Liver Function Tests &

Jaundice
Dr Rehma Dar
Assistant professor, Pathology
Learning Objectives
Tests included in LFTs
Interpretation of LFTs
Pathophysiology of Jaundice
LFTs in different types of jaundice & diseases
JAUNDICE
DEFINITION
It is the yellow discolouration of
skin,mucous membranes and sclera caused by
bilirubin deposition when plasma bilirubin
concentration reaches 2-3mg/dl(34-51micromol/L)
TYPES OF JAUNDICE
CONJUGATED
UN-CONJUGATED
Aged and damaged RBCs RETICULO
Hemoglobin
BILIRUBIN METABOLISM ENDOTHELIAL
Iron Amino acids Heme SYSTEM
+O2+heme oxygenase
Biliverdin + bilverdin reductase

+ Plasma Tetrapyrrole
General P
transferrin protein Bilirubin (free, indirect- L
pool of the reacting, A
body unconjugated,water S
insoluble) CO
M
+Albumin A

-Albumin relased L
Liver I
+Glucuronic acid +Y or Z protein
cell V
Entero E
Bilirubin diglucuronide ( direct-
hapitic R
reacting, conjugated,water soluble)
circulation
Bile
INTESTINE
Reabsorbed + intestinal flora

Urobilinogens Sterocobilin
FECES
Excreted Excreted

Excreted (more concentrated in alkaline urine) URINE

CAUSES OF JAUNDICE
An increased rate of bilirubin production exceeds
normal excretory capacity of liver (PRE-HEPATIC)
Normal load of bilirubin cannot be
conjugated/excreted by damaged liver cells
(HEPATIC JAUNDICE)
Biliary flow is obstructed so that conjugated
bilirubin cannot be excreted into intestine and is
regurgitated into systemic circulation (POST-
HEPATIC JAUNDICE)
MAJOR CAUSES OF JAUNDICE
PRE- HEPATIC

haemolysis
Ineffective erythropoiesis
HEPATIC

drugs e.g rifampicin that interfere with bilirubin uptake

 prematurity
 hepatitis e.g viral or drug induced
 Gilbert’s syndrome
 Crigler-Najjar syndrome
 Lucey-Driscoll syndrome
Impaired excretion: hepatitis ,drugs e.g rifampicin.
Methyltestosterone
Dubin-Johnson syndrome,Rotor syndrome
Intrahepatic obstruction:
cirrhosis,
infiltrations,e.g lymphoma, amyloid
Tumors
 sepsis.
POST-HEPATIC
gallstones
biliary stricture
carcinoma of head of pancreas or biliary tree
 cholangitis
 primary biliary cirrhosis
Cholangiocarcinoma
Parasitic infections
BIOCHEMICAL TESTS

They are used to investigate mechanisms underlying

hepatic disorders,these often coexist but one usually
predominates in any particular condition:
 Liver cell damage
 Cholestasis
 Reduced mass of hepatocytes
BIOCHEMICAL TESTS/LFTs
Serum Total Bilirubin
Direct(conjugated)bilirubin
Indirect(un-conjugated)bilirubin
Plasma enzymes
(ALT,AST,ALP,GGT)
Serum Albumin
Prothrombin time
Urine tests for
(urobilinogen,bilirubin)
SERUM BILIRUBIN
DIRECT BILIRUBIN- conjugated bilirubin
INDIRECT BILIRUBIN - Unconjugated bilirubin

( difference b/w total bilirubin and direct bilirubin)

URINE TESTS
URINE BILIRUBIN
Only conjugated bilirubin is excreted in urine its presence
indicates conjugated hyperbilirubinemia.

 UROBILINOGEN
increase occurs whenever hepatocellular function is
decreased or an excess of urobilinogen in the GI tract that
exceeds liver’s capacity to re-excrete it.
decrease occurs when biliary excretion of bilirubin is
impaired (cholestasis) ------ causing clay coloured stools
 TRANSAMINASES/AMINOTRANSFERASES (ALT,AST)

Sensitive indicator of damage to cytoplasmic or mitochondrial

membranes rather than hepatic function capacity.

ALT is mainly a cytoplasmic enzyme – more liver specific

AST has two fractions :

Cytoplasmic AST
Organellar AST

Hepatocytes contain more AST than ALT but lacks specificity

In Acute Hepatitis, ALT is markedly increased as
compared to AST as
only cell membrane is damaged while organelles
remain intact
In Chronic Hepatitis AST is a better marker
AST lacks specificity
So for diagnosis and monitoring of Chronic
Hepatitis (Hep B and C), ALT can be used
ALKALINE PHOSPHATASE

Derived from biliary tract, osteoblasts and

placenta.

Its activity rise in cholestatic liver disease

/obstructive jaundice because its synthesis is
increased and enzyme within biliary tract is
regurgitated into plasma.
GAMMA GLUTAMYLTRANSFERASE
Derived from endoplasmic reticulum of cells of
hepatobiliary tract
Its activity is increased in both cholestasis and
hepatocellular damage.
Its activity also increases in response to prolonged
intake of alcohol and drugs e.g phenobarbitone
,phenytoin
SERUM ALBUMIN
Useful in assessing chronicity and severity of liver
disease.
PROTHROMBIN TIME
It may be prolonged due to impaired hepatic synthesis
of clotting factors II, VII, IX, X
either

 due to hepatocellular damage.

• cholestasis; fat soluble vitamin K cannot be
absorbed.
Thank You