Liver function test presentation

1. LIVER FUNCTION
TESTS
By
Roll No.
161-170

2. INTRODUCTION:
Liver function tests are defined as tests which are
employed
For accurate diagnosis.
To assess the severity of damage.
For prognosis.
For therapy.

3. I. TESTS FOR
MANUFACTURE AND
EXCRETION OF BILE
Definition: Tests employed to assess the synthesis and
elimination of bilirubin pigment, urobilinogen and bile
acids.
Bie is produced by the liver, stored in the gallbladder and
secreted via biliary ducts into the duodenum.
Bile consists of biliary phospholipids and primary and
secondary bile acids.
Jaundice will develop if bilirubin is excessively produced,
or there is impaired hepatic uptake and conjugation of
bilirubin, or it is insufficiently excreted into the duodenum.

4. Normal
Bilirubin
Metabolism

5. 1. BILIRUBIN
Bilirubin pigment can be detected in serum, feces and urine.
1. Serum bilirubin estimation is based on van den Bergh diazo
reaction in which, diazo reagent consists of diazotized
sulphanilic acid.
Conjugated bilirubin(CB) gives direct reaction within a minute.
Unconjugated bilirubin(UB) is determined by indirect reaction.
Addition of alcohol to the reaction mixture gives positive test
for both conjugated and unconjugated bilirubin.
The serum of normal adults contains less than 1 mg/dl of total
bilirubin, out of which less than 0.25 mg/dl is conjugated
bilirubin.

6. Bilirubin level rises in diseases of hepatocytes, obstruction to biliary
excretion into the duodenum, in hemolysis, and defects of hepatic
uptake and conjugation of bilirubin pigment such as in Gilbert's
disease.
2. In feces, excretion of bilirubin is assessed by inspection of stools.
Clay-colored stool (no stercobilin in feces) : obstructive jaundice.
3. In urine, presence of bilirubin imparts deep yellow color.
Conjugated bilirubinuria can be detected by commercially available
'dipsticks', Fouchet's test or foam test method.
Bilirubinuria does not occur in normal subjects nor is UB excreted in
the urine, instead it occurs only when there is raised level of CB
because it is filterable.
Its excretion depends upon the level of CB in plasma that is not
protein-bound (available for glomerular filtration).
Bilirubinuria appears in patients of hepatitis before the patient has
jaundice.

7. Urobilinogen is normally excreted in the urine.
Its estimation in urine can be done by preparing dilutions with
Ehrlich’s aldehyde reagent and using the ‘dipstick’ method.
Increased urobilinogen in urine is seen in:
• Liver dysfunctions (e.g. alcoholic liver disease, cirrhosis, liver
malignancy)
• Hemolytic diseases
• Pyrexia
Absent urobilinogen in urine indicates: Cholestatic jaundice due
to complete biliary obstruction.
2. UROBILINOGEN

8. Primary bile acids: cholic acid & chenodeoxycholic acid (from
cholesterol in hepatocytes).
On gut entry Colonic bacteria deconjugate them form
→ →
secondary bile acids: Deoxycholic acid and Lithocholic acid.
Enterohepatic circulation reabsorbs most bile acids.
~10% excreted in feces as toxic, unabsorbable lithocholic acid.
Raised serum bile acids in cholestatic liver diseases cause
→
pruritus (itching)
Urinary excretion via: Active transport and Passive diffusion
Detected by: Hay’s test and Dipsticks
3. BILE ACIDS(BILE SALTS)

9. 4. BROMSULPHALEIN
EXCRETION
Bromsulphalein (BSP) is a dye handled by liver like
bilirubin (binding, conjugation, excretion).
Procedure:
• Inject BSP intravenously.
• Take venous blood sample after 45 minutes.
• Measure % of dye remaining in circulation.
Rarely performed now due to availability of better enzyme
tests.
Still useful in diagnosing: Dubin–Johnson syndrome.

10. II. SERUM ENZYME
ASSAYS
Determination of certain serum
enzymes is considered useful in
various types of liver injury,
whether hepatocellular or
cholestatic, as well as in
quantifying liver damage.

