![Tests to assess liver synthetic
capabilities
Used to assess functional capabilities of liver
Its synthetic products are measured
[albumin, fibrinogen, prothrombin, hepatoglobin, transferin and other proteins]](https://image.slidesharecdn.com/liverfunctiontests-170410081325/85/Liver-function-tests-9-320.jpg)
![Tests to assess liver synthetic
capabilities
Albumin:
Complete cessation of albumin production results
in only 25% decrease in serum concentrations after
8 days.
Albumin concentration remains unaltered in many
liver disease when liver function is preserved.
if disease progress its synthetic capacity
impaired[severe hepatitis, cirrhosis]](https://image.slidesharecdn.com/liverfunctiontests-170410081325/85/Liver-function-tests-13-320.jpg)
Liver function tests
- 1. Liver Function Tests Dr.laxman wagle
- 2. • Liver – the largest solid organ in human body • Weighing bet/n 1200 and 1500gm • Located in the upper quadrant of abdomen • Two sources of blood supply – Hepatic artery from aorta supplies arterial blood rich in oxygen – Portal veins shunt the venous outflow of the intestines and spleen-blood with less O2 but rich in nutrients to liver
- 4. • Liver is divided into thousands of lobules. • Each lobule composed of plates of hepatocytes (liver cells) that radiates from central vein like spokes in a wheel. • Hepatocytes continually form and secrete bile into canaliculi, which empty into terminal bile ducts.
- 5. Basic structure of a liver lobule
- 6. Functions of liver • Produces bilirubin a product of hemoglobin (Hgb) breakdown, excreted via bile ducts into intestinal tract for digestion. • Major role in amino acid and carbohydrate metabolism. • Produces many crucial proteins, including coagulation factors and albumin.
- 7. Functions of liver • Most lipid and lipoprotien metabolism, including cholesterol synthesis occurs in liver which excretes into bile. • Primary location for most drug and hormone metabolism hence in liver failure standard dosing of some medications lead to high serum concentration and toxicity.
- 8. Tests include: a) Tests to assess liver synthetic capabilities b) Tests to assess cholestatic disease and hepatocellular injury
- 9. Tests to assess liver synthetic capabilities Used to assess functional capabilities of liver Its synthetic products are measured [albumin, fibrinogen, prothrombin, hepatoglobin, transferin and other proteins]
- 10. Tests to assess liver synthetic capabilities Most commonly used tests include Albumin Prothrombin time Occasionally Total protein Globulin (with albumin) Ammonia ( controversial)
- 11. Tests to assess liver synthetic capabilities Albumin: Reference range: 3.5 to 5 gms/dl liver Synthesizes albumin using AA derived from gut/breakdown of proteins It Maintains plasma oncotic pressure. It binds numerous hormones , anions, drugs and fatty acids
- 12. Tests to assess liver synthetic capabilities Albumin: Liver synthesise 12 gm /day if needed it can double the synthesis Serum half life is20 days Serum Albumin measurements are slow to fall after the onset of hepatic dysfunction due to long lifespan
- 13. Tests to assess liver synthetic capabilities Albumin: Complete cessation of albumin production results in only 25% decrease in serum concentrations after 8 days. Albumin concentration remains unaltered in many liver disease when liver function is preserved. if disease progress its synthetic capacity impaired[severe hepatitis, cirrhosis]
- 14. Tests to assess liver synthetic capabilities Non hepatic causes: Hypoalbuminemia: Malnutrition, malabsorption, overhydration, nephrotic syndrome, protein losing enteropathy (through Gut), burns and chronic illness At very low concentration (2-2.5gm/dl) patients can develop peripheral edema, ascities or pulmonary edema
- 15. Tests to assess liver synthetic capabilities Non hepatic causes: Hyperalbuminemia: Dehydration Anabolic steroids Does not cause any symptoms
- 16. Tests to assess liver synthetic capabilities Globulin: Reference range: 2 to 3gm/dl Refers to total measurements of immunoglobulins (antibodies) in serum Synthesised by B cell lymphocytes Ig – IgA, IgD, IgE, IgG and IgM
- 17. Tests to assess liver synthetic capabilities Causes: Malabsorption Protein losing enteropathy Hepatocellular dysfunction does not lower globulin concentration (because some produced elsewhere) unless associated with malabsorption Elevation of globulins is a sign of inflammation – may present in hepatitis
- 18. Tests to assess liver synthetic capabilities Causes: In chronic hepatitis - albumin decreases and globulin increases In primary biliary cirrhosis – Increase in IgM Alcoholic patients – increase IgA
