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Jaundice Flashcards

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1
Q

What is heme?

A
  • heme is the prosthetic group of hemoglobin, myoglobin, cytochromes, catalase, and peroxidase
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2
Q

When does jaundice occur?

A
  • when serum bilirubin levels exceed 2 mg/dL

- (hyperbilirubinemia is greater than 1 mg/dL)

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3
Q

Normal Serum Bilirubin Levels

A
  • between 0.1 and 1.0 mg/dL

- (majority is unconjugated bilirubin, only a small amount is conjugated)

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4
Q

What are the two types of bilirubin? Which is water-insoluble?

A
  • unconjugated bilirubin: water insoluble (AKA indirect bilirubin)
  • conjugated bilirubin: water soluble (AKA direct bilirubin)
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5
Q

What makes up conjugated bilirubin?

A
  • bilirubin + 2 glucuronic acid

- (known as bilirubin diglucuronide)

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6
Q

What are the 5 general causes of hyperbilirubinemia/jaundice? Which type of bilirubin is increased in each?

A
  • increased unconjugated: increased bilirubin production, decreased hepatic bilirubin uptake, disrupted intracellular conjugation
  • increased conjugated: disrupted secretion of bilirubin into bile canaliculi, bile duct obstruction
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7
Q

T or F: all cells produce heme.

A
  • true!

- however, major locations are in the liver and in the bone marrow (erythroid progenitor cells)

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8
Q

What is the main enzyme involved in heme production?

A
  • ALA synthase
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9
Q

What do phenobarbitals do to heme synthesis? What about lead?

A
  • phenobarbitals induce heme synthesis by activating ALA synthase
  • lead inhibits several enzymes involved in heme production, so it prevents heme formation
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10
Q

How long do RBCs circulate the body before being degraded by the liver and/or spleen?

A
  • between 90 and 120 days
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11
Q

____% of heme degradation is of old, worn-out RBCs; what is the remaining percentage of?

A
  • 85% is old RBCs

- 15% is immature RBCs, myoglobin, and cytochromes

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12
Q

Hemoglobin gets broken down into ______ and ______.

A
  • heme and globin
  • heme –> iron + bilirubin –> excretion and/or reabsorption
  • globin –> amino acids –> recycled into hemoglobin synthesis
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13
Q

Where does heme get broken down into bilirubin? List the steps involved.

A
  • heme breakdown into bilirubin occurs in the MACROPHAGE (the bilirubin then leaves the cell and heads to the liver in the blood)
  • heme oxygenase converts heme into biliverdin –> biliverdin reductase converts biliverdin into bilirubin
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14
Q

Why do we convert biliverdin into bilirubin? (ie: why don’t we just stop at biliverdin?)

A
  • because biliverdin is very insoluble!

- bilirubin is also insoluble, but less so than its precursor

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15
Q

Bilirubin is pretty hydrophobic (water-insoluble), so how does it move around the blood and into the liver?

A
  • it gets joined by albumin! this makes it more soluble, allowing it to travel in the blood
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16
Q

What happens to bilirubin once it enters the liver?

A
  • it gets acted on by UDP-glucoronosyl transferase and gets converted into bilirubin diglucuronide (conjugated bilirubin)
  • this further increases the molecule’s solubility
17
Q

What happens to bilirubin diglucuronide once it is actively secreted into the duodenal lumen?

A
  • it gets hydrolyzed by bacterial enzymes into urobilinogen
  • some (20%) urobilinogen gets reabsorbed into the circulation where it is mainly returned via enterohepatic circulation to the liver (90%), or where it gets converted to urobilin and excreted by the kidneys (10%)
  • most (80%) urobilinogen gets converted to stercobilin and is excreted with feces
18
Q

What color is urobilinogen? Urobilin? Stercobilin? What color is conjugated bilirubin?

