Evaluations of Biochemical Panel Flashcards
Indicators of damage
Leakage enzymes- don’t correlate with severity or size of lesion
ALKP, ALT, AST, CK
Pancreatic enzymes
Lipase, PLI
Thyroid
TgAA
Renal
Casts
Cardiac
Troponin I
indicators of dysfunction
Hepatic function
Bile acid, Ammonia
Albumin, Glucose, bilirubin
Pancreatic function
TLI
Thyroid
T4, TSH
Renal
Creatinine, USG, proteinuria
Cardiac
NT-proBNP
which liver enzymes are cytosolic (within cytoplasm) of hepatocytes
ALT, AST, GDH
Which liver enzymes are in the biliary lining cells
GD, AST
Located in mitochondira- when they leak suggests a more dramatic degree of injury
Other reasons fro enzyme induction apart from damage
Pathology
Drugs or endogenous compounds
Glucocorticoids
Barbiturates
ALT
Cytosolic enzyme in hepatocytes
Almost completely liver specific in dogs and cats (not large animals)
Earlier and higher levels following hepatic damage than AST
Dog T½ = 40-60 hours
Cat T½ = 3.5 hours
Based on T½ in dog, repeat measure after 2-3 days to determine if insult passed, ongoing or worsening
Also means that its less worrying to see change in dogs but in cats is concerning even if it’s a small change
ALKP/ ALP
Membrane location (canalicular)
Induced by impaired biliary flow and medications
Not liver specific – iso-enzymes:
Bone (growth), Intestinal
Canine steroid induced
Hepatic enzyme
Dog T½ = 60-70 hrs
Cat T½ = 6 hours
Intestinal enzyme T½ <10mins
Very susceptible to non-hepatic disease and “secondary hepatic effects” including benign nodular hyperplasia and “old-dog”
Serum GGT more biliary specific
Hepatic enzyme specificity
Called “hepatic” enzymes and sensitive to hepatic impacts but recognise often not primary hepatopathy
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
AST
found in the liver cells, but is also present in other organs such as the heart and skeletal muscle.
Elevated levels of AST in the blood may indicate liver damage, but can also be a sign of heart or muscle damage.
GGT
enzyme found primarily in the liver and bile ducts. Elevated levels of GGT in the blood can be a sign of liver disease
more billary specific than other enzymes
Billiruben
Bilirubin is a waste product formed when red blood cells break down.
Elevated levels of bilirubin in the blood can be a sign of liver disease, such as hepatitis or cirrhosis, or a blockage in the bile ducts.
Albumin
protein produced by the liver.
Low levels of albumin in the blood can be a sign of liver disease, as the liver may not be producing enough albumin.
What to do about 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
Bile acids including post-prandial (not horses) for functional assessment
May have to repeat if decreasing results
Further questioning for history pointing a more specific direction
E.g., ACTH Stimulation +/- 17hydroxyprogesterone
Agree to monitor: act on further increases or appearance of clinical signs
Remember analytical variation when assessing change
significance of elevated urea and normal creatinine
Suggests pre-renal effects such as:
Reduced renal perfusion (dehydration)
Post-prandial
Unusually high urea with normal creatinine → GI bleeding
FOCUS ON CREATININE AS MEASURE OF RENAL FUNCTION
significance of USG
Assess alongside hydration
USG <1.030 Dog or <1.035 Cat with azotaemia suggests “inappropriately dilute”
Hyposthenuria (<~1.008) only possible if kidneys functional
Excessive fluid intake (primary polydipsia)
ADH production or action
Rehydrate if necessary and re-assess
UPCR for renal staging
