LFT-AN ESSENTIAL TESTING DURING PRE-OPs

3.  A LIVER DISEASE CAN BE CLINICALLY EVALUATED BY
 1.TAKING CLEAR HISTORY INCLUDING THE MAJOR RISK
FACTORS LIKE ALCOHOLISM,ILLICIT DRUG USE,BLOOD
TANSFUSIONS,OCCUPATIONAL EXPOSURE TO
TOXINS,GENETIC DISEASES SUCH AS
WILSONS,HEAMOCHROMATOSIS,ALPHA 1 ANTI TRYPSIN
DEFICIENCY.
 2.CLINICAL FINDINGS WHICH MAY BE MILD, NON SPECIFIC
LIKE LOSS OF APPETITE, EASYFATIGABILITY, MALAISE,
ALTERED SLEEP PATTERNS, CHANGES IN PERSONALITY,
PRURITUS, ABDOMINAL PAIN, INDIGESTION, CHANGES IN
URINE AND STOOL COLOUR AND PHYSICAL EXAMINATION
WHICH MAINLY FOCUSES ON ICTERUS, JAUNDICE,
ASCITES, SPIDER ANGIOMASA, XANTHELASMA,
ENCEPHALOPATHY, PALMAR ERYTHEMA AND FETOR
HEPATICUS
 3.LIVER FUNCTION TESTS

4.  LIVER FUNCTION TESTS CAN BE BROADLY
BE CLASSIFIED INTO
1.STANDARD LABORATORY TESTS
2.QUANTITATIVE LIVER TESTS
3.MEASUREMENT OF LIVER BLOOD FLOW
4.RADIOLOGIC AND ENDOSCOPIC
METHODS

5. STANDARD LABORATORY TESTS:
 DETECTION OF HEPATOCELLULAR INJURY.
 ASSESMENT OF PROTIEN SYNTHESIS.
 EVALUATING CHOLESTATIC DISORDERS

6. DETECTION OF HEPATOCELLULAR INJURY:
1.AMINOTRANSFERASES-ALT AND AST.
 ALT-ALANINE AMINOTRANSFERASE/SERUM
GLUTAMIC PYRUVIC TRANSAMINASE.
 AST-ASPARTATE AMINOTRANSFERASE/SERUM
GLUTAMIC OXALOACETIC TRANSAMINASE.
 THESE CATALYSE OF AMINE GROUP TO ALPHA
KETO GLUTARATE TO YIELD GLUTAMATE AND
PYRUVATE(ALT),OXALOACETATE(AST).

7.  ALT-CYTOPLASMIC LIVER ENZYME.
 AST-FOUND ION MANY EXTRAHEPATIC
TISSUES(HEART, MUSCLE, BRAIN, KIDNEY,
PANCREAS, ADIPOSE TISSUE, BLOOD).
 RANGES-MILD-100 TO 249 IU/L,MODERATE-250-
999IU/L,LARGE-1000 TO 1999 IU/L,EXTREME-MORE
THAN 2000.
 DE RITI’S RATIO –BETWEEN AST/ALT.
>4-WILSONS DISEASE.
2 TO 4-ALCOHOLIC LIVER DISEASE.
<1-NON ALCOHOLIC LIVER DISEASE

8. 2.LDH:
 FOUND IN LIVER AND ALSO IN EXTRAHEPATIC
TISSUES ALSO.
 BOTH DISORDERS LIKE IN LIVER DISEASE AND
EXTRA HEPATRIC LIVER DISORDERS LIKE IN
HEMOLYSIS, RHABDOMYOLYSIS, ACUTE CVA, MI,
TUMOUR NECROSIS, RENAL INFARCTION IT IS
ELEVATED.
 PROLONGED CONCURRENT INCREASE IN LDH
+ALP IS DIAGNOSTIC OF MALIGNANT
INFILTRATION OF LIVER.
 EXTREME INCREASE IS INDICATIVE OF FULMINAT
VIRAL HEPATITIS,DRUG INDUCED, HYPOXIC
HEPATITIS, ALLWAYS ACCOMPANIOED WITH
INCREASE IN ALT AND AST IN HEPATOCELLULAR
INJURY

