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Gastrointestinal System > Liver Dysfunction & Bilirubin Metabolism > Flashcards

Liver Dysfunction & Bilirubin Metabolism Flashcards

1
Q

What are the functions of the liver?

A

Key role in iontemediary metabolism
Synthetic function
Detoxification & Excretion
Storage function
Production of bile salts

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2
Q

What metabolic processes is the liver involved in?

A

Gluconeogenesis
Glycolysis
Ketogenesis

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3
Q

What synthetic functions does the liver have?

A

Plasma proteins
Coagulation factors
Cholesterol
Triglycerides
Lipoporoteins

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4
Q

What detox and excretion processes is the liver involved in?

A

Urea cycle (Ammonia to urea)
Bilirubin
Cholesterol
Drug metabolites

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5
Q

Which substances does the liver store?

A

Vitamins A, D, E and K and B12

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6
Q

What is the function of production of bile salts?

A

Helps with digestion

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7
Q

What is cholestasis?

A

Bile cannot flow from the liver to the duodenum

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8
Q

What is jaundice?

A

Yellow or greenish pigmentation of the skin and whites of the eyes due to high levels of bilirubin

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9
Q

What is hepatitis?

A

Inflammation of the liver tissue

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10
Q

What is cirrhosis?

A

Liver does not function properly due to long-term damage characterised by the replacement of normal liver tissue by scar tissue

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11
Q

What is steatosis?

A

Abmormal retention of lipids within a cell

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12
Q

What is hemochromatosis?

A

Iron storage overload

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13
Q

What are liver function tests?

A

Noninvasive methods of screening for liver dysfunction

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14
Q

What are the functions of liver function tests?

A

Help in identifying general types of liver disease
Assess severity and allow prediction of outcome
Help in monitoring the treatment of the disease

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15
Q

What are the two broad categories of liver tests?

A

Tests to assess hepatic function
Tests to detect hepatic injury

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16
Q

What is Group I of LFTs?

A

Markers of liver dysfunction

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17
Q

What are the markers of liver dysfunction?

A

Serum bilirubin
Urine
Total protein, serum albumin, and albumin/globulin ratio
Prothrombin time

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18
Q

What do you measure within serum bilirubin?

A

Total and conjugated

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19
Q

What do measure within the urine test of Group I LFTs?

A

Bile salts and urobilinogen

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20
Q

What are Group II LFTs?

A

Markers of hepatocellular injury

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21
Q

What are the markers of hepatocellular injury?

A

ALT & AST

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22
Q

What are Group III LFTs?

A

Markers of cholestasis

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23
Q

What are the markers of cholestasis?

A

ALP
GGT

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24
Q

What are the limitations of LFTs?
Why?

A
  1. Normal LFT values do not always indicate the absence of liver disease
    Because the liver has a very large reserve capacity
  2. Asymptomatic people may have abnormal LFT results
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25
Q

What is serum albumin?

A

The most abundant protein in mammals

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26
Q

Where is serum albumin synthesised?

A

The liver

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27
Q

What gene encodes serum albumin?

A

ALB gene

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28
Q

Where is serum albumin dissolved?

A

In the blood stream

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29
Q

What is the function of serum albumin?

A

Primarily a carrier protein for unconjugated bilirubin, steroids, fatty acids and thyroid hormones

Also plays a key role in stabilising extracellular fluid volume by contributing to the osmotic pressure of the plasma

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30
Q

What are the normal levels of serum albumin?

A

3.5 to 5.5 g/L

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31
Q

What does the synthesis of serum albumin depend on?

A

The extent of functioning liver cell mass

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32
Q

What is the half life of serum albumin?

A

20 days

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33
Q

In which pathology does the serum albumin levels always decrease?

A

Chronic liver diseases

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34
Q

What is the difference between globulins and albumins?

A

Globar proteins with higher molecular weights than albumins
Insoluble in pure water but dissolve in dilute salt solutions

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35
Q

Where are α & β globulins synthesised?

A

By the liver

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36
Q

What are the normal serum levels of globulins?

A

16 to 30 g/L

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37
Q

Which globulins are known as antibodies?

A

Active γ globulins

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38
Q

High serum levels of IgG are observed in which pathologies?

A

Autoimmune hepatitis

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39
Q

High serum levels of IgA are observed in which pathologies?

A

Alcoholic liver disease

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40
Q

What is prothrombin?

A

A market of liver function

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41
Q

Where is prothrombin synthesised?

A

In the liver

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42
Q

What is prothrombin converted into and when?

A

Thrombin during coagulation

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43
Q

What is the half-life of prothrombin?

A

6 hours

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44
Q

What is prothrombin time?

A

A blood test that measures how long it taken blood to clot

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45
Q

What is the reference range for PT?

A

12 to 16 seconds

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46
Q

When is PT prolonged?

A

When liver loses more than 80% of its reserve capacity

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47
Q

What are other causes of prolonged PT?

