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Clinical Chemistry II - 4378 > Test 2: Liver Function and Bilirubin Metabolism > Flashcards

Test 2: Liver Function and Bilirubin Metabolism Flashcards

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1
Q

What are the functions of the liver?

A

-carbohydrate metabolism
-protein metabolism
-lipid metabolism
-storage (glycogen, fat, vit., iron)
-detoxification
-porphyrin synthesis

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2
Q

The liver is hematopoietic organ for ______ only.

A

fetus

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3
Q

The liver is ________g in normal adult.

A

1400-1600

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4
Q

The liver functions for metabolism and synthesis includes…

A

carbohydrates, proteins, lipids, porphyrins,
and bile acids (cholesterol)

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5
Q

The liver synthesizes most plasma proteins except ______________ and ____________.

A

immunoglobulins & hemoglobin

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6
Q

The liver is responsible for storage of….

A

Iron, glycogen, metabolic end products and xenobiotics to less/
non-toxic form.

*increases water solubility for excretion

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7
Q

The liver synthesizes most plasma proteins except _____________ and ___________.

A

immunoglobulins, hemoglobin

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8
Q

Stellate cells in stimulated state are transformed into ___________ producing cells.

A

collagen*

-Responsible for Fibrosis & eventually cirrhosis

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9
Q

What is the function of Stellate cells in the normal (Quiescent state)?

A

-Vit A storage
-Nitric oxide synthesis

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10
Q

The liver is Divided into 2 primary lobes (4 total) that are abundantly vascularized (~___ ml/min) from hepatic artery to hepatic vein

A

15

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11
Q

____________ is structural unit of the liver: cords of liver cells (hepatocytes radiate from
central vein.

A

Lobule

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12
Q

Each lobule contains a branch of ________, __________, _________.

A

hepatic artery, portal vein, and bile duct.

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13
Q

What is referred to as “Triot”

A

hepatic artery, portal vein, and bile duct.

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14
Q

The lobule boundary is formed by __________ made of connective tissue.

A

portal tract

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15
Q

Lobule:

Between cords are vascular spaces (sinusoids) lined by _____________ and __________ cells.

A

endothelial and Kupffer’s cell

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16
Q

Bile _____________ are channels located between hepatocytes that interconnect and
eventually drain into larger bile ducts.

A

canaliculi

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17
Q

phagocytic macrophages that are specific to the liver

A

Kupffer’s cells

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18
Q

(parenchymal) cells that are responsible for metabolic functions

A

Hepatocytes

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19
Q

Increased ALT and AST means that __________ are damaged.

A

hepatocytes

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20
Q

The liver process endogenous and exogenous compounds by ___________.

A

biotransformation

—> a series of chemical alteration by “ENZYME ACTIVITY”

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21
Q

Carbohydrate metabolism:

(storage of glucose in form of glycogen)

A

Glycogenesis

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22
Q

Carbohydrate metabolism:

(release of glucose from glycogen)

A

Glycogenolysis

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23
Q

Carbohydrate metabolism:

(synthesis of glucose from amino acid or lactic acid precursors)*

A

Gluconeogenesis

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24
Q

What is the primary source for blood glucose?

A

Glycogen

[Glycogen]liver fluctuates depending on usage

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25
Q

The synthesis and release of glycogen from the liver is controlled by what hormones?

A

Insulin, glucagon, glucocorticoids, T3/T4 (thyroid hormone)

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26
Q

Normal blood glucose: _________ mg/dl, (regardless of last meal time)

ATP and NADH are produced by what

A

70-110***

Required for normal brain and tissue function
ATP and NADH are produced from oxidation of glucose and fatty acids.

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27
Q

Fasting blood glucose levels should be less than _______.

A

100 mg/dl

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28
Q

After meal liver has ____ hrs of glycogen reserve.
** Depletion of reserve leads to increased lipolysis (increasing the FA) and gluconeogenesis

A

14

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29
Q

All plasma proteins (except Igs & Hb) are synthesized in the liver.
* Neonates retain some ___________ synthesis

A

hemoglobin

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30
Q

under normal conditions the rate of protein synthesis =

A

rate of protein degradation.

