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CVSOH1 Clinical Pathology and Clinical Biochemistry > Clinical Biochemistry 3 > Flashcards

Clinical Biochemistry 3 Flashcards

1
Q

Functions of the liver in synthesis.

A

Protein synthesis.
- albumin
- globulin
– positive acute phase proteins
– clotting factors
Glucose synthesis
Cholesterol synthesis

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2
Q

Liver function in detoxification.

A

Encephalopathic toxins
- Ammonia > urea.
Portal contaminants
- e.g. translocated bacteria.
Bilirubin
Bile acids
Enterically-absorbed drugs.

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3
Q

Non-specific and vague clinical signs of liver disease.

A

Inappetance
V+/D+
Lethargy
Weight loss
PU/PD (multiple mechs).

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4
Q

Specific clinical signs of liver disease.

A

Icterus (>40).
- Pre- / hepatic / post-hepatic causes possible (e.g. biliary tree obstruction/pancreatic obstruction).
Coagulopathy
Ascites – due to low albumin levels.
Hepatic encephalopathy
Other; rare.

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5
Q
  1. Markers of liver damage / “stress”.
  2. Markers of reduced liver function.
A
  1. Hepatocellular enzymes (ALT, AST).
    Cholestatic enzymes (ALP, GGT).
  2. Hepatic synthetic products (reduced production).
    - urea, albumin, cholesterol, clotting times.
    Hepatic detoxification products (accumulation).
    - specific markers – bile acids (fasted; dynamic); ammonia (unreliable).
    - Bilirubin.
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6
Q
  1. What does hepatocellular damage result in in terms of hepatocellular enzymes?
  2. Where is ALT located in the cells?
  3. When is ALT released?
  4. What species is ALT useful in?
  5. In what spp is ALT not useful in?
  6. In what part of the cell is AST found?
  7. Where else is AST found?
  8. Which out of ALT and AST would be picked as a marker of liver damage in dogs and cats? – WHY?
  9. What should you do if you see AST increase w/o ALT increase to the same level?
A
  1. increased hepatocellular enzymes.
  2. Cytoplasm.
  3. Hepatocellular repair.
  4. Dogs, cats, rabbits.
  5. Horses, ruminants, pigs.
  6. Mitochondria.
  7. Muscle.
  8. ALT. – ALT more sensitive and specific marker than AST.
    But if AST is increased as well, can indicate that the damage is more severe.
  9. Measure CK as could be muscle related rather than liver related.
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7
Q
  1. Hepatocellular enzyme in horses and cattle.
    – Why can this be difficult?
  2. Hepatocellular enzyme in large animals and exotics?
    – Where is it found?
    – Compare to previous enzyme.
    – Downside.
A
  1. Sorbitol dehydrogenase (SDH).
    – Assay not readily available.
  2. Glutamate dehydrogenase (GLDH).
    – Many tissues, primary hepatocellular (mitochondrial) origin.
    – More stable.
    – Less specific for the liver itself as found in many tissues.
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8
Q
  1. Primary liver disease causes.
  2. Secondary / reactive liver disease causes.
A
  1. Hepatic inflammation, infections, trauma, neoplasia, vacuolar hepatopathy.
    Toxins (incl. drugs) – xylitol, alfatoxins, phenobarbitone, methimazole, antifungals, azathioprine.
  2. Due to inflammatory / metabolic process elsewhere in the body.
    Commonly seen with e.g. dental disease, GI disease, endocrinopathies (DM, hyperthyroidism, hyperadrenocorticism).
    Often mild unless concurrent vacuolar hepatopathy.
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9
Q
  1. What does an increase in cholestatic enzymes indicate?
  2. What is ALP/ALKP? – what about in dogs?
  3. Why is ALP/ALKP seen to be increased during growth?
  4. What is GGT in dogs?
  5. In what spp are GGT levels high in colostrum?
    – What is it therefore a good marker for?
  6. Why is GGT better marker in equines/cattle than ALP?
A
  1. Impaired biliary flow.
  2. Cholestatic isoenzyme. – steroid isoenzyme.
  3. It is a bone isoenzyme.
  4. Steroid isoenzyme.
  5. Cattle, sheep, dogs.
    – Colostrum ingestion in calves.
  6. More sensitive.
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10
Q
  1. Cholestatic causes of cholestatic enzyme activity increases.
  2. Non-cholestatic causes of cholestatic enzyme activity increases.
A
  1. Primary biliary tree disease – infectious, inflammatory, metabolic (gall bladder, musoceoles, choleliths), toxic (incl. drugs), neoplastic.
  2. Endocrinopathies/metabolic > vacuolar hepatopathy.
    - Hyperadrenocorticism, DM, hepatic lipidosis (ALP).
    Steroid induced in dogs.
    - Exogenous (iatrogenic) vs endogenous (hyperadrenocorticism).
    - NB. phenobarbitone may also cause enzyme induction (ALP, GGT).
    Bone induced (ALP) – growth (physiologic), osteolysis (bone cancer).
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11
Q

Evidence of cholestasis.

