Liver Function Flashcards
1
Q
Blood vessel that conducts blood from the gastrointestinal tract and spleen to the liver
A
Function of the portal vein
2
Q
A branch of the celiac artery that supplies oxygenated blood to the liver
A
Function of the hepatic artery
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
4
Q
Its primary function is to collect and transport the bile produced by hepatocytes, or liver cells
A
Functions of the bile canaliculi
5
Q
In a patient w/ liver disease, will GLUCOSE increase or decrease?
A
DECREASE
6
Q
In a patient w/ liver disease, will ACUTE PHASE REACTANTS increase or decrease?
A
INCREASE
7
Q
In a patient w/ liver disease, will ALBUMIN increase or decrease?
A
DECREASE
8
Q
In a patient w/ liver disease, will TRANSTHYRETIN increase or decrease?
A
DECREASE
9
Q
In a patient w/ liver disease, will IMMUNOGLOBULINS increase or decrease?
A
DECREASE (abnormal)
10
Q
In a patient w/ liver disease, will COAGULATION PROTEINS increase or decrease?
A
DECREASE
11
Q
In a patient w/ liver disease, will AMMONIA increase or decrease?
A
INCREASE
12
Q
In a patient w/ liver disease, will UREA increase or decrease?
A
DECREASE
13
Q
In a patient w/ liver disease, will CHOLESTEROL increase or decrease?
A
DECREASE
14
Q
In a patient w/ liver disease, will LIPOPROTEINS increase or decrease?
A
DECREASE
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
16
Q
Three functions of Kupffer cells
A
- Store iron (vitamins A, E, K and other substances)
- Phagocytic action
- Immune mechanism
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
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
19
Q
A patient w/ liver disease will have altered drug concentrations and ability to absorb and store vitamins…Why?
A
?
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
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
22
Q
Transport protein for unconjugated bilirubin
A
Albumin
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
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
25
Formation, reabsorption, and urine/fecal excretion of urobilinogen
- 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)
26
Pre-hepatic jaundice
| - General cause
Any process that cuases premature RBC destruction and increased production of unconjugated bilirubin
27
Pre-hepatic jaundice
| - 4 specific causes
1. Hemolysis
2. Ineffective erythropoiesis
3. Increased turnover of non-hemoglobin heme compounds
4. Hematoma
28
Pre-hepatic jaundice
- Serum total bilirubin
- Unconjugated bilirubin
- Conjugated bilirubin
- Urine bilirubin
- Urine urobilinogen
- Fecal urobilinogen
- Serum total bilirubin: increased
- Unconjugated bilirubin: increased
- Conjugated bilirubin: normal
- Urine bilirubin: negative/normal
- Urine urobilinogen: increased
- Fecal urobilinogen: increased
29
Post-hepatic jaundice
| - General cause
Caused by any process that prevents excretion of conjugated bilirubin (biliary obstructive disease)
30
Post-hepatic jaundice
| - Three specific causes
1. Ductal occlusion by stones
2. Spasms or strictures
3. Compression by neoplastic diseases (tumors)
31
Post-hepatic jaundice
- Serum total bilirubin
- Unconjugated bilirubin
- Conjugated bilirubin
- Urine bilirubin
- Urine urobilinogen
- Fecal urobilinogen
- Serum total bilirubin: increased
- Unconjugated bilirubin: normal
- Conjugated bilirubin: increased
- Urine bilirubin: positive
- Urine urobilinogen: decreased to absent
- Fecal urobilinogen: decreased to absent
32
Post-hepatic jaundice
| - Four enzymes that are elevated to a significant degree
1. ALP
2. GGT
3. LAP
4. 5'NT
33
In hepatic (hepatocellular) jaundice, the hepatocyte itself is "sick"; which functions are impaired?
- Impaired uptake
- Impaired conjugation
- Impaired excretion
34
Hepatocellular disease
| - Causes
- All 3 processes (uptake, conjugation, and excretion of bilirubin) are impaired
- Most common cause is HEPATITIS
35
Hepatocellular disease
- Expected serum total
- Unconjugated bilirubin level
- Conjugated bilirubin level
- Urine bilirubin level
- Fecal and urine urobilinogen levels
- Elevated enzymes in hepatitis
- 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!)
