Helpful

1. Uzair Mumtaz
Farah Shafiq

2.  Liver is the principle organ for maintaining
the body’s internal environment & of vital
importance in intermediary metabolism,
detoxification and the elimination of toxic
substances.

3.  Largest internal body organ
 Largest gland
 Largest organ apart from skin
 Weighs about 1.5kg
 Found in the upper abdominal cavity:
extends from right upper quadrant to left
upper quadrant of the abdomen
 Attached to diaphragm by
1. Falciform and coronary ligaments
2. Left and right triangular ligaments

4. Metabolic
function
Excretory
function
Synthetic
function
Storage
function
Detoxification
function
Functions Of
Liver

5. Hepatocytes synthesize:
 Plasma Proteins
 Coagulation factors like Prothrombin,
factors II,V,IX,X,XI,XII and XIII
 Primary bile acids
 Lipoproteins VLDL, HDL

6.  Serum Total protein
 Serum albumin
 Total proteins - Albumin = Globulin
 Prothrombin time
 Serum Cholesterol

7. Principle:
Biuret’s method: Photometric endpoint, colorimetric
assay
Proteins(3P)+Alkaline Cu tartrate= Blue-Purple
coloured substance.
Reference Range: 65-80 g/l
Interpretations:
Dehydration
Hypergammaglobulinaemia
Infection
Cirrhosis, Ascites,
Cardiac failure

8.  Estimation of Serum Albumin:
Principle: Bromocresol-Green method
Albumin+ BCG → Green coloured compound
(citrate buffer)
Reference Range: 35-50 g/l
Interpretation: Used to asses chronicity and
severity of liver disease.
↓ in Chronic liver disease.

9.  PROTHROMBIN TIME:
 Synthetic dysfunction
↑ in liver disease due to ↓ of clotting factors
Reference Range: 10-14 sec

10. Liver is the only organ that has the capacity to
rid the body of heme waste products.
Major heme waste product is Bilirubin,
principle pigment of bile derived from
breakdown of RBCs.
Hepatocytes in liver are separated by sinusoidal
spaces along walls known as Kupffer cells
present for detoxifying function.

12.  Serum bilirubin
 Urine Bilirubin
 Urine & faecal urobilinogen
 Urine bile salts
 Dye excretion tests

13.  Catabolism of Heme
 Estimated by Van den bergh reaction
 Principle:
 When diazotised sulfanilic acid reacts with
bilirubin, it forms ‘azobilirubin’, a purple
coloured product.
 ↑ Conjugated Bilirubin: gives colour immediately
→ Direct positive
 ↑ Unconjugated Bilirubin: Gives colour after
addition of methanol → Indirect positive
 ↑ Both conjugated and Unconjugated → Biphasic

14.  Ehrlich’s test:
Principle:
Urobilinogen reacts with ƿ-dimethylamino-
benzaldehyde in chloroform to form a pink
coloured aldehyde complex.

15.  Bile salts: Hay test
Principle: Bile salts have property of lowering
surface tension.Hence when sulphur powder
is sprinkled to urine containing bile salts, it
sinks to bottom.
 Bile pigments: Fouchet’s test
Principle: Bile pigments adhere to the
precipitate of barium sulphate. On addition of
fouchet’s reagent, FeClз in presence of
trichloroacetic acid oxidizes yellow colour
bilirubin to green colour biliverdin.

16. Allows important substances to reach systemic
circulation and serve as a barrier to prevent toxic
or harmful substances
Either bind with material to inactivate the
compound or chemically modify it
Drug Metabolism: Detoxification of drugs by
1. Oxidation
2. Reduction
3. Hydrolysis
4. Hydroxylation
5. Carboxylation
6. Demethyaltion

17.  HIPPURIC ACID TEST:
Principle: Hippuric is produced in the liver when
benzoic acid combines with glycine.
Procedure:
6gm of sodium benzoate is given to the patient.
Urine is collected up to 4hrs.
Hippuric excreted in urine is estimated.
Normal: >4.5g of hippuric acid
Abnormal: <3g of hippuric acid

18.  Alpha-fetoprotein – Hepatoma
 Alpha 1- antitrypsin – Congenital
deficiency, In
inflammation
 Serum copper – Wilson’s disease
 Serum Iron – Hepatocellular damage

19. METABOLISM OF CARBOHYDRATES:
 Store glucose as glycogen
 Degrade glycogen to glucose
(Glycogenolysis)
 Create glucose from non-sugar carbon
substrates e.g. pyruvate (Gluconeogenesis)

20. METABOLISM OF LIPIDS & LIPOPROTEINS:
 Gathering free fatty acids from diet to
produce Acetyl-CoA
 Greatest source of cholesterol in body
METABOLISM OF PROTEINS:
 Synthesize all proteins except
immunoglobulin's complement & adult
hemoglobin
 Transamination of amino acids to produce
ammonium ions.