A

When mild, evidence only of cholestatic enzyme activity increases.
As progresses, serum accumulation of other substances typically excreted in the bile.
- cholesterol
- bile acids
- bilirubin (bile pigment).

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12
Q

Hepatic enzyme activity interpretation.

A

Magnitude of increase indicates extent of damage expressed in terms of magnitude of increase above reference interval, not absolute number.
- Mild = ~2-3x
- Moderate = ~ 4-5x
- Marked = >10x
- Hepatocellular vs cholestatic – interrelated.
– Primarily cholestatic = secondary hepatic damage.
– Primarily hepatocellular = secondary cholestasis.
- Half-life influences significance.
– SDH short (12-24hrs) in horses.
– All short (6hrs) in cats.
– Dogs nearer 3 days.
More fussed about liver enzyme changes in cats more than in dogs.

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13
Q

Markers of liver dysfunction.

A

Liver has large functional reserve.
- May have considerate liver damage W/O dysfunction.
Non-specific – Decreased albumin, urea, cholesterol, glucose.
Specific – increased bilirubin (pre-, hepatic, post-). Hyperbilirubinaemia (<10 micromol/L) vs visible jaundice / icterus (>40micromol/L).
– Increased bile acids.
– Increased ammonia (failure of detoxification).

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14
Q

Bilirubin metabolism.

A

Bilirubin synthesised from haemoproteins.
Breakdown of red cells in macrophages (in liver / spleen / bone marrow).
Release of bilirubin due to breakdown.
Bilirubin binds to albumin and goes to the liver hepatocytes..
Bilirubin conjugated in the liver hepatocytes.
Bilirubin excreted into the bile to be transported in biliary system to the intestine.
Becomes urobilinogen and either is excreted in faeces as stercobilin or is reabsorbed back to the hepatocytes or excreted in the urine.
more common to see bilirubin in dog urine than in cat urine.

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15
Q

1.Prehepatic hyperbilirubinaemia cause?
2. Hepatic hyperbilirubinaemia cause?
3. Post-hepatic hyperbilirubinaemia cause?

A
  1. Excessive production of bilirubin through haemolysis.
  2. Significant loss of liver function or obstruction by liver swelling.
  3. Obstructive processes (w/ increases in ALP in particular).
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16
Q
  1. Hyperbilirubinaemia in cats and dogs.
  2. Hyperbilirunaemia in equines and sometime cattle.
  3. Hyperbilirubinaemia in cattle.
A
  1. Pre-hepatic – haemolysis.
    Hepatic – Hepatitis.
    Post-hepatic – Pancreatitis, biliary disease (cholangitis; obstruction – cholelith, neoplasia, mucocoele).
  2. Fast-associated jaundice.
  3. Haemolysis&raquo_space;> liver disease (except hepatic lipidosis).
    spp difference in susceptibility to infectious / toxic causes.
17
Q

Hyperbilirubinaemia investigative pathway.

A

PCV normal or PCV low?
If PCV low, consider:
- regenerative anaemia – pre-hepatic (haemolysis).
- non-regenerative anaemia – exclude pre-regenerative, then explore PCV normal pathway.
If PCV normal, consider:
- Hepatic? Look for other evidence of hepatocellular damage / dysfunction – See increased hepatocellular enzymes, decreased albumin, urea, cholesterol, glucose. Increased ammonia (NB bile acids already obsolete when already jaundiced).
- Post-hepatic? Look for other evidence of cholestasis – Primarily cholestatic enzyme elevations / hypercholesterolaemia / imaging consistent w/ cholestasis.
- Other – anorexia in horses and cattle (rare in cats and dogs).
– FIP, toxoplasmosis in cats.

18
Q
  1. What are bile acids?
  2. What are bile acids not?
  3. Where are bile acids made?
  4. Where are bile acids present?
  5. Bile acid excretion?
  6. What does amphipathic mean?
  7. Type of recycling bile acids undergo?
  8. What are bile acids used as markers to test?
  9. What sample type should be used to measure bile acids?
A
  1. Bile salts.
  2. Bilirubin.
  3. Liver.
  4. In bile.
  5. Biliary system.
  6. Aid fat digestion / absorption.
  7. Enterohepatic recycling.
  8. Liver function in absence if jaundice.
  9. Plain serum.
19
Q
  1. What does a BAST measure? and in what spp is this testing used?
  2. BAST protocol?
A
  1. hepatic clearance of enterohepatically recycled bile acids. – cats and dogs.
  2. Overnight (>12hr) fast > serum sample.
    Feed (gall bladder contracts).
    2 hours post-prandial > serum sample.
20
Q

Cause of increased serum bile acids.

A

Cholestasis – exclude based on biochemistry (enzyme increases)
+/or
Liver dysfunction
+/or
Portosystemic shunt(s)
*differentiate between liver dysfunction and portosystemic shunt(s) w/ imaging.
*sometimes end up needing liver biopsies.

