Lab D > 10 - Liver Function 1 > Flashcards

10 - Liver Function 1 Flashcards

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1
Q

What type of molecule is bilirubin?

A

Lipid soluble, derives from breakdown of RBCs by mononuclear phagocyte system.

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2
Q

Most important parameter of liver function

A

Bilirubin conc in the blood

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3
Q

Types of bilirubin

A
  • Br1: Indirect, unconjugated. Binds to albumin. Formed in MPS cells.
  • Br2: Direct, glucoronic acid conjugated, produced by hepatocytes with UDP-glucoronyl transferase enzyme, is excreted into the bile.
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4
Q

Transport molecules of bilirubin

A

Albumin and glucoronic acid

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5
Q

What is UBG?

A

Urobilinogen, the bacterially reduced form of Br (or stercobilinogen).

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6
Q

Where is UBG absorbed and excreted?

A

Absorbed in ileum and colon, into the circulation, where one part is taken up by hepatocytes and urea is formed, and the other part is filtered through the kidneys and excreted into urine. The rest is excreted from intestines into feces.

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7
Q

What samples are UBG determined from?

A

Urine samples. It is not measured from plasma.

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8
Q

Which dedicates are absorbed only at the special mucosa of the ileum?

A

UBG, vit.B12 and vile acids

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9
Q

When can Br be detected in the blood?

A
  • When only slightly elevated: lab measuring methods
  • When much higher than normal: visible yellow discolorizution of the plasma or serum. Can be depleted in fat and collagen containing tissue.
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10
Q

What disease and body region should be evaluated when we check increased Br?

A

Icterus of mucous membranes, esp. genital tract.

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11
Q

Major causes for of increased Br in serum or plasma

A

3 types of jaundices:

  • Prehepatic (haemolysis)
  • Hepatic (hepatocullular) (liver cell damage and damage of the intrahepatic structure that leads to leakage bw. sinusoids and biliary vessels)
  • Posthepatic (cholestasis, obstruction of bile vessels and/or bile ducts)
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12
Q

How can bilirubin be oxidised?

A
  • To greenish biliverdin (greenish urine)
  • By sunlight
  • If stored too long, esp at higher temp
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13
Q

Lab signs of bilirubinuria

A

Urine is dark yellow

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14
Q

Blood bilirubin measurement

  1. Methods
  2. Reagents
  3. Sample type
  4. Normal valúes
A
  1. “van den bergh” or “Grof-Jendrassik” reaction
  2. Sulphanilic avid and NaNO2
  3. Serum
  4. total Br: 8mikromol/l, horse: <40mikromol/l, direct Br: 0.2-3mikromol/l
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15
Q

Causes of increased Br 1 level in the serum

A

-Excess prod. due to incr. RBC destruction:
 acute haemolysis
 abs. of Hb following massive internal haemorrhage, or after big haematoma formation
 transfusion of stored blood, which contains many dyeing or dead RBCs
-Decr. uptake of Br.I from the blood by liver cells:
 impaired hepatic function
 (acute haemolysis)
-Decr. rate of conjugation of Br I by liver cells:
 impaired hepatic function

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16
Q

Causes of increased Br II level in the serum

A

-A few days after severe acute intravascular haemolysis (incr. prod.).
-Decr. excretion of Br II by liver cells:
 impaired hepatic function
-Obstruction of bile canaliculi within the liver, often due to inflam. causing swelling of cells, or CT proliferation:
 impaired hepatic function
-Obstruction of bile canaliculi due to blockage or compression of the bile duct: rupture of the biliary vessels or duct or gall bladder

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17
Q

What is bilirubinuria?

A

Br 2 (with glucoronic acid) in the urin

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18
Q

Where is most of the UBG taken up?

A

In the liver cells, the rest is filtered through the glomeruli from the kidneys

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19
Q

What does an increase of UBG in urine indicate?

A

Increased haemolysis or liver cell damage

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20
Q

What is indicane?

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A

A sulphated derivate of indol which is produced by bacteria in the lumen of the large intestines and abs. to the blood and filtrated by the kidneys and finally excreted in the urine.

21
Q

What happens when Indicane is oxidised?

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A

Becomes purple.

22
Q

What does appearance of indicane show?

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A

Appearance of indicane in the urine is normal in horses but in carnivores it indicates pathological enteral catabolism (enteritis, constipation).

23
Q

Tests used for examination of bilirubin derivates in urine

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A
  • Gmelin test

- Ehrlich test

24
Q

Gmelin test:

  1. Reagent used?
  2. What is evaluated?
  3. The different results?
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A
  1. Reagent used: C.c. HNO3
  2. The width of the differently coloured layers at the meeting of the two fluid phases.
  3. Differently coloured layers from the highest layer:
     condensed material on the surface of the glass tube - acidic urea
     yellow - urine itself
     white (opaque) – protein
     purple - indicane (indol-sulphate)
     green – biliverdin
     brown - urobilinogen (UBG)
     HNO3
25
Ehrlich test 1. Reagent used? 2. The different results?
1. Reagent used: Ehrlich reagent; p-dimethyl-amino-benzaldehyde in HCl 2. -Normal:  colour from above - a mild reddish discolouration  colour from the side - no colour change -Abnormal:  colour from above - intensive red colour  colour from the side - mild or intense red  colour change
26
Bilirubin derivates in faeces
Br is excreted by the bile and hydrolysed to UBG (and stercobilinogen) by the bacteria. Some of UBG (stercobilinogen) is abs from the ileum (and colon), and the rest is further oxidised to brownish coloured stercobilin.
27
What does increased Br II excretion lead to?
Increased UBG and thus increased stercobilin formation.
28
What does an intense colour in the faeces mean?
Increased stercobilin
29
What is the sign and cause of... 1. Hyperchromic, pleichrom, hypercholic 2. Hypochromic, hypocholic 3. Hypochromic, acholic
1. Hyperchromic, pleichrom, hypercholic - intense colour, due to i.e. haemolysis 2. Hypochromic, hypocholic - decreased colour (light brown), due to liver failure (as less Br II is excreted by the bile) 3. Hypochromic, acholic – very light colour (grey), due to bile duct obstruction
30
Prehepatic jaundice lab. signs
(haemolytic crisis) Incr. in unconjugated Br in the serum, stercobilin in the stool, (darker colour), and urinary UBG, in addition to increased quantity of bile pigments metabolized due to erythrocyte haemolysis.
31
Cause of increased urinary UBG?
Prehepatic jaundice + may be partly because of secondary liver damage
32
Hepatocellular jaundice lab. signs
- Incr. levels of Br conjugates in serum; lesser amount of unconjugated Br may also be elevated in the serum owing to a decreased uptake of the pigment. - Presence of Br glucuronide and incr. amounts of UBG in urine.
33
Posthepatic jaundice lab. signs
- Regurgitation to the serum and subsequently the urine of Br diglucuronides conjugated in the liver. - Biliprotein may also be present in the serum during cholestasis. - Urinary UBG and faecal stercobilin are absent.
34
Examination methods of hepatic excretory function
- Brom-sulphalein- (sulphobromtalein-) (BSP) retention test - Measurement of BSP half life - Indocyane green (ICG) retention test
35
BSP-retention test 1. Reagent used? 2. What is evaluated? 3. The different results? 4. What does it give info. about? 5. Normal range? 6. Disadvantage of the test?
1. Brom-sulphalein dye 2. Given intravenously and examination of the clearance of it from the plasma by hepatocytes. 3. BSP has a purple colour in alkaline pH. If liver function is normal, BSP is not retained in the plasma and it is split to brom and thioether by the hepatocytes. Then brom is conjugated with glucuronic acid and excreted in the bile. 4. UDP-glucuronyl transferase activity of liver cells. 5. Normally liver eliminates 95% of BSP from blood within 30-45 minutes. In dogs and sheep BSP is eliminated within 30, in cattle and horse within 40-45 minutes. In cats it is not liver specific. Normal: -dog: retention less than 5-10% -cat: retention less than 3-5% 6. BSP can be dangerous as it can cause unexpected anaphylactic reactions.
36
Indocyane green (ICG) retention test - Pros and cons? - Normal range?
``` Pros: -more liver specific -especially good for cats -less dangerous Cons: more expensive. -Normal is 20-25% retention in dog, and 15% in cat. ```
37
Causes of increased BSP retention
``` -Primary liver failure:  liver cirrhosis  liver tumour  hepatic lipidosis  "lipid mobilisation syndrome" -Decreased hepatic perfusion:  right sided heart failure  portosystemic shunt  arteriole-venous fistulas in liver  blockage in portal vessels -Other causes:  decr. UDP-glucuronyl transferase activity in liver cells ```
38
Primary and secondary bile acids
Primary: cholic acid, chenodeoxycholic acid | -Secondary: litho-cholic acid, deoxy-cholic acid
39
Where is bile acids synthetized, excreted, stored and released?
Synthetized in n the liver from cholesterol. Excreted to the bile, and it is then stored and concentrated in the gall bladder, and released into the duodenum through the bile duct.
40
How are sec. bile acids formed?
Primary bile acids are deconjugated in the intestines by bacteria, and secondary bile acids are formed by this process (litho-cholic acid, deoxy-cholic acid).
41
Where is bile acids transported and absorbed in the body?
Nearly 90% of conjugated bile acids are reabsorbed at the terminal part of the ileum and transported back to the liver via portal circulation. -Faecal loss is 2-5 % of the whole bile acid pool per day (entero-hepatic circulation).
42
Function of bile acids
- Have detergent function (emulgating big fat droplets to smaller drops with bigger surface, for lipolytic enzymes) - Key role in micelle-formation and lipid digestion - Strong anti-endotoxic effect (neutralise effects of toxins of Gram – neg. bacteria).
43
What mediates the release of bile acids?
Cholecystokinin-pancreozymin and secretin.
44
Methods for determination of bile acids
Different types - HPLC, RIA or total bile acids (TBA) - spectrophotometric method.
45
Samples used for bile acid determination
No heparin is used as an anticoagulant, or the sample is haemolysed or lipaemic. Na-EDTA or -citrate can be used as an anticoagulant.
46
Normal value of bile acids
(fasting): 6 µmol/l (carnivores) 20-30 µmol/l (other animals)
47
Causes of increased bile acid level in the blood
- liver injury, hepatic cell damage - incr outflow of BA from the damaged hepatocytes to the blood - bile duct obstruction or bile endothelial cell damage - decr. secr. of BA to bile, incr. outflow to plasma instead - decr. in liver function, therefore decr. uptake of the abs. BA - biliary stasis (cholangiohepatitis cirrhosis, hepatic or pancreatic neoplasm, pancreatitis) - portosystemic shunt (abs. BA bypass liver tissue)
48
Causes of decreased bile acid level in the blood
- decr. abs. from the intestines - intestinal wall damage or surgical removal of the ileum or lymphangiectasia - severe liver cirrhosis (or other cause of severe liver cell damage) - decr. synthesis of BA
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