Lab 10- Liver 2 Flashcards

1
Q

What can impaired protein synthesis cause?

A

decreased colloid osmotic (oncotic) pressure of the blood, quicker ESR (erythrocyte sedimentation rate) (hypoalbiminaemia), and longer PI (prothrombin time)

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2
Q

Why does the blood pressure decrease with impaired protein synthesis

A

(due to hypoalbuminaemia),

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3
Q

Why does the PI time increase with impaired protein synthesis

A

lower fibrinogen level

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4
Q

What can impaired liver function lead to?

A

hormonal imbalances

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5
Q

lysomal enzymes with severe liver necrosis

A

catepsin-D, carboxypeptidase) can be elevated in the blood

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6
Q

Parameters to be measured:

A

TP, albumin, and fibrinogen concentration by spectrophotometric, refractometric methods and fibrinogen by the thrombin time.

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7
Q

When can edema be expected?

A

if albumin concentration is < 20 g/l, and there is edema formation if albumin concentration is < 11 g/l

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8
Q

how do we measure alpha and beta globulins

A

electrophoresis

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9
Q

how are coagulation factors measured?

A

APTT and PR

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10
Q

Why do we need to measure ammonia conc?

A

1) in carnivores to diagnose severe decrease of liver function (i.e. cirrhosis), portosystemic shunt

2) in ruminants as a consequence of ruminal alkalosis, or decomposition of ruminal fluid severe systemic alkalosis can be developed due to hyperammoniaemia,

3) in case of horse, rabbit pathologic breakdown of ingest in the colon or caecum or in case of liver failure .

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11
Q

Where is ammonia produced and absorbed

A

produced in the intestines by the bacteria, it is absorbed to the portal vein

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12
Q

How is ammonia detoxified

A

in the liver
- ornithine cycle
- GLDH untilised alpha keto glutaric acid

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13
Q

After what time period can we take ammonia measurements?
How should we take samples.

A

animals should starve for 24 hours.

We take blood samples to tubes that contain EDTA or citrate as an anticoagulant.

Samples should be taken by avoiding air - contamination of them

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14
Q

Normal value for ammonia conc

A

<120 μmol/l in dogs

<175 μmol/l in cats.

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15
Q

Basis of ammonia measurement (standard) method

A

ammonia with alpha-ketoglutaric acid and NADH+ H+ and GLDH enzyme produces glutamic acid and NAD+

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16
Q

What type of sample do we need for ammonia conc measurement?

A

plasma sample for standard method
Whole blood sample for portable ammonia checker

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17
Q

Ammonia tolerance test:
- when do we perform this?

A

when basal NH3-concentration values do not show alteration and the suspect of portosystemic shunt is strong

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18
Q

Ammonia tolerance test:
pretreatment

A

with neomycin

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19
Q

Causes of increased NH3.concentration in the blood

A

 Impaired liver function - decreased urea prod
 Ruminal alkalosis or ammonia toxicosis
 Intestinal overgrowth of ammonia producing bacteria
 Congenital enzymopathies

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20
Q

mild vs severe liver damage effect on cytoplasmic and mitochondrial enzymes

A

mild - cytoplasmic increase
severe - mitochondrial ones increase

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21
Q

AST (Aspartate-aminotransferase)
- location

A

mitochondria
muscles
RBC

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22
Q

AST (Aspartate-aminotransferase)
- function

A

converts alpha-keto-glutaric acid to L-glutamic acid, and L-aspartate to oxalic acetic acid.

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23
Q

AST (Aspartate-aminotransferase)
- Basis of measurement method

A

Oxalic-acetate with NADH+H+ and malate-dehidrogenase (this is in the reagent) produces malate and NAD+ .

This NADH+H+ →NAD+ change cause absorbancy reduction. The speed of it is in correlation with AST activity.

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24
Q

AST (Aspartate-aminotransferase)
- cause of increased activity

A

muscle cells
- exercise, muscle necrosis, inflamation, injury, myocarditis
- Generally LDH and CK enzymes elevated too

Liver cells
- ethonal consumption, hepatopathy,

RBC
- haemolysis

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25
Q

AST (Aspartate-aminotransferase)
- Decreased activity

A

metronidasol (an antimicrobial drug, which can cause liver function problems), vitamin B6 deficiency,

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26
Q

liver specific enzyme in herbivores

A

AST

27
Q

ALT (Alanine-aminotranferase)
- location

A

liver cells (in carnivores liver specific), red blood cells (false increase) in the cytoplasm

28
Q

ALT (Alanine-aminotranferase)
- function

A

converts alpha-keto-glutaric acid to L-glutamic acid, and L-alanine to piruvic acid

29
Q

ALT (Alanine-aminotranferase)
- determination

A

produced piruvic acid is converted to lactic acid by lactate dehydrogenase (LDH)

30
Q

ALT (Alanine-aminotranferase)
- increased activity

A

liver cell damage (especially in carnivores), chronic active hepatitis (CAH),
cholangiohepatitis (CH)
virus hepatitis (human) (AST/ALT1)
hepatic lipidosis
cirrhosis,
bile duct obstruction,
liver neoplasm (AST/ALT1),
pancreatitis,
septicaemia
neoplasm,

31
Q

Drugs causing increased ALT

A

barbiturates, glucocorticoids, salicylates, tetracyclines
- from cell damage

32
Q

Copper storage disorder
- breeds

A

Doberman pincher, West highland white and Bedlingtone terrier !