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31
Q

Excessive amino acids are converted to ______ and _______ for excretion

A

ammonia and urea

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32
Q

Amino acids can also be used for gluconeogenesis, ___________ or _________ reactions

A

transamination or deamination

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33
Q

What are transamination reactions catalyzed by?***

A

alanine aminotransferase (ALT) &
aspartate aminotransferase (AST)

-for amino acid metabolism

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34
Q

Alkaline phosphatase (ALP) & 5’-nucleotidase (NT) signifies what kind of damage?

A

Damaged canalicular membrane and biliary obstruction

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35
Q

γ-glutamyl transferase (GGT) signifies what kind of damage?

A

Hepatocellular and obstructive disorders

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36
Q

What is important for bone metabolism and is elevated in kids?

A

Alkaline phosphatase (ALP)

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37
Q

What will increase with damage to hepatobiliary cells?

A

AST and ALT!***

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38
Q

Increased GGT can be associated with…

A

alcoholism

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39
Q

List 4 functions of proteins synthesized in liver

A

-nutrition
-oncotic blood pressure
-coagulation
-transport

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40
Q

Some key proteins include…

A

-albumin
-alpha 1 antitrypsin
-HDL
-Thyroxine binding protein
-heptoglobin

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41
Q

with acute Hepatic Diseases, what changes in plasma protein concentrations are seen?

A

not much change

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42
Q

With severe liver diseases what proteins are decreased ?

A

Short lived hepatic proteins [Transthyretin (T4 carrier), Prothrombin]

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43
Q

What is the half life of transthyretin?
prothrombin?

A

24-48 hours
about 60 hours

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44
Q

In advanced cirrhosis, what plasma proteins are decreased?

A

-all liver-synthesized plasma proteins decreases
-increased Igs (to maintain oncotic pressure)

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45
Q

What lipids dose the liver synthesize?

A

-cholesterol (free & esters)
-free fatty acids
-triglycerides
-sphingolipids
-phospholipids

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46
Q

increased or decreased lipid synthesis with dietary intake?

A

increased

-lipids are repackaged by liver with specific proteins and transported as lipoproteins (VLDL, LDL)

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47
Q

What happens with increased carbohydrate intake?

A

Acetyl CoA —> fFA —-> TG

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48
Q

70% of synthesized cholesterol is esterified with FA from phosphatidyl
choline by…

A

LCAT (lecithin cholesterol acyltransferase)

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49
Q

cholesterol synthesis is necessary for…

A

1) Cell membrane fluidity
2) Bile acid formation (helps emulsify digested lipids for absorption)

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50
Q

What is the final excretory metabolite of cholesterol?

A

bile acids

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51
Q

80% of cholesterol is converted into what 4 major bile acids?***

A

-cholic acid
-chemodeoxycholate
-deoxycholic acid
-lithocholic acid

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52
Q

Bile acids are conjugated with amino acids (________ and ________) forming
conjugated bile salts.

A

glycine & taurine

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53
Q

Bile salts are released into intestinal lumen to emulsify and absorb ______ and ________ from diet.

A

TG, cholesterol

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54
Q

what is the cofactor for lipase to work?

A

colipase

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55
Q

What is it called when the liver breaks down FAs for energy? (occurs when glycogen is depleted)

A

lipolysis

FFA —> AcetylCoA —> CO2 +NADH

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56
Q

Excess acetyl-CoA formation (as might occur in Fasting, DM or Alcohol
intoxication) and limited amounts of NAD+/NADP+ results in hepatic
synthesis of ______ bodies

A

ketone

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57
Q

What substances does the liver store?

A

Iron, glycogen, amino acids(?), vitamins (A & B12), Lipid (transient).

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58
Q

How is iron stored in the liver?

A

as ferritin (and some hemosiderrin)

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59
Q

Only the ______ & _______ contains **glucose-6-phosphatase which converts glucose-6-phosphate to glucose.

A

liver and kidneys

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60
Q

Liver is primarily responsible for detoxification of…

A

poisons, drugs and toxic
metabolic end products

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61
Q

What converts heme to biliverdin?

A

heme oxygenase

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62
Q

What converts biliverdin to bilirubin?

A

biliverdin reductase

63
Q

Two ways detoxification is done by the liver?

A
  1. Inactivation of agent by binding with serum protein (albumin binds bilirubin)
  2. Chemical modification of agent in liver to increase likelihood of excretion
64
Q

Detoxification is the _______________ function of the liver.