11. ALKALINE PHOSPHATASE
(ALP)
Produced by bone, liver, intestine, placenta.
Normal range: 33–96 U/L.
Elevated in bone & liver disease, and
pregnancy.
Greatest elevation in biliary obstruction.
Moderate elevation in hepatitis, cirrhosis,
metastatic liver disease.

12. GAMMA-GLUTAMYL
TRANSPEPTIDASE (GGT)
• Source: Liver.
• GGT level parallels ALP.
• Used to confirm ALP is hepatobiliary in
origin.
• Elevated in alcohol abuse even without
liver disease.

13. TRANSAMINASES
(AMINOTRANSFERASES)
•AST (SGOT): 12–38 U/L from liver, heart,
→
muscle, kidney.
•ALT (SGPT): 7–41 U/L specific to liver.
→
•ALT more liver-specific.
•High levels in viral hepatitis, acute necrosis.
•Mild elevation in cirrhosis, alcoholic liver
disease.

14. OTHER SERUM ENZYMES
• 5'-Nucleotidase: differentiates ALP
origin
• LDH: elevated in metastatic liver
disease
• Choline esterase: decreased in
hepatocellular damage, malnutrition

15. III. TESTS FOR
METABOLIC
FUNCTIONS

16. 1. LIPID AND LIPOPROTEIN
METABOLISM
• Liver synthesizes cholesterol,
phospholipids, triglycerides
• Cholestasis → increased cholesterol and
triglycerides
• Chronic liver disease & malnutrition →
decreased values

17. 2. AMINO ACID AND
PLASMA PROTEIN
METABOLISM
• Liver converts amino acids to ammonia and
urea.
• Synthesizes albumin, fibrinogen, prothrombin,
etc.
• Hypoalbuminaemia = hepatocyte destruction
• Hyperglobulinaemia = cirrhosis, chronic
hepatitis

18. IMMUNOGLOBULINS & CLOTTING
FACTORS
• IgA in cirrhosis.
↑
• IgG in chronic active hepatitis.
↑
• IgM in primary biliary cirrhosis.
↑
• Clotting factors in liver disease.
↓
• PT & PTT ; vitamin K may correct
↑
PT if no liver cell death.

19. SERUM AMMONIA:
Elevated in hepatic
encephalopathy, fulminant
hepatitis, cirrhosis due to
impaired urea synthesis in
damaged liver

20. 3. CARBOHYDRATE
METABOLISM
Liver maintains glucose homeostasis
Fulminant necrosis → decreased
blood glucose
Chronic liver disease impaired
→
glucose tolerance, insulin resistance

21. IV. IMMUNOLOGIC
TESTS

22. 1. NON-SPECIFIC
IMMUNOLOGICAL
REACTIONS
Smooth muscle antibody to actin component of
muscle is formed in certain hepatic disorders
with hepatic necrosis Hepatocytes have a
→
protein immunologically similar to actin.
Mitochondrial antibody develops in patients
with primary biliary cirrhosis.
Antinuclear antibody is present in some
patients of chronic hepatitis The LE cell test
→
may be positive in these cases.

23. 2. ANTIBODIES TO
SPECIFIC ETIOLOGIC
AGENTS
• Hepatitis B surface antigen (HBsAg):
Demonstrated in serum hepatitis. A confirmed
positive test is proof of hepatitis B infection.
• Hepatitis B core antibody (HBc): Detected in all
hepatitis B patients.
• Hepatitis Be antigen (HBeAg): Found in
chronic hepatitis B.
• Amoeba antibodies to Entamoeba histolytica:
Found in amoebic liver abscess.

24. V. ANCILLIARY
DIAGNOSTIC TESTS

25. 1. FNAC AND/OR
PERCUTANEOUS LIVER
BIOPSY
Used for examining hepatic morphology in:
i) Hepatocellular disease of unknown cause
ii) Suspected chronic hepatitis
iii) Hepatomegaly of various etiologies
iv) Splenomegaly of unknown cause
v) Fever of unknown origin
vi) SOLs on radiologic examination.

26. 2. ULTRASONOGRAPHY
•Ultrasound (US) examination of the liver
is indicated in:
•Cholestasis: To detect dilated intra- and
extrahepatic ducts.
•Space-occupying lesions (SOLs): To
differentiate neoplasms from cysts.
•iUS-guided FNAC or liver biopsy.

27. THANK YOU !!!!!