9. 3.GLUTHATHIONE-S-TRANSFERASE:
 BOTH SENSITIVE AND SPECIFIC FOR DRUG
INDUCED LIVER INJURY.
 PLASMA HALF LIFE OF 90MINS AND IS
RELEASED RAPIDLY INTO CIRCULATION AFTER
HEPATOCYTE INJURY.
 WHILE ALT AND AST –ACINAR ZONE 1,
GLUTHATHIONE-S-TRANSFERASE-ACINAR
ZONE 3(CENTRILOBULAR REGION)

10. ASSESMENT OF HEPATIC PROTEIN SYNTHESIS
1.SERUM ALBUMIN-
 12 -15gm/day
 Total body pool-500 gm
 YIELDS INFORMATION ABOUT
HEPATOCELLULAR FUNCTION(PROTIEN
SYNTHESIS).
 CAN BE USED TO EVALUATE CHRONIC LIVER
DISEASE.
 HAS A PLASMA HALF LIFE OF 3 WEEKS.

11.  BEFORE RULING OUT HEPATIC CAUSE FOR
HYPOALBUMINEMIA WE SHOULD RULE OUT
OTHER CAUSES LIKE RENAL LOSSES,
INCREASED ALBUMIN CATABOLISM,
EXPANSION OF BLOOD VOLUME,
MALDISTRIBUTION OF TOTAL BODY
ALBUMIN.
 NO CLEAR RELATIONSHIP BETWEEN SERUM.
ALBUMIN AND INSTANTANEOUS RATE OF
ALBUMIN SYNTHESIS.

12. 2.PROTHROMBIN TIME:
 ALL ARE LIVER DERIVED PROCOAGULANTS
EXCEPT 3,4,8.
 LIVER DERIVED PROCOAGULANTS HAVE
SHORTER HALF LIVES RANGING FROM 4HRS
FOR FACTOR 7 TO 4 DAYS FOR FIBRINOGEN.
 PT/INR IS USED TO ASEESS AND MONITOR
ACUTE LIVER DYSFUNCTION.
 PROLONGED PT DUE TO LIVER FAILURE-DUE
TO DECREASED LEVELS OF FACTOR 7a.

13.  SERUM TOTAL PROTEINS-BIURET METHOD.
 SERUM ALBUMIN-BCG DYE BINDING
METHOD.
 TOTAL PROTEINS-ALBUMIN=GLOBULIN

14. DETECTION OF CHOLESTATIC DISORDERS:
1. ALKALINE PHOSPHATASE:
 TO SCREE FOR DISORDERS OF LIVER AND
BILIARY TREE.
 ALP ISOENZYMES EXIST IN PLASMA
MEMBRANES OF BONE , INTESTINE, KIDNEY,
PLACENTA(THIRD TRIMESTER OF GESTATION),
LEUCOCYTES, NEOPLASMS.
 INCREASED ALP-DUE TO INCREASED
PRODUCTION/RELEASE OF ALP FROM
CELLS.NOT DUE TO DECREASED CLEARANCE.

15.  ALP INCREASE IN CHOLESTATIC DISORDERS
IS DUE TO ACTION OF BILE SALTS ON
PLASMA MEMBRANES OF HEPATOCYTES.
 HALF LIFE –1WEEK.
 INTIIALLY ALP LEVELS REMAIN LOW IN
BILiARY OBSTRUCTION UNLESS INCREASES
IN PRODUCTION.
EXTREME INCREASE:
 1.BLOCK IN BILIARY TREE AS IN PRIMARY
BILIARY CIRRHOSIS AND
CHOLEDOCHOLITHIASIS
 2.HEPATIC MALIGNANCY COMPRESSING

16. 3.5’NUCLEOTIDASE AND GGTP:
 USED TO DISTINGUISH BETWEEN HEPATIC
AND EXTRAHEPATIC ALP SOURCES.
 5’NT EXISTS IN MANY TISSUES BUT MORE
RELEASED FROM HEPATOCYTES DUE TO
ACTION OF BILE SALTS.
 IN BILIARY OBSTRUCTION ALP AND GGTP
BOTH INCREASE SIMULTANEOUSLY.
 SHORTHLY AFTER 5’NT BEGINS TO
INCREASE

17.  Bilirubin is a breakdown product of heme
 About 4 mg/kg body weight of bilirubin is
produced each day
 Heme is converted to biliverdin by the
microsomal enzyme heme oxygenase.
Biliverdin is then converted to bilirubin by
the cytosolic enzyme biliverdin reductase.
 Bilirubin formed in the reticuloendothelium is
lipid soluble and virtually insoluble in water .
This process of making insoluble to soluble
by liver is called conjugation.