A

Vitamin K deficiency, however, intake of vitamin K has no effect in the case of liver disease

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48
Q

Where is ALT found?

A

Plasma and in various body tissues but most common in the liver

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49
Q

What is the function of ALT?

A

Reversible transfer of an amino group from L-alanine to α-ketoglutarate

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50
Q

Which transferase is liver-specific enzyme?

A

ALT more than AST

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51
Q

What is the normal range of ALT?

A

10 to 55

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52
Q

What do high elevations of ALT indicate?

A

Acute hepatitis

53
Q

What do moderate elevations of ALT indicate?

A

Alcoholic hepatitis

54
Q

What do minor elevations of ALT indicate?

A

Cirrhosis, hepatitis C, non-alcoholic steatohepatitis

55
Q

In what cases might ALT levels be elevated but there the individuals are healthy?

A

In obese but otherwise healthy individuals

56
Q

What is the function of AST?

A

Reversible transfer of an amino group from aspartate to α - Ketoglutarate

57
Q

What is the normal range of AST?

A

10 to 40

58
Q

Where is AST found?

A

In the liver, skeletal muscle, myocardium, kidney, pancreas and RBCs

59
Q

What is AST?

A

A marker of hepatocellular damage

60
Q

In what cases are there high levels of AST?

A

Chronic hepatitis, cirrhosis and liver cancer

61
Q

What is ALP?

A

A homodimeric protein enzyme, containing two zinc atoms crucial to its catalytic function

62
Q

What is the optimal environment for ALP?

A

Optimally active in alkaline pH environments

63
Q

What is ALP’s function under alkaline environments?

A

To dephosphorylate compounds

64
Q

Is ALP a specific or non-specific marker of liver disease?

A

Non-specific

65
Q

Where is ALP produced?

A

In bone osteoblasts

66
Q

What other structures is ALP present on?

A

Hepatocyte membranę

67
Q

What is the normal range of ALP?

A

45 to 115

68
Q

When is moderate elevation of ALP seen?

A

Infective hepatitis, alcoholic hepatitis, and hepatocellular carcinoma

69
Q

When is high elevation of ALP seen?

A

Obstructive jaundice and interhepatic cholestasis

70
Q

When is very high elevation of ALP seen?

A

Bone disease

71
Q

What is GGT?

A

Transferase that catalyses the transfer of gamma-glutamyl functional groups from molecules like glutathione to an acceptor that may be an amino acid or peptide

72
Q

What is the function of GGT?

A

Key role in gamma-glutamyl cycle

73
Q

What is gamma-glutamyl cycle?

A

A pathway for the synthesis and degradation of glutathione as well as the drug and xenobiotic detox

74
Q

Where is GGT found?

A

Microsomal enzyme in hepatocytes and epithelium of small bile ducts and pancreas, kidney and intestines

75
Q

What is the normal range of GGT?

A

15 to 85

76
Q

When is moderate elevation of GGT seen?

A

Infective hepatitis and prostate cancers

77
Q

In which cases is GGT increased despite normal liver functions?

A

In alcoholics, highly sensitive to detecting alcohol abuse

78
Q

What is bilirubin?

A

A yellow bile pigment

79
Q

What is bilirubin responsible for?

A

The yellow colour in urine and the brown colour of faeces

Yellow colour of bruises

Yellow colour in jaundice

80
Q

What is the average life span of healthy RBCs?

A

120 days

81
Q

What happens to senescent RBCs?

A

They undergo erythrophagocytosis by macrophages in the spleen and liver

82
Q

What happens to global chains when RBCs are broken down?

A

Break down into amino acids

83
Q

What happens to the heme when RBCs are broken down?

A

Heme oxygenate converts heme to biliverdin

Biliverdin reductase converts biliverdin to bilirubin

84
Q

What is the function of biliverdin reductase?

A

Catalyses the conversion of biliverdin to bilirubin by transferring two hydrogen ions to the centrally located C10 carbon of bilirubin

85
Q

What is the linear structure of Bilirubin?

A

Two dipyrroles joined by a central methene bridge

86
Q

Why is bilirubin insoluble even though it has multiple polar groups?

A

Because of the internal hydrogen bonding, all polar groups are engaged and central methene bridge becomes buried

87
Q

Why is the conjugation of bilirubin crucial?

A

It increases its aqueous solubility on preparation for its transport to bile

88
Q

What does albumin function as in regards to bilirubin?

A

Carrier protein for transporting unconjugated bilirubin through the bloodstream to the liver in order for bilirubin to be conjugated

89
Q

What is unconjugated bilirubin joined with to form conjugated bilirubin?

A

Glucuronic acid

90
Q

What catalysed the conjugation of bilirubin with glucuronic acid?

A

Glucuronyl transferase

91
Q

What is the first step of bilirubin conjugation?

