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Gastrointestinal Biology > GB 18. Bile and Jaundice > Flashcards

GB 18. Bile and Jaundice Flashcards

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1
Q

Where is bile synthesized and stored?

A
  • bile is synthesized in the liver
  • bile is stored in the gall bladder
  • bile can be released from both liver and gall bladder
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2
Q

What is the function of Cholescytokinin (CCK)?

A

It stimulates the gall bladder to contract and release the stored bile into the intestine

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3
Q

What are the primary functions of bile? [2]

A

[1] Excretory

[2] Digestive

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4
Q

What is bile synthesized in the liver and gall bladder primarily made up of?

A
  • mainly made of water
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5
Q

What is the excretory function of bile? What are the principal excretory products?

A

Goal: it provides an excretory route for many substances

Principal Excretory Products include….

  • bile pigments (degradation of haem)
  • cholesterol
  • bile acids/salt
  • drugs + their metabolites
  • particulate matter (removed from blood stream by Kupffer Cells of Liver)
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6
Q

What is the digestive function of bile? What mechanisms does this work by?

A

Goal: digests biomolecules (particularly fats)

Mechanisms:
- Alkaline Secretion
( rich in bicarbonate pH 8.0 )
( neutralizes acidity of gastric content )

  • Bile Salts + Phospholipids emulsify fats into small droplets
  • Bile Salts activate pancreatic hydrolase precursors
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7
Q

How do you create a bile acid?

A
  • cholesterol is conjugated with glycine and taurine

- there are primary and secondary bile acids

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8
Q

Where is a primary bile acid created? What are some examples?

A

created in liver

  • cholic acid
  • chenodeoxycholic acid
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9
Q

Where is a secondary bile acid created? What are some examples?

A

created in gut (through bacterial alpha-hydroxylase)

  • deoxycholic acid
  • lithocholic acid
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10
Q

How is a bile salt created?

A

conjugated bile acid + (Na+) + (K+)

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11
Q

What is bilirubin? Where can bilirubin be created (2 categories)?

A

a natural degradation product of haem in erythrocytes

  • 75% of bilirubin in the body is derived from RBCs
  • process requires phagocytosis and/or lysis of senescent RBCs

bilirubin can be created..

  • intravascular
  • extravascular
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12
Q

Hemolysis can either be…

A

[1] Intravascular

[2] Extravascular

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13
Q

Explain the process of extravascular hemolysis and formation of bilirubin.

A
  • haemoglobin of RBCs split into (a) globin and (b) haem
  • haem is then split into (a) Fe2+ and (b) bilirubin
  • the bilirubin is then excreted
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14
Q

What is the difference between intravascular and extravascular hemolysis?

A

Intravascular Hemolysis: RBCs that are lysed in the blood stream and release haem into the blood circulation

Extravascular Hemolysis: RBCs are lysed in the spleen (or by spherocytes)

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15
Q

What are the main mechanisms behind the handling of free (intra-vascular) haemoglobin? (the 3 complexes)

A

[1] Haptoglobin

  • haptoglobin binds to free haemoglobin
  • haemoglobin-haptoglobin complex metabolized in liver + spleen
  • forms iron-globin complex and bilirubin
  • PREVENTS LOSS OF IRON IN URINE

[2] Haemopexin

  • binds free haem
  • haem-hemopexin complex taken up by liver
  • iron stored bound to ferritin

[3] Methaemalbumin
- complex of oxidized haem and albumin

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16
Q

What is the main function of the haptoglobin-haemoglobin complex?

A

it prevents loss of iron in urine

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17
Q

What are the main goals of andling free intra-vascular haemoglobin? [3]

A

[1] scavenge iron
[2] prevents major iron losses
[3] complex free haem (very toxic)

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18
Q

List the steps involved in haem degradation and processing. (starting from haem)

A

[1] Haem
[2] Bilirubin Formation
[3] Albumin transports Unconjugated Bilirubin in the Bloodstream
[4] Taken up by Liver
[5] Bilurubin Conjugated with Glucoronic Acid (for water solubility)
[6] Excreted into Bile
[7] Urobilinogens Formed in Intestinal Tract
(a) re-absorbed: excreted from kidney as urinary urobilin
(b) excreted as faecal stercobilin

19
Q

What are the 2 fates that urobilinogens may undergo?

A

[1] re-absorbed: excreted from kidney as urinary urobilin

[2] excreted as faecal stercobilin

20
Q

What is Urobilinogen? How is it created?

A
  • is a colorless by-product of bilirubin reduction

- formed in the intestines by bacterial action on bilirubin

21
Q

What are the steps (+ enzymes) involved with the degradation of haem to bilirubin?

A

[1] Haem
[2] Heme Oxygenase Enzyme converts Haem to BILIVERDIN
[3] Biliverdin - intermediate
[4] Biliverdin Reductase Enzyme converts Biliverdin to UNCONJUGATED BILIRUBIN

22
Q

Explain the steps involved in the metabolism of bilirubin. (slides 16 + 17)

A

[1] liver takes up bilirubin by carrier-mediated facilitated diffusion (high binding capacity)

[2] binds to cytoplasmic proteins (ligand - glutathione S-transferases + protein Y)
- prevents efflux back into the blood

[3] bilirubin conjugated with glucoronic acid

  • catalysed by UDP-glucoronyl transferase
  • UDP-glucoronoosyltransferase
  • makes bilirubin water-soluble

[4] conjugated bilirubin secreted into biliary tree

  • active transport via Multidrug Resistant-Like Protein MRP-3)
  • RATE LIMITING STEP

[5] bile excreted from liver into gut
- glucoronidases in intestinal flora de-conjugate bilirubin

[6] some fat-soluble bilirubin is absorbed

[7] most bilirubin oxidized to urobilinogens

(a) colourless urobilinogen metabolised to brown stercobilin + excreted in faeces
(b) some re-absorbed urobilinogen oxidised to yellow urobilin + excreted by kidney

23
Q

What is the rate-limiting step in the metabolism of bilirubin?

