Liver Functions tests
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Liver function tests (LFTs) are essential for detecting liver disease, estimating damage, and monitoring treatment response, but they have limitations, such as not being specific for particular diagnoses. Key tests include measurements of synthetic function (like albumin and prothrombin time), cholestasis indicators (such as bilirubin and alkaline phosphatase), and enzymes indicating hepatocyte injury (like AST and ALT). The document also discusses neonatal jaundice and the significance of the serum-to-ascites albumin gradient in evaluating portal hypertension.
![Prognostic Tools for chronic liver disease
• MELD is a prospectively developed and validated
chronic liver disease severity scoring system
that uses a patient's laboratory values for serum
bilirubin, serum creatinine, and the international
normalized ratio for prothrombin time (INR) to
predict survival.
• MELD (model for end-stage liver disease)
– Identify patients whose predicted survival post-procedure
would be three months or less
• MELD = 3.8[serum bilirubin (mg/dL)] + 11.2[INR] + 9.6[serum
creatinine (mg/dL)] + 6.4](https://image.slidesharecdn.com/p-220406175742/85/Liver-Functions-tests-39-320.jpg)
Liver Functions tests
- 1. Liver Funtion tests Dr Abdul Qayyum Khan
- 2. Liver Function profile (LFT)
- 3. LIVER FUNCTION TESTS • USED TO ; • Detect presence of liver disease. • Distinguish among different types of liver dieases. • Estimate the extent of known liver damage. • Follow the response of treatment
- 4. LIVER FUNCTION TESTS • Disadvantages ; • Rarely suggest a specific diagnosis. • Can be normal in pts with serious liver disease and abnormal in pts with diseases that do not affect the liver • Only categorises into hepatocellular or cholestatic or pre-hepatic.
- 5. Clinical Lab tests Liver Function Test (LFT) profile Synthetic function Execratory function Integrity of liver cells Bilirubin Proteins TP, Alb, A/G ratio Liver enzymes AST, ALT, GGT, ALP
- 6. Tests based on detoxification & excretory functions • Serum bilirubin • Urine bilirubin • Blood ammonia
- 7. RE cell plasma hepatocyte HEME UCB UCB + albumin UCB+ligandin BMG BDG bile urobilinogen stercobilinogen Bilirubin UDP-glucoronyltransferase
- 9. Total bilirubin = D+ ID Direct bilirubin: is conjugated (water soluble bilirubin). Indirect bilirubin: is unconjugated (water insoluble bilirubin). Normal levels are: Direct (also called conjugated) bilirubin: 0 to 0.3 mg/dL Total bilirubin: 0.3 to 1.0 mg/dL Unconjugated is calculated by subtracting direct from total and so called indirect.
- 10. Gilbert’s syndrome Benign, unconjugated hyperbilirubinemia with otherwise normal liver chemistries up to 5% of normal population Polymorphisms of gene encoding bilirubin UDP-GT impaired ability to conjugate bilirubin Prominent in fasting state, systemic illnesses, hemolysis, some medications
- 11. Blood Ammonia • Produced by normal protein metabolism, by intestinal bacteria in colon. • Liver – detoxification – converting into urea which is excreted by kidneys. • Patients with advance liver disease- significant muscle wasting contributes to hyperammonemia • Used for detecting hepatic encephalopathy or hepatic synthetic functions.
- 12. Tests for bio-synthetic function of the liver Estimation of plasma proteins Total Protein ; Serum Albumin ; Serum Globulins Tests for reversal of A:G ratio Tests for coagulability of blood ; PT ,INR Plasma protein Normal levels Total 6.4 – 8.3 g% S. Albumin 3 – 5 g% Serum globulin 2 – 3 g% Serum fibrinogen 0.3 g% Serum prothrombin 40 mg% A:G ratio 1.7 : 1
- 13. Serum albumin • Produced by hepatocytes Normal : 3.5 – 5 g/dl • S. albumin <3 g/dl suspect chronic liver disease. • About six months stores are present in liver therefore S. Albumin is not a good indicator of acute/mild hepatic dysfunction • Hypoalbuminemia – not specific for liver disease – Protein malnutrition of any cause – Protein losing enteropathies – Nephrotic syndrome – Chronic infections – Burns • Reversal of A : G ratio chronic liver dysfunction.
