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Chemistry 1 > Liver Function > Flashcards

Liver Function Flashcards

1
Q

How are most water soluble drugs and substances excreted?

A

Usually unchanged

Excreted in urine or bile

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2
Q

How are lipid soluble compounds dealt with in the body?

A

Usually accumulate and affect cells unless they are converted to less active compounds or more soluble metabolites for excretion

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3
Q

What is a first stage reaction?

A

Reactions that involve chemical modification of reactive groups
Usually involving enzymatic systems

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4
Q

What are some processes a first stage reaction might achieve?

A

Inactivate or detoxify drugs
Activation of drugs
Conversion of nontoxic compounds to toxic ones
(ex acetaminophen, carcinogens)

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5
Q

What might induce a first stage reaction?

A

Drugs like ethanol and barbiturates

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6
Q

What might inhibit a first stage reaction?

A

Drugs

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7
Q

What is a second stage reaction?

A

Conjugation and conversion of substances to permit excretion in bile or urine

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8
Q

What is the most common second stage reaction?

A

Conjugation catalyzed by UDP-glucuronyltransferase to form glucuronide derivatives

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9
Q

What are the major constituents of bile?

A

Cholesterol
Bile salts
Bilirubin

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10
Q

How are hepatic cells involved with metabolism?

A

Exclusive metabolism of galactose and fructose, channels them to glucose pathways

Glycolysis
Glycogenesis
Glycogenolysis
Gluconeogenesis

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11
Q

How are hepatic cells involved with amino acids and proteins?

A

Synthesis of majority of serum proteins
Synthesis of many enzymes
Metabolism of amino acids

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12
Q

How do hepatic cells metabolize amino acids?

A

Gluconeogenesis (conversion to glucose)
Formation of urea from ammonia during deamination
Deamination
Transamination

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13
Q

How are hepatic cells involved with lipid metabolism?

A 
Synthesis of:
fatty acids from acetyl-CoA
cholesterol
bile acids from cholesterol
formations of ketons
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14
Q

What are diseases associated with the liver?

A

Hepatitis
Cirrhosis
Cholestasis

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15
Q

What is hepatitis?

How is it caused?

A

Inflammation of the liver

Caused by infection, drugs, toxins, autoimmune

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16
Q

What is cirrhosis?

How is it caused?

A

Hepatocellular damage leading to scar tissue

Alcohol

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17
Q

What is cholestasis?

A

Blockage of normal bile flow

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18
Q

How is bilirubin formed?

A

Catabolism of heme from hemoglobin

Some from cytochromes, myoglobin, peroxidase

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19
Q

How does hemoglobin breakdown create bilirubin?

A

Hemoglobin -> globin + heme
Heme -> iron + protoporphyrin
Protoporphyrin -> biliverdin
Biliverdin -> unconjugated / indirect bilirubin

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20
Q

Where does hemoglobin catabolism take place?

A

In macrophages

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21
Q

What are features of indirect bilirubin?

A

Non-polar, non water soluble

Bound to albumin in plasma

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22
Q

How does bilirubin enter the liver?

A

In the sinusoids it attaches to receptors on the cell membranes and release from the albumin

Attaches to ligandin in the cell

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23
Q

What happens to bilirubin once it enters liver cells?

A

Indirect bilirubin is converted to conjugated / direct bilirubin

Attaches to glucuronic acid

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24
Q

Where does bilirubin go after being conjugated?

A

Secreted into the bile

Enters duodenum

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25
Q

What happens to bilirubin in the intestines?

A

Unconjugated
Bilirubin converted to urobilinogen
Small amount absorbed but most is excreted

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26
Q

What happens to reabsorbed urobilinogen?

A

Goes through liver and GI again

Small amount secreted by kidneys

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27
Q

What lab tests are done to assess liver function?

A 
Serum and urine bilirubin
ALP
AST
ALT
GGT

sometimes protein, urine urobilinogen, serum ammonia

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28
Q

How should a sample for bilirubin analysis be handled?

A

Serum or plasma
Avoid hemolysis and lipemia
Should be tested quickly or protected from light

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29
Q

What can interfere with bilirubin analysis?

A

Hemolysis (decreases)

Extended light exposure (decreases)

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30
Q

What are 4 methods that cane be used to measure bilirubin?

