Biochemistry Flashcards
Interpreting
‘abnormal’ results
- In vitro
- Artefactual
- Post prandial
- Age or breed related
- Potential to be significant
- Accounts for clinical signs
Age related changes
Persistence of foetal RBC:
* \/Hct, /\MCV, regenerative picture
Catecholamine response
* Generalised leucocytosis
Antigenic stimulation
* Lymphocytosis
Bone metabolism/growth
* /\ALP, /\Phosphorus, /\Ca
Immature immune-system
* \/Globulin
Limited hepatic function
* \/albumin
* Dietary lipid dependency- Hypertriglyceridemia ,
hypercholesterolemia
Renal parameter
- Urea (tubular flow rate, diet, proteolysis, GI blood loss)
- Creatinine (muscle mass)
- SDMA
Phosphorus
Calcium
Amylase& Lipase
Albumin
Assessment of GFR:
- Urea (tubular flow rate, diet, proteolysis, GI blood loss)
- Creatinine (muscle mass)
- SDMA
Urine specific gravity
- Some veterinary
refractometers have
different scales, use the
correct one - Remember to calibrate
- Turbid urine, use
supernatant - Some scales have “ND”
which is refractometive
index (ignore
▪ Although protein and glucose are soluble, it takes a LOT to
have a very small impact on USG (e.g. every 10 g/L of glucose
raises USG by only 0.004)
▪ Contribution of protein and Glucose is typically negligible
▪ Should always be correlated with hydration
▪ Essential information for interpretation of changes in renal
parameters
dipstick
- pH
- Protein
- Glucose
- Ketones
- Bilirubin
- Blood
Check urine only at room temperature
If you have dipsticks for human, don’t read:
˟Leukocytes (false positives in animals)
˟Nitrates
˟USG by dipstick
Azotemia with decreased renal concentrating ability
Acute or chronic renal disease
* CKD
* Pyelonephritis
* Primary renal glucosuria
* Post obstructive diuresis
Pre-renal azotemia with impaired concentrating ability-
Lack of response to ADH
* Hypercalcemia
* Pyometra (E.coli)
* (Hyperadrenocorticism)
Osmotic diuresis (e.g. diabetes mellitus)
Decreased medullary hypertonicity
* Prolonged hyponatremia/hypochloremia
* Loop diuretics
Electrolyte disturbances: Sodium/chloride
Think about fluid balance-
Intake vs loss
* GI
* PUPD/diuresis
* Third space effusions
* Panting
* Fluid therapy
Chloride typically follows sodium……
with exceptions
* Vomiting
* Excessive bicarbonate loss
* Artefactual (KBr)
Remember to consider impact on acid base balance
Electrolyte disturbances: Potassium
Serum [K+] may not reflect total body potassium
Hypokalemia
* \/ intake
* /\loss
* Intracellular shift
Hyperkalemia
* Artefactual (EDTA contamination)
* /\ intake (not usually an issue)
* \/ excretion
* Extracellular shift
* Insulin deficiency
Metabolic acidosis
Titrational: HCO3-
consumed to buffer
excess [H+]- can be Organic and inorganic:
Uraemic acids
▪ Renal disease (uremic acid!)
▪ Azotemic patient
Dehydrated dog
▪ Lactate (acidic! so causes acidosis)
▪ Beta hydroxy butyrate
▪ (DKA)
▪ Negative energy balance
Toxins
Secretory: HCO3- lost
from GIT or kidneys;
characterised by
hyperchloraemia
strong Ion difference
(Dilutional)- Na+ decreases more
than Cl- if excess H20
dilutes electrolytes
proportionately
Interpreting dysproteinemia
Hypoalbuminemia:
<18-20g/L unlikely chronic inflammation
Correlate with clinical signs/ effusions/ UPC/ other biochem data
<15g/L may develop transudative effusions
* Especially if acute
* Perform full fluid analysis
Hyperglobulinemia:
Suspect neoplasia?
* Perform serum protein electrophoresis
Take in to account hydration statuS
CRP
C-reactive protein (CRP) is a protein made by the liver. The level of CRP increases when there’s inflammation in the body. A simple blood test can check your C-reactive protein level
- Identify inflammation before it is visible on leukogram
- Identify inflammation when leukogram is ambiguous ( on the way down or when inflammation is
sequestrated) - When investigating significance of neutropenia (decreased production vs consumption)
- Monitoring inflammatory condition – Classic for monitoring for IMPA , minimize repeatable joint taps
Biochemical evaluation of the live
Assays for liver disease:
Enzymes that detect hepatocyte injury
(ALT, AST)
Enzymes that detect cholestasis
(ALP, GGT)
Liver function tests
(Bilirubin, bile acids, Urea, albumin, cholesterol, ammonia)
* Substances normally produced or removed by the liver
Enzyme assays:
Magnitude of change is exponential
May reflect ‘leakage’ or induction….. and what does that mean?
* Active damage
* Solubilisation by bile salts (cholestasis)
* Drug-induction
* Tissue repair (ALT)
Diagnosing pancreatitis
1.Spec cPL Assay (Texas A&M University, Gastrointestinal Laboratory):
1. Studies indicate sensitivity ranging from 70% to 90.9% and specificity
from 74.1% to 88%.