A

Formation of bilirubin monoglucuronide, sufficient soluble for transport

92
Q

In which cases in bilirubin monoglucuronide the predominant form of conjugated bilirubin?

A

In fetal and early neonatal life

93
Q

What happens if you add another glucuronic acid to bilirubin monoglucuronide?

A

It becomes bilirubin diglucuronide, which is the fully conjugated form

94
Q

What does conjugated bilirubin do?

A

Passes through the bile and reaches the intestines

95
Q

What substances deconjugate bilirubin?

A

Intestinal bacteria

96
Q

What happens to the free bilirubin in the small intestine?

A

Reduced to urobilinogen and then into stercobilinogen

97
Q

What percentage of bilirubin is converted into stercobilinogen?

A

Over 80%

98
Q

Where is stercobilin excreted?

A

In the faeces, gives the brown colour

99
Q

What happens to the remainder urobilinogen?

A

Reabsorbed from the intestine and enters portal blood

Some of it returns to the liver and is re-excreted (enter-hepatic circulation)

100
Q

What happens to the urobilinogen that does not return to the liver?

A

Passes through the kidney and is converted into urobilin that is excreted in the urine and gives it its yellow colour

101
Q

What is the bilirubin that is conjugated with the glucuronic acid called?

A

Direct or conjugated bilirubin

102
Q

What is the bilirubin that is not conjugated with glucuronic acid called?

A

Indirect or unconjugated bilirubin

103
Q

What is all the bilirubin in the blood called?

A

Total bilirubin

104
Q

What is the normal levels of the different kinds of bilirubin?

A

Total: 0.3 to 1mg/dl
Unconjugated: 0.2 to 0.7 mg/dl
Conjugated: 0.1 to 0.3 mg/dl

105
Q

What happens if serum bilirubin > 1?

A

Hyperbilirubinemia

106
Q

What happens if serum bilirubin > 2?

A

Jaundice

107
Q

What is neonatal jaundice?

A

Jaundice in newborns, especially seen in premies

108
Q

When does neonatal jaundice appear?

A

Appears after 24 hours, picks up after 4 to 5 days and then disappears after 14 days

109
Q

What causes neonatal jaundice?

A

Bilirubin accumulates as glucurynol transferase is low at birth
Unconjugated bilirubin is increased in blood > albumin
Diffuses into basal ganglia and cause toxic encephalopathy

110
Q

What is the treatment for neonatal jaundice?

A

Blue fluorescent ligt, convers bilirubin to more polar –> water soluble isomers –> which can be excreted unto bile without glucuronic acid

111
Q

What are the causes for haemolytic jaundice?

A

Excessive hemolysis
Low haemoglobin levels
Increased levels of indirect bilirubin
Sickle cell anemia, thalassemia, malaria and haemolytic transfusion reaction

112
Q

What causes hepatic jaundice?

A

Impaired uptake of bilirubin by hepatocytes
Impaired conjugation of bilirubin with hepatocytes
Impaired secretion of bilirubin by hepatocytes

113
Q

What happens to the elevates of both direct and indirect bilirubin in hepatic jaundice?

A

Both increase

114
Q

What happens to AST and ALT during hepatic jaundice?

A

Significant increase

115
Q

What happens to aLP during hepatic jaundice?

A

Moderate increase

116
Q

What can cause hepatic jaundice?

A

Hepatitis, cirrhosis, Crigler-Najjar syndrome, gilbert’s syndrome, dubin-johsnon syndrome, rotor syndrome, drug toxicity

117
Q

What cause obstructive jaundice?

A

Impaired excretion of bilirubin due to obstruction in the bile flow from the liver to the ntestien

118
Q

What happens to the levels of direct bilirubin in obstructive jaundice?

A

Increase

119
Q

What happens to ALP levels in obstructive jaundice?

A

Significant increase

120
Q

What happens to AST and ALT levels in obstructive jaundice?

A

Moderate increase

121
Q

What can cause obstructive jaundice?

A

Gallstones, inflammation, carcinoma of head of pancreas

122
Q

What is congenital hyperbilirubinemia?

A

Bilirubin is elevated in blood due to inherited defects in the bilirubin metabolic pathway

123
Q

What is the Crigler-Najjar syndrome?

A

Low activity of glucuronyltransferase

124
Q

What does Crigler-Najjar syndrome present like?

A

Severe hyperbilirubinemia in neonates

Complicated by kernicterus and early death

125
Q

What is Gilbert’s syndrome?

A

Decreased production of glucuronyltransferase due to mutations

126
Q

What population is Gilbert’;s syndrome more common in?

A

In men, 2 to 3% of men

127
Q

How does Gilbert’s syndrome present?

A

Usually asymptomatic
LFT’s are normal

128
Q

What is the Dubin-Johnson/Rotor syndrome?

A

Defect in transfer of conjugated bilirubin into biliary canaliculi
Conjugated hyperbilirubinemia

129
Q
A

Gastrointestinal System (29 decks)

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