CLINICAL CHEMISTRY 1 CC1 TOPIC

LIVER
LECTURER: SHIRLEY O.SOLITARIO,RMT
BACHELOR OF SCIENCE IN MEDICAL LABORATORY SCIENCE
LECTURE 7
TRANSCRIBED BY: ANSHERINA MAY G. RAMOS
THIRD YEAR – FIRST SEMESTER
8
LIVER FUNCTION PROFILE (LFT)  HEPATOCYTES are cuboidal epithelial cells that
 Excretion functions (Bilirubin measurement) line the sinusoids and make up the majority of cells
LIVER in the liver. Hepatocytes perform most of the
 The liver is a large, meaty organ that sits on the liver’s functions – metabolism, storage, digestion,
right side of the belly. Weighing about 3 pounds, and bile production.
the liver is reddish-brown in color and feels  Tiny bile collection vessels known as bile canaliculi
rubbery to the touch. run parallel to the sinusoids on the other side of
 Normally you can't feel the liver, because it's the hepatocytes and drain into the bile ducts of
protected by the rib cage. the liver.
 The liver has two large sections, called the right BLOOD VESSELS
and the left lobes.  Hepatic Artery - supplies oxygen to the liver
 The gallbladder sits under the liver, along with  Portal vein - transports absorbed nutrients from
parts of the pancreas and intestines. the intestines to the liver
 The liver and these organs work together to digest, MICROSTRUCTURE OF THE LIVER
absorb, and process food. LIVER LOBULES

 The liver's main job is to filter the blood coming  Central vein
from the digestive tract, before passing it to the  Branches of the hepatic vein and the hepatic artery
rest of the body.  Sinusoids
 The liver also detoxifies chemicals and metabolizes  Hepatic plates
drugs. As it does so, the liver secretes bile that  Bile canaliculi
ends up back in the intestines.  Bile ducts
 The liver also makes proteins important for blood FUNCTIONS OF THE LIVER
clotting and other functions. DETOXIFICATION OF BLOOD (EXCRETION)
 Phagocytosis by Kupffer cells
 Metabolism and excretion of steroid hormones,
drugs and foreign compounds
 Production of urea, uric acid and other molecules
that are less toxic than their parent compound
 Bile pigments, bile salts and cholesterol are
excreted in bile into intestine.
METABOLIC FUNCTIONS –ACTIVELY PARTICIPATES
 Carbohydrate metabolism
 Lipid metabolism
LOBULES
 Protein metabolism
 The internal structure of the liver is made of  Hormone metabolism
around 100,000 small hexagonal functional units  Mineral and vitamin metabolism
known as LOBULES. SECRETION OF BILE
 Each lobule consists of a central vein surrounded
 Metabolism (conjugation) and excretion of
by 6 hepatic portal veins and 6 hepatic arteries.
bilirubin
 These blood vessels are connected by many  Synthesis of bile salts or bile acids
capillary-like tubes called sinusoids, which extend STORAGE
from the portal veins and arteries to meet the
 Glycogen
central vein like spokes on a wheel.
 Vitamin A
Each sinusoid passes through liver tissue containing 2
 Vitamin B12
main cell types: Kupffer cells and hepatocytes.
 Traced element Iron
 KUPFFER CELLS are a type of macrophage that
HEMTOLOGICAL FUNCTION:
capture and break down old, worn out red blood
 Liver participates in formation of blood
cells passing through the sinusoids.
(particularly in embryo)
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  Liver is also produces clotting factors like factor V. VII.  Degradation occurs in the spleen, bone marrow
 Fibrinogen involved in blood coagulation is also and liver
synthesized in liver. HEME AND BILIRUBIN
 It synthesize plasma proteins & destruction of  Heme four pyrrols rings connected together to
erythrocytes. form (porphyrin).
PROTECTIVE FUNCTION & DETOXIFICATION:  Bilirubin consists of open chain of four pyrrols-like
 Ammonia is detoxified to urea. rings
 kupffer cells of liver perform phagocytosis to
eliminate foreign compounds.
 Liver is responsible for the metabolism of xenobiotics
BILE
 Components:
o bile acids- are synthesized form
cholesterol
o Exists mainly as conjugated (bile salts)
o Phospholipids HEMOGLOBIN DEGRADING AND BILIRUBIN FORMATION
- Major ones are the lecithins
o Bile pigments (Bilirubin, breakdown
product of RBCs)
o cholesterol
o urobilinogen, and
o electrolytes
 Important in lipid digestion: formation of micelles
 Cholic acid and chenodeoxycholic acid
REVIEW: LIVER
 The liver is the largest organ in the body.
 It is located below the diaphragm in the right upper
quadrant of the abdominal cavity and extended
approximately from the right sth rib to the lower
border of the rib cage. BILIRUBIN METABOLISM
 The working cells of the liver are known as hepatocytes.
LIVER FUNCTION TEST (LFT) PROFILE
1. UNCONJUGATION PROCESS :
 RBCs are phagocytized in the spleen. Hemoglobin
is catabolized into amino acids, iron and heme.
 Heme ring is broken open and converted to
unconjugated (indirect ) bilirubin.
 This unconjugated bilirubin is not soluble in water,
BILIRUBIN due to intramolecular hydrogen bonding.
DEFINITION OF BILIRUBIN  It is then bound to albumin and sent to the liver.
 Bilirubin is the water insoluble breakdown product 2. CONGUGATION PROCESS:
of normal heme catabolism  In liver: Bilirubin is conjugated with Glucouronic
 It’s a yellow pigment present in bile ( a fluid made acid to produce bilirubin diglucuronides, which is
by the liver) , urine and feces . water soluble and readily transported to bile. and
 Heme is found in hemoglobin, a principal thus out into the small intestine.
component of RBCs [Heme: iron + organic
compound “porphyrin”].
 Heme source in body:
o 80% from hemoglobin  Then conjugated bilirubin is excreted in bile through
o 20% other hemo-protein: cytochrome, bile duct to help in food digestion (mainly fat).
myoglobin)  The excess amount transferred to intestine to be
BILIRUBIN excreted in urine and stool.
 Bile pigment that results from the catabolism of  However 95% of the secreted bile is reabsorbed by
the heme moiety of the hemoglobin molecule due the small intestine. This bile is then resecreted by
to old age or trauma the liver into the small intestine.

