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LIVER FUNCTION TEST

LIVER FUNCTION TEST. BY Dr Grace Ann Varghese. ALBUMIN. Normal Range: 3.5 to 5.5 g/dl 3 Important protein synthesized in liver. 10-15 g/day in healthy individual. About 60% is located in interstitial compartment of ECF High Concentration are seen in serum compartment.

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LIVER FUNCTION TEST

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  1. LIVER FUNCTION TEST BY Dr Grace Ann Varghese

  2. ALBUMIN Normal Range: 3.5 to 5.5 g/dl3 • Important protein synthesized in liver. • 10-15 g/day in healthy individual. • About 60% is located in interstitial compartment of ECF • High Concentration are seen in serum compartment. • A reduction in serum albumin concentration results in edema [an abnormal accumulation of fluid in intracellular spaces of the body] • Serum concentration of Albumin depends on its • Rate of synthesis • Volume of Distribution • Rate of catabolism.

  3. Synthesis falls in parallel with increasing severity of liver disease. • Low serum albumin concentration when the volume of distribution of albumin increases, such as cirrhosis (interstitial inflammation of liver) • Pregnancy ( fluid retention) • Shift of albumin from serum to interstitial fluid, this causes dilution hypoalbuminaemia after parenteral infusion of excess protein free fluid. • Movement of albumin from serum into interstitial fluid is often associated with increased capillary permeability in post- operative patients.

  4. A shift of protein is known to occur physiologically when moving from lying down to the upright position. • This can account for an increase in the serum albumin level of up to 10g/L Hypoalbuminaemia: Causes: • Catabolic states associated with a a variety of illness and increased loss of albumin, either in urine from damaged kidneys [Nephrotic Syndrome via skin following burns (or)psoriasis. • Albumin serum half life is approximately 20 days. Hyperalbuminaemia: • Seen in patients with marked dehydration (which concentration their plasma) • Concurrent elevation in BUN and Hematocrit. It is Asymptomatic.

  5. BILIRUBIN (5 – 17 micromole/L) • At the end of their life RBC’s are broken down in the spleen. • Hemoglobin molecules are liberated and are split into Globin and Haem. • Globin enters general protein pool. • Iron in haem is reutilized. • Remaining tetrapyrrole ring of haem is degraded to Bilirubin.

  6. Bilirubin is of two types unconjugated and conjugated.

  7. Elevated Bilirubin can be caused by: • Increased production of Bilirubin (Eg: Haemolysis, ineffective erythropoiesis. Impaired transport into hepatocytes. Eg: interference with bilirubin uptake by drugs such as Rifampicin) • Decreased excretion Eg: with the drugs such as Rifampicin.

  8. Liver produces 300 mg of bilirubin each day. • Mature liver can metabolize and excrete upto 3g/ day • Hence serum bilirubin concentration are not a sensitive test of liver function. • An elevation of serum bilirubin concentration approximately 2.5 times the normal upper limit will reveal itself as jaundice, seen best in the skin. • Bilirubin in serum is normally unconjugated, bound to protein, not filtered by the Glomeruli and does not normally appear in the urine. • Bilirubin in the urine is usually the result of increase in serum concentration of conjugated bilirubin.

  9. CLINICAL IMPLICATIONS: • Hepatocellular jaundice results from injury (or) disease of parenchymal cells of the liver and can be caused by following conditions: • Viral hepatitis • Cirrhosis • Infectious mononucleosis • Reactions to certain drugs such as chlorpromazine.

  10. Obstructive jaundice is usually the result of Obstruction of the common bile (or) hepatic ducts due to stones. • The obstruction produces high conjugation bilirubin levels due to bile regurgitation. • Hemolytic jaundice is due to over production of Bilirubin resulting from hemolytic process that produce high levels of unconjugated bilirubin. • Pernicious • Sickle cell Anemia

  11. Elevated indirect (unconjugated) bilirubin levels occur in: • Crigler- Najjar Syndrome • Glibert’s Disease. • Elevated Direct Conjugated bilirubin levels occur in • Cancer of the head of pancreas • Choledocholithiasis • Dubin- Johnson Syndrome

  12. ALKALINE PHOSPHATASE Normal: Males: < 12 yrs : <350 U/L 12-14yrs: <500 U/L > 20 yrs : 25- 100 U/L Females: 1 – 12 yrs : <350 U/L >15 yrs : 25 – 100 U/L

  13. This enzyme is present in canalicular (narrow tube passage) and sinusoidal (blood channel) membranes of liver and many other tissues such as bone. • Elevated levels of this enzyme originates predominantly from two sources i.e. liver and bone. • Elevation of the enzyme - glutamyl transpeptidase confirms the hepatic origin of elevated alkaline phosphatase. • Each site of origin produces a specific isoenzyme of alkaline phosphatase, it can be separated electorphoreticallyif concentrations are very high.

