Liver Function

- Rene Ritche C Gorospe, RMT, MT(ASCPi), MSMT(c)

Unit Objectives:
At the end of the unit, the learner should be
able to:
O Identify the parts of the liver,
O Explain the physiologic role of the liver,
O Discuss the pathway of bilirubin
metabolism,
O Differentiate between conjugated and
unconjugated bilirubin, and
O Classify and identify the causes of
jaundice

Liver
O responsible for several vital physiologic tasks

O receives approx. 1500 mL of blood per minute

O has a unique capacity to regenerate by cell division

and hypertrophy of the remaining tissue in case of

injury due to biliary obstruction or toxic exposure
O severe loss of function are reflected by diagnostic
changes in its physiologic activities
O to abolish liver function, 80% of the liver must be
destroyed

Anatomy of the liver

Location: ___________________________
Liver is divided into 2 lobes by the
_____________________
Two sources of blood:
____________________
____________________

Excretory system of the liver

O Excretory products of the liver are drained

via the ________________

O Bile canaliculi Intrahepatic duct
hepatic ducts common bile duct

Microanatomy of the liver

O 2 major cell types of the liver:
_________________________________
_________________________________

O Functional units of the liver: __________

Liver Physiology
Several vital bodily processes are being
carried out by the liver, namely:
O excretion and secretion functions
O metabolic functions
O detoxifying functions
O Storage functions

Excretory and Secretory

Functions of the Liver
O The liver processes and excretes

substances into bile or urine, such as the

heme waste product: __________.
O ___________ is composed of bile acids or
salts, pigments, cholesterol, and other
substances extracted from blood, with
____________ as its main pigment.

Metabolic Functions of the

Liver
O Carbohydrate metabolism
O Lipid metabolism
O Protein metabolism
O Hormone metabolism

Detoxifying Functions of the

Liver
O The liver detoxifies drugs through

oxidation, reduction, hydrolysis,

hydroxylation, carboxylation, and
demethylation
O These processes take place in the
__________________ via the
___________________ isoenzymes.

Storage Functions of the Liver

O Glycogen
O Iron
O Fat-soluble and water-soluble vitamins
O Amino acids

Bilirubin Metabolism

Characteristics

B1

B2

Solubility
Water
Alcohol

+
+

Affinity to serum alb

Lipid membrane
permeability

Renal excretion

Indirect

Direct

Van den Berg rxn

Synonyms

Non

polar bilirubin
Unconjugated
bilirubin
Indirect-reacting
bilirubin
Hemobilirubin
Hemolytic bilirubin

Bilirubin

diglucoronide
Direct-reacting
bilirubin
Prompt bilirubin
Water soluble
Polar bilirubin
Cholestatic
bilirubin

Delta Bilirubin
O _____________________________
O Longer half-life than other forms
O Formed due to prolonged elevation of Bc

in biliary obstruction
O Delta bilirubin = TB (DB + IB)

Bilirubin reference values

O (conversion factor: 17.10)
O Adult:
O Bc: 0 0.3 mg/dL (0 5 mol/L)
O Bu: 0.1 1.0 mg/dL (2 17 mol/L)

O Total: 0.1 1.2 mg/dL (2 21 mol/L)

O Delta: <0.2 mg/dL (<3 mol/L)

O Neonate:
O Total: 1.0 12.0 mg/dL (17 205 mol/L)

Jaundice
O aka. _____________
O caused by hyperbilirubinemia and

subsequent deposition of bilirubin to the

_______________________
O TB > ___________
O Hyperbilirubinemia may be caused by:
O Increased cellular breakdown
O Impaired liver cell uptake
O Impaired conjugation
O Impaired excretion

Classifications of jaundice:
O Physiologic Jaundice (Jaundice of the

newborn)
O Prehepatic (Hemolytic) Jaundice
O Hepatic (Hepatocellular) Jaundice
O Posthepatic (Obstructive Jaundice

