Liver function tests Dr.r.mallika
- 1. LIVER FUNCTION TESTS Dr (tmty)R.Mallika Associate professor &HEAD, DEPARTMENT OF PG BIOCHEMISTRY V.V.VANNIAPERUMAL COLLEGE FOR WOMEN, VIRUDHUNAGAR.
- 7. 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
- 8. Facts About Liver Disease Obesity, drinking alcohol and using drugs are the leading causes of liver disease. A liver disease may even be genetic. A healthy liver has the amazing ability to grow back, or regenerate when it is damaged. In the early stage of any liver disease, your liver may become inflamed which shows that your body is trying to fight an infection or heal an injury. Liver failure means that your liver is losing or has lost all of its function
- 10. Hepatocellular disease Cholestasis (obstruction of bile flow) Cirrhosis Hepatitis Jaundice Liver cancer Steatosis (fatty liver) Genetic Disorders ◦ Hemochromatosis (iron storage)
- 11. 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
- 12. Broadly classified as: Tests to detect hepatic injury: • Mild or severe; acute or chronic • Nature of liver injury (hepatocellular or cholestasis) 1.Tests to assess hepatic function
- 13. Group I: Markers of liver dysfunction ▫ Serum bilirubin: total and conjugated ▫ Urine: bile salts and urobilinogen ▫ Total protein, serum albumin and albumin/globulin ratio ▫ Prothrombin Time
- 14. Group II: Markers of hepatocellular injury ▫ Alanine aminotransferase (ALT) ▫ Aspartate aminotransferase (AST)
- 15. Normal LFT values do not always indicate absence of liver disease ◦ Liver a has very large reserve capacity Asymptomatic people may have abnormal LFT results ◦ Diagnosis should be based on clinical examination
- 16. Group III: Markers of Cholestasis ▫ Alkaline phosphatase (ALP) ▫ g-glutamyltransferase (GGT)
- 18. A byproduct of red blood cell breakdown It is the yellowish pigment observed in jaundice High bilirubin levels are observed in: ◦ Gallstones, acute and chronic hepatitis
- 20. Normal ◦ 0.2 – 0.8 mg/dL Unconjugated (indirect): ◦ 0.2 – 0.7 mg/dL Conjugated (direct): ◦ 0.1 – 0.4 mg/dL Latent jaundice: ◦ Above 1 mg/dL Jaundice: ◦ Above 2 mg/dL
- 29. Class of Jaundice Causes Pre-hepatic or hemolytic Abnormal red cells; antibodies; drugs and toxins; thalessemia Hemoglobinopathies, Gilbert’s, Crigler-Najjar syndrome Hepatic or Hepatocellular Viral hepatitis, toxic hepatitis, intrahepatic cholestasis Post-hepatic Extrahepatic cholestasis; gallstones; tumors of the bile duct, carcinoma of pancreas
- 31. Diagnosis Bilirubin test The level of bilirubin in their blood will need to be tested using: a small device called a bilirubinometer, which shines light on to your baby's skin (it calculates the level of bilirubin by analysing how the light reflects off or is absorbed by the skin) A blood test of a sample of blood taken by pricking your baby's heel with a needle (the level of bilirubin in the liquid part of the blood called the serum is then measured) Blood tests are usually only necessary if your baby developed jaundice within 24 hours of birth or the reading is particularly high. The level of bilirubin detected is used to decide whether any treatment is needed.
- 32. Most UBG is metabolized in the large intestine but a fraction is excreted in urine (less than 4 mg/day) Normally bile salts are NOT present in urine Obstruction in the biliary passages causes: ◦ Leakage of bile salts into circulation ◦ Excretion in urine
- 33. 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
- 34. Normal serum levels: 2.5 – 3.5g/dL a and b-globulins mainly synthesized by the liver They constitute immunoglobulins (antibodies) High serum g-globulins are observed in chronic hepatitis and cirrhosis: ◦ IgG in autoimmune hepatitis ◦ IgA in alcoholic liver disease
- 35. Normal A/G ratio: 1.2/1 – 1.5/1 Globulin levels increase in hypoalbuminemia as a compensation
- 36. 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
- 37. Normal range: 8 – 20 U/L A marker of hepatocellular damage High serum levels are observed in: ◦ Chronic hepatitis, cirrhosis and liver cancer
- 38. • More liver-specific than AST • Normal range (U/L): ▫ Male: 13-35 ▫ Female: 10-30 • High serum levels in acute hepatitis (300- 1000U/L) • Moderate elevation in alcoholic hepatitis (100- 300U/L) • Minor elevation in cirrhosis, hepatitis C and non- alcoholic steatohepatitis (NASH) (50-100U/L)
- 39. 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
- 40. A non-specific marker of liver disease Produced by bone osteoblasts (for bone calcification) Present on hepatocyte membrane Normal range: 40 – 125 U/L Moderate elevation observed in: ◦ Infective hepatitis, alcoholic hepatitis and hepatocellular carcinoma
- 41. High levels are observed in: ◦ Extrahepatic obstruction (obstructive jaundice) and intrahepatic cholestasis Very high levels are observed in: ◦ Bone diseases
- 42. Used for glutathione synthesis Normal range: 10 – 30U/L Moderate elevation observed in: ◦ Infective hepatitis and prostate cancers GGT is increased in alcoholics despite normal liver function tests ◦ Highly sensitive to detecting alcohol abuse
- 46. Deaths from cirrhosis rose between 1999- 2016, with increase seen most often among young adults- a new study shows In 2016 alone, 11,073 lives were lost to liver cancer which was doubled the number of deaths in 1999. Liver cirrhosis is the 12th leading cause of mortality worldwide and approximately half of those the deaths are due to alcohol abuse.
- 47. Alcoholism is associated with bacterial overgrowth in the intestines. Determined by measuring plasma levels of a liver enzyme called alanine aminotransferase and levels of liver triglycerides. More protein after weight loss may reduce fatty liver disease Increasing the amount of protein in the diet may reduce the liver’s fat content and lower the risk of diabetes in people with nonalcoholic fatty liver disease (NAFLD).
- 48. Hepatitis delta virus (HDV) causes the most aggressive form of viral hepatitis, putting at least 20 million people worldwide at risk of developing liver fibrosis, cirrhosis, and liver cancer. HDV is a small, RNA-based “Satellite” virus that products just a single protein of its own and therefore requires additional proteins provided by another liver virus, hepatitis B virus(HBV) . HDV can infect patients already carrying HBV, or both viruses can infect patients simultaneously.
- 49. LFTs help detect liver injury and function. LFTs do have some limitations.
Editor's Notes
- #33: Obstruction can occur in obstructive jaundice and also in hepatic jaundice due to obstruction of microbiliary channels caused by inflammation