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LEAH FCP > Evaluation of biochemical panel > Flashcards

Evaluation of biochemical panel Flashcards

1
Q

How are reference intervals determined?

A

Based on central 95% of clinically normal animals

Ideally, derived from ≥120 healthy animals, but often estimated from smaller groups

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2
Q

What is a cut-off value in diagnostic testing?

A

fixed threshold with defined sensitivity & specificity for disease

More useful in high-prevalence diseases

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3
Q

How can we use standard deviations to establish if a biochem result is normal or not?

A

Mean +- 2SD = normal

3-4SD = very unlikely to be healthy

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4
Q

Why should borderline results be interpreted cautiously?

A

Lab imprecision (Coefficient of Variation CV%) affects reliability

Example: If cut-off is 10, with a CV of 19%, result of 12 might actually be between 7.3–16.6.

Pre-analytical factors (haemolysis, lipaemia, contamination) can affect results

Repeat tests or use alternative methods if in doubt

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5
Q

Give examples of factors that can cause biochem result to be incorrect

A

Haemolysis, icterus and lipaemia
Post-prandial
EDTA contamination
Unphysiological values
Limits of techniques (min and max reportable conc)

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6
Q

What are the different methods of profile interpretation?

A

Step by step (go down list of abnormal results creating differential lists & carrying on adding & eliminating differentials)

Pattern match (using experience to identify trends)

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7
Q

What steps should you take when interpreting lab results?

A

Review results objectively—don’t be biased by previous differentials

Check if “normal” values align with case

Don’t ignore outliers without reason—they may be relevant

Create pathophysiological story that explains all abnormalities

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8
Q

Why is clinical context crucial when interpreting lab results?

A

Same abnormality can mean different things in different patients

Example:
- High glucose in 2 cats: One may be stressed, other truly diabetic
- Isosthenuria in 2 dogs: One may be azotaemic, other not

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9
Q

What markers indicate liver damage vs. dysfunction?

A

Damage (Leakage Enzymes): ALT, AST, ALKP, CK

Dysfunction: Bile acids, ammonia, albumin, glucose, bilirubin

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10
Q

What markers indicate pancreatic damage vs. dysfunction?

A

Damage: Lipase, PLI (pancreatic lipase immunoreactivity)

Dysfunction: TLI (Trypsin-like Immunoreactivity)

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11
Q

What markers indicate thyroid damage vs. dysfunction?

A

Damage: TgAA

Dysfunction: T4, TSH

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12
Q

What markers indicate renal damage vs. dysfunction?

A

Damage: Casts in urine (indicate tubular damage)

Dysfunction: Creatinine, USG (urine specific gravity), proteinuria

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13
Q

What markers indicate cardiac damage vs. dysfunction?

A

Damage: Cardiac Troponin I

Dysfunction: NT-proBNP (marker of heart failure)

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14
Q

How can we assess the degree of liver damage using biochemistry?

A

ALT & AST are cytoplasmic enzymes that increase with significant hepatocellular damage

AST & GDH (Glutamate Dehydrogenase) are also found in mitochondria, requiring severe damage for elevation

ALP is located in biliary tree & can increase with mild cholestasis or enzyme induction

Non-liver sources: AST can rise due to muscle injury, while ALP may originate from bone, GIT, or steroid induction

Magnitude of enzyme elevation does NOT correlate with prognosis—small injuries can release large amounts of enzymes

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15
Q

What causes enzyme induction rather than true cell damage?

A

Enzyme induction by pathology or drugs/endogenous compounds (e.g. glucocorticoids or barbiturates)

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16
Q

Describe use of ALT measurement in biochemistry

A

Liver specific in dogs & cats (not large animals)

Earlier & higher levels following hepatic damage than AST

17
Q

Why should ALT & ALKP measurements be repeated in dogs after 2-3 days?

A

to determine if the cause has passed, is ongoing or worsened

Half life in dog = 40-60hrs
Half life in cats = 3.5hrs

(pathology must be ongoing for this result in cats)

18
Q

How is ALKP used in biochemistry?

A

Located in canalicular membranes; induced by biliary stasis & medications

Not liver-specific—isoenzymes also come from:
- Bone growth (young animals)
- Intestinal mucosa
- Steroid induction (dogs)

Half-life (T½):
- Dogs: 60–70 hours
- Cats: 6 hours
- Intestinal ALKP: <10 minutes (rarely detected in blood).

Increases in non-hepatic conditions: Age-related (“old dog”), secondary liver effects.