- 14. Prothrombin Time ,INR Normal : 11.5 – 12.5 sec Prolongation of PT by 2 sec / more – Abnormal. PT – factors II,V, VII, X Rapid turnover – Best measure of hepatic synthetic functions & helpful for diagnosis of acute parenchymal liver disease. • Most present in excess, clotting abnormality occurs only when substantial impairment in ability of liver to synthesise the Clotting factors. PT prolonged – hepatitis, cirrhosis, vit K deficency ( obs.jaundice, fat malabsorption)
- 15. Serum Enzymes • Aminotransferases (AST,ALT) . Sensitive indicators of liver cell injury Helpful in recognizing hepatocellular disease such as hepatitis.
- 16. Evaluation of abnormalities of ALT (SGPT) and AST (SGOT) levels AST and ALT are markers of hepatocellular injury AST present in cytosol and mitochondria in liver, cardiac muscle, skeletal muscle, kidney, brain, pancreas, lungs, WBC and RBC. ALT a cytosolic enzyme, highest concentration in the liver. ALT considered a “liver specific” enzyme.
- 17. Alanine Aminotransferase(SGPT) Normal : 7 – 41 U/L ALT found primarily in liver. Upto 300U/L – Nonspecific , any type of liver disorder(CLD…cirrhosis /malignancy) >1000U/L – Extensive hepatocellular damage ( viral hepatitis, ischemic liver injury , toxin /drug induced liver injury )
- 18. Aspartate Aminotransferase (SGOT) Normal – 12 – 38U/L Two Iso enzymes- cytoplasmic, mitochondrial Mild degree of tissue injury – cytoplasmic form in serum Severe injury – mitochondrial type in serum Significant elevation – Myocardial Infarction. Moderate elevation – liver disease AST – liver , cardiac muscles, skeletal muscle, kidneys, brain, pancreas, lungs, leucocytes, RBC in decreasing order.
- 19. Serum Enzymes – that reflect cholestasis Three enzymes Alkaline Phosphatase 5’Nucleotidase Gamma glutamyl transpeptidase
- 20. Alkaline Phosphatase • Normal :40 – 125 U/L • Iso enzymes • Alpha -1 ALP – Epithelial cells of biliary canaliculi , increased in obs.jaundice. • Alpha-2 heat labile ALP – Hepatic cells , increased in hepatitis • Alpha -2 heat stable ALP – Placental origin, normal pregnancy • Pre Beta ALP – Bone origin , increased in bone disease. • Gamma ALP – Intestinal cells, increased in Ulcerative colitis • Leucocyte ALP – Increase – lymphoma, Decrease – CML .
- 22. Gamma glutamyl transpeptidase • Used in body for synthesis of glutathione • 11 iso enzymes. • Present in liver, kidney, pancreas, intestinal cells, prostate. • Normal : 9 – 58 U/L. • Unlike ALP , the level is unrelated with osteoblastic activity ie.. Unaffected by bone disease. • Slightly high normally in males due to prostate. • To detect alcohol abuse.
- 23. GGT • Raised even when other LFT are normal in alcohalics. • GGT falls rapidly within few days after abstinence. • Mod rise – infectious hepatitis, prostate Ca • High rise – Alcoholism, Obstructive jaundice, Neoplasms of liver
- 24. Take home message Classified in 3 groups 1. Synthetic function : albumin, clotting time. 2. Cholestasis : bilirubin, ALP, GGT 3. Hepatocyte injury : AST, ALT
- 25. Patterns of Abnormal • Elevations in ALT & AST only: Suggests cellular injury • Elevations in Alk Phos & Bilirubin: Suggests cholestasis or obstruction • Mixed pattern: ALT, AST, AP & Bili: Probably the most common scenario
- 26. Summary • Liver tests are numerous and somewhat confusing. • Not all liver disease is associated with abnormal test results. • Some of the worst liver disease has relatively normal appearing LFT’s and can only be noticed with a look at synthetic functions.