19.  The terms direct and indirect bilirubin, which
correspond roughly to conjugated and unconjugated
bilirubin, respectively.
 Test is called as vandenbergh test or diazo reaction.
 In this assay, bilirubin is exposed to diazotized sulfanilic
acid.
 The conjugated fraction of bilirubin reacts promptly,
or “directly,” with the reagent without the need for an
accelerant ,and thereby allows measurement of the
conjugated bilirubin fraction by photometric analysis
within 30 to 60 seconds.
 The total bilirubin is measured 30 to 60 minutes after
the addition of an accelerant such as alcohol or
caffeine.
 The unconjugated, or indirect, fraction is then
determined by subtracting the direct component
from the total bilirubin.

20.  Total serum bilirubin 1.0 -1.5 mg/dL, with
95% of a normal population falling
between 0.2 and 0.9 mg/dL.
 If the direct acting fraction is less than 15%
of the total, the bilirubin can be
considered to be entirely indirect.
 The most frequently reported upper limit of
normal for conjugated bilirubin is 0.3
mg/dL.
 Indirect component 0.8-1.2 mg/dL.

21.  Presence of conjunctival icterus suggests
a total serum bilirubin level of at least 3.0
mg/dL but does not allow differentiation
between conjugated and unconjugated
hyperbilirubinemia.
 Tea- or cola-colored urine may indicate
the presence of bilirubinuria and thus
conjugated hyperbilirubinemia

22.  Isolated elevation of the serum bilirubin
level
 Patient with an elevated bilirubin
associated with elevated liver enzyme
levels

23.  Hemolytic Disorders
 Ineffective Erythropoiesis
 Drugs like Rifampin, Probenecid impairs
hepatocellular uptake.
 Inherited Conditions : Crigler-Najjar
syndrome types I and II and Gilbert’s
syndrome causes Impaired conjugation
of bilirubin.
 Hematoma most common in neonates.

24.  Inherited Conditions causing impaired
excretion of conjugated bilurubin.
 Dubin-Johnson syndrome
 Rotor’s syndrome

26. Quantitive Liver Tests:
 Total hepato cellular mass can be
assessed by clearance of a substance
that is extracted by liver like
bromsulphalein, ICG, Rose Bengal.
Factors affecting :
Variations in Blood flow
Extra hepatic retention or clearance of
substance
Hepato Biliary function

27. Drug Metabolising Capacity:
 Caffeine Clearance
 Galactose Elemination Capacity
 Amino pyrine breath test
 Antipyrine clearance
 Monoethylglycinexylidide(MEGX)

28. Measurement of Liver Blood Flow:
 Clearance Technique-
ICG Dye,
propranolol,
lidocaine,
colloidal particles
 Indicator Dilution Techniques –
Radio Label Indicator(Iodinated albumin)
 Direct Measurement

29. Radiologic and Endoscopic Methods:
ERCP- Provides intraductal access to
the biliary tree and pancreatic duct.
 To Diagnose and treat extrahepatic
biliary disorders such as gallstones,
tumors, inflammatory strictures or post
surgical anastomotic leaks
 Complication – Pancreatities etc
PTHC- Percutaneus Trans Hepatic
Cholangiography
 Evaluation of Intra hepatic bileduct

30.  Esophagogastroscopy
 Splenoportography
 Portal Venography
 Fibroscan Test
 Fibrosure/ Fibro Test-
Alpha2 Macroglobulin, HaptoGlobulin,
Apolipo protein A1, Bilurubin, GGT, ALT

31. Testing for Specific Diseases:
 Serologic Testing to identify viral,
autoimmune, microbial causes
 Genetic Testing to identify hereditary
disorders
 Tumour Markers for malignancy

34.  NORMAL RANGES
1. TOTAL BILURUBIN - 0.3-1.3 mg/dl
2. DIRECT - 0.1-0.4 mg/dl
3. INDIRECT - 0.2-0.9 mg/dl
4. AST - 12- 38 IU/L
5. ALT - 7- 41 IU/L
6. TOTAL PROTEINS- 5.5 -9.0 gm/dl
7. ALBUMIN – 3.5- 5.5 gm/dl
8. Globulin – 2.0- 3.3 gm/dl

35. THANK
U