Bile and Its Components Quiz
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Questions and Answers

What is the primary function of bile in fat digestion?

  • It emulsifies and solubilizes fats. (correct)
  • It acts as a solvent for sugars.
  • It provides an energy source.
  • It reduces the temperature of the food.

    • Which factor induces the release of bile from the gallbladder?

  • Insulin
  • Secretin
  • Gastrin
  • Cholecystokinin (CCK) (correct)

    • Which component is NOT a principal excretory product of bile?

  • Bile acids
  • Glucose (correct)
  • Bile pigments
  • Cholesterol

    • What is the typical daily production of bile in adults?

    <p>500 mL</p> Signup and view all the answers

    Jaundice can be classified based on which of the following criteria?

    <p>Location of the bilirubin-handling defect</p> Signup and view all the answers

    What role do bile acids play in the composition of bile?

    <p>They act as emulsifiers for fats.</p> Signup and view all the answers

    Which part of the digestive system is primarily responsible for inducing the release of cholecystokinin?

    <p>Duodenum</p> Signup and view all the answers

    Which type of bilirubin is primarily dealt with in the liver?

    <p>Conjugated bilirubin</p> Signup and view all the answers

    What is the function of bile acids during digestion?

    <p>To facilitate fat digestion and absorption</p> Signup and view all the answers

    Where are primary bile acids synthesized in the body?

    <p>Liver</p> Signup and view all the answers

    What percentage of bile acids are reabsorbed in the ileum?

    <p>95%</p> Signup and view all the answers

    What leads to the conversion of primary bile acids into secondary bile acids?

    <p>Bacterial metabolism in the colon</p> Signup and view all the answers

    How are most senescent red blood cells (RBCs) destroyed in the body?

    <p>Through phagocytosis and/or lysis</p> Signup and view all the answers

    What is the primary characteristic of pre-hepatic jaundice?

    <p>Excess bilirubin production from haemolysis</p> Signup and view all the answers

    Which condition is associated with intra-hepatic jaundice?

    <p>Generalized liver dysfunction</p> Signup and view all the answers

    Which of the following could cause post-hepatic jaundice?

    <p>Biliary tract obstruction</p> Signup and view all the answers

    What type of bilirubin is typically elevated in pre-hepatic jaundice?

    <p>Unconjugated bilirubin</p> Signup and view all the answers

    Which biochemical markers are typically elevated in intra-hepatic jaundice?

    <p>AST and ALT</p> Signup and view all the answers

    What is the primary consequence of free iron ($Fe^{2+}$) being released during hemolysis?

    <p>It promotes tissue damage and inflammation.</p> Signup and view all the answers

    Which two enzymes are primarily involved in the degradation of hemoglobin to bilirubin?

    <p>Heme Oxygenase and Biliverdin reductase</p> Signup and view all the answers

    Which protein binds free hemoglobin in the blood to prevent iron loss through urine?

    <p>Haptoglobin</p> Signup and view all the answers

    What percentage of bilirubin in the body is derived from the breakdown of red blood cells?

    <p>75%</p> Signup and view all the answers

    What is the role of UDP-glucuronyl transferase in bilirubin metabolism?

    <p>To make bilirubin water-soluble</p> Signup and view all the answers

    What happens to conjugated bilirubin after it is synthesized in the liver?

    <p>It is secreted into bile ducts and excreted into the gut.</p> Signup and view all the answers

    Which of the following statements is true regarding jaundice?

    <p>It is characterized by hyperbilirubinemia.</p> Signup and view all the answers

    What is a common symptom associated with jaundice?

    <p>Pale feces</p> Signup and view all the answers

    How is excess bilirubin typically excreted from the body?

    <p>Through bile as stercobilin and via urine as urobilin</p> Signup and view all the answers

    What is the implication of high levels of bilirubin (> 35 µM/L) in the body?

    <p>It signifies potential hemolytic disease or liver dysfunction.</p> Signup and view all the answers

    What is a common consequence of complete bile duct obstruction?

    <p>Dark urine due to increased conjugated bilirubin</p> Signup and view all the answers

    Which condition is characterized by mild, fluctuating unconjugated hyperbilirubinaemia?

    <p>Gilbert's Syndrome</p> Signup and view all the answers

    What factor can aggravate jaundice in patients with Dubin-Johnson Syndrome?

    <p>Dehydration</p> Signup and view all the answers

    What is the typical treatment for Type I Crigler-Najjar Syndrome?

    <p>Liver transplant</p> Signup and view all the answers

    What is a typical complication of severe unconjugated hyperbilirubinaemia in newborns?

