The liver function tests typically include alanine transaminase (ALT) and aspartate transaminase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), serum bilirubin, prothrombin time (PT), the international normalized ratio (INR), total protein and albumin.
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liver_function_tests.ppt
1.
2. Synthetic Function
Plasma proteins (albumin, globulins), cholesterol, triglycerides and
lipoproteins
Detoxification and excretion
Ammonia to urea (urea cycle), bilirubin, cholesterol, drug metabolites
Storage Function
Vitamins A, D, E, K and B12
Production of bile salts
Helps in digestion
3. Hepatocellular disease
Cholestasis (obstruction of bile flow)
Hepatitis
Icterus
Liver cancer
Steatosis (fatty liver)
4. Noninvasive methods for screening of liver dysfunction
Help in identifying general types of disorder
Assess severity and allow prediction of outcome
Disease and treatment follow up
5. 1. Protein synthesis (albumin, α- and β-globulins, clotting factors)
2. Uptake and excretion of bilirubin and bile acids
3. Uptake of ammonia and conversion of ammonia to urea (BUN)
4. Glucose homeostasis and glycogen storage
6. Broadly classified as:
1.Tests to detect hepatic injury:
• Mild or severe; acute or chronic
• Nature of liver injury (hepatocellular or cholestasis)
2.Tests to assess hepatic function
7. Group I: Markers of liver dysfunction
▫ Serum bilirubin: total and conjugated
▫ Urine: bile salts and urobilinogen
▫ Total protein, serum albumin and albumin/globulin ratio
8. Group II: Markers of hepatocellular injury
▫ Alanine aminotransferase (ALT)
▫ Aspartate aminotransferase (AST)
9. Group III: Markers of cholestasis
▫ Alkaline phosphatase (ALP)
▫ g-glutamyltransferase (GGT)
10. Normal LFT values do not always indicate absence of liver
disease
Liver a has very large reserve capacity
Asymptomatics may have abnormal LFT results
Diagnosis should be based on clinical examination
11.
12. A byproduct of red blood cell breakdown
It is the yellowish pigment observed in icterus
High bilirubin levels are observed in:
Gallbladder stones
acute and chronic hepatitis
14. Hepatocellular disease may cause increased concentrations of both
unconjugated bilirubin and conjugated bilirubin.
(1) The presence of unconjugated bilirubin is due to decreased
bilirubin uptake and conjugation by damaged hepatocytes.
(2) The presence of conjugated bilirubin is due to intrahepatic
cholestasis from hepatocyte swelling.
Post-hepatic biliary obstruction is expected to increase conjugated
bilirubin concentration, but hepatic injury secondary to cholestasis
also may result in increased concentration of unconjugated bilirubin.
15. Dogs and cats with pre-hepatic or post-hepatic hyperbilirubinemia often have a
mixture of conjugated and unconjugated bilirubin.
Evaluation of other laboratory parameters may provide more information about
the cause of hyperbilirubinemia than does the percentage of conjugated vs.
unconjugated bilirubin.
(1) Anemia suggests hemolytic disease, particularly with evidence of a hemolytic
anemia (spherocytes, positive Coombs’ test, Heinz bodies, etc.).
(2) Increased GGT or ALP activity in conjunction with hyperbilirubinemia
suggests cholestatic disease
16.
17. Most UBG is metabolized in the large intestine but a fraction is
excreted in urine
Normally bile salts are NOT present in urine
Obstruction in the biliary passages causes:
Leakage of bile salts into circulation
Excretion in urine
18. The most abundant protein synthesized by the liver
Normal serum levels: 3.5 – 5 g/dL
Synthesis depends on the extent of functioning liver cell mass
Longer half-life: 20 days
Its levels decrease in all chronic liver diseases
19. Normal serum levels: 2 – 3.5g/dL
a and b-globulins mainly synthesized by the liver
They constitute immunoglobulins (g-globulins-antibodies)
High serum g-globulins are observed in chronic hepatitis and
cirrhosis:
20. Normal A/G ratio: 0.5-1.7
Globulin levels increase in hypoalbuminemia as a
compensation
21. Prothrombin: synthesized by the liver, a marker of liver
function
Half-life: 6 hrs. (indicates the present function of the liver)
PT is prolonged only when liver loses more than 80% of its
reserve capacity
Vitamin K deficiency also causes prolonged PT
Intake of vitamin K does not affect PT in liver disease
22. Also present in erythrocytes and myocytes
Normal range: 10– 40 U/L
A marker of hepatocellular damage
High serum levels are observed in:
Chronic hepatitis, cirrhosis and liver cancer
23. More liver-specific than AST
Normal range (U/L):10-60
High serum levels in acute hepatitis (300-1000U/L)
Mild to moderate increases in ALT activity may occur with
anticonvulsants, corticosteroids(dog), and thiacetarsemide.
This is most likely due to mild hepatocellular injury rather
than induction.
24. Appears in plasma many days before clinical signs appear
A normal value does not always indicate absence of liver damage
Obese but otherwise normal individuals may have elevated ALT
levels
25. The liver of all animals contains high SDH activity. Increases
in serum SDH activity generallyare considered liver specific in
all species studied.
26. SDH is the enzyme of choice to detect hepatocellular injury in
horses, sheep, goats, and cattle, because it is more specific for
hepatic disease than AST and ALT in these species.
(1) AST is not a liver-specific enzyme.
(2) Hepatic ALT activity is too low to serve as a marker of
hepatocellular injury in these species.
27. A non-specific marker of liver disease
Produced by bone osteoblasts (for bone calcification)
Present on hepatocyte membrane
Normal range: 40 – 150U/L
Modearte elevation observed in:
Infective hepatitis and hepatocellular carcinoma
28. High levels are observed in:
Extrahepatic obstruction and intrahepatic cholestasis
Very high levels are observed in:
Bone diseases
29. Increased serum ALP activity may occur in:
(1) Cholestatic diseases
(2) Bone lysis or remodeling (e.g., bone tumors, young,
growing animals)
(3) Corticosteroid treatment or Cushing’s disease (dogs)
(4) Phenobarbital treatment (likely due to hepatic
injury/cholestasis)
(5) Hepatic nodular hyperplasia (dogs)
(6) Colic in horses
(7) Feline hepatic lipidosis
(8) Hyperthyroidism in cats
30. Used for glutathione synthesis
Normal range: <10 U/L
Moderate elevation observed in:
Infective hepatitis
GGT is increased in fatty liver
Editor's Notes
Obstruction can occur in obstructive jaundice and also in hepatic jaundice due to obstruction of microbiliary channels caused by inflammation