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GI test 2 > Jaundice and Bilirubin > Flashcards

Jaundice and Bilirubin Flashcards

1
Q

Bilirubin

A
  • orange-yellow toxic waste product derived from seescent blood cells
  • Hgb broken down to heme and globin. Globin reused as an AA, heme is taken up by reticoendothelial cells of the spleen and made to unconjugated bilirubin.
  • Unconjugated bilirubin is transported to liver in blood stream bound to albumin and is taken up by hepatic cells
  • In liver bilirubin is conjugated by addition of glucoronic acid via UDP-GT
  • Conjugated bilirubin flows into bile ducts and secreted with bile into intestines
  • converted to urobilinogen and is excreted in stool as stercobilin or urobilin. Small portion is reabsorbed and another portion is filtered into kideny and excreted in urine
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2
Q

What is bilirubin conjugated into in the liver

A

made into bilirubin diglucuronide

  • this is done by enzyme UDP-GT
  • bilirubin is thus conjugated/water soluble and moves into the bile duct to the intestines
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3
Q

glucuronyltransferase

A

= UDP-GT

- necessary enzyme to form conjugated bilirubin: only found in the liver

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4
Q

clear/clay colored stool

A
  • no stercobilin present
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5
Q

clear urine

A

no urobilin present

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6
Q

direct bilirubin

A

= conjugated/water-soluble

  • -> done by UDP-GT
  • it is conjugated with glucoronic acid
  • Conjugation increases the solubility of bilirubin and prevents its reuptake from the intestinal lumen.

Bilirubin conjugates can be eliminated in the urine if biliary outflow is blocked.

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7
Q

urobilinogen

A

bacterial proteases in the intestine remove the glucuronic acid from conjugated bilirubin to form urobilinogen –> further converted into urobilin in kidneys or stercobilin in intestines.

Bilirubin is deconjugated and further metabolized by colonic bacteria; some of the products may circulate enterohepatically–notably urobilinogen, which also enters the urine.

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8
Q

Bacterial beta glucuronidases

A
  • anaerobic flora of distal ileum and colon that hyrolyze conjugated bilirubin to unconjugated bilirubin to form urobilinogens.
  • oxidation of unconjugated bilirubin results in brown stercobilinogen and mesobilinogen.
  • urobilinogen is also reabsorbed from intestine and converted to urobilin in kidney
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9
Q

3 urobilinogens that oxidize to produce orange-brown color of stool?

A
  • stercobilin
  • mesobilin
  • urobilin
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10
Q

Jaundice/Icterus

A
  • normal serum bilirubin = 0.2-1.2 mg/dL , of this usually conjugated is <0.2 mg/dL
  • elevation of serum bilirubin cause depostiion in tissues and sclera of eyes
  • jaundice appears when bilirubin exceeds 2-3 mg/dL
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11
Q

Causes of jaundice?

A
  • excessive production of bilirubin
  • reduced hepatocyte uptake: caused by cirrhosis
  • impaired bilirubin conjugation: enzyme UDP-GT defect
  • impaired bile flow: gall stone/tumor blocking
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12
Q

Kernicterus

A
  • in infants, if bilirubin exceeds 15-20 mg/dL
  • brain damage resulting from excessive jaundice
  • when babies are born, only have fetal Hgb which can’t carry O2 - it is all lysed and the liver has to conjugate the bilirubin. If enzymes aren’t efficient then infantile jaundice will ensue.
  • bilirubin crosses an immature blood-brain barrier and precipitates in basal ganglia and other areas of the brain
  • can lead to severe neurological deficits to death
  • must be treated with phototherapy
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13
Q

pre-hepatic jaundice

A
  • elevated unconjugated serum bilirubin
  • negative urine bilirubin
  • urinary urobilinogen increased resulting in dark urine
  • normal stool because some conjugation still takes place
  • seen with excessive hemolysis
  • hemolytic neonatal jaundice: Rh/ABO incompatibilities, hepatic immaturity
  • malaria, sickle cell anemia, thalassemia, G6PD deficiency, AI’s, drugs
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14
Q

inrahepatic jaundice

A
  • elevated conjugated or unconjugated bilirubin
  • Viral hep, drugs, Alcoholic hep, cirrhosis, prenancy, acetaminophen, sepsis, carcinoma
  • Gilbert’s, Crigler-Najjar, Dubin-Johnson, Rotor’s syndrome
  • neonatal physiological jaundice due to delayed expression of UDPGT
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15
Q