A
  • urobilinogen: colorless
  • urobilin: yellow (urine)
  • stercobilin: brown (feces)
  • conjugated bilirubin: dark brown
19
Q

4 Classifications of Jaundice

A
  • pre-hepatic/hemolytic, hepatic/hepatocellular, post-hepatic/obstructive, and neonatal
20
Q

Pre-Hepatic Jaundice

A
  • AKA hemolytic jaundice
  • increased hemolysis results in overproduction of bilirubin beyond liver’s capacity to take it in
  • main increase is in unconjugated bilirubin levels
  • more bilirubin in blood = more in liver = more in bile, so patients will also have darker urine (b/c increased urobilin) and darker feces (b/c increased stercobilin)
21
Q

What are three examples of disorders that can cause pre-hapatic jaundice?

A
  • incompatible blood transfusion, malaria, and sickle-cell anemia
22
Q

Post-Hepatic Jaundice

A
  • AKA obstructive jaundice
  • obstruction prevents bile secretion, leading to build-up of bilirubin
  • main increase is in conjugated bilirubin levels
  • lack of bilirubin in bile, so patients will have light colored, floating feces (no stercobilin and steatorrhea), but will have DARK urine
  • conjugated bilirubin in serum also results in nausea and anorexia (loss of appetite)
23
Q

In post-hepatic jaundice, bilirubin isn’t entering the duodenal lumen, explaining why these patients have light colored, floating feces; why, then, do patients have dark urine? (ie: why isn’t their urine also colorless?)

A
  • because the elevated conjugated bilirubin enters the blood and the kidneys, and this gives urine a very dark color
24
Q

Hepatic Jaundice

A
  • AKA hepatocellular jaundice
  • liver dysfunction and/or damage results in a loss of function, causing an increase in unconjugated AND conjugated bilirubin
  • patients will have light, floating feces, dark urine, nausea, and anorexia
25
Q

Neonatal Jaundice

A
  • jaundice is common in many neonates because it takes about 2 weeks for the hepatic machinery to mature and develop
  • mainly an increase in unconjugated bilirubin
  • worrying because excess bilirubin can cross the immature blood-brain barrier, resulting in toxic encephalopathy
26
Q

What are the most common causes of jaundice?

A
  • hepatitis, biliary obstruction, and hemolytic anemia
27
Q

Gilbert Syndrome

A
  • a benign (not associated with any increased morbidity), inherited condition resulting in mild, fluctuating increases in unconjugated bilirubin
  • a result of decreased levels of bilirubin UDP glucuronyl transferase and decreased bilirubin uptake
28
Q

Dubin-Johnson Syndrome

A
  • an inherited defect in the transport protein needed for hepatocellular excretion of bilirubin, leading to large increases in conjugated bilirubin
  • patients have a VERY dark liver (but the color is NOT due to the conjugated bilirubin!)
29
Q

Unconjugated bilirubin is also known as ______ bilirubin; conjugated bilirubin is also known as _______ bilirubin.

A
  • unconjugated = indirect

- conjugated = direct

30
Q

What is a major complication of physiologic jaundice of the newborn if left untreated? How do we treat this type of jaundice?

A
  • kernicterus: a bilirubin induced brain dysfunction (can be fatal)
  • (unconjugated bilirubin is very fat soluble and can therefore deposit in the brain)
  • treat this jaundice with phototherapy, which makes unconjugated bilirubin water-soluble (note that it does NOT make it into conjugated bilirubin)
31
Q

Crigler-Najjar Syndrome (types I and II)

A
  • absence of UDP-glucuronosyltransferase, resulting in early and rapid onset of elevated unconjugated bilirubin, jaundice, kernicterus and death within a few years if untreated
  • treat with plasmapheresis and phototherapy
  • type I is more severe than type II
32
Q

What is the difference between jaundice and cholestasis?

A
  • jaundice = excess bilirubin that manifests as discoloration
  • cholestasis = retention of bile (excess bilirubin, bile salts, and cholesterol) that manifests as pruritis and xanthomas
  • (obstructive jaundice usually results in cholestasis as well)
33
Q

Rotor Syndrome

A
  • a milder form of Dubin-Johnson syndrome (inability of liver to excrete the conjugated bilirubin. Into biliary tract)
  • unlike Dubin-Johnson, patient’s liver is NOT black here

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