33
Q

GLDH (glutamate-dehydrogenase)
- locatiom

A

liver specific, small amount is found in nerves and muscles in mitochondria only !

Liver specific in ruminants, horses and dogs.

34
Q

GLDH (glutamate-dehydrogenase)
- function

A

binds NH3 to form glutamic acid.

35
Q

GLDH (glutamate-dehydrogenase)
- determination

A
36
Q

GLDH (glutamate-dehydrogenase)
- causes of increased activity

A

severe liver cell necrosis that leads to mitochondrial membrane damage.

37
Q

BILE DUCT OBSTRUCTION ENZYMES

A

ALKP
GGT

38
Q

ALKP (AP-Alkaline-phosphatase)
- location

A

every cell really
- hepatic and bone ALKP appears in blood

39
Q

ALKP (AP-Alkaline-phosphatase)
- what causes ALKP increase in urine

A

Tubular Cell damage

40
Q

ALKP (AP-Alkaline-phosphatase)
- isoenzymes

A

liver one - heat stabile
bone one - heat labile

41
Q

ALKP (AP-Alkaline-phosphatase)
- optimum pH
- function

A
  • 10
  • phosphotransferases and not phosphatases. Generally phosphate-esters are translocated to one alcohol or phenol hydroxyl groups to another by ALKP.
42
Q

ALKP (AP-Alkaline-phosphatase)
- determination

A

yellow colour detected by spectrophotometrically

43
Q

ALKP (AP-Alkaline-phosphatase)
- causes of increased activity

A

bone
- young dogs, pregnant animals, bone tumours

Paraneoplastic processes

Liver
- cholestasis, bile acids, acute hepatic, necrosis, bilary obstruction

SIAP synthesis
- hyperadenocorticism
- Chronic stress

44
Q

ALKP (AP-Alkaline-phosphatase)
- causes of decreased activity

A

severe cirrhosis

45
Q

ALKP (AP-Alkaline-phosphatase)
- what causes ALKP increase in urine

A

Tubular Cell damage

46
Q

GGT (gamma glutamyl-transferase)
- location

A

produced by different organs
- endothelial cells of bile ducts concentrates it

47
Q

GGT (gamma glutamyl-transferase)
- specific to

A

horses (and cats)

48
Q

GGT (gamma glutamyl-transferase)
- function

A

L-alpha-aminoacids can be attached to reduced glutathione and transported through the membrane by GGT (GGT is bound to glutathione).

49
Q

GGT (gamma glutamyl-transferase)
- determination

A

yellow

50
Q

GGT (gamma glutamyl-transferase)
- increased activity

A

biliary stasis (cholestasis),
cholangiohepatitis
cirrhosis,
neoplasm (hepatic, pancreatic),
hepatic lipidosis,
barbiturates,
ethanol specifically exaggerates the GGT excertion (human)

51
Q

GGT (gamma glutamyl-transferase)
- Decreased activity

A

cirrhosis,

52
Q

More liver specific enzymes in large animals

A

OCT (ornityl-carbamyl-tranferase,
Ar (arginase),
SDH (sorbite dehydrogenase).

53
Q

What is SDH specific in?

A

swine, cattle, horse

54
Q

OCT specific in?

A

Dogs

55
Q

AR specific in?

A

Equine

56
Q

What do we measure in
- dogs

A

ALT, (AST, GLDH), ALKP, GGT

57
Q

What do we measure in
- cat

A

ALT, (AST, GLDH), GGT, (ALKP in acute processes)

58
Q

What do we measure in
- ru

A

AST, GLDH, (GGT)

59
Q

What do we measure in
- eq

A

AST, GGT, (Arg)

60
Q

What do we measure in
- swine

A

AST, GGT, ALKP, OCT, SDH

61
Q

What does decreased total cholesterol conc cause

A

decreased esterification ability
decreased apolipoprotein synthesis

62
Q

What does increased FFA conc cause

A

decreased FFA utilisation

63
Q

What does lipid accumulation in the liver cause?

A

decreased ability to perform beta-oxidation (decreased lipid breakdown)

decreased synthesis of lipid-transporting apolipoprotein molecules