A

Jendrassik-Grof Method
Vitros Method
Direct Spectrophotometry
Evelyn-Malloy Method

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31
Q

How does the Jendrassik-Grof Method work?

A

Diazo reaction with conjugated bili produces colored product

Measured spectrophotometrically

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32
Q

What are the steps of the Jendrassik-Grof Method?

A

Diazotized sulphanilic acid converts direct bili to azobilirubin
Ascorbic acid stops the reaction
Tartrate shifts absorbance from 585 to 600nm for reading

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33
Q

How can the Jendrassik-Grod Method measure total bilirubin?

A

Accelerator like caffeine-sodium benzoate quickly separates indirect bili from albumin

Then sulphanilic acid can convert all bili to azobilirubin

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34
Q

How can indirect bilirubin be calculated?

A

Total - direct

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35
Q

What is the reference range for direct bilirubin?

A

0-4 umol/L

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36
Q

What is the reference range for indirect bilirubin?

A

0-16 umol/L

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37
Q

What is the reference range for total bilirubin?

A

0-20 umol/L

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38
Q

What are the steps of the vitros bilirubin method?

A

Spreading layer contains caffeine-sodium benzoate to separate indirect bili from albumin

Screening layer traps other substances and lets bilirubin pass

Reaction layer is where bili binds to mordant

Reflectance measured at 400 for direct bili and 460 for indirect bili

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39
Q

How is bilirubin measured spectrophotometrically?

A

Bilirubinometer with capillary sample

Measures bili+hemoglobin at 454 nm
Hemoglobin only at 540

Hemoglobin - hemoglobin + bili = bili

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40
Q

Why is a bilirubinometer only used on babies?

A

After 3 months lipochromes can interfere

Absorb at 454 nm and cause positive interference

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41
Q

What are the reference ranges for bilirubin in babies?

A 
birth < 34
24 hrs 34-103
48 hrs 103-120
3-5 days 68-103
1 week < 34
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42
Q

Why might premature babies have higher bilirubin levels?

A

Lack glucuronyltransferase
Cannot conjugate bili
Unconjugated bili builds up

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43
Q

What happens if bilirubin exceeds 225 umol/L?

A

Can cause kernicterus

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44
Q

What is kernicterus?

A

Bili entering the brain and nervous tissue and depositing causing neurological disorders

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45
Q

What is a critical level of bilirubin in babies?

A

> 300 umol/L

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46
Q

How is kernicterus treated?

A

Phototherapy or exchange transfusions

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47
Q

At what bilirubin level could kernicterus start to occur?

A

225 umol/L

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48
Q

What is jaundice?

A

Yellowing of skin and eyes due to bilirubin

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49
Q

When can jaundice occur?

A

Total bilirubin exceeds 35 umol/L

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50
Q

How does the Evelyn-Malloy method work?

A

Diazo reaction at acid pH
Direct bili measured at 1 minute
Methanol added to make indirect bili more soluble to read total bilirubin level

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51
Q

What causes pre-hepatic jaundice?

A

Increased RBC destruction

  • hemolytic anemias
  • ineffective erythropoiesis
  • HDN/TR
  • drugs
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52
Q

What blood results are expected with pre-hepatic jaundice?

A

Increased indirect bili
Decreased hemoglobin
Decreased LD

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53
Q

What effect does pre-hepatic jaundice have on excretions?

A

Presence of increased urobilinogen

Increased indirect bili = increased direct bili = increased urobilinogen

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54
Q

What might cause hepatic jaundice?

A

Necrosis from viruses, drugs, poison (alcohol)

Diseases impairing direct bili from entering bile

Cholestasis caused by cirrhosis or inflammation of bile ducts

Diseases causing failure of or decreased conjugation of bili

Impaired uptake of bilirubin into the liver

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55
Q

What is Gilbert’s disease?

A

Most common inherited cause of hepatic jaundice

Causes impaired uptake of bilirubin into hepatic cells

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56
Q

What blood results are expected with hepatic jaundice?

A

Increased indirect bili

Possible increased direct bili if conjugation can occur

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57
Q

What effect does hepatic jaundice have on excretions?

A

Decreased direct bili in bile

Decreased urobilinogen in excretion

If direct bili increased in blood, may be found in urine

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58
Q

What might cause post-hepatic jaundice?

