Bile and jaundice Flashcards

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1
Q

What is bile?

A
  • A brownish-yellow or green fluid that is secreted by liver and stored in gallbladder.
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2
Q

What are the functions of bile?

A
  • Excretory
  • Digestive
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3
Q

Discuss the excretory function of bile.

A
  • Exogenous and endogenous products can accumulate in bile and be excreted.
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4
Q

What are the names of the macrophages of the liver?

A
  • Kupffer cells: maintain liver function.
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5
Q

Discuss the digestive function of bile.

A
  • Associated mainly with fats.
  • Increases pH to neutralise acidity of gastric content. Alkaline secretion.
  • Bile salts and phospholipids emulsify fats into smaller droplets.
  • Bile salts activate pancreatic hydrolyse precursors.
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6
Q

Where do we get bile acids and salts from?

A
  • Come from breakdown of cholesterol.
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7
Q

Name 2 primary bile acids (Liver).

A
  • Cholic acid
  • Chenodeoxycholic acid.
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8
Q

Name 2 secondary bile acids (Gut).

A
  • Deoxycholic acid
  • Lithocholic acid
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9
Q

What is bilirubin?

A
  • A natural degradation product of haem in erythrocytes.
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10
Q

What processes need to happen for production of bilirubin?

A
  • Phagocytosis and/or lysis of RBCs.
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11
Q

Describe extra-vascular formation of bilirubin.

A
  1. RBC undergoes phagocytosis and/or lysis.
  2. Haemoglobin is released and broken into Haem and Globin.
  3. Globin is further degraded into AAs.
  4. Haem is broken into Fe2+ and a product of its breakdown is bilirubin.
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12
Q

Discuss haem degradation and processing.

A
  1. Haem is degraded into bilirubin.
  2. Bilirubin binds to albumin and is transported in bloodstream.
  3. Then taken up by liver.
  4. It is then conjugated with glucuronic acid to make it water soluble.
  5. It is then excreted into bile.
  6. Urobilinogens then form in intestinal tract.
    - Can either be re-absorbed and excreted from kidney as urinary urobilin, or excreted as faecal stercobilin
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13
Q

How exactly is haem degraded into bilirubin?

A
  • Via 2 enzymes:
    1. Haem oxygenate
    2. Biliverdin reductase
  • Haem–biliverdin—unconjugated bilirubin
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14
Q

Discuss the metabolism of bilirubin.

A
  1. Haem is degraded and produces bilirubin.
  2. Bilirubin binds to albumin, transported into bloodstream then is taken up by liver.
  3. In the liver, binds to cytoplasmic proteins: ligand + protein Y.
  4. Then conjugated with glucoronic acid is catalysed by UDP-glucuronyl transferase to make it water soluble.
  5. Conjugated bilirubin is secreted into biliary tree.
  6. Bile excreted from liver to gut and de-conjugated.
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15
Q

What pigment gives faeces brown colour?

A
  • Stercobilin.
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16
Q

What gives urine yellow colour?

A
  • Urinobilin.
17
Q

What is jaundice?

A
  • Hyperbilirubinemia.
18
Q

Discuss the classifications of jaundice.

A
  1. Pre-hepatic: haemolytic.
  2. Intra-hepatic: viral, drugs
  3. Post-hepatic: obstruction
19
Q

What is pre-hepatic jaundice?

A
  • Haemolytic jaundice.
  • Bilirubin production is exceeding liver uptake capacity.
  • Commonly due to autoimmune dx: Rh- incompatibility, sickle cell dx, haemolytic disease of newborn.
  • Unconjugated
20
Q

What is intrahepatic jaundice?

A
  • Hepatocellular jaundice.
  • Problem within hepatocytes function.
  • Impaired uptake, conjugation or secretion.
  • Unconjugated or conjugated.
21
Q

What is post-hepatic jaundice?

A
  • Obstructive/ choleostatic jaundice.
  • Obstruction in biliary tract.
  • Conjugated bilirubin regurgitated back into systemic circulation.
  • Pale stools + dark urine.
22
Q

What is Kernicterus (bilirubin encephalopathy)?

A
  • Results from untreated hyperbilirubinemia w/bilirubin levels 25 or higher.
  • Signs: lethargy, tonic motions such as backward arching of the neck and trunk, hypotonia.
23
Q

What is Gilbert’s syndrome?

A
  • Benign congenital unconjugated hyperbilirubinemia.
  • Defect in UDP glucuronyl transferase.
  • Treatment: phenobarbitone.
24
Q

What is Crigler-Najjar syndrome?

A
  • Congenital unconjugated hyperbilirubinemia.
  • Defect in UDP glucuronyl transferase.
  • Type 1&2.
25
Q

What is Dubin- Johnson syndrome and Rotor Syndrome?

A
  • Benign autosomal recessive disorders presenting with conjugated hyperbilirubinemia.
  • Characterised by impaired biliary secretion of conjugated bilirubin.
  • Grossly black liver. Benign.
  • Mutation in MRP2 (DJS).