A

excretory

65
Q

Detoxification by chemical Modifications can also occur via ____________ system located in
microsomes

A

cytochrome P-450

66
Q

Detoxification by chemical Modification includes…

A

hydroxylation, sulfation or conjugation (to make more water soluble) with a
carbohydrate or amino acid.

67
Q

_______________ are chemical intermediates in the synthesis of hemoglobin,
myoglobin and Respiratory cytochromes

A

Porphyrins

68
Q

▪ (Within the liver), heme synthesis is controlled by…

A

aminolevutinic acid
(ALA) Synthase

69
Q

What is the rate-limiting enzyme that converts Succinyl CoA —-> d-aminoluevulic acid

A

ALA synthase***

70
Q

What enzyme converts d-aminoluevulic acid —-> Porphobilinogen

A

ALA dehydrogenase

71
Q

What are the types of accelerators for bilirubin testing?***

A

Methanol, DMSO, urea

72
Q

Conjugated bilirubin: should be less than…

A

0.3 mg/dL (5.1 µmol/L)

73
Q

Total bilirubin: _______mg/dL

A

0.1 to 1.2 mg/dL (1.71 to 20.5 µmol/L)

74
Q

What causes jaundice?

A

hyperbilirubinemia (25-50 mg/L)

by Interference of bilirubin metabolism

75
Q

Jaundice CANNOT be present in many individual with liver diseases such as…

A

chronic liver disease

76
Q

How are conditions that interfere with bilirubin metabolism classified?

A

-Prehepatic (overproduction)
-Hepatic (impaired uptake by hepatocytes, conjugation defects, reduced excretion into bile)
-Posthepatic (obstruction of bile flow

77
Q

Prehepatic, hepatic, or postherpetic?

▪ Over production: **Excessive hemolysis (e.g. chronic hemolytic
anemia, pernicious anemia) exceeds liver’s capacity to clear bilirubin

A

Pre-hepatic

78
Q

Prehepatic:

-Serum bilirubin rarely exceeds _____ mg/L [almost entirely “Unconjugated”]

Chronic bilirubin production may lead to formation of bilirubin containing
gallstones.

A

50

79
Q

Prehepatic, hepatic, or postherpetic?

Impaired hepatocyte uptake

A

HEPATIC

80
Q

What are two things that can cause impaired hepatocyte uptake?

A

1) drugs (competition for ligand binding)
2) a hereditary disorder (**Gilbert’s syndrome: GS)

81
Q

____________ syndrome:

✴ Degree of hyperbilirubinemia is variable but is made worse with fasting.
✴ No other apparent symptoms.

A

Gilbert’s syndrome: GS**

82
Q

What syndromes has Lack/defect of conjugating enzyme (glucuronysltransferase)

A

Crigler-Najjar Syndrome (type I / II) & Neonates

83
Q

What is type 1 Crigler-Najjar Syndrome?

A

inherited, complete lack of enzyme, leads to infant mortality by 1 year

84
Q

What is type 2 Crigler-Najjar Syndrome?

A

inherited, partial deficiency: bilirubin levels not as high as with type I

85
Q

caused by immaturity of glucuronysltransferase enzyme

A

Neonatal physiologic jaundice

86
Q

What are the risks of Neonatal physiologic jaundice?

A

-Decreased albumin and incomplete blood-brain barrier (BBB) place infant at great risk of encephalopathy.
-Increased deposition of bilirubin in the Brain can result in kernicterus.

87
Q

How is neonatal jaundice treated?

A

UV radiation (phototherapy) or exchange transfusion

88
Q

Crigler-Najjar Syndrome (type I / II) & Neonates lead to increased _________ bilirubin.

A

unconjugated

89
Q

glucuronysltransferase is also known as…

A

UDP-glucuronidase

90
Q

What are the four types of “hepatic” jaundice?

A

-Impaired hepatocyte uptake
-Lack/defect of conjugating enzyme
-.Defective excretion to the bile
-Hepatocellular damage & necrosis

91
Q

Excretion of bile is rate-limiting step of metabolism, what are two rare hereditary disorders of excretion?

A

Dubin-johnson & Rotor syndromes***

92
Q

What type of bilirubin is increased with “hepatic” jaundice?

A

**Serum conjugated bilirubin

93
Q

Dubin-Johnson syndrome is distinguished by ___________ in hepatocytes

A

dark pigment

94
Q

What causes “post hepatic” jaundice?