A

Obstruction of bile duct preventing bile excretion

Bile duct cancer
Tumor compression of bile duct
Gallstones
Common bile duct inflammation

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59
Q

What are other names for post-hepatic jaundice?

A

Obstructive jaundice

Extrahepatic cholestasis

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60
Q

What blood results are expected in post-hepatic jaundice?

A

Increased direct bili (unable to enter bile)

Indirect usually normal but may build up if severe

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61
Q

How does post-hepatic jaundice affect excretions?

A

Direct bili present in urine
Decreased urobilinogen in stool and urine
Pale colored stool

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62
Q

Where does ALP come from?

A

Bone (osteoblasts)

Liver sinusoid cells, bile canaliculi

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63
Q

When would ALP be elevated?

A

Bone disease, pregnancy growth

Markedly elevated in cholestasis
Moderately in liver damage

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64
Q

Why is ALP so increased in cholestasis?

A

ALP is usually excreted into bile

When there is a blockage it spills over massively into the blood just like direct bilirubin

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65
Q

Serum ALP is increased but bilirubin is normal. Why might this be?

A

Bone disease

or

Possible lesion/carcinoma or obstruction of one of the radicles of the common bile duct

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66
Q

Where does GGT come from?

A

Widespread

Highest levels in cells lining bile canaliculi and ducts

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67
Q

What might cause elevated GGT?

A

Markedly elevated in cholestasis
Moderately in liver damage

Acute hepatitis, cirrhosis, tca abuse

Often first enzyme to rise
Increases with alcohol

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68
Q

How can GGT and ALP levels be used together for diagnosis?

A

GGT + ALP elevated = liver

ALP only elevated = bone

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69
Q

Where are ALT and AST found?

A

Highest in hepatocytes and heat and skeletal muscle

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70
Q

When might ALT and AST be elevated?

A

Markedly in hepatocellular damage

Moderately in cholestatis

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71
Q

How can the ratio of AST to ALT be used?

A

AST:ALT < 1.0 = acute (viral or toxic hepatitis)

AST:ALT = 1.0 obstructive jaundice

AST:ALT > 2.0 = chronic (hepatitis, alcoholism, cirrhosis)

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72
Q

Where is 5’-Nucleotidase found?

A

Bile canaliculi lining cells

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73
Q

When might 5’-Nucleotidase be increased?

A

Markedly in cholestasis

Moderately in liver damage

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74
Q

When might lactate dehydrogenase be elevated?

A

Mostly in liver conditions but not like other enzymes
Not as sensitive

LD-4 and LD-5 elevated in liver disease

75
Q

Where is albumin synthesized?

76
Q

When might albumin level be decreased?

A

Decrease gradually in acute liver disease

Markedly decreased in chronic liver disease

77
Q

When might a-fetoprotein (AFP) be elevated?

A

Hepatocellular carcinoma

78
Q

Is a-fetoprotein (AFP) usually found in adults?

A

No

Maximum concentration at 12-15 weeks gestation

79
Q

When might gamma globulins be increased?

A

Chronic active hepatitis

Increase in both IgG and IgM

80
Q

What is beta-gamma bridging in electrophoresis?

A

Elevated levels of IgA and beta-globulins showing a bridge between beta and gamma on an electrophoresis gel

Caused by cirrhosis

81
Q

When might ammonia be increased?

A 
Liver damage (cirrhosis, failure, necrosis)
Cannot be quickly converted to urea
82
Q

What hematology tests might be affected by liver problems?

A

INR

RBC morphology

83
Q

How is INR affected by liver disease?

A

Increased

Not corrected with vitamin K

84
Q

How is RBC morphology affected by liver disease?

A

Target cells
Acanthocytes
Macrocytes

85
Q

Define hepatitis

A

Inflammation of liver caused by infection, toxins, drugs, autoimmune disorders

86
Q

Define cirrhosis

A

Heptocellular damage leading to scar tissue effecting flow of blood and bile

87
Q

Define cholestasis

A

Blockage of bile flow

88
Q

What is intrahepatic cholestasis?

A

Blockage of bile inside the liver

In bile canaliculi and ducts

89
Q

What is extrahepatic cholestasis?

A

Blockage after the liver
In common bile duct, gallbladder

May be caused by gallstones

90
Q

What blood tests might be elevated with cholestasis?

A

ALP, GGT, 5’NT

91
Q

What is the reference range for ALP?

