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Lab D MT2 > Lab 9 - liver 1 > Flashcards

Lab 9 - liver 1 Flashcards

1
Q

Why do we measure Br?

A

evaluate different types of jaundice

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2
Q

What is Br derived from?

A

breakdown of aged RBC by the MPS

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3
Q

Br1 or indirect Br

A

unconjugated bound to albumin and formed in MPS

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4
Q

BrII

A

produced by hepatocytes
- conjugated with glucuronic acid

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5
Q

UBG
- absorption

A

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

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6
Q

UBG
- where is it measured from?

A

urine

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7
Q

3 derivates absorbed in ileum

A
  • UBG
  • Vit B12
  • Bile acids
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8
Q

where is the first place we see jaundice

A

mucous membrane of the genital tract

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9
Q

3 types of jaundice

A
  • prehepatic (haemolysis)
  • hepatic
  • post hepatic (cholestasis, obstruction of bile vessels and/or bile duct)
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10
Q

What is bilirubin oxidised into?
- how

A

Biliverdin
- exposed to UV light or stored too long

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11
Q

Causes of increase BrI in serum

A

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

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12
Q

Causes of increased BrII level in serum

A

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

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13
Q

What does an increase in UBG mean

A
  • haemolysis or liver cell damage
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14
Q

gmelin test colours

A

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

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15
Q

What does Erlich test show?

A

UBG

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16
Q

Examination of Br in faeces

A

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

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17
Q

Faeces:
Intense colour

A

Hyperchromic, pleichrom, hypercholic

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18
Q

Hypochromic, hypocholic

A

decreased colour due to liver failure

19
Q

Hypochromic, acholic

A

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

20
Q

Parameters - learn off table in handout!!

A
21
Q

Examination of hepatic excretory function
- tests?

A

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

Indocyane green (ICG) retention test

22
Q

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

A

renal clearance by hepatocytes

23
Q

BSP test
- colour?

A

purple in alkaline pH

24
Q

BSP test
- what does it break down into?

A

thioether and brom

brom is conjugated with glucaronic acid and excreted in bile

25
Q

BSP test
- elimation rate?

A

normally 95% gone from blood in 30-45 mins

dog and sheep - 30
cattle and eq - 40-45

26
Q

BSP test
- cons

A

Cats not liver specific
CAn cause anaphylactic shock

27
Q

BSP retention in
- dogs
- cats

A
  • 5-10%
  • 3-5%
28
Q

ICG test
- pros?

A

more liver specific in cats
- less dangerous

29
Q

ICG test: retention
- dogs
- cats

A

20-25%
15%

30
Q

Causes of increased BSP retention (main)?

A
  • primary liver failure
  • decreased hepatic perfusion
31
Q

what can cause primary liver failure?

A

 liver cirrhosis
 liver tumour
 hepatic lipidosis
 “lipid mobilisation syndrome”

32
Q

What can cause decreased hepatic perfusion

A

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

33
Q

congenital disease that may increase the BSP?§

A

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

34
Q

name the bile acids?

A

Cholic acid and chenodeoxycholic acid

35
Q

Bile acids:
what are they synthesised from?

A

cholesterol

36
Q

Bile acids:
Where do they travel from and to?

A

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

37
Q

Secondary bile acids
- names
- how are they formed?

A
  • lithocholic acid and deoxycholic acid
  • deconjugated from primary bile acids by the bacteria in the intestines
38
Q

Function of bile acids

A

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

39
Q

Bile acid conc after eatinfg?

A

increased

40
Q

What mediates bile acid release?

A

cholecystokinin-pancreozymin and secretin.

41
Q

When do we take a sample for bile acid analysis

A

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.

42
Q

Bile acids:
What anticoagulant do we use?

A

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

43
Q

Bile acids
- normal value

A

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

44
Q

Causes of increased bile acids in the blood?

A

 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)

Lab D MT2 (5 decks)

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