Post-hepatic jaundice

A
  • see high levels of direct bilirubin
  • see pale stools and dark urine
  • due to common duct stones, carcinoma of bile duct/ pancreas/ ampulla
  • intrahepatic bile duct failure due to drugs, cirrhosis or cholangitis
  • extrahepatic cholestasis due to gall stones, pancreatic tumor or cholangiocarcinoma, pancreatitis, cholangitis
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16
Q

hemolytic anemia

A

= excess hemolysis

  • increased unconjugated bilirubin in blood
  • increased conjugated bilirbuin released to bile duct
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17
Q

hepatitis

A
  • hepatic jaundice
  • increased unconjugated bilirubin in blood AND
    increased conjugated bilirubin in blood
  • results from hepatocyte damage or destruction.
  • Total serum bilirubin in Hep B may reach 5-10 mg/dL
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18
Q

biliary stone duct

A
  • increased unconjugated bilirubin in blood
  • increased conjugated bilirubin in blood (though 90% is conjugated)
  • bilirubin is cannot reach intestinal tract, not converted to urobilinogen or stercobilin, thus will have clay colored stools
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19
Q

dark urine

A

increased urinary urobilinogen (or conjugated bilirubin)

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20
Q

gray/clay stool

A

bilirubin not being conjugated, no stercobilin or urobilinogen in stool
- often due to obstruction such as gallstones

21
Q

Gilbert’s syndrome

A
  • intra-hepatic jaundice due to UDP-GT mutation/impaired hepatocellular uptake
  • also called “familial non-hemolytic non-obstructive jaundice”
  • will see total serum bilirubin <4.0mg/dL
  • mild unconjugated hyperbilirubinemia
  • increased urinary urobilinogen
  • results in mild jaundice during illness or stress
  • up to 12% of population has this
22
Q

Crigler-Najjar type I

A
  • intra-hepatic jaundice due to defective UDP-GT
  • very severe, seen only in babies, often die before 1 year from kernicterus.
  • findings: serum unconjugated bilirubin >5.0 mg/dL
  • increased urinary urobilinogen
  • profound jaundice
  • early liver transplant is only effective therapy
23
Q

Dubin-Johnson syndrome

A
  • intra-hepatic jaundice
  • benign, autosomal recessive condition
  • moderate jaundice resulting from mutation of MRP2, resulting in abnormal transport of conjugated bilirubin due to defect in canlicular excretion. Results in back up of conjugated bilirubin and it spilling into circulation and serum.
  • will find increased serum conjugated bilirubin
  • minor amounts of unconjugated bilirubin
  • will always see BLACK liver due to dark brown pigment in hepatocytes and Kupffer cells
  • brown urine
24
Q

Rotor’s syndrome

A

intra-hepatic jaundice

  • increased serum conjugated bilirubin, but no black liver
  • jaundice due to impaired hepatic secretion or storage of conjugated bilirubin
25
Q

hepatitis virus

A

intra-hepatic jaundice

- se increased serum direct and indirect bilirubin with levels of 5-10 mg/dL

26
Q

post-hepatic jaundice

A
  • seen due to obstruction of bile duct at any point due to gall stones or tumor, resulting in impaired excretion of bilirubin
  • Findings: increased serum AND urine conjugated bilirubin, decreased level of urobilin/stercobilin in stool (clay-colored stools)
  • negative urinary urobilinogen
  • CLEAR/CLAY colored stool
26
Q

Kernicterus

A
  • brain encephalopathy is form of permanent damage to infants caused by excessive jaundice
  • The concentration of bilirubin in serum is so high that Free bilirubin can move into brain tissue by crossing the fetal blood-brain barrier

This condition develops in newborns with prolonged jaundice due to:

  • Polycythemia
  • Rh incompatibility between mother & fetus

Sx: muscle tone changes, drowsiness, poor feeding, intellectual defecits

26
Q

Crigler-Najjar Syndrome Type II

A
  • rare autosomal dominant disorder characterised by partial deficiency of UDP-GT
  • worse than Gilbert’s syndrome
  • unconjugated bilirubin between: 5-20 mg/dL
  • Unlike Crigler_Najjar Syndrome Type I, Type II responds dramatically to phenobarbital and a normal life can be expected
28
Q

MRP2

A
  • bilirubin mono- and diglucuronides are excreted across canalicular plasma membrane into bile canaliculi by an ATP dependent transport process mediated by canalicular membrane protein called
    multidrug resistance –associated protein 2 (MRP2).
  • Mutations of MRP2 results in Dubin-Johnson syndrome
29
Q

Bilirubin in gut

A
  • bilirubin in GIT is converted by bacteria to water soluble colorless urobilinogen
  • 80-90% of urobilinogen is excreted in feces, either unchanged or oxidized to orange derivates called urobilins
  • 10-20% of urobilinogens are passively absorbed, enters portal venous blood and re-excreted by the liver
  • a small fraction escapes hepatic uptake, filters across the renal glomerulus and is excreted in urine
  • unconjugated bilirubin* does not reach the gut except in neonates and in severe unconjugated hyperbilirubinemia (e.g. Crigler-Nijjar syndrome I)
30
Q

