Lab 9 - liver 1

Question 1

Why do we measure Br?

Answer 1

evaluate different types of jaundice

Question 2

What is Br derived from?

Answer 2

breakdown of aged RBC by the MPS

Question 3

Br1 or indirect Br

Answer 3

unconjugated bound to albumin and formed in MPS

Question 4

BrII

Answer 4

produced by hepatocytes
- conjugated with glucuronic acid

Question 5

UBG
- absorption

Answer 5

bacterially reduced
- absorbed in ileum and colon and gets into circ

Question 6

UBG
- where is it measured from?

Answer 6

urine

Question 7

3 derivates absorbed in ileum

Answer 7

• UBG
• Vit B12
• Bile acids

Question 8

where is the first place we see jaundice

Answer 8

mucous membrane of the genital tract

Question 9

3 types of jaundice

Answer 9

• prehepatic (haemolysis)
• hepatic
• post hepatic (cholestasis, obstruction of bile vessels and/or bile duct)

Question 10

What is bilirubin oxidised into?
- how

Answer 10

Biliverdin
- exposed to UV light or stored too long

Question 11

Causes of increase BrI in serum

Answer 11

Excess production of Br I due to increased RBC destruction.
 acute haemolysis
 absorption of haemoglobin following massive internal haemorrhage, or after big
haematoma formation (so called ”resorption icterus”)
 transfusion of stored blood, which contains many dyeing or dead RBCs

Decreased uptake of Br I from the blood by liver cells:
 impaired hepatic function
 (acute haemolysis)

Decreased rate of conjugation of Br I by liver cells
 impaired hepatic function

Question 12

Causes of increased BrII level in serum

Answer 12

after severe acute intravascular haemolysis (increased production).

Decreased excretion of Br II by liver cells:

Obstruction of bile canaliculi within the liver,

Obstruction of bile canaliculi due to blockage or compression of the bile duct:
Rupture of the biliary vessels or duct or gall bladder –> bile peritonitis

Question 13

What does an increase in UBG mean

Answer 13

• haemolysis or liver cell damage

Question 14

gmelin test colours

Answer 14

 yellow - urine itself
 white (opaque) – protein
 purple - indicane (indol-sulphate)
 green – biliverdin
 brown - urobilinogen (UBG)

Question 15

What does Erlich test show?

Answer 15

UBG

Question 16

Examination of Br in faeces

Answer 16

Increased BrII –> Increased UBG –> increased stercobilin in faeces –> orange colour

Question 17

Faeces:
Intense colour

Answer 17

Hyperchromic, pleichrom, hypercholic

Question 18

Hypochromic, hypocholic

Answer 18

decreased colour due to liver failure

Question 19

Hypochromic, acholic

Answer 19

very light colour (grey), due to bile duct obstruction

Question 20

Parameters - learn off table in handout!!

Question 21

Examination of hepatic excretory function
- tests?

Answer 21

Brom-sulphalein- (sulphobromtalein-) (BSP) retention test

Indocyane green (ICG) retention test

Question 22

Examination of hepatic excretory function
- What do we examine in BSP test?

Answer 22

renal clearance by hepatocytes

Question 23

BSP test
- colour?

Answer 23

purple in alkaline pH

Question 24

BSP test
- what does it break down into?

Answer 24

thioether and brom

brom is conjugated with glucaronic acid and excreted in bile

Question 25

BSP test - elimation rate?

Answer 25

normally 95% gone from blood in 30-45 mins dog and sheep - 30 cattle and eq - 40-45

Question 26

BSP test - cons

Answer 26

Cats not liver specific CAn cause anaphylactic shock

Question 27

BSP retention in - dogs - cats

Answer 27

- 5-10% - 3-5%

Question 28

ICG test - pros?

Answer 28

more liver specific in cats - less dangerous

Question 29

ICG test: retention - dogs - cats

Answer 29

20-25% 15%

Question 30

Causes of increased BSP retention (main)?

Answer 30

- primary liver failure - decreased hepatic perfusion

Question 31

what can cause primary liver failure?

Answer 31

 liver cirrhosis  liver tumour  hepatic lipidosis  "lipid mobilisation syndrome"

Question 32

What can cause decreased hepatic perfusion

Answer 32

 right sided heart failure  portosystemic shunt  arteriole-venous fistulas in liver  blockage in portal vessels

Question 33

congenital disease that may increase the BSP?§

Answer 33

decreased UDP-glucuronyl transferase activity in liver cells (congenital disorder)

Question 34

name the bile acids?

Answer 34

Cholic acid and chenodeoxycholic acid

Question 35

Bile acids: what are they synthesised from?

Answer 35

cholesterol

Question 36

Bile acids: Where do they travel from and to?

Answer 36

excreted to bile --> stored in gallbladder --> released into duodenum

Question 37

Secondary bile acids - names - how are they formed?

Answer 37

- lithocholic acid and deoxycholic acid - deconjugated from primary bile acids by the bacteria in the intestines

Question 38

Function of bile acids

Answer 38

detergent character - have a key role in micelle formation and lipid digestion - anti endotoxin effect

Question 39

Bile acid conc after eatinfg?

Answer 39

increased

Question 40

What mediates bile acid release?

Answer 40

cholecystokinin-pancreozymin and secretin.

Question 41

When do we take a sample for bile acid analysis

Answer 41

1) after 12 hours starvation, 2) after eating, postprandial value - postprandial value can be 10 times (dog), 5-6 times (cat) more than the value measured after starvation.

Question 42

Bile acids: What anticoagulant do we use?

Answer 42

Na- EDTA or Na- citrate bc heparin diturbs the measurement

Question 43

Bile acids - normal value

Answer 43

Normal value (fasting): 6 µmol/l (carnivores) 20-30 µmol/l (other animals).

Question 44

Causes of increased bile acids in the blood?

Answer 44

 liver injury, hepatic cell damage - increased outflow of bile acids from the damaged hepatocytes to the blood,  bile duct obstruction or bile endothelial cell damage - decreased secretion of bile acids to the bile, increased outflow to the plasma instead,  decrease in liver function, therefore decreased uptake of the absorbed bile acids (note: increased urobilinogen level !)  biliary stasis (cholangiohepatitis cirrhosis, hepatic or pancreatic neoplasm, pancreatitis)  portosystemic shunt (absorbed bile acids bypass liver tissue)