    <p>Kernicterus</p> Signup and view all the answers

    Which type of bilirubin is primarily increased in post-hepatic jaundice?

    <p>Conjugated bilirubin</p> Signup and view all the answers

    What is the typical timeframe for newborn jaundice to resolve without treatment?

    <p>Within 10 days</p> Signup and view all the answers

    What laboratory finding is typically normal in pre-hepatic jaundice?

    <p>Conjugated bilirubin levels</p> Signup and view all the answers

    Which medication can induce synthesis of UDP-glucuronyl transferase in Gilbert's Syndrome?

    <p>Phenobarbitone</p> Signup and view all the answers

    What is a key difference in the urine findings between intra-hepatic and post-hepatic jaundice?

    <p>Urine urobilinogen is absent in intra-hepatic jaundice</p> Signup and view all the answers

    Which statement accurately describes the pathway of bile acids in the body?

    <p>Primary bile acids are synthesized in the liver and conjugated before storage.</p> Signup and view all the answers

    What role does CCK play in bile acid metabolism?

    <p>It stimulates the release of bile from the gallbladder after a meal.</p> Signup and view all the answers

    How are primary bile acids modified before they are stored in the gallbladder?

    <p>They are conjugated to taurine or glycine.</p> Signup and view all the answers

    Which of the following accurately describes bilirubin's origin?

    <p>Bilirubin is a breakdown product of the degradation of hemoglobin from senescent erythrocytes.</p> Signup and view all the answers

    What occurs to bile acids following their initial release into the intestine?

    <p>They are mostly reabsorbed in the ileum and returned to the liver.</p> Signup and view all the answers

    What distinguishes intra-hepatic jaundice from the other forms of jaundice?

    <p>It is characterized by impairment in bilirubin uptake and conjugation.</p> Signup and view all the answers

    Which condition is most commonly associated with pre-hepatic jaundice?

    <p>Hemolytic disease of the newborn.</p> Signup and view all the answers

    What is a hallmark biochemistry finding in post-hepatic jaundice?

    <p>High levels of conjugated bilirubin in the plasma.</p> Signup and view all the answers

    Which of the following conditions might lead to intra-hepatic jaundice?

    <p>Genetic liver disorders.</p> Signup and view all the answers

    What plasma bilirubin level is considered normal, and how does this relate to conditions associated with excessive bilirubin?

    <p>Normal level is ~17μmol/L, but levels can rise in hemolytic conditions.</p> Signup and view all the answers

    What is the primary alkaline pH range of bile produced by adults?

    <p>7.5 – 8</p> Signup and view all the answers

    Which of the following is NOT a principal function of bile?

    <p>Storage of bile salts</p> Signup and view all the answers

    What initiates the release of bile from the gallbladder?

    <p>Cholecystokinin (CCK)</p> Signup and view all the answers

    Which component is directly responsible for the emulsification of fats in bile?

    <p>Bile acids</p> Signup and view all the answers

    Which type of bilirubin is primarily formed from the breakdown of hemoglobin?

    <p>Unconjugated bilirubin</p> Signup and view all the answers

    What term describes the clinical condition with yellowing of the skin due to excess bilirubin?

    <p>Jaundice</p> Signup and view all the answers

    What is a common cause of post-hepatic jaundice?

    <p>Bile duct obstruction</p> Signup and view all the answers

    Which organ is primarily responsible for the removal of particulate matter from the bloodstream as part of bile function?

    <p>Liver</p> Signup and view all the answers

    What is the primary consequence of the detoxification process of free haem in the blood?

    <p>Formation of bilirubin and preventing iron loss</p> Signup and view all the answers

    Which enzyme is responsible for the conversion of haem to biliverdin during bilirubin formation?

    <p>Heme Oxygenase</p> Signup and view all the answers

    How is unconjugated bilirubin made water-soluble in the liver?

    <p>By conjugation with glucuronic acid</p> Signup and view all the answers

    What initiates the process of bilirubin metabolism in the liver?

    <p>Facilitated diffusion by OATP transporter</p> Signup and view all the answers

    What primarily distinguishes post-hepatic jaundice from other forms of jaundice?

    <p>Obstruction in the biliary tract</p> Signup and view all the answers

    Why is free haem in the blood considered toxic?

    <p>It causes tissue damage and inflammation</p> Signup and view all the answers

    What percentage of bilirubin is derived from heme-containing proteins other than RBCs?

    <p>25%</p> Signup and view all the answers

    How does the liver handle free haem in the blood?