Classifications of Jaundice:

A

Unconjugated hyperbilirubinemia:

  1. excessive production of bilirubin
  2. reduced hepatic uptake
  3. impaired conjugation

Conjugated hyperbilirubinemia:

  1. decreased hepatocellular excretion
  2. impaired intra and extra hepatic bile flow
31
Q

Physiologic Neonatal Jaundice

A
  • massive fetal Hgb lysis occurs soon after birth, bilirubin is not cleared effectively b/c UDPGT levels are low.
  • intestinal flora that convert bilirubin to urobilinogen are underdeveloped, so enterohepatic circulation of unconjugated bilirubin increases.
  • most neonates dev. mild unconjugated hyperbilirubinemia (2-5 days)
  • risk for kernicterus if concentration is greater than 20 mg/dL
32
Q

phototherapy

A

converts insoluble bilirubin (trans form) to water soluble bilirubin (cis form)

33
Q

maternal fetal blood group incompatability

A

(Rh, ABO)
- jaundice due to incompatibility between
blood types of the mother and fetus
- increased bilirubin levels from the
breakdown of fetus’ RBC (hemolysis)

34
Q

Breast milk Jaundice

A
  • jaundice in breastfeeding newborns, usually end of first week
  • certain chemicals in breast milk inhibits UDPGT, resolves by stopping breastfeeding
35
Q

hepatocellular disease

A
  • could be due to hepatitis
  • hepatic jaundice
  • dark urine
  • low grade fever, RUQ discomfort
  • enlarged tender liver
36
Q

primaquine induced hemolytic anemia, progressing to jaundice

A
  • prehepatic jaundice
  • Glucose-6-P dehydrogenase (G6PD) deficiency seems to be underlying defect
  • High fever due to: malaria
  • Pallor and icterus due to: hemolytic anemia
  • Jaundice due to: high bilirubin
  • Urine dark brown: hemolytic jaundice, hemoglobunuria
  • G6PD deficiency lead to massive breakdown of RBCs, produced bilirubin faster that it can conjugate.
  • More bilirubin is excreted in bile
  • Amount of urobilinogen entering enterohepatic circulation increased
  • Urinary urobilinogen also increased
  • Unconjugated bilirubin levels become elevated in blood causing jaundice
37
Q

Hx: A 15 y/o boy received a sulfonamide antibiotic as prophylaxis for recurrent urinary tract infections. Although he was previously healthy and well nourished, he became progressively ill and presented with pallor and irritability. A blood count revealed that he was severely anemic with jaundice due to hemolysis of the red blood cells.

A

This child is suffering from: G6PD deficiency, resulting in RBC lysis and ensuing jaundice

G6PD deficiency presents with excessive hemolysis on exposure to: - certain drugs – antibiotics, analgesics, antimalarials, etc

38
Q

G6PD deficiency

A
  • In RBCs, G6PD is only source of reduced nicotinamide dinucleotide
    Phosphate (NADPH)
  • NADPH directly and via glutathione (GSH) protects RBCs against oxidative stress

G6PD deficiency presents with excessive hemolysis on exposure to: - certain drugs – antibiotics, analgesics, antimalarials, etc

Acute hemolytic anemia can be triggered by:
1) fava beans 2) infections (malaria) 3) drugs

39
Q

Clinical manifestation of G6PD deficiency

A
  • Vast majority of people with G6PD deficiency remain clinically asymptomatic throughout their life time
  • However, all of them have an increased risk of developing neonatal jaundice and risk of developing acute hemolytic anemia when challenged by oxidative agents
  • Typically, hemolytic anemia attack starts with malaise, weakness, and abdominal or lumbar pain.
  • Within 2-3 days, jaundice develops and often dark urine due to hemoglobinuria
  • Anemia can be moderate to extreme
  • Jaundice is pre-hepatic
40
Q

lab tests to test for G6PD deficiency?

A
  • test enzyme activity of G6PD
  • obtain CBC with retic. count to determine levels of anemia and bone marrow fn.
  • indirect bil. occurs with excessive hgb. degredation and can produce clinical jaundice
  • urinary urobilinogen is high
41
Q

hx: A 55 y/o female had a 8 day history of loss of appetite, nausea and flu like
symptoms. She had noticed that her urine had been dark in color over the
past two days. On examination she had tenderness in the RUQ.

