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CC LEC > Liver Functions Prt. 2 > Flashcards

Liver Functions Prt. 2 Flashcards

1
Q

JAUNDICE
• From the french word____ which means “yellow”

A

jaune

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2
Q

One of the oldest known pathologic conditions reported & described by Hippocratic physicians

A

Jaundice

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3
Q

Jaundice

• Yellowish discoloration of the (3).
• Due to the retention of____
• May also occur due to the retention of other substances

A

skin, eyes and mucous membranes

bilirubin

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4
Q

The normal level of bilirubin is

A

0.2-1.0 mg/dL

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5
Q

Jaundice will only become overt or noticeable to the naked eye at above____

A

3.0 mg/dL.

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6
Q

_______- term used in the laboratory to refer to a serum or plasma with a yellowish discoloration due to bilirubin.

• Dark yellow discoloration of serum/plasma

• Yellow serum will stay in the walls of the test tube once tilted

• Will have effects in other test results

A

Icterus

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7
Q

Total Bilirubin Upper Limit -

A

1.0 to 1.5 mg/dL

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8
Q

Overt Jaundice - Not noticeable by the naked eye until it reaches

A

3.0 to 5.0 mg/dL

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9
Q

Normal

Noticeable

TB upper limit

Overt jaundice

A

0.2-1.0 mg/dL

3.0 mg/dL.

1.0 to 1.5 mg/dL

3.0 to 5.0 mg/dL

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10
Q

Liver function test based upon bile pigment metabolism

A

licteric index

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11
Q

Icteric serum
[Bilirubin concentration)
1+=
2+ =
3+=
4 =

A

2.5 mg/dL

5.0 mg/dL

10.0 mg/dL

20.0 mo/dL

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12
Q

TYPES OF JAUNDICE

A

Pre-Hepatic
Hepatic
Post-Hepatic

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13
Q

• Excessive amount of bilirubin is presented to the liver due to excessive hemolysis.

• Excessive amount of bilirubin is presented to the liver for metabolism
Due to processes/diseases before conjugation in the liver

A

PRE-HEPATIC JAUNDICE

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14
Q

Elevated unconjugated bilirubin (B1) in serum.

A

PRE-HEPATIC JAUNDICE

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15
Q

Hemolysis, Hemolytic Anemia, Malaria

Increased breakdown of RBCs
Increased conjugated bilirubin in the blood = unconjugated hyperbilirubinemia

A

PRE-HEPATIC JAUNDICE

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16
Q

• Impaired cellular uptake, defective conjugation or abnormal secretion by the liver cell (= intrinsic liver defect/diseases)

A

HEPATIC JAUNDICE

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17
Q

Both conjugated and unconjugated bilirubin may be elevated in serum.

A

HEPATIC JAUNDICE

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18
Q
  • Increased B1
A

Unconjugated Hyperbilirubinemia

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19
Q

Unconjugated Hyperbilirubinemia (2)

A

Gilbert Syndrome

Crigler-Najjar Syndrome

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20
Q

Gilbert Syndrome -› Benign autosomal recessive hereditary disorder

Genetic mutation of _____

A

UGT1A1 = UDP Glucuronosyltransferase
Family 1 Member A1

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21
Q

Gene that encodes the
UDPGT enzyme = can’t
conjugate B1 to B2

A

UGT1A1

uridine diphosphate glucuronosyltransferase 1A1 gene (UGT1A1)

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22
Q
  • Elevated B1
  • 30% of the liver is still functional = some conjugation may still be possible
  • May have no symptoms but w/ mild icterus
A

Gilbert Syndrome

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23
Q
  • More serious than Gilbert syndrome
A

Crigler-Najjar Syndrome

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24
Q

Crigler-Najjar Syndrome

Deficiency of _____ enzyme

A

uridine diphosphate-glucuronosyltransferase (UDPGT)

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25
Q
  • Complete absence of UDPGT

Accumulation of bilirubin in the brain = neuronal degeneration = Kernicterus

<1 year life expectancy

Some may reach 1 year = phototherapy

A

Crigler-Najjar Syndrome Type 1

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26
Q

Severe/partial deficiency of UDPGT = decreased B2

• Px. can still survive w/ phototherapy

A

Crigler-Najjar Syndrome Type 2

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27
Q

UV rays can oxidize bilirubin to_____

If bilirubin is exposed to light = falsely decreased = must be covered upon testing

A

biliverdin

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28
Q
  • Increased B2
A

Conjugated Hyperbilirubinemia

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29
Q

Conjugated Hyperbilirubinemia (2)

