Zoobia Zaheeruddin

 Plays a major role in protein, CHO and Lipid metabolism

 Metabolize, detoxify and excrete

 Excretion of digestive aids (bile acids)

 Why?

 LFTs are measurements of blood components

which simply provide a lead to existence, the
extent and type of liver damage
 Bilirubin – total and direct
 Aminotransferases – ALT(SGPT) and AST(SGOT)
 Alkaline Phosphatase

SERUM – RED TOP

 Serum Albumin
 GGT
 PT
INVESTIGATION:
• Test for excretory function/ cholestasis:
• Total bilirubin, direct bilirubin
• Test for liver damage/ parenchymal injury:
•AST, ALT
• Synthetic Function:
•Total protein, Albumin
•Test for Obstruction:
•γGT, ALP
  Pre-hepatic – Hemolysis -IB INCREASED
- Prematurity

- ALT/AST INCREASED
 Hepatic
(acute hepatocellular damage)

 Post-hepatic -DB INCREASED

(cholestasis, - ALP
- GGT
obstruction to bile flow)
Cholestasis is any condition in which the flow of bile from the liver
is blocked.

CHRONIC LIVER DISEASE – ALBUMIN DECREASES

 Results from excess production of bilirubin
(beyond the livers ability to conjugate it)
following hemolysis

 High plasma concentrations of unconjugated

bilirubin
 Impaired uptake, conjugation, or secretion of
bilirubin

 Reflects a generalized liver (hepatocyte)

dysfunction

 In this case, hyperbilirubinemia is usually

accompanied by other abnormalities in
biochemical markers of liver function
 Caused by an obstruction of the biliary tree

 Plasma bilirubin is conjugated, and other biliary

metabolites, such as bile acids accumulate in
the plasma

 Characterized by pale colored stools (absence

of fecal bilirubin), and dark urine (increased
conjugated bilirubin)
 Total
 Direct ( conjugated )
 Indirect ( unconjugated )

 N/V: TB: 0.0-1.0 mg/dl

 DB: 0.0-0.3 mg/dl
 Benign liver disorder

 ½ of the affected individuals inherited it

 Characterized by mild, fluctuating increases in

unconjugated bilirubin caused by decreased
ability of the liver to conjugate bilirubin

 Onset of symptoms in teens, early 20’s or 30’s

 Characterized by a complete absence or marked
reduction in bilirubin conjugation

 Present with a severe unconjugated

hyperbilirubinemia that usually presents at birth

 Condition is fatal when the enzyme is

completely absent
 Characterized by impaired biliary secretion of
conjugated bilirubin

 Present with a conjugated hyperbilirubinemia that is

usually mild
 ALT / AST
 Sensitive, acute damage to hapatocytes
 Causes:
- Hepatitis
- Toxic injury
- Drug overdose
- Severe hypoxia
- Acute cardiac failure
 N.V: ALT upto 31 U/L
AST in M upto 37 U/L , In F: upto31 U/L
 Sources: - Bone (enzyme rich osteoblasts)
- Liver
Placenta – 3rd trimester
- Small Intestine
Kidney

 Increase in ALP activity in liver disease due to extra

hepatic function of bile flow, usually in response to
cholestasis –> both intra and extra-hepatic
 Also in Cirrhosis (b/c of obstruction)
 N.V: Child: 117-390 U/L
Adult: 39-117 U/L
 Microsomal enzyme, widely distributed in liver and
renal tubule
 Activity increases in cholestasis
 Very sensitive index of liver pathology
 Induced by: ethanol, phenobarbitone, phenytoin
(even in the absence of recognizable liver disease)
 Acute hepatic damage: changes in GGT activity
parallel those of aminotransferases
 Pregnancy: GGT is inhibited by gestational
hormones so that it tends to remain normal despite
the presence of hepatic disease
 N/V: In M: 11-50 U/L, In F: 5-50 U/L
 Hepatic synthetic function

 Albumin – major protein product of liver

 Long biological half life in plasma, therefore,

significant falls in albumin concentration are slow to
occur if synthesis is suddenly reduced

 Hypoalbuminemia is a feature of advanced chronic

liver disease

 Can also occur in severe acute liver damage

 N/V: TP: 6.6-8.7 gm/dl
 Albumin: 3.8-4.4 gm/dl
 Globulin: 1.9-2.8 gm/dl