    <p>Via binding to hemopexin and haptoglobin</p> Signup and view all the answers

    What is a common associated symptom of jaundice?

    <p>Abdominal pain</p> Signup and view all the answers

    Which protein is crucial for the secretion of conjugated bilirubin into bile?

    <p>MRP-3</p> Signup and view all the answers

    What is the primary genetic cause of Crigler-Najjar Syndrome?

    <p>Mutation in the gene coding for UDP-glucuronyl transferase</p> Signup and view all the answers

    Which laboratory finding is distinctively absent in post-hepatic jaundice?

    <p>Urinary urobilinogen</p> Signup and view all the answers

    What characterizes Gilbert’s Syndrome?

    <p>Mild, fluctuating unconjugated hyperbilirubinaemia</p> Signup and view all the answers

    Which treatment option is specifically indicated for Type I Crigler-Najjar Syndrome?

    <p>Liver transplant</p> Signup and view all the answers

    What is a common consequence of severe jaundice in newborns?

    <p>Kernicterus</p> Signup and view all the answers

    Which of the following conditions is typically associated with conjugated hyperbilirubinaemia?

    <p>Dubin-Johnson Syndrome</p> Signup and view all the answers

    Which aggravating factor can lead to worsening of jaundice in patients with Dubin-Johnson Syndrome?

    <p>Dehydration</p> Signup and view all the answers

    What is the usual course of treatment for newborn jaundice that is transient?

    <p>No treatment required</p> Signup and view all the answers

    What enzyme is primarily affected in Gilbert’s Syndrome?

    <p>UDP-glucuronyl transferase</p> Signup and view all the answers

    In which type of jaundice is urine bilirubin typically absent?

    <p>Pre-hepatic jaundice</p> Signup and view all the answers

    Study Notes

    Bile

    • Produced by the liver (~500mL daily in adults)
    • Yellow-green in colour
    • Alkaline pH (7.5-8)
    • Stored in the gall bladder
    • Released by cholecystokinin (CCK) after eating
    • Principal functions:
      • Fat digestion and absorption
      • Excretion of excess cholesterol and metabolites
      • Neutralisation of stomach acid

    Components of Bile

    • Bile acids
    • Bile pigments
    • Cholesterol
    • Drugs and metabolites
    • Particulate matter

    Bile Acids

    • Primary bile acids are synthesised in the liver from cholesterol
    • Conjugated with glycine or taurine
    • Stored in the gall bladder
    • Released in response to a meal to facilitate fat digestion and absorption
    • Primary bile acids are converted to secondary bile acids by bacteria in the colon
    • Excreted in faeces

    Bilirubin

    • Natural degradation product of haem
    • Erythrocytes (RBCs) have a finite lifespan (~60-120 days)
    • Senescent RBCs destroyed by phagocytosis/lysis
    • Haem is toxic and must be metabolised to bilirubin in a 2-step process
    • Most bilirubin in the body is derived from RBCs

    Bilirubin Formation

    • Haem is converted to biliverdin by Heme Oxygenase
    • Biliverdin is converted to bilirubin by Biliverdin reductase
    • Bilirubin binds to albumin and is transported to the liver
    • Bilirubin is conjugated with glucuronic acid by UDP-glucuronyl transferase (UDP-glucuronosyltransferase) to make it water-soluble
    • Conjugated bilirubin is secreted into bile ducts and excreted

    Causes of Jaundice

    • Pre-hepatic jaundice
      • High bilirubin production
      • Haemolytic disease of newborn
      • Structurally abnormal RBCs
      • Breakdown of extravasated blood
    • Intra-hepatic jaundice
      • Impaired uptake, conjugation or secretion of bilirubin
      • Liver disease
      • Neonatal jaundice
    • Post-hepatic jaundice
      • Obstruction of biliary flow
      • Gallstones
      • Cancer
      • Pale stools
      • Dark urine

    Newborn Jaundice

    • Common, particularly in premature infants
    • Occurs 2-4 days after birth
    • Caused by immaturity of enzymes involved in bilirubin conjugation
    • Usually transient, resolving within first 10 days of life
    • Complications:
      • Kernicterus
    • Treatment:
      • Phototherapy
      • Phenobarbitone administration
      • Exchange blood transfusion

    Gilbert's Syndrome

    • Most common inherited disorder of bilirubin conjugation
    • Mild, fluctuating unconjugated hyperbilirubinaemia
    • Onset typically during adolescence
    • Reduced activity of UDP-glucuronyl transferase
    • Can be treated with phenobarbitone