A

Dubin-Johnson Syndrome

Rotor’s Syndrome

30
Q

-› Autosomal recessive disease

• Presents shortly after birth

Increased B2 w/o elevation of liver
enzymes (ALT & AST) = can also
see Delta Bilirubin

A

Dubin-Johnson Syndrome

31
Q

Defective excretion of bilirubin by
hepatocytes to bile canal = B2
returns to bloodstream

Deficiency in______

A

Dubin-Johnson Syndrome

canalicular multidrug resistance/multispecific organic anionic transporter protein (MDR2/cMOAT)

32
Q
  • Liver granules aren’t pigmented = liver biopsy
  • Increased B2
    • Unknown etiology w/ good prognosis
A

Rotor’s Syndrome

33
Q

Same symptoms w/ Dubin-Johnson Syndrome

> Differentiated through liver
biopsy = absence of liver granules

A

Rotor’s Syndrome

34
Q

T or F

Physiologic Jaundice of the Newborn - Newborn
Jaundice is normal

A

True

35
Q

Physiologic Jaundice of the Newborn

Deficiency of _____= last enzyme to be fully developed = liver isn’t fully developed

A

UDPGT

36
Q
  • Bilirubin-conjugation inhibition
A

Lucey-Driscoll Syndrome

37
Q

Lucey-Driscoll Syndrome

AKA

A

Transient Familial Neonatal
Hyperbilirubinemia

38
Q

Circulating inhibitor of bilirubin conjugation

Increase of B1 = can’t be conjugated

A

Lucey-Driscoll Syndrome

39
Q

• Impaired bilirubin excretion due to mechanical obstruction to bile flow.

Due to processes/diseases after conjugation in the liver

A

POST-HEPATIC JAUNDICE

40
Q

Elevated conjugated bilirubin (B2) in serum.

A

POST HEPATIC JAUNDICE

41
Q

Biliary Obstructive Diseases - Gallstones, Tumor

Increased conjugated bilirubin in the blood

Can’t be fully excreted to the
feces/urine = goes back to the
bloodstream

A

POST HEPATIC JAUNDICE

42
Q

Slightly increased unconjugated bilirubin = lesser than B2

Duct obstruction = buildup of
pressure = liver injury = impaired
conjugation function

Not all B1 will be converted to B2

A

POST HEPATIC JAUNDICE

43
Q

It is most commonly caused by an increased amount of bilirubin being presented to the liver such as that seen in acute and chronic hemolytic anemias.

occurs when the problem causing the jaundice occurs prior to liver metabolism.

A

Prehepatic jaundice

44
Q

Other term for pre hepatic jaundice

_______ because the fraction of bilirubin increased in people with prehepatic jaundice is the unconjugated fraction.

A

unconjugated hyperbilirubinemia

45
Q

are hepatic causes of jaundice that result in elevations in unconjugated bilirubin.

A

Gilbert’s disease
Crigler-Najjar syndrome
physiologic jaundice of the newborn

46
Q

Conditions such as _____ and_____ are hepatic causes of jaundice that result in elevations in conjugated bilirubin.

A

Dubin-Johnson
Rotor’s syndrome

47
Q

________, first described in the early twentieth century, is a benign autosomal recessive hereditary disorder that affects approximately 5% of the US population.

A

Gilbert’s syndrome

48
Q

Gilbert’s syndrome results from a genetic mutation in the______ gene that produces the enzyme_______ important for bilirubin metabolism.

The UGT1A1 gene is located on chromosome 2, and other mutations of this same gene produce Crigler-Najjar syndrome, a more severe and dangerous form of hyperbilirubinemia.

A

UGT1A1

uridine diphosphate glucuronosyltransferase

49
Q

occurs when the problem causing the jaundice occurs prior to liver metabolism.

It is most commonly caused by an increased amount of bilirubin being presented to the liver such as that seen in acute and chronic hemolytic anemias.

A

Prehepatic jaundice

50
Q

The liver responds by functioning at maximum capacity; therefore, people with______ rarely have bilirubin levels that exceed 5.0 mg/dL because the liver is capable of handling the overload.

A

prehepatic jaundice

51
Q

This type of jaundice may also be referred to as________ because the fraction of bilirubin increased in people with prehepatic jaundice is the unconjugated fraction.

A

unconjugated hyperbilirubinemia

52
Q

is not water soluble, is bound to albumin, is not filtered by the kidneys, and is not seen in the urine.

A

unconjugated bilirubin

53
Q

Type of jaundice

intrinsic liver defect or disease

A

Hepatic

54
Q

Hepatic jaundice

A

Crigler-Najjar syndrome
Dubin-Johnson syndrome
Gilbert’s disease
neonatal physiologic jaundice of the newborn

55
Q

(3) are hepatic causes of jaundice that result in elevations in unconjugated bilirubin.