A

Obstruction of bile flow by gallstones or tumors which increase conjugated serum bilirubin.

95
Q

Memorize liver disease chart

A

!!!

96
Q

Bilirubin + glucuronic acid —> conjugated bilirubin + bile is done by what enzyme?

A

Glucuronyl Transferase

97
Q

What is the bacterial enzyme that deconjugated bilirubin in the intestines to make urobilinogen?

A

B-glucuronidase

98
Q

What type of bilirubin is increased in hemolytic diseases?

A

unconjugated bilirubin

(think pre-hepatic)

99
Q

What type of bilirubin is increased with parenchymal liver disease?

A

Unconjugated and conjugated bilirubin

(think “hepatic”)

100
Q

What type of bilirubin is increased with liver obstruction?

A

Conjugated bilirubin

(think post-hepatic)

101
Q

What is the carrier for unconjugated bilirubin?

A

albumin

102
Q

Why is bilirubin seen in urine with liver obstruction?

A

conjugated bilirubin is increased and it is water soluble

103
Q

What is the ratio seen with Non-alcoholic fatty liver disease?

A

less than 1 but AST and ALT are both increased

104
Q

Inflammation of the liver may be _____ or _____ origin.

A

viral, drug

105
Q

What are the most common causes of viral hepatitis?

A

A,B,C,D,E, cytomegalovirus, coxsackie virus B and
Epstein-Barr virus

106
Q

How is viral hepatitis diagnosed?

A

1) antibodies directed toward virus or 2) patient specific antibodies
produced by viral antigens.

107
Q

What are the lab findings for acute hepatitis infections?

A

Liver initially retains ability to excrete bilirubin, but analyte enzyme levels AST and ALT will be increased.

108
Q

What are the lab findings for chronic hepatitis infections?

A

elevate serum bilirubin, ALP, and ALT/AST (ALT>AST).

(ALT has a longer half life)

109
Q

What is a normal AST:ALT ratio?

A

less than 1

110
Q

Increased ALP could indicate…

A

bile duct obstruction

111
Q

The most common drug induced hepatic damage is alcohol, what is the most significant laboratory finding?

A

induction of GGT (γ-glutamyl transferase)

112
Q

Other drugs that can cause drug induced hepatic damage?

A

Barbituates, tricyclic antidepressants, antiepileptics, acetaminophen,
chemotherapeutics

113
Q

True of false:

Drug induced hepatic damage is usually reversed with removal of drug?

A

True

114
Q

AST:ALT ratio greater than 2:1 with increased GGT could indicate…

A

Alcoholic liver damage***

115
Q

-Typically occurs in children between the age of 2-13 years
-after recovery from Virus Infection such as flu and chickenpox.

A

REYE’S SYNDROME (CNS disorder)

116
Q

What are the effects of Reye’s syndrome?

A

-Associated with increased fatty infiltration, necrosis and **cholestasis (blockage of bile flow)
-Encephalopathy develops with increased NH3.

117
Q

caused by congenital deficiencies in porphyrin
synthesis pathway
How many types are there?

A

Porphyrias (six types)

118
Q

hereditary disorder leads to accumulation of copper in liver —> jaundice —> cirrhosis

A

Wilson’s disease

119
Q

congenital deficiency: Decreased ceruloplasmin, increased urinary copper excretion, glycosuria, phosphaturia, and
aminoaciduria.

A

Wilson’s disease

120
Q

genetic disorder leading to accumulation of iron —> cirrhosis

A

Hemohromatosis

121
Q

What are the clinical manifestations of Hemohromatosis?

A

increased serum iron and ferritin, decreased iron binding capacity.

122
Q

How can Hemohromatosis lead to diabetes?

A

from the iron accumulation in the pancreas (causes damage)

123
Q

How is Hemochromatosis monitored?
What is the treatment?

A

Phlebotomy treatment. 2-6 units/year
Monitoring with ferritin level
To make less then blank***

124
Q

The term for iron induced cell death?

A

Ferroptosis

125
Q

Hemochromatosis:

At what ferritin levels is treatment needed?
At what level is the treatment stopped?

A

-more than 200 mg/ml ferritin
-20-50ng/ml

126
Q

Wilsons disease:

copper is elevated in ________ but not in _______.