A
  • the conjugated bilirubin being secreted into the biliary tree
  • active transport via Multidrug Resistant-like Protein MRP-3
24
Q

What is Icterus?

A

Jaundice

25
Q

Why does Jaundice arise? What is normally the upper limit? When number value does jaundice arise at?

A

Hyperbilirubinemia

  • normal upper limit for plasma [bilirubin] = 17umol/L
  • arises when patient has plasma [bilirubin] of approx. 35 umol/L
26
Q

What are the external signs of icterus?

A
  • yellow discolouration of skin and sclera
27
Q

What are the 3 classifications of jaundice? Give a brief overview of each.

A

[1] Pre-Hepatic Jaundice
- bilirubin production exceeds uptake capacity of liver

[2] Intra-Hepatic Jaundice

  • bilirubin cannot be taken up, conjugated and/or excreted because hepatocytes somehow damaged
  • e.g. liver damage (cirrhosis)

[3] Post-Hepatic Jaundice

  • obstruction to biliary flow
  • conjugated bilirubin “regurgitated” back into systemic circulation
  • e.g cancer of head of pancreas
28
Q

What are some other names for pre-hepatic jaundice?

A
  • haemolytic jaundice

- hematogenous jaundice

29
Q

What are some causes of pre-hepatic jaundice?

A
  • excess RBC lysis due to autoimmune disease (e.g. haemolytic disease of newborn, structural abnormal RBCs [sickle cell anaemia]…)
  • excess production of bilirubin following haemolysis
30
Q

What are some other names for intra-hepatic jaundice?

A
  • hepatic jaundice

- hepatocellular jaundice

31
Q

What are some causes of intra-hepatic jaundice?

A
  • impaired uptake, conjugation or secretion of bilirubin
  • reflects generalized liver cell (hepatocyte) dysfunction
  • hyperbilirubinaemia usually accompanied by other abnormal biochemical markers of liver function
  • – ELEVATED AST OR ALT
32
Q

What are some other names for post-hepatic jaundice?

A
  • obstructive jaundice

- choleostatic jaundice

33
Q

What are some of the causes of post-hepatic jaundice?

A
  • obstruction to biliary tract
  • plasma bilirubin conjugated
  • – other biliary metabolites (such as bile acids) accumulate in the plasma
34
Q

What is post-hepatic jaundice characterized by?

A
  • pale stools (absence of faecal bilirubin or stercobilin)

- dark urine (increased conjugated bilirubin)

35
Q

In complete obstruction of the biliary tract, what happens (in the case of post-hepatic jaundice)?

A

urobilin absent from urine

36
Q

What causes Newborn Jaundice? List some of the causes as well

A
  • unconjugated hyperbilirubinaemia
  • due to immaturity of enzymes involved in bilirubin conjugation

Causes:

  • immature/impaired hepatic uptake/conjugation of bilirubin
  • RBC destruction
37
Q

What is a major complication that may arise in Newborn Jaundice?

A
  • the free (unbound) unconjugated bilirubin may be deposited in the brain
  • can cause Kernicterus (rare form of brain damage)
38
Q

What is Kernicterus?

A
  • rare form of brain damage

- can arise when free (unbound) unconjugated bilirubin may be deposited in the brain

39
Q

What are some aggravating factors of Newborn Jaundice?

A
  • haemolysis
  • sulphonamides (displaces bilirubin from albumin)
  • Novobiocin - inhibits glucoronyltransferase
40
Q

What are some treatments for Newborn Jaundice?

A
  • Phototheraphy (UV Light) converts bilirubin to water-soluble, non-toxic form
  • exchange blood transfusion to remove excess bilirubin
  • Maternal Phenobarbitone prior to induction of labour of premature infant
  • – crosses placenta and induces synthesis of UDP-glucoronyl transferase [UDP-glucoronosyltransferase]
41
Q

What is Gilbert’s Syndrome? What is a possible treatment?

A
  • characterized by mild, fluctuating UNCONJUGATED HYPERBILIRUBINEMIA (often correlated with fasting or illness)
  • 50% of cases are inherited (mainly males than females)
  • caused by….
  • – reduced activity of UDP-glucoronyl transferase (UDP-glucoronosyltransferase)
  • – defect in bilirubin uptake

Treatment:
- treated with small doses of Phenobarbitone to stimulate UDP-glucoronyl transferase (UDP-glucoronosyltransferase) activity

42
Q

What is Crigler-Najjar Syndrome? What are the treatments for it?

A
  • autosomal recessive disorder presenting with UNCONJUGATED HYPERBILIRUBINEMIA
  • caused by mutation in gene coding for UDP-glucoronyl transferase
  • – type I: complete absence
  • – type II: marked reduction in enzyme activity
  • affected individuals at high risk for kernicterus

Treatment:

  • Type I by Liver Transplant (by 5 years of age)
  • Type II with Phenobarbitone or Phototherapy (10-12 hours/day)
43
Q

What is Dubin-Johnson and Rotor’s Syndrome?

A
  • benign autosomal recessive disorder presenting with CONJUGATED HYPERBILIRUBINEMIA
  • characterized by impaired biliary secretion of conjugated bilirubin (!)
  • mutation in gene coding for MRP-2 (Dubin-Johnson Syndrome)

Gastrointestinal Biology (15 decks)

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