21. CARBOHYDRATE METABOLISM
• Glucose tolerance test
Interpretation:
Normal: 2h PG level less than 7.8 mmol/l
IGT: between 7.8-11.1 mmol/l
DM: greater than 11.1 mmol/l
LIPID METABOLISM
• Serum cholesterol

22. Protein metabolism
• Serum Ammonia:
Liver detoxicates ammonia to form urea
Normal: 40-70µg /100ml
 Congenital defect in urea cycle
 Ornithine transcarbamylase deficiency
 Liver cirrhosis
 Hepatic failure
 Acute & sub acute liver necrosis
Sample: Arterial Blood

23. LFTs help in diagnosis of liver disease to
evaluate severity, monitor therapy and asses
the prognosis.

25. ALANINE AMINO TRANSFERASE:
 Highest in liver
 Principle: Coupled enzyme technique with
continuous UV monitoring of NADH
disappearance
ɖ -oxoglutarate + L- Alanine→L-glutamate+
pyruvate
Pyruvate+ NADH + H⁺→Lactate+ NAD⁺
Calculations:
ALT U/l = 1746 ӿ ∆A (340nm/min)
Reference range: Up to 42U/l

26. ASPARTATE AMINOTRANSFERASE
Principle:
Coupled enzyme technique with UV
monitoring of NADH disappearance.
Reaction:
2-oxoglutarate+ L-aspartate → L-glutamate+oxaloacetate
Oxaloacetate+NADH+H⁺ → L-Malate+ NAD⁺
Calculations:
AST U/l = 1746 ӿ ∆A (340nm/min)
Reference range: Up to 0-37 U/l

27.  Sample: Serum heparinized, EDTA plasma
stable for 1 week at 2-8ºC
Serum shouldn't be hemolysed
 Interpretation:
Markers of Hepatocellular damage.
Raised in Acute Hepatitis
Cytoplasmic Damage:↑ALT
Mitochondrial damage:↑AST

28.  Derived from Liver, osteoblasts and placenta
 Principle:
Alkaline phosphatase catalyses the hydolysis of p-
nitropheylphosphatse in the presence of Mg ions at
alkaline pH
4-PNPP + H₂O → ƿ-Nitrophenol + PO₄
ALP U/l = 2760 ӿ ∆A/min @ 405nm
Reference Range= Adults 65-306 U/l
Children 0-645 U/l
 ↑ in cholestatic liver disease

29.  Marker of severe Alcoholic Liver disease.
 Extremely sensitive test
 Reference Range: 11-60 U/l
5 Nucleotidase
 Hydrolysis of nucleoside 5’ phosphate esters.
 Increased in hepatobiliary diseases
Measurement of GGT & 5- Nucleotidase tends to
parallel Alp levels in hepato-biliary diseases.

31.  Yellow colour of conjunctiva, mucous membrane,
and skin due to increased bilirubin level
Pre hepatic Jaundice: ↑metabolism
In Acute & chronic hemolytic anemia's
Hepatic Jaundice: Intrinsic liver defect or disease
Due to disorders of bilirubin metabolism & transport
defects.
 Crigler najjar syndrome
 Dubin-johnson syndrome
 Gilbert’s disease
 Physiologic jaundice(Newborn)
Post hepatic jaundice: biliary obstructive disease
Physical obstructions gall stones and tumors

32. Gilbert syndrome:
 Benign autosomal recessive hereditary
disorder
 Due to mutation in gene UGT1A1
Crigler najjar syndrome:
 Due to defect in gene involved in bilirubin
conjugation.
Dubin Johnson syndrome:
 Rare autosomal recessive inherited disorder
 ↑ in delta bilirubin

33. Rotor syndrome:
 Similar to dubin johnson
 ↓ ligandin
Physiological jaundice of Newborn:
 ↓ glucoronyl transferase

34. Cholestasis is an hepatic disorder
characterized by retention of conjugated
bilirubin & ALP
Cholestasis may be either:
 INTRAHEPATIC: Bile secretion from
hepatocytes into canaliculi is impaired
 EXTRAHEPATIC: Due to obstruction to the
flow of bile through biliary tract

35.  Inflammation in liver tissue
 INFECTIOUS: viral, bacterial & fungal
infections
 NON-INFECTIOUS: Drugs, chemicals & toxins
 Symptoms: Jaundice, dark urine, fatigue,
nausea, vomiting & abdominal pain

36.  Clinical condition in which scar tissue replaces
normal
 SIGNS & SYMPTOMS: fatigue, nausea, weight loss,
jaundice, bleeding from GIT
 COMMON CAUSES: Chronic Alcoholism,
HBV,HCV,HDV
Inherited disorders: ɖ1-antitrypsin deficiency, Wilson
disease, hemochromatosis
Albumin , Total
protein, Total
Cholesterol
Prothrombin time

37.  Hepatitis B
 HBsAg
 HBeAg
 Anti-HBs
 Anti-HBc
 HBV DNA
 Hepatitis C
 Anti HCV
 HCV RNA
 Auto-immune hepatitis:
 ANA
 ASTHMA

38. It is indicated in patients in whom ALT & AST
are persistently greater than two-fold
elevation.