36
Gilbert's disease
| - Causes
Pre-conjugation transport failure
37
Gilbert's disease
| - Mechanism
- Normal amt of unconjugated bilirubin to the "sick" liver
- Impaired uptake of unconjugated bilirubin
- Decreased conjugated bilirubin to gut
38
Gilbert's disease
- Serum total
- Unconjugated level
- Conjugated level
- Urine bilirubin
- Urine and fecal urobilinogen
- Serum total: increased
- Unconjugated: increased
- Conjugated: decreased
- Urine bilirubin: negative
- Urine and fecal urobilinogen: decreased (normal)
39
Crigler-Najjar Syndrome
| - Causes
Conjugation failure
40
Crigler-Najjar Syndrome
| - Mechanism
- Normal amt of unconjugated bilirubin to "sick" liver
| - No conjugation occurs → unconjugated bilirubin leaks back into blood
41
Crigler-Najjar Syndrome
- Serum total
- Unconjugated level
- Conjugated level
- Urine bilirubin
- Urine and fecal urobilinogen
- Serum total: increased
- Unconjugated: increased
- Conjugated: decreased
- Urine bilirubin: negative
- Urine and fecal urobilinogen: decreased
42
Physiologic jaundice of the newborn
| - Causes
Conjugation failure (common/normal), liver not yet producing UDP-glucuronyl transferase yet b/c immature
43
Physiologic jaundice of the newborn
| - Mechanism
- 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
44
Physiologic jaundice of the newborn
- Serum total
- Unconjugated level
- Conjugated level
- Urine bilirubin
- Urine and fecal urobilinogen
- Serum total: increased?
- Unconjugated: increased
- Conjugated: None
- Urine bilirubin: ?
- Urine and fecal urobilinogen: ?
45
Dubin-Johnson Syndrome
| - Causes
Post-conjugation transport failure
46
Dubin-Johnson Syndrome
| - Mechanism
- 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
Dubin-Johnson Syndrome
- Serum total
- Unconjugated level
- Conjugated level
- Urine bilirubin
- Urine and fecal urobilinogen
- Serum total: increased
- Unconjugated: normal
- Conjugated level: increased
- Urine bilirubin: positive
- Urine and fecal urobilinogen: decreased/normal
48
Specific range of total bilirubin levels in the blood at which jaundice is observed
> 2.0-3.0 mg/dL
49
7 clinical manifestations of liver disease
1. Jaundice
2. Portal hypertension
3. Hepatic failure/encephalopathy
4. Altered drug metabolism
5. Disordered hemostasis
6. Endocrine abnormalities
7. Ig abnormalities
50
Causes of toxic hepatitis
- Acetomenophen
- Heavy metals
- Drugs
- Poison causing liver necrosis
51
Fecal-oral transmission; infection is often transmitted in restaurants or households
Hepatitis A
52
Routes of transmission of this disease include heterosexual sex, homosexual sex, mother to child, sharing needles, receipt of blood products, and needlestick injury
Hepatitis B
53
Routes of transmission of this disease include blood transfusions, sharing of needles, mother to baby, body piercing, tattooing, and unprotected sex with multiple partners
Hepatits C
54
This disease coexists with Hep B and shares similar routes of transmission
Hepatitis D
55
This disease is transmitted by fecal-oral route; raw sewage can spread this disease to contaminate food and drinking water
Hepatitis E
56
This virus can live in humans without causing infection; can act as a co-infection with Hep C in order to show symptoms
Hepatitis G
57
A two-phase illness associated with a previous viral illness (flu, cold, chicken pox, etc) for which aspirin or salicylate-containing medications were given
Reye's Syndrome
58
In Reye's Syndrome, abnormal accumulations of fat develop in the ____., along w/ a severe increase of pressure in the brain
Liver
59
Symptoms of Reye's Syndrome as it progresses
- 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
Four lab results that are increased in Reye's Syndrome
- ALT/AST
- PLASMA AMMONIA
- Hypoglycemia in infants
- Fatty deposits in liver
61
Causes of cirrhosis
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
Metal involved in Wilson's Disease
Copper
63
Results in deposits of copper in brain, liver, kidney, and cornea; neurological degeneration; cirrhosis; and Kayser-Fleischer Rings
Wilson's Disease
64
Wilson's Disease
- Plasma ceruloplasmin
- Serum copper levels
- Urine copper levels
- Plasma ceruloplasmin: decreased
- Serum copper levels: increased
- Urine copper levels: increased
65
Metal involved in primary hemochromatosis
Iron
66
Primary hemochromatosis
- Iron levels
- Ferritin levels
- Transferrin levels
- TIBC levels
- Iron levels: increased
- Ferritin levels: increased
- Transferrin levels: increased
- TIBC levels: decreased
67
Treatment of primary hemochromatosis
Therapeutic phlebotomy
68
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
Primary Biliary Cirrhosis
69
Inflammation and scarring of the bile ducts; primarily in males 20-30; associated with ulcerative colitis
Primary Sclerosing Cholangitis
70
Significance of neonatal jaundice
- Reaction of mother's milk due to immature liver;
| - Can cause kernicterus, infiltrating the brain and causing severe damage
71
Treatment for neonatal jaundice
- Discontinue breast feeding
- Treat w/ UV light source (phototherapy)
- Exchange transfusion in extreme cases
72
Three stages of Alcoholic Liver Disease
1. Alcoholic fatty liver
2. Alcoholic hepatitis
3. Alcoholic cirrhosis
73
Earliest stage of alcoholic liver disease, few symptoms; advanced cases may have hepatomegaly, vomiting, and jaundice
Progressive clinical characteristics used to make a diagnosis of alcoholic fatty liver
74
Alcohol liver disease with acute liver necrosis and inflammation; hepatomegaly, jaundice, and ascites
Progressive clinical characteristics used to make a diagnosis of alcoholic hepatitis
75
Alcohol liver disease with jaundice, ascites, hepatosplenomegaly, malnutrition, and edema
Progressive clinical characteristics used to make a diagnosis of alcoholic cirrhosis
76
Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Alkaline phosphatase (ALP)
1-3x ULN
77
Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Aspartate aminotransferase (AST)
> 8x ULN (ALT > AST)
78
Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Alanine aminotransferase (ALT)
> 8x ULN (ALT > AST)
79
Relative increase above the upper limit of normal for enzyme in hepatocellular disease
- Lactate dehydrogenase (LD)
increased LD4 and LD5
80
Relative increase above the upper limit of normal for enzyme in BILIARY OBSTRUCTION
- Alkaline phosphatase (ALP)
10-12x ULN
81
Relative increase above the upper limit of normal for enzyme in BILIARY OBSTRUCTION
- Gamma glutamyltransferase (GGT)
5-30x ULN
82
Why is ALBUMIN altered in liver disease and is it increased or decreased?
