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Liz's Clinical Chemistry Module 2 > Liver Function > Flashcards

Liver Function Flashcards

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1
Q

Blood vessel that conducts blood from the gastrointestinal tract and spleen to the liver

A

Function of the portal vein

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2
Q

A branch of the celiac artery that supplies oxygenated blood to the liver

A

Function of the hepatic artery

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3
Q

Low pressure vascular channels that receive blood from terminal branches of the hepatic artery and portal vein at the periphery of lobules and deliver it into central veins

A

Function of sinusoids

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4
Q

Its primary function is to collect and transport the bile produced by hepatocytes, or liver cells

A

Functions of the bile canaliculi

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5
Q

In a patient w/ liver disease, will GLUCOSE increase or decrease?

A

DECREASE

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6
Q

In a patient w/ liver disease, will ACUTE PHASE REACTANTS increase or decrease?

A

INCREASE

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7
Q

In a patient w/ liver disease, will ALBUMIN increase or decrease?

A

DECREASE

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8
Q

In a patient w/ liver disease, will TRANSTHYRETIN increase or decrease?

A

DECREASE

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9
Q

In a patient w/ liver disease, will IMMUNOGLOBULINS increase or decrease?

A

DECREASE (abnormal)

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10
Q

In a patient w/ liver disease, will COAGULATION PROTEINS increase or decrease?

A

DECREASE

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11
Q

In a patient w/ liver disease, will AMMONIA increase or decrease?

A

INCREASE

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12
Q

In a patient w/ liver disease, will UREA increase or decrease?

A

DECREASE

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13
Q

In a patient w/ liver disease, will CHOLESTEROL increase or decrease?

A

DECREASE

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14
Q

In a patient w/ liver disease, will LIPOPROTEINS increase or decrease?

A

DECREASE

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15
Q

Two hepatic mechanisms for detoxification and excretion of xenobiotic materials and toxic metabolic products

A
  • Excreted directly into the bile for fecal excretion

- Circulated to the kidney for renal excretion

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16
Q

Three functions of Kupffer cells

A
  1. Store iron (vitamins A, E, K and other substances)
  2. Phagocytic action
  3. Immune mechanism
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17
Q

Most potent Ag-presenting cells of the immune system and also serve to characterize the pathogenicity of invading Ags

A

Function of dendritic cells

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18
Q

They store vitamin A in a normal liver, limit fibrosis upon senescence, and secrete collagen upon liver damage

A

General functions of stellate cells

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19
Q

A patient w/ liver disease will have altered drug concentrations and ability to absorb and store vitamins…Why?

A

?

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20
Q

Metabolic degradation of hemoglobin including the final deposition of iron, heme, and globin

A
  • Senescence of RBCs are picked up by the spleen, liver and bone marrow.
  • RES breaks the RBCs down into heme and and globinand iron; heme goes on to bilirubin; globin returned to amino acid pool; and iron returns to the iron stores
  • Bilirubin leaves the RES as unconjugated bilirubin (toxic) and is taken up by the liver
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21
Q

Metabolic conversion of heme to unconjugated bilirubin, then conjugated to bilirubin

A
  • The hepatocyte conjugates the bilirubin by adding one or two glucuronide molecules via catalysis by UDP-Glucuronyl transferase and it enters the small intestine through the common bile duct
  • Conjugated bilirubin has 3 fates
    1. 50% absorbed into plasma; of that 50%, 30% goes back to liver and 20% is filtered by the kidney as urinary urobilinogen then excreted as urobilin
    2. 50% is not reabsorbed and excreted as fecal urobilinogen —> urobilin
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22
Q

Transport protein for unconjugated bilirubin

A

Albumin

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23
Q

Formation of bilirubin mono- or diglucuronide (conjugated bilirubin), including the name of the enzyme that catalyzes the reaction

A
  • Conjugated bilirubin is formed by conjugation w/ one or two glucuronide molecules via catalysis by UDP-glucuronyl transferase
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24
Q

Structure in the hepatocyte into which conjugated bilirubin is secreted

A

Once conjugated, it’s secreted into the common bile duct (bile canaliculus) on to the small intestine

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25
Q

Formation, reabsorption, and urine/fecal excretion of urobilinogen

A
  • Once in the intestine, conjugated bilirubin is transformed to urobilinogen
  • 50% is excreted as fecal urobilinogen
  • Other 50% is reabsorbed into the plasma (3% back to the liver, 20% is excreted as urinary urobilinogen)
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26
Q