A

30 - 130 U/L

92
Q

What is the reference range for GGT?

A

M 0 - 60 U/L

F 0 - 35 UL

93
Q

What is the reference range for AST?

A

0 - 40 U/L

94
Q

What is the reference range for ALT?

A

0 - 60 U/L

95
Q

What is the reference range for albumin?

A

35 - 55 g/L

96
Q

What is the reference range for ammonia?

A

10 - 45 umol/L

97
Q

Describe the purpose of first stage reactions

A

Chemically modify substances to

  • detoxify
  • activate
  • convert from non-toxic to toxic
98
Q

Describe the purpose of second stage reactions

A

Convert substances to more water soluble forms by conjugation

99
Q

Name the enzyme most commonly used to second stage reactions

A

UDP-glucuronyltransferase

100
Q

List the 3 classes of substances the liver displays metabolic functions for

A

Carbohydrates
Amino acids and proteins
Lipids

101
Q

Identify the source of bilirubin in the body

A

Hemoglobin breakdown

Heme -> protoporphyrin -> biliverdin -> bilirubin

102
Q 
Describe unconjugated bilirubin including
alternate name
solubility
transport in plasma
if it can be excreted in urine
A

indirect bilirubin/alpha bilirubin
not water soluble
transported attached to albumin
cannot be excreted in urine

103
Q 
Describe conjugated bilirubin
alternate name
types
solubility
if it can be excreted in urine
A

direct bilirubin
water soluble
one glucuronide group (beta bilirubin) two glucuronide groups (gamme bilirubin)
can be excreted in urine

104
Q

Describe delta bilirubin

A

Levels rise when conjugated bilirubin levels are very high

Irreversiblely bound to albumin

105
Q 
Describe urobilinogen
where it is formed
color
how is it primarily excreted
the yellowed color product it is oxidized to in feces and urine
A

formed in the duodenum
colorless
excreted mostly in feces
urobilin

106
Q

Name the specimen type for analysis including cautions for the specimen integrity and result of failing to follow precautions

A

Serum or plasma
Run quickly or protect from light
Too much light = decreased bili

107
Q

Describe the Jendrassik-Grof method

- purpose of each reagent

A
  • diazoitized sulphanilic acid converts bilirubin to azobilirubin
  • ascorbic acid stops reaction
  • tartrate shifts A from 585 to 600 nm
108
Q

Describe the Jendrassik-Grod method

- final product measured

A

Azobilirubin

109
Q

Describe the Jendrassik-Grof method

- difference in the method for total vs direct

A

Original reaction measures direct bilirubin

Accelerator like caffeine-sodium-benzoate is added to measure indirect bili

Total - direct = indirect

110
Q

Name the 3 layers of the Vitros dry slide method and what occurs on each

A

Spreading layer - contains caffeine-sodium-benzoate to separate indirect bili from albumin

Screening layer - traps proteins but allows bili to pass

Reaction layer - bilirubin binds to mordant, reflectance measured

111
Q

Describe spectrophotometric measurement of bili

  • what it is used for
  • the substances measured
  • reason for using 2 wavelengths
  • reason it cannot be used on adults
A
  • measuring bili in babies < 3 months
  • oxyhemoglobin and bilirubin
  • oxyhemoglobin measured at 1, bilirubin and hemoglobin measured at the other
  • carotenoid interferes
112
Q

List the reference range for bilirubin in adults

A

Direct 0 - 4 umol/L
Indirect 0 - 16 umol/L
Total 0 - 20 umol/L

113
Q

Describe neonatal bilirubin

  • type of bilirubin
  • reason for increased levels
  • treatments
  • critical bilirubin level
A
  • indirect bili
  • lack glucuronyltransferase to convert it to direct for excertion
  • phototherapy or exchange transfusion
  • > 300 umol/L
114
Q

Describe jaundice including at what plasma bilirubin level it occurs

A

Yellowing of skin and eyes
Occurs around 35 umol/L
May be pre-hepatic, hepatic, or post-hepatic

115
Q

For pre-hepatic jaundice list

  • primary cause
  • two common examples of a condition that will produce the cause
  • primary form of increased bilirubin
  • relative bilirubin and urobilinogen levels in plasma, feces, and urine
A
  • increased hemolysis
    • hemolytic anemia
    • ineffective erythropoiesis,
      HDN, transfusion reactions
  • increased total bili due to increased indirect bili
  • increased direct bili = increased urobilinogen
116
Q