Prehepatic Jaundice
O Aka. hemolytic/retention jaundice
O Due to excessive destruction of RBCs
O Free bilirubin is increased
O EF/Malaria
O Prolonged fasting, drug intake
O Decreased activity off UDPG (neonatal

jaundice)
O Gilbert disease
O Crigler-Najjar syndrome

Post-hepatic Jaundice
O Aka. regurgitative, obstructive or cholestatic

jaundice.
O Due to obstruction of the biliary flow
O Dubin-Johnson syndrome
O Rotor syndrome
O Intra-hepatic cholestasis
O Obstruction in the extra-hepatic biliary tree
O Gallstone (cholelithiasis)
O Strictures
O Spasms
O Atresia
O Parasite or bacteria
O Cancer of the pancreas

Cholestasis
O Hyperbilirubinemia with bilirubinuria
O Elevation of ALP, GGT, 5-nucleotidase

and LAP
O Hypercholesterolemia
O High serum bile salts (cholate and
chenodeoxycholate)

Hepatic Jaundice
O Aka. hepatocellular or infectious jaundice
O Due to severe damage to hepatocytes
O Both free and conjugated bilirubin is

elevated
O Due to alcohol or microorganisms

Differential Diagnosis
PRE-HEPATIC JAUNDICE POST-HEPATIC
JAUNDICE
O

Elevated

free bilirubin Elevated conjugated

Negative urine bilirubin bilirubin
Positive urine bilirubin
Elevated urine
urobilinogen
Decreased urine
urobilinogen
Darkly-colored stool
Kernicterus (deposition Clay-colored (acholic
or putty) stool
of bilirubin in brain
tissues) may occur
Steatorrhea
Increased ALP and 5nucleotidase

Derangements of Bilirubin
Metabolism:
O Gilberts Syndrome
O Crigler-Najjar Syndrome
O Dubin-Johnson Syndrome
O Rotor Syndrome
O Lucey-Driscoll Syndrome

Derangements of Bilirubin
Metabolism:
O Gilberts Disease
O Characterized by decreased conjugation and decreased

uptake of bilirubin
O Pre-conjugation failure
O Increased B1
O Crigler-Najjar Syndrome
O Type 1: autosomal recessive
O Absence of UDPGT
O Severe increase of B1 death
O Type 2: autosomal dominant
O Partial defect of the conjugating enzyme
O Increased B1 survival to adulthood

Derangements of Bilirubin
Metabolism:
O Dubin-Johnson Syndrome
O Characterized by a decreased hepatic

excretion of bilirubin
O Increased B2 with hepatic pigmentation
(melanin)
O Rotor Syndrome
O Cause is still unknown
O Similar to Dubin-Johnson but without hepatic

pigmentation
O Increased B2
O Prognosis is excellent

Derangements of Bilirubin
Metabolism:
O Lucey-Driscoll syndrome:
O Familial unconjugated hyperbilirubinemia
O Due to a circulating inhibitor of conjugation
O Hyperbilirubinemia usually lasts for the first 2-3

weeks of life

References:
[1] Bishop, M. L., Fody, E. P., & Schoeff, L. E. (2013). Clinical
Chemistry: principles, techniques, and correlations (7th
Ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
[2] Burtis, C. A., Ashwood, E. R., & Bruns, D. E. (2013). Tietz
textbook of Clinical Chemistry and Molecular Diagnostics
(5th Ed.).Singapore: Elsevier Pte Ltd.
[3] Crook, M. A. (2012). Clinical Biochemistry and Metabolic
Medicine (8th Ed.). London, UK: Hodder & Stoughton Ltd.
[4] McPherson, R. A., & Pincus, M. R. (2011). Henrys clinical
diagnosis and management by laboratory methods (22nd
Ed.). Singapore: Elsevier Pte Ltd.

References:
[5] Rabor, R. R. (2005). Clinical Chemistry review outline.

[6] Rodriguez, M. T. T. (2014). Clinical Chemistry review handbook

for medical technologists.