Jaundice and Cholestasis
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Questions and Answers

What is the characteristic feature of hepatitis A virus regarding chronic infection?

  • It does not cause chronic hepatitis. (correct)
  • It has a high carrier state.
  • It is often asymptomatic in adults.
  • It causes chronic hepatitis.

What is the typical incubation period for hepatitis A virus infection?

  • 6 to 8 weeks.
  • 1 to 2 weeks.
  • 4 to 6 weeks.
  • 2 to 4 weeks. (correct)

Which of the following is a reliable marker for acute hepatitis A infection?

  • IgM anti-HAV. (correct)
  • IgG anti-HAV.
  • Fecal viral shedding.
  • Total anti-HAV.

What percentage approximately indicates the fatality rate associated with hepatitis A virus?

<p>0.1% (D)</p> Signup and view all the answers

In which environment is hepatitis A virus most commonly endemic?

<p>Countries with substandard hygiene and sanitation. (C)</p> Signup and view all the answers

What symptom is least likely to be associated with hepatitis A infections?

<p>Chronic fatigue. (B)</p> Signup and view all the answers

What occurs after the IgM antibody response to hepatitis A virus declines?

<p>IgG anti-HAV appears and persists. (C)</p> Signup and view all the answers

What characteristic of hepatitis A infections complicates the identification of previous exposure?

<p>Rarity of IgG anti-HAV testing. (D)</p> Signup and view all the answers

Which group is least likely to show clinical symptoms from hepatitis A infection?

<p>Children under 10 years. (A)</p> Signup and view all the answers

How does the presence of IgG anti-HAV contribute to immunity?

<p>It confers lifelong immunity against all HAV strains. (D)</p> Signup and view all the answers

What characterizes cholestasis in the context of bile form alterations?

<p>Systemic retention of bilirubin and other bile solutes. (D)</p> Signup and view all the answers

Which of the following describes unconjugated bilirubin?

<p>It exists in tight complexes with serum albumin and is not water-soluble. (D)</p> Signup and view all the answers

What is the serum bilirubin level threshold for the clinical appearance of jaundice?

<p>2.0 to 2.5 mg/dL (D)</p> Signup and view all the answers

Which condition is associated with impaired bilirubin conjugation?

<p>Gilbert syndrome (A)</p> Signup and view all the answers

Which mechanism primarily leads to unconjugated hyperbilirubinemia?

<p>Excessive extrahepatic bilirubin production. (B)</p> Signup and view all the answers

What is kernicterus and how is it related to bilirubin levels?

<p>Toxic injury to the brain due to unbound bilirubin in infants. (A)</p> Signup and view all the answers

What contributes to the development of neonatal jaundice?

<p>Breastfeeding that increases bilirubin levels. (D)</p> Signup and view all the answers

Which condition is most likely associated with conjugated hyperbilirubinemia?

<p>Dubin-Johnson syndrome (B)</p> Signup and view all the answers

Which of the following is a mechanism that leads to increased bilirubin production?

<p>Excessive extrahepatic RBC destruction. (B)</p> Signup and view all the answers

What defines conjugated bilirubin compared to unconjugated bilirubin?

<p>It can be easily excreted in urine. (D)</p> Signup and view all the answers

What is the inheritance pattern of Dubin-Johnson syndrome?

<p>Autosomal recessive (D)</p> Signup and view all the answers

Which condition is characterized by absent UGT1A1 activity?

<p>Crigler-Najjar syndrome type I (A)</p> Signup and view all the answers

Which disorder is likely to result in kernicterus, albeit occasionally?

<p>Crigler-Najjar syndrome type II (A)</p> Signup and view all the answers

What distinguishes Gilbert syndrome from Crigler-Najjar syndrome type II?

<p>Gilbert syndrome does not cause kernicterus. (B)</p> Signup and view all the answers

Which syndrome is associated with impaired biliary excretion of bilirubin glucuronides?

<p>Dubin-Johnson syndrome (C)</p> Signup and view all the answers

Flashcards

Jaundice

A yellow discoloration of the skin and sclera caused by the retention of bilirubin.

Cholestasis

Systemic retention of bilirubin and other solutes normally eliminated in bile.

Unconjugated bilirubin

Bilirubin that is not water-soluble and requires albumin for transport. It cannot be excreted in urine.

Conjugated bilirubin

Bilirubin that is water-soluble and can be excreted in urine.

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Unconjugated hyperbilirubinemia

A condition where unconjugated bilirubin levels in the blood are high.

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Conjugated hyperbilirubinemia

A condition where conjugated bilirubin levels in the blood are high.

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Neonatal jaundice

A transient and mild unconjugated hyperbilirubinemia that occurs in almost every newborn.

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Gilbert syndrome

A group of disorders where the liver cannot effectively conjugate bilirubin.

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Obstructive jaundice

A condition where bile flow is obstructed, leading to conjugated hyperbilirubinemia.

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Kernicterus

A condition where bilirubin diffuses into the brain causing neurologic damage.

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Hepatotropic Viruses

A group of viruses that specifically target and infect the liver, causing hepatitis.

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Hepatitis A

A type of viral hepatitis known for its generally mild and self-limiting nature. It does not usually lead to chronic infection or long-term liver damage.

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Incubation Period of HAV

The time between exposure to the hepatitis A virus and the appearance of symptoms, usually 2 to 4 weeks.

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Fulminant Hepatitis (HAV)

The rare and severe form of hepatitis A infection that can lead to liver failure.