For hepatic jaundice list

  • primary cause
  • two common examples of a condition that will produce the cause
  • primary form of increased bilirubin
  • relative bilirubin and urobilinogen levels in plasma, feces, and urine
A
  • liver disease
    • necrosis -> cirrhosis
    • Gilbert’s disease (impaird bilirubin uptake)
    • impairment of conjugation
  • indirect bilirubin
  • increased indirect bili in plasma
    decreased urobilinogen in feces and urine
117
Q

For post-hepatic jaundice list

  • primary cause
  • two common examples of a condition that will produce the cause
  • primary form of increased bilirubin
  • relative bilirubin and urobilinogen levels in plasma, feces, and urine
A
  • cholestasis
    • gallstones
    • tumors
  • direct bili
  • increased direct bili in blood
    decreased urobilinogen in feces and urine
    direct bilirubin present in urine
118
Q

Name the most common inherited cause of jaundce and the defect involved

A

Gilbert’s disease

Impaired uptake of bilirubin into liver cells

119
Q

For ALP list

  • where it is primarily found
  • conditions that levels are most increased
A
  • liver canaliculi and bile ducts, bone
  • post-hepatic jaundice
    cholestasis

moderate in liver damage and bone conditions

120
Q

For GGT list

  • where it is primarily found
  • conditions that levels are most increased
A
  • liver canaliculi and bile ducts
  • post-hepatic janudice
    cholestasis

moderate in liver damage, alcohol use

121
Q

For AST list

  • where it is primarily found
  • conditions that levels are most increased
A
  • hepatocytes, heart, skeletal muscle
  • hepatocellular damage

moderate in cholestasis

122
Q

For ALT list

  • where it is primarily found
  • conditions that levels are most increased
A
  • hepatocytes, heart, skeletal muscle
  • hepatocellular damage

moderate in cholestasis

123
Q

For 5’NTD list

  • where it is primarily found
  • conditions that levels are most increased
A
  • liver canaliculi and bile ducts
  • cholestasis

moderate in liver damage

124
Q

Describe how ALP and GGT can be used together to identify liver issues

A

ALP and GGT elevated = liver issue, likely cholestasis

ALP only elevated = bone related

125
Q

Describe how AST and ALT can be used together to identify liver issues

A

AST : ALT < 1.0 = acute (viral / toxic hepatis)

AST : ALT = 1.0 = post-hepatic jaundice

AST : ALT > 2.0 = chronic (hepatitis, alcoholism, cirrhosis)

126
Q

Indicate the levels of albumin observed in acute and chronic liver disease, as well as pre and post heptic conditions

A

Acute - gradual decrease
Chronic - markedly decreased
Norma in pre and post hepatic jandice

127
Q

Indicate the condition that AFP can be elevated in

A

Hepatocellular carcinoma

128
Q

Indicate the changes observed in gamma globulin levels in liver disease, including characteristic finding in electrophoresis

A

Increased IgG and IgM in chronic acute hepatitis

Elevated IgA and beta-globulins in cirrhosis

Beta-gamma bridging

129
Q

Describe when ammonia levels can be elevated, and the significance related to this

A

Elevated in cirrhosis, failure, and necrosis

May lead to coma

130
Q

Name the hematology and coagulation findings associated with liver disease

A

Increased INR not corrected with vitamin K

Target cells, acantocytes, macrocytes

131
Q

Name some appropriate followup testing for cholestasis

A

Liver biopsy

132
Q

Name some appropriate followup testing for hepatitis

A

Hepatitis serology

Toxicology

133
Q

Name some appropriate followup testing for cholestasis

A

Ultrasound

134
Q

Where does catabolism of hemoglobin into globin, iron, and biliverdin take place?

A

Macrophages of liver and spleen

135
Q

What is the source of bilirubin

A

Heme -> protoporphyrin -> biliverdin -> bilirubin

136
Q

In normal persons how is most bilirubin transported in plasma?

A

Bound to albumin

137
Q

Where does the conjugation of bilirubin with glucuronic acid take place? What is the enzyme involved?

A

Liver

Glucuronyltrasferase

138
Q

What portion of the bilirubin excreted by normal persons is derived from hemolysis and catabolism of circulating erythrocytes?