A

Gilbert’s disease
Crigler-Najjar syndrome
physiologic jaundice of the newborn

56
Q

Conditions such as _____ and_____ are hepatic causes of jaundice that result in elevations in conjugated bilirubin.

A

Dubin-Johnson
Rotor’s syndrome

57
Q

Gilbert’s syndrome results from a genetic mutation in the______ gene that produces the enzyme UDPGT — uridine diphosphate glucuronosyltransferase, one of the enzymes important for bilirubin metabolism.

A

UGT1A1

58
Q

The UGT1A1 gene is located on chromosome 2, and other mutations of this same gene produce_______ syndrome, a more severe and dangerous form of hyperbilirubinemia.

A

Crigler-Najjar syndrome

59
Q

Of the many causes of jaundice,______ is the most common cause, and interestingly, it carries no morbidity or mortality in the majority of those affected and carries generally no clinical consequences.

It is characterized by intermittent unconjugated hyperbilirubinemia, underlying liver disease due to a defective conjugation system in the absence of hemolysis.

A

Gilbert’s syndrome

60
Q

Crigler-Najjar syndrome may be divided into two types:

type 1, where there is a ______ of enzymatic bilirubin conjugation

type II, where there is a______ causing a severe_____ of the enzyme responsible for bilirubin conjugation.

A

complete absence

mutation; deficiency

61
Q

Unlike Gilbert’s syndrome,______ is rare and is a more serious disorder that may result in death.

A

Crigler-Najjar syndrome

62
Q

Dubin-Johnson syndrome and Rotor’s syndrome are characterized as_______

A

conjugated hyperbilirubinemias

63
Q

is a rare autosomal recessive inherited disorder caused by a deficiency of the canalicular multidrug resistance/multispecific organic anionic transporter protein (MDR2/cMOAT).

In other words, the liver’s ability to uptake and conjugate bilirubin is functional; however, the removal of conjugated bilirubin from the liver cell and the excretion into the bile are defective.

This results in accumulation of conjugated and, to some extent, unconjugated bilirubin in the blood, leading to hyperbilirubinemia and bilirubinuria.

A

DubinJohnson syndrome

64
Q

______ is a condition that is obstructive in nature, so much of the conjugated bilirubin circulates bound to albumin.

This type of bilirubin (conjugated bilirubin bound to albumin) is referred to as_____.

A

Dubin-Johnson

delta bilirubin

65
Q

reacts as conjugated bilirubin in the laboratory method to measure conjugated or direct bilirubin.

A

delta bilirubin

66
Q

A distinguishing feature of_______ syndrome is the appearance of______ (thought to be pigmented lysosomes) on a liver biopsy sample.

have a normal life expectancy, so no treatment is necessary.

A

Dubin-Johnson

dark-stained granules

67
Q

T or F

the defect causing Rotor’s syndrome is not known

A

True

68
Q

Physiologic jaundice of the newborn is a result of a deficiency in the enzyme_____, one of the last liver functions to be activated in prenatal life since bilirubin processing is handled by the mother of the fetus.

Premature infants may be born without ____, the enzyme responsible for bilirubin conjugation.

A

UDPGT

69
Q

UDPGT deficiency results in the rapid buildup of unconjugated bilirubin, which can be life threatening.

When unconjugated bilirubin builds up in the neonate, it cannot be processed and it is deposited in the nuclei of brain and degenerate nerve cells, causing______.

A

kernicterus

70
Q

Infants with this type of jaundice are usually treated with_____ to destroy the bilirubin as it passes through the capillaries of the skin.

It lowers serum bilirubin levels by using____ or ____ lights to transform bilirubin into watersoluble isomers that can be eliminated without conjugation in the liver.

During this process, the baby is undressed so that as much of the skin as possible is exposed to the light, his/her eyes are covered to protect the nerve layer at the back of the eye (retina) from the bright light, and the bilirubin levels are measured at least once a day.

A

phototherapy

halogen or fluorescent

71
Q

results from biliary obstructive disease, usually from physical obstructions (gallstones or tumors) that prevent the flow of conjugated bilirubin into the bile canaliculi.

A

Posthepatic jaundice

72
Q

the liver cell itself is functioning, bilirubin is effectively conjugated; however, it is unable to be properly excreted from the liver.

Since bile is not being brought to the intestines, stool loses its source of normal pigmentation and becomes clay-colored.

A

Post hepatic jaundice

CC LEC (38 decks)

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