    Crigler-Najjar Syndrome

    • Rare autosomal recessive disorder
    • Severe unconjugated hyperbilirubinaemia
    • Mutation in gene coding for UDP-glucuronyl transferase
    • Type l - complete absence of enzyme
    • Type ll - marked reduction in enzyme activity
    • Affected individuals at high risk for kernicterus
    • Treatment:
      • Type l - Liver transplant
      • Type ll - Phenobarbitone or phototherapy

    Dubin-Johnson Syndrome

    • Benign genetic disorder
    • Impaired biliary secretion of conjugated bilirubin
    • Mutation in gene coding for MRP-2
    • Jaundice may worsen with aggravating factors
    • Treatment not usually necessary

    Bile

    • Complex fluid produced by the liver
    • ~500mL produced daily by adults
    • Yellow-green color
    • Alkaline pH (7.5 – 8)
    • Stored in the gallbladder
    • Released into the duodenum in response to cholecystokinin (CCK)
    • CCK is released from I cells in the duodenum after eating a meal
    • CCK induces gallbladder contraction

    Bile Functions

    • Facilitates fat digestion and absorption
    • Excretes excess cholesterol and metabolites
    • Neutralizes stomach acid

    Bile Composition

    • Bile acids
    • Bile pigments (from haem degradation)
    • Cholesterol
    • Drugs and their metabolites
    • Particulate matter (removed from the bloodstream by Kupffer cells in the liver)

    Bile Acids

    • Amphipathic molecules - charged (hydrophilic) on one side, uncharged (hydrophobic) on the other
    • Primary bile acids are synthesized in the liver from cholesterol
    • Conjugated to glycine or taurine
    • Stored in the gallbladder
    • Released in response to a meal to facilitate fat digestion and absorption
    • Primary bile acids are converted to secondary bile acids by bacteria in the colon
    • Provide a pathway for excess cholesterol excretion from the body

    Bilirubin

    • A natural degradation product of haem
    • Released from senescent red blood cells (RBCs)
    • RBCs have a finite lifespan (~60-120 days)
    • Most RBCs are destroyed extravascularly (in the liver, spleen, or bone marrow)
    • Intravascular haemolysis also occurs, usually as a consequence of disease
    • Free haem is toxic and must be metabolised
    • 75% of the bilirubin in the body is derived from RBCs
    • The remainder comes from other heme-containing proteins (e.g., myoglobin, cytochromes)
    • Bilirubin metabolism is a 2-step detoxification process

    Handling of Free Haemoglobin

    • Free haem is toxic and must be bound to serum proteins for detoxification
    • Haptoglobin binds to haemoglobin, forming a complex that is metabolized in the liver and spleen
    • Haemopexin binds to free haem, forming a complex that is taken up by the liver
    • Albumin binds to oxidized haem, forming Met-haemalbumin

    Degradation of Haem to Bilirubin

    • Occurs mostly in the spleen
    • Requires 2 enzymes:
      • Heme oxygenase (primarily in the spleen)
      • Biliverdin reductase

    Metabolism of Bilirubin

    • Taken up by the liver by carrier-mediated facilitated diffusion (transporters OATP)
    • Binds to cytoplasmic proteins in hepatocytes (e.g., Ligandin, Protein Y)
    • Bilirubin is conjugated with glucuronic acid by UDP-glucuronyl transferase (UDP-glucuronosyltransferase), making it water-soluble
    • Conjugated bilirubin is secreted into the bile ducts (active transport via MRP-3)
    • Bile is excreted from the liver into the gut
    • Glucoronidases in colonic bacteria de-conjugate bilirubin to urobilinogen (colorless)
    • Urobilinogen is oxidized by bacteria to stercobilin (brown pigment)
    • Most stercobilin is excreted in feces
    • Some urobilinogen is reabsorbed into the portal blood
    • Some urobilinogen is excreted into the urine as urobilin.

    Jaundice

    • Yellowing of the skin, whites of the eyes, and mucous membranes due to high bilirubin levels (hyperbilirubinemia)
    • Indicates underlying disease involving abnormal heme metabolism, liver dysfunction, or biliary tract obstruction
    • Typically occurs when serum bilirubin levels are > 35µM/L (normal = 17uM/L)
    • Common in newborns
    • Can lead to neurological damage (kernicterus) in severe cases
    • Treatment depends on the underlying cause

    ### Classification of Jaundice

    • Pre-hepatic (haemolytic) jaundice: Bilirubin production exceeds the uptake capacity of the liver.
    • Intra-hepatic (hepatocellular) jaundice: Bilirubin cannot be taken up, conjugated, and/or excreted due to hepatocellular damage.
    • Post-hepatic (cholestatic) jaundice: Obstruction to biliary flow.