Serum GGT is more biliary/liver-specific than ALKP

19
Q

Give examples of non-primary hepatopathies that cause elevated liver enzymes

A

Enzyme induction/toxin in other disease:
- Stress, Glucocorticoids, e.g. pyometra

Liver central to a lot of metabolic processing
- Diabetes, fatty liver, hyperlipaemia

Portal circulation
- Hepatocyte impact of pancreatic and GI pathology

Blood supply and oxygenation
- Cardiac congestion, anaemia

20
Q

What are the next steps after identifying elevated liver enzymes?

A

Rule out therapies (including topical eye, ear and skin)

Rule out systemic, pancreatic, GI disease

Multiple enzyme abnormalities, very high results +/- bilirubin – can’t ignore (possible primary liver disease)

Further tests:
- bile acids
- ACTH stim (test for HAC)

Monitor and act if worsened

21
Q

What does elevated urea & normal creatinine suggest?

A

Pre-renal effects:
- Reduced renal perfusion (dehydration) (measure USG to assess hydration)
- Post-prandial
- Unusually high urea with normal creatinine → GI bleeding

Focus on creatinine as measure of renal function

22
Q

What does hypostenuria with azotaemia suggest?

A

‘inappropriately dilute’

Functional kidneys:
- excessive fluid intake (primary polydipsia)
- ADH production or action

23
Q

What is the significance of the Na:K ratio?

A

Na:K <22 suggests hypoadrenocorticism (Addison’s disease)

Other causes: GI disease, renal dysfunction, effusions.

Check Na+ and K+ separately before interpreting

Mild abnormalities may not be Addison’s—confirm with ACTH stimulation test

24
Q

What should you consider with elevated glucose?

A

Cats: Stress-induced hyperglycemia common

Persistent hyperglycemia → Pre-diabetes or diabetes mellitus

Fructosamine helps differentiate stress vs. true diabetes.

25
Q

Give examples of causes of hypercalcaemia

A
26
Q

Give examples of differentials for hhypocalcaemia

A

Parathyroid dependent - primary hypoparathyroidism:
- immune mediated
- post-surgical

demand exceeds supply/mobilisation:
- periparturient tetany (eclampsia)
- nutritional deficiency of Ca or Vit D
- pancreatitis with fat necrosis

27
Q

Which biochem tests relate to hydration?

A

TP
Albumin

28
Q

Which biochem results are nutrition related?

A

albumin
glucose
bilirubin

29
Q

What biochem tests are pancreatic related?

A

ALKP
ALT
Lipase
Glucose
Ca

30
Q

Which do biochem electrolyte levels (Na, Cl, K) relate to?

A

Hydration
Renal
GI
Endocrine

31
Q

Which biochem tests are muscle related?

A

CK
AST
myoglobinuria

32
Q

Which biochem tests are hepatic related?

A

Liver enzymes
bile acids
urea
albumin
glucose

33
Q

Which biochem tests are renal related?

A

Urea
Creatinine
Phosphate
Ca
Urinalysis

34
Q

Describe the variation in ALT results in biochem between species

A

Dog T½ = 40–60h, Cat T½ = 3.5h

Mild ALT (& ALKP) increases are more concerning in cats

Not liver-specific in horses & ruminants—use GLDH & SDH instead

35
Q

Why is urea unreliable for assessing renal function in some species?

A

Equids & ruminants: GI excretion reduces its reliability for kidney assessment

Uric acid is used instead in uricotelic species (birds, reptiles)

Creatinine is a better renal function marker in large animals

36
Q

How does calcium metabolism vary between species?

A

Horses excrete excess Ca via kidneys, so renal failure can cause true hypercalcemia

Egg-laying species (birds, reptiles) have high tCa due to protein-bound Ca (ovalbumin) but maintain normal iCa

Always check iCa when interpreting hypercalcemia

36
Q

Why is bilirubin elevated in anorexic horses and cattle?

A

Fasting/anorexia leads to bilirubin buildup without liver disease

Horses lack a gallbladder, so bilirubin metabolism differs from other species

Bilirubin elevation ≠ liver dysfunction in these species

37
Q

What are the key acute phase proteins (APPs) (inflammatory markers) in different species?

A

Equine: Serum Amyloid A (SAA), fibrinogen

Cattle: Haptoglobin

Dogs: C-reactive protein (CRP)

Cats: Alpha-1 acid glycoprotein (AGP)

Large animals rely more on APPs than neutrophil counts for inflammation detection

38
Q

What electrolyte imbalances are common in large animals?

A

Large animal diarrhea → Low Na, Cl, high K

Less common in small animals

LEAH FCP (77 decks)

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