is done to unconjugated bilirubin to make it soluble?

A

It is bound to serum albumin

114
Q

What occurs to bilirubin once it is bound to albumin?

A

It is transported to the liver where it is conjugated with two molecules of glucuronic acid

115
Q

What is unconjugated bilirubin also called?

A

Indirect bilirubin

116
Q

What occurs to conjugated bilirubin once it has been conjugated with two molecules of glucuronic acid?

A

It is secreted into the small intestine via the bile

117
Q

What occurs to conjugated bilirubin once it has been secreted into the small intestine via the bile?

A

It is converted to bilinogen by gut flora

118
Q

What are three potential pathways bilinogen may follow?

A

It can be reabsorbed into the bloodstream where it is excreted into the urine to give urobilinogen, it can be taken back to the liver, or it can be excreted into the faeces

119
Q

What are three potential pathways bilinogen may follow?

A

It can be reabsorbed into the bloodstream where it is excreted into the urine to give urobilinogen, it can be taken back to the liver, or it can be excreted into the faeces

120
Q

What gives urine its classic straw colour?

A

Urobilinogen

121
Q

What is bilinogen in the faeces called?

A

Stercobilinogen

122
Q

What gives faeces its stereotypical dark brown colour?

A

Stercobilinogen

123
Q

What is conjugated bilirubin also called?

A

Direct bilirubin

124
Q

What is unconjugated bilirubin also called?

A

Indirect bilirubin

125
Q

Once bilirubin is covalently conjugated with glucuronic acid, what is formed?

A

Direct bilirubin

126
Q

Direct (or conjugated) bilirubin makes up about what fraction of total bilirubin?

A

Around a third

127
Q

Is it common in practice to assess the direct to indirect bilirubin ratio?

A

No

128
Q

What is total bilirubin the sum of?

A

All conjugated (direct) bilirubin and unconjugated (indirect) bilirubin

129
Q

Is there a particular form of bilirubin (i.e. conjugated or unconjugated) which tends to rise in liver disease?

A

It can be either

130
Q

When do bilirubin levels tend to rise?

A

They can rise in almost any liver disease

131
Q

What are three causes of unconjugated hyperbilirubinaemia?

A
  1. Increased load
  2. Immature liver
  3. Congenital disease of bilirubin transport
132
Q

What are two examples of causes of increase bilirubin load contributing to unconjugated hyperbilirubinaemia?

A

Haemolysis
Ineffective erythropoiesis

133
Q

What is an example of liver immaturity which can lead to unconjugated hyperbilirubinaemia?

A

Neonatal physiological jaundice

134
Q

What is an example of a congenital disease of bilirubin transport leading to unconjugated hyperbilirubinaemia?

A

Gilbert’s syndrome

135
Q

What is the most common cause of conjugated hyperbilirubinaemia?

A

Any cause of cholestasis causing backflow of bilirubin into the blood stream

136
Q

When are very high levels of conjugated bilirubin typically seen?

A

In biliary obstruction (i.e. obstructive jaundice)

137
Q

What is a rare cause of conjugated hyperbilirubinaemia?

A

It is also seen in rare congenital conditions

138
Q

If conjugated hyperbilirubinaemia is constant, what is the common cause?

A

Malignancy

139
Q

If conjugated hyperbilirubinaemia is fluctuating, what are the common causes?

A

Stones, strictures, inflammation, etc

140
Q

Why does it make sense that conjugated hyperbilirubinaemia is more common in chlestatic disease?

A

The liver is still conjugated glucuronic acid to the bilirubin, it just can’t facilitate appropriate flow of it to the intestine via the bile and thus it flows back into the blood

Residency Exam (22 decks)

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