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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?

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A

Cat – they have a shorter half life – 3.5 hours

24
Q

Do we use ALT in large animal?

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A

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

25
What does AST stand for? Where is this in the cell?
Aspartate aminotransferase | cytosol and mitochondria
26
What tissues are involved in AST increase? What must this increase be used in combination with?
Liver Muscle RBC ALT, SDH, CK
27
What blood change can lead to a false AST increase?
hemolyzed specimen
28
What animals is AST useful in? What are their half lifes?
Large and Small animal Horse (possibly the cow?) ~ 4-7 days Dog and cat ~ 24 hours
29
What does ALP stand for? Where is it located in the cell?
Alkaline phosphatase | Bound mostly to membrane
30
What is special about ALP only in domestic animals?
two isoenzymes (gene products) modified into two tissue specific isoforms by glycosylation
31
What are the two types of ALP isoenzymes? What are the isoforms in each group?
1. Tissue unspecific: hepatic, bone (osteoblasts), placental, renal 2. Intestinal: intestinal and corticosteroid induced hepatic
32
What three isoforms mostly contribute to serum ALP? What is half life for Dog?
hALP, cALP, bALP | ~ 3 days
33
What is the ALP half life for cats?
~ 6 hours
34
How should you interpret horse ALP half life?
Similar to cat -- 6 hours
35
Which ALP isoenzyme is specific only in dogs?
cALP
36
What three things can cause an ALP increase in dogs?
1. Corticosteroid administration (corticosteroids, phenobarbitol) 2. Cholestasis 3. Bone formation in young animals
37
When is ALP increase specific for cholestasis in the dog? What else may it indicate?
``` 4x increase (600) isoenzyme induction -- cALP ```
38
What are three possible scenarios if there is a 4x increase in dog ALP?
1. Cholestasis 2. Pure isoenzyme induction - cALP 3. Both 1 and 2
39
What is it called when both hALP and cALP are responsible for increased ALP?
Drug-associated hepatopathy
40
When is ALP increase considered specific for cholestasis in cats? Why?
Any increase! | short half life
41
What is one situation when you may see an increase ALP in a cat with no other support for cholestasis?
Pregnant queen (pALP)
42
When is it appropriate to say a horse has cholestasis based on the ALP value? When wouldn't this be the case?
Increases in mature animals = cholestasis | Increase in young animals = normally high ALP
43
How long will there be a mild to moderate increase (1000-3000) in ALP for neonates?
1-2 weeks ~ 4 weeks -- osteoblastic activity in bone
44
When does ALP finally reach
~ 6 months
45
What does GGT stand for?
gamma glutamyltransferase
46
What is GGT half life for horse, dog, and cat?
3 days | best documented in horse
47
Where is GGT found and is it constitutively expressed or induced?
Membrane of bile duct epithelium, less extent hepatocyte Induced
48
What enzymes are specific for liver -- ALP, AST, SDH, GGT, ALT?
GGT - dogs and cats | SDH
49
What does increase GGT indicate in small animals? large animals?
``` SA -- cholestasis LA - cholestasis - acute severe injury - neonates: colostral GGT markedly in calves and lambs but not foals ```
50
What can you look at in horses to determine biliary hyperplasia?
GGT
51
What can be used as an indirect indication for confirming passive transfer?
High GGT -- NOT in foals!! | May increase 5x during first 24 hours if colostrum is received (kids)
52
What does SDH stand for? Where is it located?
Sorbital dehydrogenase | cytosolic enzyme
53
What is SDH half life?
minutes - few hours
54
What enzyme does SDH substitute for on LA panels?
ALT
55
Why don't many labs run SDH values?
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
Does the cALP or hALP increase have to happen in direct association with cholestasis?
No | They can both happen independently from cholestasis from induction from corticosteroids
57
What is a very suggestive pattern for feline hepatic lipidosis?
``` 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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