    Pre-hepatic Jaundice

    • Also called haemolytic jaundice
    • Excess production of bilirubin following massive hemolysis
    • Excess RBC lysis is often due to:
      • Autoimmune disease (e.g., haemolytic disease of the newborn)
      • Structurally abnormal RBCs (e.g., sickle cell disease)
      • Breakdown of extravasated blood
    • Characterized by high plasma levels of unconjugated bilirubin

    Intra-hepatic Jaundice

    • Also called hepatocellular jaundice
    • Impaired uptake, conjugation, or secretion of bilirubin
    • Reflects generalized liver cell dysfunction (e.g., hepatitis, cirrhosis, genetic abnormalities)
    • Hyperbilirubinaemia usually accompanied by other abnormal biochemical markers of liver function (e.g., elevated AST, ALT)

    Post-hepatic Jaundice

    • Also called obstructive jaundice or cholestatic jaundice
    • Caused by obstruction to the biliary tract (e.g., gallstones, cancer)
    • Plasma bilirubin is primarily conjugated
    • Other bile constituents (e.g., bile acids) also accumulate in plasma
    • Characterized by
      • Pale stools (absence of faecal bilirubin or stercobilin)
      • Dark urine (increased conjugated bilirubin)

    Differential Diagnosis of Jaundice

    • Pre-hepatic: Elevated unconjugated bilirubin; normal ALT, AST, and ALP; absent urine bilirubin; present urine urobilinogen.
    • Intra-hepatic: Elevated conjugated and unconjugated bilirubin; increased ALT, AST, and ALP; present urine bilirubin; present urine urobilinogen.
    • Post-hepatic: Elevated conjugated bilirubin; normal ALT, AST; increased ALP; present urine bilirubin; absent urine urobilinogen.

    Newborn Jaundice

    • Common, particularly in premature infants
    • Occurs 2-4 days after birth
    • Due to immaturity of enzymes involved in bilirubin conjugation (e.g., UDP-glucuronyl transferase)
    • Usually transient, resolving within the first 10 days of life

    ### Newborn Jaundice Complications

    • Unconjugated bilirubin can deposit in the brain, leading to kernicterus (rare form of brain damage)
    • Aggravating factors
      • Haemolysis (infants have increased RBC turnover)
      • Breastfeeding (dehydration can increase RBC lysis)
      • Sulphonamides (displace bilirubin from albumin)
      • Antibiotics (can inhibit glucuronyltransferase)

    Newborn Jaundice Treatment

    • Usually resolves on its own within 10 days
    • Phototherapy (UV light) converts bilirubin to a water-soluble, non-toxic form.
    • Phenobarbital administration (induces synthesis of UDP-glucuronyl transferase)
    • Exchange blood transfusion to remove excess bilirubin
    • Jaundice within the first 24 hours of birth or that persists beyond 10 days is usually pathological

    Gilbert's Syndrome

    • Most common inherited disorder of bilirubin conjugation
    • Characterized by mild, fluctuating unconjugated hyperbilirubinaemia
    • Onset of symptoms is typically during adolescence
    • Caused by reduced activity of UDP-glucuronyl transferase (UDP-glucuronosyltransferase), preventing bilirubin conjugation in the liver
    • Can be treated with phenobarbital to stimulate UDP– glucuronyl transferase

    Crigler-Najjar Syndrome

    • Extremely rare autosomal recessive disorder presenting with severe unconjugated hyperbilirubinaemia
    • Caused by a mutation in the gene coding for UDP-glucuronyl transferase (UDP-glucuronosyltransferase)
      • Type I: complete absence
      • Type II: marked reduction in enzyme activity
    • Affected individuals are at high risk for kernicterus
    • Treatment:
      • Type I: by liver transplant in some cases (by 5 years old)
      • Type II: with phenobarbital or phototherapy (10-12 hours per day)

    Dubin-Johnson Syndrome

    • Benign genetic disorder presenting with conjugated hyperbilirubinaemia
    • Most patients have lifelong, recurrent mild symptoms of jaundice
    • Characterized by impaired biliary secretion of conjugated bilirubin (intrahepatic jaundice)
    • Mutation in the gene coding for MRP-2
    • Jaundice may worsen with aggravating factors (e.g., pregnancy, oral contraceptives)
    • Treatment is not usually necessary

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