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Clin Chem exam 2 > Hepatobiliary - abnormality types and enzymes > Flashcards

Hepatobiliary - abnormality types and enzymes Flashcards

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1
Q

What happens during hepatocellular injury?

A

Enzymes are released resulting in increase serum levels – blebbing
Swelling –> secondary cholestasis

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2
Q

What are 3 injury enzymes?

A

ALT
AST
SDH

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3
Q

What are the two types of cholestasis?

A

Physical

Functional

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4
Q

How is cholestasis recognized biochemically?

A

Increased bile product in blood or urine (bilirubin, bile acids)
Induction of membrane bound enzymes associated with cholestasis (ALP, GGT)

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5
Q

How does cholestasis induce secondary hepatocellular injury and associated injury enzyme increase?

A

decreased secretion –> bile acids build up in canaliculi –> emulsify fats (cell membrane) –> release cytoplasmic enzymes (ALT, SDH, AST)

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6
Q

What are two general mechanisms for decreased functional mass?

A
  1. decreased number of viable hepatocytes

2. vascular abnormalities –> functional hepatocytes are bypassed

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7
Q

What things may cause decreased number of viable hepatocytes?

A 
injury
cirrhosis
atrophy
neoplasia
lipidosis
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8
Q

What may cause vascular abnormalities causing decreased functional mass?

A

shunts: congenital or aquired

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9
Q

What is next if there is evidence of decreased functional mass on the biochem? Why?

A

other testing modalities to determine which of the 2 mechanisms is causing this
Both mechanisms present similarly biochemically

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10
Q

When will we see proof of decreased functional mass on the biochem?

A

Once 70-80% of functional mass is lost

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11
Q

What three things does decreased function involve?

A

clearance
synthesis
metabolism

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12
Q

Why would we see increased gamma globulins with decreased functional mass?

A

decreased antigen clearance (Kupffer cells) and increased Ig half life

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13
Q

What 4 factors are influencing enzyme interpretation?

A

Tissue specificity
Circulating half life
Sequential data
Localization and Expression

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14
Q

What tissues is LDH found in? Why isn’t LDH recommended?

A

Liver
RBC

5 different isoenzymes which can be used to determine tissue of origin – not practical and unspecific!

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15
Q

How can understanding half life help us in diagnosis?

A

some enzymes are not tissue specific (i.e. AST) – compare

Use SDH and AST at the same time. SDH = short half life –> make sure we know half life to measure when both are elevated, not just one!!

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16
Q

What is the estimated half life of AST in horses?

A

~ 1 week

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17
Q

How can sequential data help?

A

resolving?
progressing?
persisting?

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18
Q

Are injury enzymes constitutively expressed or induced? Cholestasis?

A

INJURY ENZYMES
Constitutively = don’t increase easily. level and fnx are maintained
+/- induced

CHOLESTASIS
Induced
+/- constitutive

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19
Q

Where are injury enzymes located?

A

cytoplasm

mitochondria

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20
Q

What does ALT stand for?

A

Alanine aminotransferase

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21
Q

What tissues are involved in ALT increase? What is it more specific for?**

A

Liver (hepatocytes) **

Muscle

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22
Q

What is ALT half life in dog and cat?

A

Dog ~ 2.5 days

Cat ~ 3.5 hours

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23
Q

What is more significant… ALT of 500 in dog or cat? Why?

A

Cat – they have a shorter half life – 3.5 hours

24
Q

Do we use ALT in large animal?

A

Not useful – hepatocyte levels are low and or non-specific

25
Q

What does AST stand for? Where is this in the cell?

A

Aspartate aminotransferase

cytosol and mitochondria

26
Q

What tissues are involved in AST increase? What must this increase be used in combination with?

A

Liver
Muscle
RBC

ALT, SDH, CK

27
Q

What blood change can lead to a false AST increase?

A

hemolyzed specimen

28
Q

What animals is AST useful in? What are their half lifes?

A

Large and Small animal

Horse (possibly the cow?) ~ 4-7 days
Dog and cat ~ 24 hours

29
Q

What does ALP stand for? Where is it located in the cell?