Pre-hepatic jaundice

- General cause

A

Any process that cuases premature RBC destruction and increased production of unconjugated bilirubin

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27
Q

Pre-hepatic jaundice

- 4 specific causes

A
  1. Hemolysis
  2. Ineffective erythropoiesis
  3. Increased turnover of non-hemoglobin heme compounds
  4. Hematoma
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28
Q

Pre-hepatic jaundice

  • Serum total bilirubin
  • Unconjugated bilirubin
  • Conjugated bilirubin
  • Urine bilirubin
  • Urine urobilinogen
  • Fecal urobilinogen
A
  • Serum total bilirubin: increased
  • Unconjugated bilirubin: increased
  • Conjugated bilirubin: normal
  • Urine bilirubin: negative/normal
  • Urine urobilinogen: increased
  • Fecal urobilinogen: increased
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29
Q

Post-hepatic jaundice

- General cause

A

Caused by any process that prevents excretion of conjugated bilirubin (biliary obstructive disease)

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30
Q

Post-hepatic jaundice

- Three specific causes

A
  1. Ductal occlusion by stones
  2. Spasms or strictures
  3. Compression by neoplastic diseases (tumors)
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31
Q

Post-hepatic jaundice

  • Serum total bilirubin
  • Unconjugated bilirubin
  • Conjugated bilirubin
  • Urine bilirubin
  • Urine urobilinogen
  • Fecal urobilinogen
A
  • Serum total bilirubin: increased
  • Unconjugated bilirubin: normal
  • Conjugated bilirubin: increased
  • Urine bilirubin: positive
  • Urine urobilinogen: decreased to absent
  • Fecal urobilinogen: decreased to absent
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32
Q

Post-hepatic jaundice

- Four enzymes that are elevated to a significant degree

A
  1. ALP
  2. GGT
  3. LAP
  4. 5’NT
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33
Q

In hepatic (hepatocellular) jaundice, the hepatocyte itself is “sick”; which functions are impaired?

A
  • Impaired uptake
  • Impaired conjugation
  • Impaired excretion
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34
Q

Hepatocellular disease

- Causes

A
  • All 3 processes (uptake, conjugation, and excretion of bilirubin) are impaired
  • Most common cause is HEPATITIS
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35
Q

Hepatocellular disease

  • Expected serum total
  • Unconjugated bilirubin level
  • Conjugated bilirubin level
  • Urine bilirubin level
  • Fecal and urine urobilinogen levels
  • Elevated enzymes in hepatitis
A
  • Serum total bilirubin: increased
  • Unconjugated bilirubin: increased
  • Conjugated bilirubin: increased
  • Positive
  • Normal to decreased
  • Elevated enzymes: ALT > AST, ALP, LD4/LD5, NH4+ (can’t be detoxified to urea, so BUN will be low!)
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36
Q

Gilbert’s disease

- Causes

A

Pre-conjugation transport failure

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37
Q

Gilbert’s disease

- Mechanism

A
  • Normal amt of unconjugated bilirubin to the “sick” liver
  • Impaired uptake of unconjugated bilirubin
  • Decreased conjugated bilirubin to gut
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38
Q

Gilbert’s disease

  • Serum total
  • Unconjugated level
  • Conjugated level
  • Urine bilirubin
  • Urine and fecal urobilinogen
A
  • Serum total: increased
  • Unconjugated: increased
  • Conjugated: decreased
  • Urine bilirubin: negative
  • Urine and fecal urobilinogen: decreased (normal)
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39
Q

Crigler-Najjar Syndrome

- Causes

A

Conjugation failure

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40
Q

Crigler-Najjar Syndrome

- Mechanism

A
  • Normal amt of unconjugated bilirubin to “sick” liver

- No conjugation occurs → unconjugated bilirubin leaks back into blood

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41
Q

Crigler-Najjar Syndrome

  • Serum total
  • Unconjugated level
  • Conjugated level
  • Urine bilirubin
  • Urine and fecal urobilinogen
A
  • Serum total: increased
  • Unconjugated: increased
  • Conjugated: decreased
  • Urine bilirubin: negative
  • Urine and fecal urobilinogen: decreased
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42
Q