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Carrier State

A condition where a virus remains in the body for a long time, typically without causing symptoms. This is not typical of HAV.

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IgM Antibody Against HAV

The presence of specific antibodies against the HAV in the blood. It indicates a current infection.

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Fecal Shedding of HAV

The shedding of the HAV virus in the stool, which stops as the IgM antibody levels increase.

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IgG Anti-HAV

The antibodies against HAV that persist for a long time after an infection, potentially providing lifelong protection from reinfection.

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Endemic Prevalence of HAV

A common way for populations in areas with poor sanitation to develop immunity to HAV.

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Nonspecific Symptoms

Symptoms that are not specific to a particular disease. Examples include fatigue and loss of appetite.

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Crigler-Najjar syndrome type I

A rare, autosomal recessive disorder characterized by the complete absence of the enzyme UDP-glucuronosyltransferase (UGT1A1). This results in the inability to conjugate bilirubin, leading to extremely high levels of unconjugated bilirubin in the blood.

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Crigler-Najjar syndrome type II

An autosomal dominant disorder with variable penetrance, where there is decreased, but not absent, activity of the enzyme UDP-glucuronosyltransferase (UGT1A1). The reduced enzyme activity leads to increased levels of unconjugated bilirubin in the blood, but the symptoms are generally milder than in Crigler-Najjar syndrome type I.

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Dubin-Johnson syndrome

An autosomal recessive disorder characterized by defects in the biliary excretion of conjugated bilirubin. This is due to mutations in the canalicular multidrug resistance protein 2 (MRP2), which is responsible for transporting bilirubin glucuronides across the canalicular membrane.

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Rotor syndrome

A rare autosomal recessive disorder characterized by defective hepatic uptake and/or storage of bilirubin, as well as impaired biliary excretion. However, the exact mechanism is not fully understood, and it may involve a combination of factors.

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Study Notes

Jaundice and Cholestasis

  • Jaundice (and icterus) is yellow discoloration of skin & sclera due to bilirubin retention
  • Cholestasis is systemic retention of bilirubin and other bile solutes
  • Bilirubin exists in two major forms: unconjugated and conjugated

Pathophysiology of Jaundice

  • Unconjugated Bilirubin: Virtually insoluble, tightly bound to albumin, cannot be excreted in urine, can cross blood-brain barrier (potentially causing kernicterus).
  • Conjugated Bilirubin: Water-soluble, non-toxic, loosely bound to albumin, can be excreted in urine; normal serum levels are 0.3-1.2 mg/dL, above 2.0-2.5 mg/dL causes jaundice
  • Jaundice results from an imbalance between bilirubin production and clearance due to:
    • Excessive bilirubin production (e.g., hemolytic anemias, thalassemia)
    • Reduced hepatocyte uptake (e.g., some cases of Gilbert syndrome, drugs)
    • Impaired bilirubin conjugation (e.g., newborn physiologic jaundice, breast milk jaundice, Gilbert syndrome, hepatitis)
    • Decreased hepatocellular excretion (e.g., transporter deficiencies like Dubin-Johnson or Rotor syndrome)
    • Impaired bile flow
  • First three mechanisms typically lead to unconjugated hyperbilirubinemia
  • Last two mechanisms typically lead to conjugated hyperbilirubinemia
  • Genetic Mutations: Multiple genetic mutations can cause hereditary hyperbilirubinemia.
    • Unconjugated Hyperbilirubinemia:
      • Crigler-Najjar syndrome type I: Absence of UGT1A1 activity, fatal neonatal period.
      • Crigler-Najjar syndrome type II: Decreased UGT1A1 activity, Generally mild, occasional kernicterus.
      • Gilbert syndrome: Decreased UGT1A1 activity, Most common form, often innocuous.
    • Conjugated Hyperbilirubinemia:
      • Dubin-Johnson syndrome: Impaired biliary excretion of bilirubin glucuronides, generally innocuous, pigmented cytoplasmic globules; also, epinephrine metabolites
      • Rotor syndrome: Decreased hepatic uptake and storage, decreased biliary excretion Innocuous

Neonatal Jaundice

  • Newborn infants often experience transient, mild unconjugated hyperbilirubinemia (physiologic jaundice) due to immature hepatic machinery for bilirubin conjugation & excretion.
  • Breastfeeding may exacerbate this jaundice due to bilirubin-deconjugating enzymes in breast milk.

Viral Hepatitis (General)

  • Viral hepatitis is liver infection caused by hepatotropic viruses (HAV, HBV, HCV, HDV, HEV).

Hepatitis A Virus (HAV)

  • HAV causes a self-limiting, benign disease with 2-4 week incubation.
  • It rarely progresses to fulminant hepatitis and has a low fatality rate (<0.1%).
  • Commonly found in areas with poor sanitation, acquiring antibodies common by age 10.
  • Mild or asymptomatic illness, rare in adults.
  • Symptoms: Fatigue, loss of appetite, jaundice.
  • Diagnosis: Elevated IgM anti-HAV at illness onset (reliable marker).
  • Fecal shedding stops with rising IgM: IgM declines in months, followed by IgG anti-HAV development for years, conferring long-term immunity.
  • Chronic carrier state and hepatitis are uncommon
  • IgG levels are inferred by the difference between total and IgM anti-HAV. No direct IgG test commonly available.

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Description

This quiz explores the concepts of jaundice and cholestasis, including their definitions, causes, and the types of bilirubin involved. Understand the pathophysiology of jaundice and how it affects bilirubin production and clearance in the body. Test your knowledge on these critical topics in medical science.

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