A

80-90%

rest derived from other heme proteins

139
Q

What happens to urobilinogen in the intestine?

A

Converted to urobilin and excreted

Small amount reabsorbed

140
Q

What happens to urobilinogen in the intestine?

A

Mostly converted to stercobilin and excreted

Small amount reabsorbed

141
Q

What’s the principle of the Evelyn-Malloy method for bilirubin?

A

direct bili soluble in acid, reacts with diazo reagent

methanol makes indirect soluble and reactive

direct and total measured at the same time

indirect = total - direct

142
Q

What are the reference ranges for bilirubin in adults?

A

Direct 0 - 3 umol/L
Indirect 0 - 14 umol/L
Total 0 - 17 umol/L

143
Q

Compare total bilirubin in full term and premature infants

A 
FT                    PM
24h       34-103          17-103
48h       103-120        103-137
3-5d      68-103         171-205
1w          =34           higher
144
Q

In cases of sever hemolytic anemia, how high can the urinary excretion of indirect bilirubin reach

a. very high
b. moderately high
c. only slightly elevated
d. not elevated
e.

A

d. not elevated

145
Q

In cases where there is large scale liver necrosis and normal renal function, the serum urea level would be

a. greatly elevated
b. moderately elevated
c. normal decreased
d. decreased

A

a. greatly elevated

146
Q

Hepatic cellular plates are composed of

a. parenchyma cells
b. hepatocytes
c. Kuppfer cells
d. endothelial cells
e. all of the above
f. a and b only
g. c and d only

A

f. a and b

147
Q

Sinusoids are composed of

a. parenchyma cells
b. hepatocytes
c. Kuppfer cells
d. endothelial cells
e. all of the above
f. a and b only
g. c and d only

A

g. c and d

148
Q

The phagocytic function of the liver is carried out by

a. parenchyma cells
b. hepatocytes
c. Kuppfer cells
d. endothelial cells
e. all of the above
f. a and b only
g. c and d only

A

c. Kuppfer cells

149
Q

Which of the following is/are part of the bile

a. cholesteol
b. bilirubin
c. bile salts
d. enzymes
e. all of the above

A

e. all of the above

150
Q

Crigler-Najjar Syndrome is caused by

a. congenital lack of glucuronic acid
b. failure of bilirubin transport
c. hemolysis
d. congenital lack of glucuronyl transferase
e. a and d

A

d. a and d

151
Q

Rotor Syndrome

a. results in hepatic jaundice
b. results in lack of transport of direct bilirubin to bile canaliculi
c. is a type of hepato-cellular jaundice
d. all of the above
e. a and c only

A

d. all of the above

152
Q

The purpose of caffeine/sodium benzoate in the Jendrassik-Grof procedure is/are

a. to destroy excess bilirubin
b. to convert bilirubin to azobiliruin
c. an accelerating agent
d. all of the above
e. b and c only

A

c. and accelerating agent

153
Q

The beta gamma briding noted on serum electrophoresis

a. occurs in post hepatic jaundice
b. is characteristic of cirrhosis
c. is the result of elevated IgD and IgM
d. results from and elevation of IgA
e. a, b, and c
f. b and d
g. c and d

A

f. b and d

154
Q

An increased prothrombin time that fails to respond to vitamin-K is typical of

a. hepatocellular jaundice
b. obstructive jaundice
c. pre-hepatic jaundice
d. post-hepatic jaundice

A

a. hepatocellular jaundice

155
Q

In cases where there is large scale liver necrosis and normal renal function, the serum urea level would be

a. greatly elevated
b. moderately elevated
c. normal decreased
d. decreased

A

d. decreased

156
Q

The synthesis of bilirubin diglucuronide occurs

a. in hepatocyte cytosol
b. while bilirubin is attached to ligandin
c. in Kuppfer cells
d. all of the above
e. a and b

A

e. a and b

157
Q

In the Jendrassik-Grof procedure for bilirubin, ascorbic acid is used to

a. react with bilirubin
b. stop the reaction
c. destroy excess sulphanilic acid
d. all of the aove
e. a and b
f. b and c

A

f. b and c

158
Q

The purpose of sodium nitrite in the Jendrassik-Grof procedure is

a. to form nitrous acid
b. to provide acidity
c. to convert bilirubin to azobilirubin
d. a and c
e. b and c

A

a. to form nitrous acid

159
Q

The enterohepatic circulation involves

a. intestine-colon-blood-liver
b. liver-bile duct-intestine-portal vein
c. liver-bile duct-colon-feces
d. portal vein-liver-kidney-bile duct
e.