Physiologic jaundice of the newborn

- Causes

A

Conjugation failure (common/normal), liver not yet producing UDP-glucuronyl transferase yet b/c immature

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43
Q

Physiologic jaundice of the newborn

- Mechanism

A
  • Normal amt of unconjugated bilirubin to immature liver
  • No conjugated bilirubin to gut b/c liver isn’t producing UDP-glucuronyl transferase yet
  • Unconjugated bilirubin leaks into blood
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44
Q

Physiologic jaundice of the newborn

  • Serum total
  • Unconjugated level
  • Conjugated level
  • Urine bilirubin
  • Urine and fecal urobilinogen
A
  • Serum total: increased?
  • Unconjugated: increased
  • Conjugated: None
  • Urine bilirubin: ?
  • Urine and fecal urobilinogen: ?
45
Q

Dubin-Johnson Syndrome

- Causes

A

Post-conjugation transport failure

46
Q

Dubin-Johnson Syndrome

- Mechanism

A
  • Normal amt of unconjugated bilirubin to “sick” liver
  • Normal uptake and conjugation
  • Impaired transport of conjugated bilirubin to bile duct
  • Conjugated leaks into blood
47
Q

Dubin-Johnson Syndrome

  • Serum total
  • Unconjugated level
  • Conjugated level
  • Urine bilirubin
  • Urine and fecal urobilinogen
A
  • Serum total: increased
  • Unconjugated: normal
  • Conjugated level: increased
  • Urine bilirubin: positive
  • Urine and fecal urobilinogen: decreased/normal
48
Q

Specific range of total bilirubin levels in the blood at which jaundice is observed

A

> 2.0-3.0 mg/dL

49
Q

7 clinical manifestations of liver disease

A
  1. Jaundice
  2. Portal hypertension
  3. Hepatic failure/encephalopathy
  4. Altered drug metabolism
  5. Disordered hemostasis
  6. Endocrine abnormalities
  7. Ig abnormalities
50
Q

Causes of toxic hepatitis

A
  • Acetomenophen
  • Heavy metals
  • Drugs
  • Poison causing liver necrosis
51
Q

Fecal-oral transmission; infection is often transmitted in restaurants or households

A

Hepatitis A

52
Q

Routes of transmission of this disease include heterosexual sex, homosexual sex, mother to child, sharing needles, receipt of blood products, and needlestick injury

A

Hepatitis B

53
Q

Routes of transmission of this disease include blood transfusions, sharing of needles, mother to baby, body piercing, tattooing, and unprotected sex with multiple partners

A

Hepatits C

54
Q

This disease coexists with Hep B and shares similar routes of transmission

A

Hepatitis D

55
Q

This disease is transmitted by fecal-oral route; raw sewage can spread this disease to contaminate food and drinking water

A

Hepatitis E

56
Q

This virus can live in humans without causing infection; can act as a co-infection with Hep C in order to show symptoms

A

Hepatitis G

57
Q

A two-phase illness associated with a previous viral illness (flu, cold, chicken pox, etc) for which aspirin or salicylate-containing medications were given

A

Reye’s Syndrome

58
Q

In Reye’s Syndrome, abnormal accumulations of fat develop in the ____., along w/ a severe increase of pressure in the brain

A

Liver

59
Q

Symptoms of Reye’s Syndrome as it progresses

A
  • Viral illness
  • Repetitive vomiting
  • Lethargy
  • Delirium
  • Decorticate coma
  • Decerebrate comma, flaccid comma
    Unless diagnosed and treated successfully, death is common w/in a few days or a few hours
60
Q

Four lab results that are increased in Reye’s Syndrome

A
  • ALT/AST
  • PLASMA AMMONIA
  • Hypoglycemia in infants
  • Fatty deposits in liver
61
Q

Causes of cirrhosis

A
  1. Viral Hep B or Hep C
  2. Toxic alcohol or methotrexate administration
  3. Wilson’s Disease
  4. Alpha-1-antitrypsin deficiency
  5. Hemochromatosis
62
Q

Metal involved in Wilson’s Disease

A

Copper

63
Q

Results in deposits of copper in brain, liver, kidney, and cornea; neurological degeneration; cirrhosis; and Kayser-Fleischer Rings

