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Chemical Pathology > Liver Chemical Pathology > Flashcards

Liver Chemical Pathology Flashcards

0
Q

Which organs does the hepatic portal vein drain? What does blood from each organ normally carry?

A

Spleen - bilirubin
GI - nutrients, toxins, bacteria
Pancreas - insulin, glucagon

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1
Q

Which blood vessels drain into the liver?

A 
Hepatic artery (25% of liver blood flow)
Hepatic portal vein (75% of liver blood flow)
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2
Q

Where do the hepatic artery and portal vein enter the liver?

What happens to these vessels at this area?

A

Enter at the porta hepatis.

Each artery then divides into two branches > further divide to give hepatic arterioles and portal venules

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3
Q

What are varices?

A

A type of varicose vein that develops in veins in the linings of the esophagus and upper stomach when these veins fill with blood and swell due to an increase in blood pressure in the portal veins.

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4
Q

Name the three anastomotic connections between the the systemic and portal circulation?

A

Paraumbilical veins
Lower oesophagus
Rectal veins

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5
Q

What is the significance of anastomotic connections between portal and systemic circulation?

A

Varices and portal-systemic shunting occur at these points in portal hypertension.

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6
Q

Venous drainage of the liver?

A

Hepatic venules > form three hepatic veins > drain into inferior vena cava.

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7
Q

How can one subdivide the acinus of a liver lobule and how is this of use?

A

Peri portal area:
- highest O2 content therefore least susceptible to ischemic damage
Mediolobular area:
- intermediate area
Centrilobular area:
- lowest O2 content therefore most susceptible to ischemic damage
- involved in drug metabolism
- most susceptible to drug induced damage

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8
Q

What are the sources of bilirubin?

A

Haemoglobin:
- RBC breakdown (RES in spleen) ~ 70-80%
- ineffective erythropoiesis (bone marrow)
Other haem-containing proteins:
- myoglobin and cytochrome P450 in liver

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9
Q

What is ineffective erythropoiesis?

A

Active erythropoiesis with premature death of RBC’s.

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10
Q

What is Haemoglobin broken down into?

A

Globin (a protein) > constituent amino acids

Haem > CO, Fe, bilirubin (via biliverdin)

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11
Q

What colour is biliverdin and why is this interesting?

A

Is green > gives the green colour sometimes seen in bruises.

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12
Q

Features of unconjugated bilirubin?

A

Is a hydrophobic molecule.
Binds to hydrophobic sites on albumin.
DOES NOT APPEAR IN URINE.
Can be displaced from albumin by drugs Eg) salicylates, sulphonamides

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13
Q

Normal levels of unconjugated bilirubin exist at <3umol/L. Why is it dangerous if these levels rise?

A

Free unconjugated bilirubin is neurotoxic!

High concentrations > deposits in cell membrane > kernicterus

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14
Q

What is kernicterus?

A

Bilirubin-induced brain dysfunction.

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15
Q

How is bilirubin taken up by the liver?

A

Unconjugated bilirubin > carried in plasma to sinusoids > enters space of Disse > dissociates from albumin at hepatocyte membrane > taken up by hepatocyte by carrier-mediated process.

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16
Q

Within the hepatocyte what does bilirubin bind to?

A

Ligandin.

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17
Q

How is bilirubin conjugated by the liver?

A

Bilirubin conjugated with glucuronic acid by UDPGT1 > bilirubin monoglucuronide(BMG) > UDPGT2 > bilirubin diglucuronide(DMG)

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18
Q

Why does the liver have to conjugate bilirubin?

A

Because conjugated bilirubin is more water-soluble and can therefore be excreted in bile or urine.

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19
Q

Is conjugated bilirubin found in plasma under normal circumstances?

A

No.

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20
Q

Where and how is conjugated bilirubin transported to by hepatocytes?

A

Into bile canaliculi via an energy-dependent carrier-mediated process.

  • is sensitive to injury
  • canalicular step thought to be rate-limiting step in bilirubin metabolism
21
Q

Where does bile flow from biliary canaliculi?

A

Canaliculi > bile ducts > duodenum

22
Q

What happens to conjugated bilirubin in the GIT?

A

Conjugated bilirubin is converted to urobilinogen by bacterial flora.

23
Q

What happens to urobilinogen in the GIT?

A

Further converted into stercobilin and urobilin.