A

Alkaline phosphatase

Bound mostly to membrane

30
Q

What is special about ALP only in domestic animals?

A

two isoenzymes (gene products) modified into two tissue specific isoforms by glycosylation

31
Q

What are the two types of ALP isoenzymes? What are the isoforms in each group?

A
  1. Tissue unspecific: hepatic, bone (osteoblasts), placental, renal
  2. Intestinal: intestinal and corticosteroid induced hepatic
32
Q

What three isoforms mostly contribute to serum ALP? What is half life for Dog?

A

hALP, cALP, bALP

~ 3 days

33
Q

What is the ALP half life for cats?

A

~ 6 hours

34
Q

How should you interpret horse ALP half life?

A

Similar to cat – 6 hours

35
Q

Which ALP isoenzyme is specific only in dogs?

A

cALP

36
Q

What three things can cause an ALP increase in dogs?

A
  1. Corticosteroid administration (corticosteroids, phenobarbitol)
  2. Cholestasis
  3. Bone formation in young animals
37
Q

When is ALP increase specific for cholestasis in the dog? What else may it indicate?

A 
4x increase (600)
isoenzyme induction -- cALP
38
Q

What are three possible scenarios if there is a 4x increase in dog ALP?

A
  1. Cholestasis
  2. Pure isoenzyme induction - cALP
  3. Both 1 and 2
39
Q

What is it called when both hALP and cALP are responsible for increased ALP?

A

Drug-associated hepatopathy

40
Q

When is ALP increase considered specific for cholestasis in cats? Why?

A

Any increase!

short half life

41
Q

What is one situation when you may see an increase ALP in a cat with no other support for cholestasis?

A

Pregnant queen (pALP)

42
Q

When is it appropriate to say a horse has cholestasis based on the ALP value? When wouldn’t this be the case?

A

Increases in mature animals = cholestasis

Increase in young animals = normally high ALP

43
Q

How long will there be a mild to moderate increase (1000-3000) in ALP for neonates? </= 800?

A

1-2 weeks

~ 4 weeks – osteoblastic activity in bone

44
Q

When does ALP finally reach </= 200-300s in neonates?

A

~ 6 months

45
Q

What does GGT stand for?

A

gamma glutamyltransferase

46
Q

What is GGT half life for horse, dog, and cat?

A

3 days

best documented in horse

47
Q

Where is GGT found and is it constitutively expressed or induced?

A

Membrane of bile duct epithelium, less extent hepatocyte

Induced

48
Q

What enzymes are specific for liver – ALP, AST, SDH, GGT, ALT?

A

GGT - dogs and cats

SDH

49
Q

What does increase GGT indicate in small animals? large animals?

A 
SA -- cholestasis 
LA
- cholestasis
- acute severe injury
- neonates: colostral GGT markedly in calves and lambs but not foals
50
Q

What can you look at in horses to determine biliary hyperplasia?

A

GGT

51
Q

What can be used as an indirect indication for confirming passive transfer?

A

High GGT – NOT in foals!!

May increase 5x during first 24 hours if colostrum is received (kids)

52
Q

What does SDH stand for? Where is it located?

A

Sorbital dehydrogenase

cytosolic enzyme

53
Q

What is SDH half life?

A

minutes - few hours

54
Q

What enzyme does SDH substitute for on LA panels?

A

ALT

55
Q

Why don’t many labs run SDH values?

A

unstable in serum or frozen
assay is not convenient – must run in 8-12 hours of collection
activity decreases by 25% within 1 week, even if frozen

56
Q

Does the cALP or hALP increase have to happen in direct association with cholestasis?

A

No

They can both happen independently from cholestasis from induction from corticosteroids

57
Q

What is a very suggestive pattern for feline hepatic lipidosis?

A 
High ALP in the face of minimal increase to normal GGT
Hepatomegally
Weight loss
Anorexia
Decrease muscle mass

Clin Chem exam 2 (6 decks)

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