A

tissues and urine but not in the blood

127
Q

What three lab values will be elevated with bile duct obstruction and Hepatomas?

A

Increased serum alkaline phosphatase (ALP), 5’ nucleotidase & GGT

128
Q

What is a good marker for liver cancer?

A

Increased α-fetoprotein (AFP) (yolk sac and liver in fetal development, should not be seen in adults otherwise)

129
Q

Protein that reduces “PROTEASE ACTIVITY”

A

α1-ANTITRYPSIN

130
Q

α1-ANTITRYPSIN makes up ____% of α1 fraction of serum proteins.

A

80

131
Q

What causes lack of α1-antitrypsin?

A

a genetic disorder

132
Q

How does α1-ANTITRYPSIN DEFICIENCY manifest itself?

A

as Emphysema and Liver Cirrhosis

133
Q

pH at which particular molecule carries no NET electrical charge

A

Isoelectric point

134
Q

How is phenotyping performed for α1-ANTITRYPSIN DEFICIENCY?

A

using Isoelectric Focusing

  • Run samples on polyacrylamide gel/Immobilized pH gradient Strip
  • Individual proteins are immobilized in the pH gradient as they approached
    its own specific isoelectric point (IP)

*electrical flow is (-) to (+)

135
Q

What converts Bilirubin – glucuronides to unconjugated bilirubin?

What converts unconjugated bilirubin to urobilinogen?

A

β-glucuronidase

Reduction by anaerobic
bacteria

136
Q

Urobilinogen (serum and urine) is increased in…

A

hemolysis (hereditary
spherocytosis) and hepatocellular injury without cholestasis

137
Q

Urobilinogen is decreased with…

A

1) with cholestasis and 2) when there is a lack
of intestinal bacteria (i.e. after antibiotic therapy).

138
Q

True or flase:

urobilinogen is useful in the detection of liver disease.

A

False. of little use in the detection of liver disease.

139
Q

What hepatitis type is most likely to become chronic?

A

Hepatitis C

140
Q

How is hepatitis A virus measured?

A

(1) Total Ab ! persist forever with natural infection to HAV
(2) IgM anti-HAV ! Rapidly develop with acute exposure (detectable: 3-6 mo)

141
Q

What is the most common chronic viral infection
Transmitted through body fluid (parenteral or sexual contact)
From mom to baby at birth or after birth

A

hepatitis B virus

142
Q

42nm DNA virus (hepadna virus family)
Made from RNA template [Reverse transcriptase] –> prone to mutation

A

HBV

143
Q

most common cause of chronic hepatitis in north America, Europe,
Japan
Primarily occur through plasma: drug injection, transfusion 80% ↓ over the past decade

A

HCV

144
Q

Witch hepatitis virus is associated with increased cancer risk?

A

HCV

145
Q

HBV mutant is resistant to…

A

RT inhibitor

146
Q

What is the problem with Mutation with HBsAg?

A

not detected by routine lab test

Cf. HBsAg: used as a routine test Anti HBcAg is also commonly detected Ab
against HBV

147
Q

Post hepatic bilirubin levels

A

Increased total bilirubin
Increased conjugated
Positive bilirubin In urine
Decreased urobilinogen
Pigment is brown

148
Q

Neonatal bilirubin

A

Increased total bilirubin
Increased uncojugated bilirubin
Negative urine Bilirubin

149
Q

Dubin Johnson bilirubin

A

Increased total and conjunction bilirubin
Positive bilirubin in urine
Decrease urobilinogen

150
Q

Criglers syndrome bilirubin
Gilbert syndrome

A

Increased total and unconjugated bilirubin
Decreased conjugation bilirubin normal in Gilbert syndrome
Decreased urobilinogen

151
Q

Hepatocellular bilirubin

A

Increased total bilirubin conjugated and unconjugated bilirubin
Positive bilirubin in urine
Decreased urobilinogen

152
Q

Pre-hepatic bilirubin

A

Increased total and unconjugated and urobilinogen levels
Negative bilirubin in urine

153
Q

Emphysema

A

A lung disease that causes shortness of breath

154
Q

A1 anyitrypsin deficiency effects lungs by

A

Not removing over reactive immunoglobulins that will eventually cause emphysema

Clinical Chemistry II - 4378 (28 decks)

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