Evaluation of biochemical panel Flashcards
(47 cards)
How are reference intervals determined?
Based on central 95% of clinically normal animals
Ideally, derived from ≥120 healthy animals, but often estimated from smaller groups
What is a cut-off value in diagnostic testing?
fixed threshold with defined sensitivity & specificity for disease
More useful in high-prevalence diseases
How can we use standard deviations to establish if a biochem result is normal or not?
Mean +- 2SD = normal
3-4SD = very unlikely to be healthy
Why should borderline results be interpreted cautiously?
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
Give examples of factors that can cause biochem result to be incorrect
Haemolysis, icterus and lipaemia
Post-prandial
EDTA contamination
Unphysiological values
Limits of techniques (min and max reportable conc)
What are the different methods of profile interpretation?
Step by step (go down list of abnormal results creating differential lists & carrying on adding & eliminating differentials)
Pattern match (using experience to identify trends)
What steps should you take when interpreting lab results?
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
Why is clinical context crucial when interpreting lab results?
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
What markers indicate liver damage vs. dysfunction?
Damage (Leakage Enzymes): ALT, AST, ALKP, CK
Dysfunction: Bile acids, ammonia, albumin, glucose, bilirubin
What markers indicate pancreatic damage vs. dysfunction?
Damage: Lipase, PLI (pancreatic lipase immunoreactivity)
Dysfunction: TLI (Trypsin-like Immunoreactivity)
What markers indicate thyroid damage vs. dysfunction?
Damage: TgAA
Dysfunction: T4, TSH
What markers indicate renal damage vs. dysfunction?
Damage: Casts in urine (indicate tubular damage)
Dysfunction: Creatinine, USG (urine specific gravity), proteinuria
What markers indicate cardiac damage vs. dysfunction?
Damage: Cardiac Troponin I
Dysfunction: NT-proBNP (marker of heart failure)
How can we assess the degree of liver damage using biochemistry?
ALT & AST: ↑ with hepatocellular damage (ALT = cytoplasmic; AST = also mitochondrial)
GDH: Mitochondrial, ↑ only with severe liver damage
ALP: From bile ducts, ↑ with cholestasis or induction (e.g. steroids)
Non-liver sources:
- AST: ↑ with muscle injury
- ALP: Can come from bone, GIT, or drugs
Note: Enzyme levels don’t reflect severity — minor injury can cause large increases
What causes enzyme induction without actual liver cell damage?
Drugs or hormones (e.g. steroids, barbiturates)
Trigger liver cells to produce more enzymes (esp. ALP)
No actual cell injury
Describe use of ALT measurement in biochemistry
Liver specific in dogs & cats (not large animals)
Earlier & higher levels following hepatic damage than AST
Why should ALT & ALKP measurements be repeated in dogs after 2-3 days?
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)
How is ALKP used in biochemistry?
Found in bile canaliculi; ↑ with cholestasis or enzyme induction (e.g. steroids)
Not liver-specific: also from bone (young animals), intestine, steroids, and age-related isoenzymes (e.g. “old dog” ALKP)
T½: Dogs ~60–70h, Cats ~6h, Intestinal ALKP <10 min (rare in serum)
May ↑ in non-hepatic illness (e.g. systemic disease)
GGT is more liver-specific and biliary-focused
Give examples of non-primary hepatopathies that cause elevated liver enzymes
Enzyme induction: Stress, steroids (e.g. pyometra)
Metabolic disease: Diabetes, lipidosis, hyperlipidaemia
Portal circulation: GI/pancreatic disease affecting hepatocytes
Hypoxia/congestion: Cardiac disease, anaemia
What are the next steps after identifying elevated liver enzymes?
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
What does elevated urea & normal creatinine suggest?
Suggests pre-renal cause, not true renal failure
Common reasons:
- Dehydration (↓ perfusion) → check USG
- Post-prandial (esp. high protein meal)
- GI bleeding (↑ protein digestion → ↑ urea)
Creatinine is a more reliable marker for renal function
What does hypostenuria with azotaemia suggest?
‘inappropriately dilute’
Kidneys are functional but failing to concentrate
Suggests issue with ADH (↓ production or response) or primary polydipsia
What is the significance of the Na:K ratio?
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
What should you consider with elevated glucose?
Cats: Stress-induced hyperglycemia common
Persistent hyperglycemia → Pre-diabetes or diabetes mellitus
Fructosamine helps differentiate stress vs. true diabetes.