2. Agreement with clinical diagnosis ranged from a kappa score of 0.33 to
0.78.
2.SNAP cPL Assay (IDEXX Laboratories, Inc):
1. Sensitivity ranged from 73.9% to 100% with specificity from 59% to
77.8%.
2. Agreement with Spec cPL had a kappa score of 0.33 to 0.78 and an ICC
of 0.92.
3.VetScan cPL Rapid Test (Abaxis, Inc):
1. Sensitivity ranged from 73.9% to 83.3% with specificity from 76.9% to
83.8%.
2. Agreement with Spec cPL was reported with an ICC of 0.96.
4.Vcheck cPL Assay (Bionote):
1. There’s a lack of published studies evaluating its clinical performance or
agreement with Spec cPL.
5.DGGR Assays:
1. Various studies reported sensitivity ranging from 85.7% to 93% and
specificity from 53% to 74.3%.
2. Agreement with Spec cPL ranged from kappa scores of 0.55 to 0.68 and
ICC of 0.89
Cushing disease
is a clinical diagnosis. laboratory data are
only meaningful when there is clinical suspicion.
▪ Remember diagnostic test and differentiating tests are
driftnet
Sensitivity :
Low does Dex > ACTH stimulation test
Specificity
ACTH stimulation test > Low does Dex
* Low does Dex within normal range essentially
exclude Cushing’s unless clinical picture is
overt
* Urine cortisol/ creatinine ratio- useful for
exclusion
* Low does Dex should not be attempted on a
diabetic dog
Polyuria and polydipsia
*Polyphagia
*Panting
*Abdominal distention (pot belly)
*Hepatomegaly
*Muscle weakness
*Dermatologic changes
* Symmetric truncal alopecia
* Hyperpigmentation
* Thin skin
* Poor hair regrowth
The Addisonian dog
Typically, nonspecific clinical presentation
* Profile can also be nonspecific
* Remember differentials for reduced NA: potassium ratio
* In most differentials (acidosis, renal disease, poorly controlled DKA,
the reduced ratio is mostly driven by high potassium. In Addison, the
low sodium is the more prominent drive for reduced ratio
* Azotemia and hyposthenuria without renal failure-loss of sodium drives reduced medullary tonicity
Specific diagnostic tests :
* ACTH stimulation test gold standard- Remember impact of any recent steroid treatment when interpreting resultd
* Basal cortisol is very effective in excluding Addison in these severely sick
patients who mimic Addison
* Low does Dex is clearly useless
Hyperthyroidism
Classical presentation:
* skinny scruffy ravenous cat, often vocal & agitated
* State of hypercatabolic which impact the wider symptoms and changes in profile
(tachycardia, PUPD, open moth breathing, are all possible symptoms.
* Diagnosis
* Most commonly Increase in total T4 is diagnostic
* Cats with mild/early disease may present with Total T4 within the normal range in the upper half
of reference range
* Free T4 is more sensitive for the diagnosis of hyperthyroidism than TT4; up to 95%
of hyperthyroid cats with normal TT4 may have an elevated
* Testing for Free T4
* Equilibrium dialysis (ED), considered as the gold standard
* Chemiluminescent enzyme immunoassay – cost effective but less sensitive
Hypothyroidism
Common presentation
* Lethargy /dull mentation
* Inactivity or unwillingness to exercise
* Weight gain
* Cold intolerance/heat seeking
*Dermatologic changes
* Symmetric, nonpruritic hair loss
* Post-clipping alopecia
* Dry, dull hair coat
* Scaling
* Hyperpigmentation
* Recurrent pyoderma or otitis externa
Total T4 then TSH
if boh low but high clinical suspission- Free T4
Diabetes
Glucose levels
* Remember in vitro consumption
* Submit promptly spun serum
* Stress related hyperglycaemia can get very high (particularly in cats )
* Prove persistency of high glucose levels :
* Urinalysis
* Fructosamin
* Glycosylated haemoglobin
Don’t forget to check for ketone bodies (urine and blood)
* Urinalysis is key in the diagnosis (remember susceptibility to bacterial cystitis)
* Remember the impact on renal function (osmotic diuresis and medullary
washout)
* Difficult to balance diabetic patient ? Seek predisposing factors for insuling
resistance
* Acromegaly (cats)
* Heat
* Concurrent Cushing’s disease
Insulinoma
Clinical Presentation:
Patients presenting symptoms related to hypoglycemia should
consider insulinoma as a differential diagnosis, especially if plasma
glucose concentration is 40 mg/dl or less.
Diagnostic approach :
Simultaneous interpretation of serum
insulin and glucose concentrations.
Fasting samples for insulin levels should
be obtained when glucose is less than
50 mg/dl
In vitro consumption-
For true hypoglycaemia :
▪ Extrapancreatic tumors
▪ severe hepatic dysfunction
▪ Toxemia of pregnancy,
▪ sepsis,
▪ Insulin overdose,
▪ Hypoadrenocorticism
▪ Starvation
▪ Malabsorption
▪ Hunting dog hypoglycaemia
History and physical
examination help eliminate
many of these possibilities.