24
Q

What colour is:

  • urobilinogen
  • stercobilin
  • bilirubin
A

Urobilinogen - colorless
Stercobilin - brown (gives faeces characteristic colour)
Bilirubin - yellow

25
Q

Why may newborns and people on broad spectrum antibiotic therapy excrete yellow faeces?

A

Die to the absence of bacterial flora > conjugated bilirubin is yellow

26
Q

Is all urobilinogen excreted in the faeces?

A

No, some is reabsorbed into the portal circulation.

  • taken up by liver and re-excreted (enterohepatoc circulation)
  • some urobilinogen appears in urine
27
Q

How can one test for urobilinogen in the urine?

A

Dipstick test.

28
Q

What gives urine it’s characteristic yellow colour?

A

Urobilinogen > urobilin (yellow)

29
Q

Comment on re uptake of urobilinogen into the liver?

A

Is sensitive to liver damage.

30
Q

What can increased urinary urobilinogen be due to?

A

Increased bilirubin production (haemolysis)

Liver disease *not if obstruction prevent bilirubin reaching GIT

31
Q

What are bile acids formed from?

A

Cholesterol.

32
Q

What are primary bile acids? Name the two.

A

Bile acids of hepatic origin.
Chenodeoxycholic acid.
Cholic acid.

33
Q

What is the rate limiting and regulated step in the formation of primary acids?

A

7-alpha-hydroxylation of cholesterol.

34
Q

What needs to be done to primary bile acids before they are secreted into bile canaliculi? Why is this done?

A

Chenodeoxycholic acid and colic acid are conjugated to glycine or taurine. Is done to increase their solubility?

35
Q

How are conjugated primary bile acids moved into the bile canaliculi?

A

Via an energy-dependent carrier-mediated process.

*independent of bilirubin transport mechanism

36
Q

What happens to conjugated primary bile acids in the GIT?

A

Bacterial enzymes deconjugate and alpha-dehydroxylate the conjugated primary bile acids into secondary bile acids.

37
Q

Name the two secondary bile acids.

A

Lithocolic acid.

Deoxycholic acid.

38
Q

What happens to secondary bile acids in the GIT?

A

They are re absorbed by the ileum (75%) and colon (10%) > taken up by liver again and re-excreted.
ENTEROHEPATIC CIRCULATION

39
Q

Relate re-uptake of bile acids to liver damage and the efficiency of this process.

A

Re-uptake of bile acids by the liver is highly efficient.

Process is sensitive to liver damage.

40
Q

Are bile acids ever found in systemic circulation?

A

A small fraction of bile acids escape re-absorption and appear in the systemic circulation.

41
Q

What is a side-effect of high systemic bile acid concentrations?

A

Pruritis (itching)

42
Q

How may bile acids reach relatively high or low concentrations in systemic circulation?

A
  • Biliary tree obstruction > back pressure of bile acids into systemic circulation
  • Liver damage > impaired reabsorption of bile acids > more gradually reabsorbed
  • Ileal disease > bile acids not reabsorbed
43
Q

Outline the structure of bile acids.

A

Amphipathic molecules > results in detergent properties

44
Q

What are the functions of bile acids?

A

Solubilise cholesterol for excretion.
Solubilise dietary fat for absorption.
Stimulate bile formation and flow.

45
Q

Why is unconjugated bilirubin not normally found in plasma?

A

Because it is normally bound to albumin which is not filtered in the glomerulus.

46
Q

When are increased amounts of unconjugated bilirubin found in the plasma?

A

Increased bilirubin production.
Decreased uptake or conjugation of bilirubin.
Generalized hepatocellular dysfunction.
Rare inherited syndromes (Gilbert’s and Criggler-Najjar syndromes)

47
Q

When are increased amounts of conjugated bilirubin found in the plasma?

A

Obstructive liver disease.
Rare inherited syndromes (Rotors and Dubin-Johnson syndromes).
*decreased excretion of bilirubin!

48
Q

What can happen in prolonged obstructive jaundice?

A

Delta-bilirubin:

  • conjugated bilirubin covalently linked to albumin.
  • explains why conjugated hyperbilirubinaemia may occasionally persist even after bilirubinuria has disappeared
49
Q

What may result in increased urobilinogen in the urine? How is this measured?

A

Increased bilirubin production.
Decreased re-uptake into liver due to hepatocellular dysfunction (not if dysfunction prevent bilirubin reaching GIT)
*urobilinogen measured qualitatively using a dipstick

Chemical Pathology (1 decks)

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