DECREASED ALBUMIN in liver disease b/c it's made in the liver
83
Why is PROTHROMBIN TIME altered in liver disease and is it increased or decreased?
INCREASED PT in liver disease b/c it has trouble clotting
84
Why are SERUM LIPIDS altered in liver disease and are they increased or decreased?
DECREASED SERUM LIPIDS in liver disease b/c it's synthesized in the liver, cannot make cholesterol
85
Why is AMMONIA altered in liver disease and is it increased or decreased?
INCREASED AMMONIA in liver disease b/c detox method is interrupted
86
Why are BILE ACIDS altered in liver disease and is it increased or decreased?
INCREASED BILE ACIDS in cholestatic disease; in recovery, bile acids will decrease
87
3 bilirubin methods
- Jendrassik-Grof
- Evelyn Malloy
- Directe Spectrophometry
88
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
Jendrassik-Grof → finding only total bilirubin
89
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
Jendrassik-Grof → finding only direct bilirubin
90
In Jendrassic-Grof, diazotized sulfanilic acid is added as a reagent in finding TOTAL bilirubin. What is its purpose?
Reacts w/ bilirubin to form colored azobilirubin
91
In Jendrassic-Grof, ascorbic acid is added as a reagent in finding both TOTAL and DIRECT bilirubin. What is its purpose?
Stops reaction and destroys excess diazo reagent
92
In Jendrassic-Grof, alkaline tartrate is added as a reagent in finding both TOTAL and DIRECT bilirubin. What is its purpose?
Changes pH and converts purple azobilirubin to blue azobilirubin
93
In Jendrassic-Grof, sodium acetate is added as a reagent in finding TOTAL bilirubin. What is its purpose?
Buffers reaction
94
In Jendrassic-Grof, caffeine sodium benzoate is added as a reagent in finding TOTAL bilirubin. What is its purpose?
Accelerates coupling of bilirubin to diazo reagent (it allows direct and indirect to react so you get total bilirubin not just direct)
95
Jendrassic-Grofspecimen specimen requirements
Use serum or heparinized plasma?
96
Jendrassic-Grof reference ranges
- Total adult
- Total infant
- Total adult: 0.2-1.0 mg/dL
| - Total infant: 4.0-8.0 mg/dL
97
Jendrassic-Grof reference ranges
- Conjugated adult
- Conjugated infant
- Conjugated adult: 0.0-0.4 mg/dL
| - Conjugated infant: 0.0-0.2 mg/dL
98
Jendrassic-Grof reference ranges
- Unconjugated adult
- Unconjugated infant
- Unconjugated adult: 0.2-0.6 mg/dL
| - Unconjugated infant: 4.0-7.8 mg/dL
99
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
Evelyn and Malloy bilirubin
100
In Evelyn and Malloy bilirubin, Diazotized sulfanilic acid is added as a reagent in finding DIRECT bilirubin. What is its purpose?
Reacts w/ bilirubin to form colored azobilirubin
101
In Evelyn and Malloy bilirubin, Methanol is added as a reagent in finding TOTAL bilirubin. What is its purpose?
Accelerates coupling of indirect bilirubin to diazo (allows indirect bilirubin to react)
102
Evelyn and Malloy bilirubin specimen requirements
?
103
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
Bilirubin by direct spectrophotometry
104
WHAT TEST?
| Principle: Take 2-oxoglutarate plus NH4 plus NADPH. Measure absorbance at 340nm
Ammonia
105
Ammonia specimen requirements
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
Ammonia reference range
14-45 ug/dL
107
WHAT TEST:
| principle: Urobilinogen plus Ehrlich's reagent leads to a red color read spectrophotometrically
Fecal and urine urobilinogen
108
Fecal and urine urobilinogen specimen requirements
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
Fecal and urine urobilinogen reference ranges
- Fecal urobilinogen: 0.1-1.0 EU/hours
| - Urine urobilinogen: 0.0-4.0 EU/day