- 19. Tests to assess liver synthetic capabilities Non – hepatic causes: increases globulin Chronic infections, chronic inflammatory states, multiple myeloma In non hepatic condition – globulin increases than albumin concentration and thus G:A ratio will be >1 (normal – 0.6)
- 20. Tests to assess liver synthetic capabilities Total protein: Reference range: 5.5 to 9gm/dl Refers to sum of albumin and globulin Any symptoms increase either albumin/ globulin also increases total protein Its value is limited if albumin and globulin results are already known
- 21. Tests to assess liver synthetic capabilities Prothrombin time: It is one of the coagulation factor Liver synthesises SIX coagulation factors: I, II, V, VII, IX and X Normal range: 10 to 13 seconds PT is not specific for liver disease
- 22. Tests to assess liver synthetic capabilities Causes for prolongation of PT: - inadequate vitamin K in the diet - poor fat absorption - poor / inadequate nutrition - drugs – warfarin, salicylates, moxalactum, cefoperazone, tetracycline
- 23. Tests to assess liver synthetic capabilities If PT remains prolonged despite parenteral vitamin K (10mg), it is considered a sign of substantial hepatic dysfunction Treat the patient with vitamin K if no bleeding If bleeding present, treat with fresh frozen plasma
- 24. Tests to assess cholestatic disease and hepatocellular injury Liver disease: Cholestatic Hepatocellular damage Mixed
- 25. Tests to assess cholestatic disease and hepatocellular injury Cholestatic – primary interference with the metabolism or secretion of bilurubin from its initial production in hepatocytes to its secretion into duodenum. Hepatocellular damage – damage to hepatocytes or inflammation of hepatocytes Mixed type is due to: back pressure Cholestatic hepatocellular damage swelling
- 26. Tests to assess cholestatic disease and hepatocellular injury Elevation of liver enzymes are common findings in clinical practice The significance of the elevation has to be assessed whether or not mild non-specific elevation (e.g., viral / drug / liver disease)
- 27. Tests to assess cholestatic disease and hepatocellular injury Useful tests Enzymes Reference range ALP 30 – 120 U/L GGT 0 - 30U/L AST 0 – 35 U/L ALT 0 – 35 U/L LDH 110 – 220 U/L
- 28. Tests to assess cholestatic disease and hepatocellular injury Useful tests Reference range Bilurubin total 2 - 18 mmol/L direct (conjugated) 0 - 4 mmol/L indirect (unconjugated) ? Albumin 3.5 – 5.0 gms/dl Globulin 2.0 – 3.0 gms/dl Prothrombin time 10 – 13 seconds
- 29. Liver enzymes are most useful in differentiating hepatocellular damage from cholestasis ALP extra-cellular GGT (present in cells lining biliary canaliculi) AST intra-cellular enzymes ALT (present in cytosol of liver cells) LDH
- 30. CHOLESTASIS Intra-hepatic (obstruction in bile ducts within liver) Causes: – metastasis Extra-hepatic (obstruction in bile ducts outside the liver) Causes: – gall stones – cancer of head of pancreas – inflammation
- 31. • Jaundice is usually obvious to the eye • Confirmed by ALP and GGT • ALP & GGT Bone disorder (pagets disease, osteomalacia, 10 , 20 malignancy of bone) GGT (100-140 U/L) Chronic alcoholism without any abnormality or in liver phenytoin
- 32. • If chronic alcoholism is associated with hepato- cellular damage, ALT increase along with GGT • Chronic alcoholism can lead to fatty infiltration, alcoholic hepatitis and cirrhosis
- 33. Hepatocellular damage • In hepatocellular damage, AST, ALT and LDH increases • Both AST and ALT runs parallel • Measure ALT as it is very specific to liver
- 34. Causes: Paracetamol overdose, ischemic / hypoxic hepatitis Marked elevation of ALT and LDH, both of the same order (800-3000 U/L) The ratio of ALT / LD is 0. 8 - 1.2 Chronic alcoholism chronic alcoholics with under lying disease when gives therapeutic dose of paracetamol, can sustain liver damage with the marked rise ALT/LDH as paracetamol toxicity Viral hepatitis - both ALT and LDH increases - ALT elevation is significantly > LDH - ALT/LDH ratio is 1.2-2.0
- 35. Rhabdomylosis - LD level will be markedly elevated (800-20,000 U/L) than ALT - ALT: LDH ratio is < 0. 8 - Due to muscle destruction CK level also increase (2,000 – 1,00,000 U/L) - Increase CK does not occur in liver damage (liver does not contain CK) Infections mono-nucleousis Simultaneous increased level of ALP, GGT, LD and ALT between (200-600 U/L) occur.
- 36. Drugs involved in liver disorders • Predominantly hepatocellular – Allopurinol, aspirin, cytotoxic, diclofenac, anti TB drugs, methotrexate, paracetamol, phenytoin, propylthiouracil and quinidine • Predominantly cholestasis - Augmentin, CBZ, chlorpromazine, chlorpropamide, flucloxacillin, dicloxacillin, indomethacin, phenothiazines and tolbutamide • Mixed – Methyldopa, halothane, norfloxacin, PAS, ranitidine, sulindac, valproate co-trimaxozole
- 38. Thank you