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GI/Liver > Lec 20 jaundice LFTs > Flashcards

Lec 20 jaundice LFTs Flashcards

1
Q

Where is bilirubin primarily derived from?

A

mostly from breakdown of hemoglobin from old/injured RBCs or ineffective erythropoiesis

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2
Q

Where is bilirubin formed?

A

in liver and spleen

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3
Q

What are 3 causes of jaundice?

A
  • increased bilirubin production
  • impaired hepatic handling
  • benign lab finding
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4
Q

AT what level of bilirubin do you see jaundice?

A

bilirubin > 2.5 mg/dL

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5
Q

What 2 enzymes involved in formation of bilirubin from heme?

A
  • heme oxygenase

- biliverdin reductase

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6
Q

What is the reaction heme oxygenase catalyzes?

A

heme —> biliverdin

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7
Q

What is the reaction biliverdin reductase catalyzes?

A

biliverdin –> unconjugated bilirubin

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8
Q

Where are heme oxygenase/biliverdin reductase located in the body?

A
  • spleen
  • hepatocytes
  • renal tubular epithelium
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9
Q

How is bilirubin primarily present in blood?

A

primarly present as unconjugated bilirubin bound to albumin

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10
Q

Why do you see greenish hue in resolving hematoma?

A

sign of biliverdin before it is converted to bilirubin

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11
Q

What is normal total bilirubin in plasma? % conjugated vs unconjugated?

A

1-1.5 mg/dl normal value
90% unconjugated
10% conjugated

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12
Q

Which type of bilirubin is soluble?

A

conjugated is soluble

unconjugated is insoluble –> must be bound to albumin

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13
Q

What are the 4 steps of bilirubin elimination via biliary tract?

A
  • hepatocellular uptake
  • intracellular binding
  • conjugation
  • excretion of conjugates into bile
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14
Q

What enzyme mediates bilirubin conjugation?

A

UDP-glucoronosyl transferase

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15
Q

What happens to bilirubin once it is secreted into small intestine?

A
  • travels to ileum/colon where bacterial enzymes metabolize some of it to urobilinogen –> absorbed and recycled back to liver and to kidneys
  • some converted to stercobilinogen –> excreted in feces
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16
Q

What is the rate limiting step in bilirubin metabolism?

A

excretion of conjugated bilirubin into bile canaliculus by MRP2 protein

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17
Q

What form of bilirubin excreted in feces?

A

stercobilin

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18
Q

What form of bilirubin excreted in urine normally?

A

urobilinogen

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19
Q

Does bilirubin in urine indicated conjugated or unconjugated hyperbilirubinemia?

A

indicated conjugated hyperbilirubinemia

unconjugated is bound to albumin so is not filtered by glomerulus

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20
Q

What percent of urobilinogen in gut is excreted as stercobilin vs reasbrobed?

A

80% secreted as stercobilin

20% reabsorbed

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21
Q

What are 3 possible causes of unconjugated hyperbilirubinemia?

A
  • increased production of bilirubin
  • reduced hepatic clearance of bilirubin
  • inherited disorders of bilirubin metabolism
22
Q

What are some potential causes of increased production of bilirubin leading to unconjugated hyperbilirubinemia?

A
  • hemolysis
  • inherited hemolytic anemias
  • acquired hemolytic anemias
  • ineffective erythropoiesis
23
Q

What are 4 things you should think if unconjugated hyperbilirubinemia?

A
  • hemolytic cause [inherited or acquired hemolytic anemia]
  • physiologic
  • crigler-najjar
  • gilbert syndrome
24
Q

What is mech of neonatal jaundice? What level/type of bilirubin

A
  • occurs 2-5 days after birth –> have total bilirubin < 5-10 mg/dl
  • due to hepatic immaturity
  • unconjugated hyperbilirubinemia
25
Q

What is treatment for neonatal jaundice?

A

phototherapy

26
Q

What are 2 inherited disorders of bilirubin conjugation?

A
  • gilbert’s syndrome
  • Crigler-Najjar

thus have high unconjugated hyperbilirubinemia

27
Q

What is pathology of GIlbert’s syndrome?