A

Wilson’s Disease

64
Q

Wilson’s Disease

  • Plasma ceruloplasmin
  • Serum copper levels
  • Urine copper levels
A
  • Plasma ceruloplasmin: decreased
  • Serum copper levels: increased
  • Urine copper levels: increased
65
Q

Metal involved in primary hemochromatosis

A

Iron

66
Q

Primary hemochromatosis

  • Iron levels
  • Ferritin levels
  • Transferrin levels
  • TIBC levels
A
  • Iron levels: increased
  • Ferritin levels: increased
  • Transferrin levels: increased
  • TIBC levels: decreased
67
Q

Treatment of primary hemochromatosis

A

Therapeutic phlebotomy

68
Q

Autoimmune etiology; many patients have AMA’s (anti-mitochondrial antibodies), damage in bile duct causing scarring and altered immunity; itching, weight loss, fatigue; primarily in women 40-60

A

Primary Biliary Cirrhosis

69
Q

Inflammation and scarring of the bile ducts; primarily in males 20-30; associated with ulcerative colitis

A

Primary Sclerosing Cholangitis

70
Q

Significance of neonatal jaundice

A
  • Reaction of mother’s milk due to immature liver;

- Can cause kernicterus, infiltrating the brain and causing severe damage

71
Q

Treatment for neonatal jaundice

A
  • Discontinue breast feeding
  • Treat w/ UV light source (phototherapy)
  • Exchange transfusion in extreme cases
72
Q

Three stages of Alcoholic Liver Disease

A
  1. Alcoholic fatty liver
  2. Alcoholic hepatitis
  3. Alcoholic cirrhosis
73
Q

Earliest stage of alcoholic liver disease, few symptoms; advanced cases may have hepatomegaly, vomiting, and jaundice

A

Progressive clinical characteristics used to make a diagnosis of alcoholic fatty liver

74
Q

Alcohol liver disease with acute liver necrosis and inflammation; hepatomegaly, jaundice, and ascites

A

Progressive clinical characteristics used to make a diagnosis of alcoholic hepatitis

75
Q

Alcohol liver disease with jaundice, ascites, hepatosplenomegaly, malnutrition, and edema

A

Progressive clinical characteristics used to make a diagnosis of alcoholic cirrhosis

76
Q

Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Alkaline phosphatase (ALP)

A

1-3x ULN

77
Q

Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Aspartate aminotransferase (AST)

A

> 8x ULN (ALT > AST)

78
Q

Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Alanine aminotransferase (ALT)

A

> 8x ULN (ALT > AST)

79
Q

Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Lactate dehydrogenase (LD)

A

increased LD4 and LD5

80
Q

Relative increase above the upper limit of normal for enzyme in BILIARY OBSTRUCTION
- Alkaline phosphatase (ALP)

A

10-12x ULN

81
Q

Relative increase above the upper limit of normal for enzyme in BILIARY OBSTRUCTION
- Gamma glutamyltransferase (GGT)

A

5-30x ULN

82
Q

Why is ALBUMIN altered in liver disease and is it increased or decreased?

A

DECREASED ALBUMIN in liver disease b/c it’s made in the liver

83
Q

Why is PROTHROMBIN TIME altered in liver disease and is it increased or decreased?

A

INCREASED PT in liver disease b/c it has trouble clotting

84
Q

Why are SERUM LIPIDS altered in liver disease and are they increased or decreased?

A

DECREASED SERUM LIPIDS in liver disease b/c it’s synthesized in the liver, cannot make cholesterol

85
Q

Why is AMMONIA altered in liver disease and is it increased or decreased?

A

INCREASED AMMONIA in liver disease b/c detox method is interrupted

86
Q

Why are BILE ACIDS altered in liver disease and is it increased or decreased?

A

INCREASED BILE ACIDS in cholestatic disease; in recovery, bile acids will decrease

87
Q

3 bilirubin methods

A
  • Jendrassik-Grof
  • Evelyn Malloy
  • Directe Spectrophometry
88
Q

WHAT TEST?
Principle: sample is mixed with sodium acetate, caffeine sodium benzoate, and diazotixed sulfanilic acid. After incubation, ascorbic acid and alkaline tartrate are added. The absorbance is read at 600nm

A

Jendrassik-Grof → finding only total bilirubin

89
Q

WHAT TEST?
Principle: sample is mixed with a dilute acid solution and diazo reagent. After incubation, ascorbic acid and alkaline tartrate are added. The absorbance is read at 600nm

A

Jendrassik-Grof → finding only direct bilirubin

90
Q

In Jendrassic-Grof, diazotized sulfanilic acid is added as a reagent in finding TOTAL bilirubin. What is its purpose?