A

b. liver-bile duct-intestine-portal vein

160
Q

Hyperbilirubinemia of premature infants is caused by

a. lack of glucuronic acid
b. immaturity of hepatic cells
c. destruction of hemoglobin
d. none of the above

A

b. immaturity of hepatic cells

161
Q

Diazotization of sulphanilic acid introduces the following function groups on the molecule

a. NH2
b. SO3H
c. COOH
d. NO2
e. N:N

162
Q

In the dry chemistry method of total bilirubin the following is used to dissociate bilirubin from albumin

a. a cationic hydrophobic polymer
b. caffeine-sodium benzoate
c. bilirubin filter
d. a carotenoid compound
e. b and c

A

b. caffeine-sodium benzoate

163
Q

In the dry chemistry method for total bilirubin, the compound that ensures the reaction of unconjugated bilirubin is

a. oxyhemoglobin
b. delta bilirubin
c. lipid
d. dyphylline

A

d. dyphylline

164
Q

Which of the following are true
In most types of hepatic jaundice

a. urobilinogen synthesis is increased
b. urobilin excretion is increased
c. urine shows reduced levels of urobilinogen
d. there is urinary excretion of conjugated bilirubin

165
Q

In a space occupying lesion of the liver the following may be observed

a. fecal urobilinogen is elevated
b. serum direct bili is elevated
c. urinary urobilinogen is elevated
d. serum ALP is elevated
e.

166
Q

The following are observed in post-hepatic jaundice

a. decreased excretion of urobilinogen in urine
b. elevated urobilinogen in feces
c. presense of bilirubin diglucuronide in urine
d. increased excretion of direct bilirubin in bile

167
Q

In normal adults plasma bilirubin should consists of the following factors

a. delta bilirubin
b. gamma bilirubin
c. beta biliruin
d. alpha bilirubin

168
Q

Which of the following are true. In a bilirubinomter

a. measurement of A at 454 nm
b. measurement of A at 540nm
c. subtraction of A at 540 from A at 454
d. difference in solubility of bilirubin at 454 nm and 540 nm

A

a, b, and c

169
Q

The following is/are characteristics of jaundice caused by hemolytic anemia

a. elevated urine urobilinogen
b. presence of indirect bili in urine
c. elevated serum indirect bili
d. elevated serum direct bili
e.

170
Q

The following enzymes are greatly increased in obstructive jaundice

a. ALP
b. 5’NTD
c. GGT
d. LDH

A

a, b, and c

171
Q

An elevation in AST greater than twice the amount of ALT is suggestive of

a. cirrhosis
b. chronic hepatic disease
c. alcoholism
d. viral hepatitis

A

a, b, and c

172
Q

TRUE OR FALSE

Dublin-Johnson syndrome is a type of hepatic jaundice

173
Q

TRUE OR FALSE

Kernicterus is pigmentation of basal ganglia by indirect bili

174
Q

TRUE OR FALSE

AST and ALT levels are normal in hemolytic jaundice

175
Q

TRUE OR FALSE

5’NTD occurs in the membrane of the cells lining bile canaliculi

176
Q

TRUE OR FALSE

Serum albumin is lowered in obstructive jaundice

A

False
Normal

Lowered in hepatic jaundice

177
Q

TRUE OR FALSE

Chronic alcoholism results in an increase in gamma glutamyl transferase

178
Q

TRUE OR FALSE

Inflammation of the walls of the bile ducts is termed cholangitis

179
Q

TRUE OR FALSE

ALP is found in the membrane of cells lining the bile canaliculi

180
Q

TRUE OR FALSE

The enzyme that results in the release of glucuronic acid from direct bili is beta-glucuronidase

181
Q

TRUE OR FALSE

Urobilin is a colorless oxidation product of urobilinogen

A

False

Orange brown

182
Q

TRUE OR FALSE

Bilirubin has a hydrophobic non-polar structure

183
Q

TRUE OR FALSE

Cholesteol is not a normal constituent of bile

Chemistry 1 (5 decks)

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