A

partial deficiency of UDP-glucoronosyltransferase

have asymptomatic or mild jaundice with high unconjugated bilirubin that increases with fasting or stress

28
Q

What is pathology of Crigler Najjar syndrome type I?

A

no functional UDP-glucoronosyltransferase activity

have high indirect bilirubin 18-45 mg/dl

29
Q

When does Crigler Najjar type I usually present?

A

presents in neonatal period

30
Q

What are signs of Crigler-Najjar type 1?

A
  • jaundice
  • kernicterus [bilirubin deposition in brain] –> neuro impairment
  • undetectable UDP-glucoronyltrasnferase
  • normal liver histology
  • often fatal w/in first 15 mos of life
31
Q

What are total bilirubin levels in crigler-najjar type 1?

A

> 20 mg/dl

32
Q

What are total bilirubin levels in crigler najjar type 2?

A

< 20 mg/dl

33
Q

What is treatment for Crigler-Najjar type 1?

A

phototherapy
plasmapheresis
liver transplant

34
Q

What is pathology of crigler-najjar syndrome type II?

A

associated with > 10 different mutations in gluconyl transferase
have very reduced by detectable enzyme activity

35
Q

How does phenobarbital effect serum bilirubin in Gilberts vs Crigler type 1 vs Crigler type 2?

A

phenobarbital decreases serum bilirubin by A LOT in crigler type 2; has modest decrease in gilbert’s, and no change in crigler type 1

36
Q

What are total bilirubin levels in gilberts?

A

< 6 [usually < 3]

37
Q

What are 5 general causes of conjugated hyperbilirubinemias?

A
  • genetic
  • chronic liver disease
  • intrahepatic cholestasis of pregnancy
  • biliary obstruction
  • drugs
38
Q

What are two excretion defects of bilirubin?

A
  • Dubin Johnson syndrome

- Rotor syndrome

39
Q

What are two biliary tract diseases that can lead to conjugated hyperbilirubinemia?

A
  • primary sclerosing cholangitis

- primary biliary cirrhosis

40
Q

What is pathology of dubin johnson syndrome?

A
  • mutation in gene encoding for MRP2 transporter of conjugated bilirubin
  • leads to chronic intermittent jaundice with pigmented black bliver
41
Q

What are clinical features of dubin johnson syndrome?

A
  • asymptomatic direct jaundice in early adulthood
  • hepatosplenomegaly
  • black pigmented liver
42
Q

What is pathology of rotor’s syndrome?

A
  • due to unknown mutation

- have total bilirubin < 10

43
Q

What is intrahepatic cholestasis of pregnancy? What lab values?

A

occurs in 2nd or 3rd trimester

  • high ALT
  • high conjugated bilirubin
  • high serum bile acids
  • high alk phosphatase

disappears after delivery

44
Q

What are the 2 markers of hepatocyte damage?

A
  • aspartate aminotransferase [AST]

- alanine aminotransferase [ALT]

45
Q

What are the 3 markers of cholestasis?

A
  • bilirubin
  • alkaline phosphatase
  • gamma glutamyl transpeptidase [GGTP]
46
Q

What are the 2 markers of liver function?

A
  • albumin

- prothrombin time [PT] / INR

47
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in acute hepatocellular injury?

A
  • very high ALT
  • very high AST
  • normal or high alk phos, GGTP
  • high bilirubin
  • normal PT, albumin
48
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in chronic viral hepatitis?

A
  • high ALT
  • high AST
  • normal or high alk phos, GGTP
  • normal bilirubin, PT, albumin
49
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in NAFLD?

A
  • high ALT
  • high AST
  • normal or high alk phos, GGTP
  • normal bilirubin, PT, albumin
50
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in alcoholic hepatitis?

A
  • high ALT
  • higher AST
  • high alk phos, GGTP
  • high bilirubin
  • normal PT, albumin
51
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in cirrhosis?

A
  • normal or high ALT, AST, alk phos, GGTP, bilirubin
  • increased prothrombin time
  • decreased albumin
52
Q

What levels of ALT, AST, alk phos, GGTP, bilirubin, INR in biliary obstruction / cholestasis?

A
  • normal or high ALT, AST
  • high alk phos, GGTP, bilirubin
  • normal PT, albumin

GI/Liver (36 decks)

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