A

Reacts w/ bilirubin to form colored azobilirubin

91
Q

In Jendrassic-Grof, ascorbic acid is added as a reagent in finding both TOTAL and DIRECT bilirubin. What is its purpose?

A

Stops reaction and destroys excess diazo reagent

92
Q

In Jendrassic-Grof, alkaline tartrate is added as a reagent in finding both TOTAL and DIRECT bilirubin. What is its purpose?

A

Changes pH and converts purple azobilirubin to blue azobilirubin

93
Q

In Jendrassic-Grof, sodium acetate is added as a reagent in finding TOTAL bilirubin. What is its purpose?

A

Buffers reaction

94
Q

In Jendrassic-Grof, caffeine sodium benzoate is added as a reagent in finding TOTAL bilirubin. What is its purpose?

A

Accelerates coupling of bilirubin to diazo reagent (it allows direct and indirect to react so you get total bilirubin not just direct)

95
Q

Jendrassic-Grofspecimen specimen requirements

A

Use serum or heparinized plasma?

96
Q

Jendrassic-Grof reference ranges

  • Total adult
  • Total infant
A
  • Total adult: 0.2-1.0 mg/dL

- Total infant: 4.0-8.0 mg/dL

97
Q

Jendrassic-Grof reference ranges

  • Conjugated adult
  • Conjugated infant
A
  • Conjugated adult: 0.0-0.4 mg/dL

- Conjugated infant: 0.0-0.2 mg/dL

98
Q

Jendrassic-Grof reference ranges

  • Unconjugated adult
  • Unconjugated infant
A
  • Unconjugated adult: 0.2-0.6 mg/dL

- Unconjugated infant: 4.0-7.8 mg/dL

99
Q

WHAT TEST?
Principle: Direct bilirubin is measured first: sample plus water plus diazotixed sulfanilic acid is incubated, then absorbance is taken at 600 nm. Next total bilirubin is measured by adding methanol to the above reactants, incubate then read at 600nm

A

Evelyn and Malloy bilirubin

100
Q

In Evelyn and Malloy bilirubin, Diazotized sulfanilic acid is added as a reagent in finding DIRECT bilirubin. What is its purpose?

A

Reacts w/ bilirubin to form colored azobilirubin

101
Q

In Evelyn and Malloy bilirubin, Methanol is added as a reagent in finding TOTAL bilirubin. What is its purpose?

A

Accelerates coupling of indirect bilirubin to diazo (allows indirect bilirubin to react)

102
Q

Evelyn and Malloy bilirubin specimen requirements

A

?

103
Q

WHAT TEST?
Principle: this method is resricted to blood specimens from a healthy newborns in which unconjgated bilirubin is the predominant species. Measure blood at two wavelengths (455 and 575nm) to correct for oxyhemoglobin that also absorbs at 455nm

A

Bilirubin by direct spectrophotometry

104
Q

WHAT TEST?

Principle: Take 2-oxoglutarate plus NH4 plus NADPH. Measure absorbance at 340nm

A

Ammonia

105
Q

Ammonia specimen requirements

A

Place specimen on ice after drawing and analyze within 20 minutes. Ammonia in freshly-drawn blood rises 2 to 3 fold if left at room temp. Plasma is specimen of choice.

106
Q

Ammonia reference range

A

14-45 ug/dL

107
Q

WHAT TEST:

principle: Urobilinogen plus Ehrlich’s reagent leads to a red color read spectrophotometrically

A

Fecal and urine urobilinogen

108
Q

Fecal and urine urobilinogen specimen requirements

A

Fresh urine collected over 2 hour period or 24- hour specimen collected in a dark bottle with 5 grams sodium bicarbonate to minimize oxidation and toulene to minimize bacterial growth and to protect from oxygen in the air

109
Q

Fecal and urine urobilinogen reference ranges

A
  • Fecal urobilinogen: 0.1-1.0 EU/hours

- Urine urobilinogen: 0.0-4.0 EU/day

Liz's Clinical Chemistry Module 2 (9 decks)

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