  14. Liver disorders can elevate alkaline phosphatase, include space occupying lesions such as Tumors( swelling) (or) Abscess (localized collection of pus in a cavity formed by disintegration of Tissue) and hepatitis (inflammation of liver) • Physiological increase in serum alkaline phosphatase activity also can occur on pregnancy due to the release of placental isoenzyme and • During periods of Growth in children and Adolescent when bone isoenzyme is released.

  15. Pathological increase in serum alkaline phosphatase of bone origin may arise in disorders such as Osteomalacia (inadequate mineralization of Osteoid (organic matrix of bone) in matured cortical and spongy bone. • Plasma alkaline phosphatase activity may be raised upto 4 – 6 times the normal limit.

  16. TRANSAMINASES: AST: Aspartate transaminase ALT: Alanine transaminase • These are two intracellular enzymes present in hepatocytes which are released into the blood of patients as a consequence of hepatocyte damage (or) Death. • These are elevated in cases of hepatocellular disease such as hepatitis. • Serum AST levels are increased in variety of Disorders including liver Diseases: • Severe Tissue Hypoxia • MI • Muscle disease, etc.

  17. ALT is elevated to similar extent in the disorders listed which involve the liver, though to a lesser extent. • These are elevated in cases of hepatocellular diseases such as hepatitis. • Extremely high valves where transaminases are recorded in the thousands. Occur in acute liver damage (disease) owing to massive levels of hepatocyte killing or damage. • In context of liver diseases increased transaminase activity indicated hepatocyte necrosis. Bilirubin in serum is normally unconjugated, bound to protein, not filtered by the Glomeruli and does not normally appear in the urine. • Bilirubin in the urine is usually the result of increase in serum concentration of conjugated bilirubin

  18. AMMONIA (NH3) Normal: Adults: 15 to 60 μg/dl • Generally ammonia is produced by protein metabolism. • And it is taken up by liver and it is converted to urea. • And this phenomenon of ammonia → urea cycle. • Ammonia concentration in the blood increased. • And urea cycle destruction is seen in Hepatic Disease (damage)

  19. Clinical signs of hyperammonaemia occurs at concentrations >60 mmol/L • Symptoms of Hyperammonaemia include • Anorexia • Somnolence • Irritability • Cerebral oedema • Coma and death • Above symptoms are proportional to ammonia concentration.

  20. Causes of hyperammonaemia: • Genetic defects in urea cycle and disorders resulting in significant hepatic dysfunction. • Ammonia plays an important role in increase in brain water which occurs in liver failure.

  21. ɣ- GLUTAMYL TRANSPEPTIDASE (ɣ- Glutamyl Transferase) Normal: Men: 7 to 47 U/L Women: 5 to 25 U/L • It is present in high concentration in the liver, kidney, and pancreases, where it is found with in the endoplasmic reticulum of cells. • It does not differentiate a cholestatic (stoppage or suppression of bile flow) disorder from hepatocellular ( affecting liver cells) disease.

  22. It can also be elevated in Alcoholic liver disease, hepatitis, cirrhosis, pancreatitis and CCF. • Serum levels of ɣ- glutamyl transpeptidase activities can be raised by enzyme induction by certain drugs such as phenytoin, phenobarbital and rifampicin. • Also raised in an individual with alcoholic liver disease. • It can also be raised in heavy drinkers of alcohol who do not have liver damage due to enzyme induction. • Its activity can remain elevated for upto 4 weeks after stopping alcohol intake.

  23. AMYLASE Normal: Adults: 25 – 125 U/L • Serum amylase concentration rises within the 1st 24 hours of an attack or pancreatitis (inflammation of pancreas) and declines to normal over the following week.

  24. References: • A MANUAL OF LABORATORY AND DIAGNOSTIC TESTS BY FRANCES FISCHBACH, MARSHALL B. DUNNING III,EDITION 8 • CLINICAL PHARMACY AND THERAPEUTICS- ROGER AND WALKER, CHURCHILL LIVINGSTONE PUBLICATIONS. • BASIC SKILLS IN INTERPRETING LABORATORY DATA BY MARY LEE, EDITION-IV

  25. THANK YOU

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