- 27. Misnomer – Does not effectively assess actual function – Not always specific for the liver – limited information regarding presence or severity of complication Liver Function Tests
- 28. Liver Synthetic Function • Total Protein and serum albumin • Total Bilirubin • Prothrombin Time (PT / INR) • These are “true” tests of liver function
- 29. LFTs • 1) Markers of acute hepatocyte injury & death: AST (SGPT), ALT (SGOT), Alk Phos. • 2) Measures of hepatocyte synthetic functions : PT, Albumin • 3) Indicators of hepatocyte catabolic activity: Direct & indirect bilirubin , ammonia • 4) Others: Lactate dehydrogenase, viral hepatitis serology
- 30. Neonatal Jaundice Neonatal jaundice is common 50% healthy term infants Chances of kernicterus In utero bilirubin is handled by placenta and mother’s liver After birth, neonate to has cope with increase in bilirubin production and the immature liver can not handle for a few days
- 31. Basis of photo therapy • UCB is not water soluble in its form • Blue light confrontational change in UCB • Its Photo Isomers are water soluble • Blue light converts the UCB into its photo isomers • The soluble photo isomers pass through the Glomerular filter and get excreted • Thus conjugation in liver is by passed.
- 33. Liver Cirrhosis
- 35. Serum-to-ascites albumin gradient • The serum-to-ascites albumin gradient (SAAG) accurately identifies the presence of portal hypertension and is more useful than the protein-based exudate/transudate concept. • The SAAG is easily calculated by subtracting the ascitic fluid albumin value from the serum albumin value, which is obtained on the same day. • The presence of a gradient 1.1 g/dL (11 g/L) indicates that the patient has portal hypertension with 97 percent accuracy. • A gradient <1.1 g/dL (<11 g/L) indicates that the patient does not have portal hypertension . The SAAG need not be repeated after the initial measurement.
- 36. Indirect markers of liver fibrosis • Liver fibrosis may be predicted by using • A single routine laboratory test that reflects alteration in hepatic function, or • A combination of such tests.
- 37. Individual serum indirect markers of fibrosis • Serum ALT levels • AST / ALT ratio • Platelet count (PLT);Trombocytopenia is a valuable marker of advanced liver disease, but it may be related to many mechanisms: hypersplenism, myelosuppression by HCV, decreased trombopoetin production, autoimmune process. • Combined assessment of the AST/ALT ratio and PLT had a high diagnostic value for cirrhosis.
- 38. Multicomponent indirect serologic markers for liver fibrosis • AST /platelet count. • Protrombin index, GGT, apolipoprotein A1. • Protrombin index, GGT, apolipoprotein A1, α2- macroglobulin • Age, platelet count, GGT. • Age, sex, ALT, GGT, bilirubin. • apolipoprotein A1, α2-macroglobulin, haptoglobin
- 39. Prognostic Tools for chronic liver disease • MELD is a prospectively developed and validated chronic liver disease severity scoring system that uses a patient's laboratory values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. • MELD (model for end-stage liver disease) – Identify patients whose predicted survival post-procedure would be three months or less • MELD = 3.8[serum bilirubin (mg/dL)] + 11.2[INR] + 9.6[serum creatinine (mg/dL)] + 6.4
- 40. Acute liver failure (ALF) • Prognostic criteria are based primarily either on clinical and laboratory (coagulation tests, serum bilirubin) parameters, or on other parameters like liver volume. • The criteria from one institute found prothrombin time >25 s, serum bilirubin >15 mg/dL, age >40 years, and cerebral edema to be bad prognostic markers.