Serum total bilirubin 4.5 mg/dL
Direct bilirubin 2.5 mg/dL
Indirect bilirubin 2.0 mg/dL
Serum AST – 80 IU/L (normal 6– 40 IU/L)
Serum ALT – 115 IU/L (normal 40-80 IU/L)
Serum ALP – 220 IU/L (normal 30-120 IU/L)
A
  • Viral hepatitis, results in hepatic jaundice
  • Damage to liver cells: Can cause unconjugated bilirubin
  • Conjugated bilirubin is not sufficiently secreted in the bile, but instead diffuses into the blood
  • Urobilinogen is increased in urine because hepatic damage decreases the enterohepatic circulation of this compound allowing more to enter
    blood, from which it is filtered into urine
  • Urine becomes dark in color
  • Stools pale colored
  • Plasma levels of AST and ALT are elevated
42
Q

hx: A 50 y/o old obese female, presents with intolerance to fatty foods, pain in the right side of abdomen, yellowing of eyes and passage of clay colored stools.

Laboratory investigations revealed 
Serum total bilirubin – 20 mg/dL
Direct bilirubin – 16 mg/dL
Urine color – deep yellow
Bilirubin ++
Stool – clay colored
High levels of alkaline phosphatase
A

ddx: obstructive jaundice due to gall stones

  • Pain develops when stones pass from gallbladder into cystic duct,
  • Common bile duct, or ampulla of Vater and block the duct.
  • Gallbladder dilates, causing pain called biliary colic.
  • Liver regurgitates conjugated bilirubin into blood (hyperbilirubinemia)
  • High conjugated hyperbilirubinemia
  • High alkaline phosphatase = marker of cholestasis
  • Absence of urobilinogen : Stool clay colored, urine yellow

Treatment:
Surgical removal of stone, gallbladder.
Prolonged obstruction of bile duct can lead to liver damage and rise in unconjugated hyperbilirubinemia

43
Q

high alk phos levels?

A
  • High alkaline phosphatase = marker of cholestasis
44
Q

hx: recent abrupt severe episodes of epigastric pain, nausea, and vomiting. The patient describes the pain as “going to my back”. Her history indicates heavy alcohol use. Physical examination reveals a pain which worsens on walking and lying supine. On palpation, upper abdomen is tender without guarding, rigidity or rebound. Patient appears slightly jaundiced.

Glucose: 130 mg/dL(70-110mg/dL)
BUN: 40 mg/dL (7-18 mg/dL)
Total bilirubin: 4.2 mg/dL (0.1-1.2 mg/dL)
Amylase: 400 U/L (25-125 U/L)
Lipase: 220 U/L (20-70 U/L)
Unconjugated bilirubin: 0.5 mg/dL (0.1-1.0 mg/dL)
Conjugated bilirubin: 3.7 mg/dL (

A
  • posthepatic jaundice due to gallstones with secondary pancreatitis
  • Chronic alcoholism is associated with a higher incidence of cholestasis, cholelithiasis and pancreatitis
  • Acute pancreatitis results from digestive enzyme activation within the pancreatic tissue
  • The resulting tissue digestion causes severe pain
  • Based on her history, this patient is at higher risk to form gallstones with resulting obstruction and hyperbilirubinemia

Confirm with abdominal radiograph (see a “sentinel loop” - segment of air-filled LUQ of small intestine)
and CT scan (see enlarged pancreas)

45
Q

ERCP

A

endoscopic retrograde cholangiopancreatogram - a means of diagnosing gall stones
- can also use ultrasound 90% of the time, or a CT

46
Q

hx: 4 day old, 36 week gestation caucasian female is brought to her primary care physician due to worsening jaundice. The blood type of the infant’s mother is O+. The infant was discharged home on day 2 of life after successfully breast-feeding for 24 hours. Discharge exam indicated mild jaundice and a cephalohematoma

Total bilirubin is 27 mg/dL 
Direct bilirubin is 1 mg/dL
Blood type is A+
Direct coombs test is positive
G6PD is normal
CBC shows mild anemia, anisopoikilocytosis and polychromasia

She is admitted to the hospital for phototherapy

A

ddx: ABO incompatibility resulting in jaundice
- Anti-A in mother’s circulation has attached to baby’s RBCs (reason for + direct Coomb’s test)
- Causes premature destruction of the baby’s cells with resulting anemia and hyperbilirubinemia

47
Q

Coomb’s test

A

+ indicates that mother’s antibodies were attached to babies RBC’s

48
Q

Neonatal hyperbilirubinemia

A
  • Approximately 50% of term neonates
  • Usually due to PNJ (lack of full liver function at birth)
  • ABO incompatibility second most common cause
  • Usually treated by phototherapy
  • Converts “trans” isomer of bilirubin to “cis” isomer
    which is more water soluble and easier to excrete
  • Severe cases may be treated by exchange transfusion

GI test 2 (14 decks)

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