21
Q
  1. What is ammonia a product of?
  2. What is ammonia converted to and by what organ?
  3. Why is laboratory measurement of urea challenging?
  4. What happens to ammonia in hepatic dysfunction or portosystemic shunts?
A
  1. GI bacterial metabolism.
  2. Urea by liver.
  3. Labile, EDTA whole blood, on ice, urgent.
  4. Increases.
22
Q
  1. In what other instances may hyperammonaemia occur?
A
  1. Urea toxicosis in ruminants from contaminated feed.
    Strenuous exercise in horses.
    Seen (rarely) in dogs with little B12.
    Kidney issues.
23
Q
  1. What is CK?
  2. Where is CK released? – And why would it be released?
  3. Good about CK as a marker?
  4. CK half-life?
  5. What is CK measured alongside? – why?
A
  1. Creatine kinase.
  2. Muscle cells. – response to muscular damage.
  3. Very sensitive.
  4. 2 hours (v short).
  5. AST – longer half-life.
24
Q

Causes of creatine kinase increase.

A

Muscle trauma – overly-firm handling, IM injections, traumatic accidents.
Muscle belly hypoxia – e.g. aortic thromboembolism (esp. cats).
Myopathies
- Inflammatory / infectious, degenerative (hereditary), toxic (e.g. snake bite).
- Recumbency in large animals.
- Equine rhabdomyolysis (‘tying up’).

25
Q
  1. Endocrine pancreatic disease examples. – and observations of these.
  2. Exocrine pancreatic disease examples – tests for these.
A
  1. Diabetes mellitus – hyperglycaemia, w/ glucosuria; fructosamine.
    Insulinoma – episodic collapse.
    Other diseases are rare.
  2. Exocrine pancreatic insufficiency (EPI) (reduced enzyme production).
    – cTLI / fTLI (trypsin-like immunoreactivity). sensitive / specific measure of functional pancreatic mass.
    Pancreatitis.
    – Routine biochemistry (cholestatic picture).
    – Non-specific lipase / amylase assays are inadequate and no longer used.
    – cPLI / fPLI (pancreatic lipase immunoreactivity) or DGGR lipase.
26
Q

Technology behind PLI tests.

A

Spp-spec monoclonal AB = spec cPL and spec fPL.
Licensed by IDEXX.
Quantitative assay (at ext. lab) vs qualitative assay in-house test.
Qualitative assay
- SNAP cPL and SNAP fPL = v sensitive, lots of false positives.
- Useful as a screen (i.e. negative usually excludes disease).
- If positive, need to follow-up assay w/ quantitative test.

27
Q
  1. Dog spec PL normal
  2. Dog spec PL equivocal
  3. Dog spec PL positive
  4. Cat spec PL Normal
  5. Cat spec PL equivocal
  6. Cat spec PL positive
  7. SNAP PL normal
  8. SNAP PL equivocal or positive.
A
  1. <200
  2. 200-400
  3. > 400
  4. <3.5
  5. 3.5-5.3
  6. > 5.3
  7. Test spot (right) lighter than reference spot (left).
  8. Same colour or darker.
28
Q
  1. Marker used as evidence of malabsorption? – and what would be seen in these markers if malabsorption was the issue?
  2. What type of this marker is absorbed in the proximal s. intestine (jejunum)?
  3. What type of this marker is absorbed in the distal s. intestine (ileum)? – what does this absorption require?
  4. Why are these markers so important to measure for?
A
  1. B vitamins. – see levels too low.
  2. Folate (vit B9).
  3. Cobalamin (vit B12). – Requires intrinsic factor, which is exclusively pancreatic in cat, and primarily pancreatic and lesser gastric in dog.
  4. So low levels can be supplemented as B vits are important in many different pathways and consequences can range from encephalopathies, dysfunction in healing, blood cell dycrasias, dysfunctional immune systems.
29
Q
  1. What is term for low B12?
  2. Clinical signs of low B12?
  3. Differentials when B12 low?
A
  1. Hypocobalaminaemia.
  2. Chronic diarrhoea
    Weight loss and failure to thrive.
    Hyperammonaemia > encephalopathy
    Blood cell changes – neutropenia, increased MCV (mean corpuscular volume), hyper-segmented neutrophils.
  3. Rule out exocrine pancreatic insufficiency w/ trypsin-like immunoreactivity test.
    Ileal malabsorption – carry out GI ultrasound; biopsy (e.g. endoscopic).
    Bacterial dysbiosis? (uncommon).
    Other causes rare (e.g. Imerslund-Grasbeck syndrome).
30
Q
  1. What about hypercobalaminaemia?
  2. What about hyperfolataemia?
  3. What about hypofolataemia?
A
  1. Limited clinical significance.
    Seen w/ supplementation, some meds, hepatopathy, neoplasia, others.
  2. Can be seen w/ dysbiosis (esp. following antimicrobials).
    No clinical significance.
  3. Often seen alongside hypocobalaminaemia.
    Limited clinical significance.
    Easy to supplement.(Cobalaplex).
    Jejunal malabsorption.

CVSOH1 Clinical Pathology and Clinical Biochemistry (8 decks)

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