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  This process is known as enterohepatic circulation Characteristic B1 B2
 About half of the conjugated bilirubin remaining in Solubility
the large intestine (about 5% of what was Water - +
originally secreted) is metabolized by colonic Alcohol + +
bacteria to form urobilinogen , which may be Affinity to + -
further oxidized to urobilin and stercobilin . serum alb
 Urobilin, stercobilin and their degradation Lipid membrane + -
products give feces its brown color. permeability
 Elevated levels of bilirubin in blood and urine Renal excretion - +
indicate certain diseases. Van den Berg Indirect Direct
rxn
Synonyms Non polar Bilirubin
bilirubin/water diglucoronide
insoluble Direct-reacting
Unconjugated bilirubin
bilirubin Prompt bilirubin
Indirect-reacting Water soluble
bilirubin Polar bilirubin
Hemobilirubin Cholestatic
Hemolytic bilirubin
bilirubin Post hepatic
Free hemoglobin bilirubin
One minute
bilirubin

TYPES OF BILIRUBIN IN SERUM:

 Direct bilirubin: is conjugated (water soluble
bilirubin) in aqueous solution it reacts rapidly with
reagent (direct reacting).
 Indirect bilirubin: is unconjugated (water insoluble
bilirubin) because it is less soluble in it reacts more
slowly with reagent (reaction carried out in
methanol).
o in this case both conjugated and
unconjugated bilirubin are measured
given total bilirubin.
o Unconjugated will calculated by
subtracting direct from total and so called
indirect.
 Total bilirubin = DB+ IB Indirect Bilirubin = TB-DB
 knowing the level of each type of bilirubin has
diagnostic important.
PLASMA BILIRUBIN
 Normal plasma bilirubin: 0.2-0.8 mg/dl.
 Unconjugated bilirubin: 0.2-0.6 mg/dl.
 Conjugated bilirubin: 0-0.2 mg/dl.
 If the plasma bilirubin level exceeds 1mg/dl. the
condition is called hyperbilirubinemia.
 Levels between 1 & 2 mg/dl are indicative of latent
jaundice.
JAUNDICE:
 It is a medical term describes the elevation of
bilirubin in blood result in yellow color of skin and
sclera.
 Other symptoms include nausea, vomiting, dark-
colored urine and fatigue.
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  Types of Jaundice: according to the cause of o Biliary stricture
jaundice o Cancer of the pancreas or gallbladder
 it is classified to three main types: o Gallstones
o Pre-hepatic jaundice PHYSIOLOGIC JAUNDICE OF THE NEWBORN:

o Hepatic jaundice  High bilirubin levels is common in newborns age

o Post-hepatic (most common type) (1-3 days).
 After birth the newborns breaking down the
excess RBCs they are born with and, because the
newborn’s liver is not fully mature, (unable to
process the extra bilirubin) leads to elevate its
level in blood and other body tissues.
 This situation usually resolves itself within a few
days
SO, WHAT TYPE OF JAUNDUCE IS THIS ???
 Note:Your child's doctor must consider the
following when deciding whether your baby's
PRE-HEPATIC JAUNDICE (OBSTRUCTIVE JAUNDICE) bilirubin levels are too high:
CAUSES o How fast the level has been rising
 Due to increase in RBCs breakdown due to o Whether the baby was born early
hemolytic anemia. o How old the baby is
 The rate of RBCs lysis and bilirubin production NEW BORN JAUNDICE TREATMENT:
more than ability of liver to convert it to the  Usually newborn is treated by phototherapy which
conjugated form breakdown bilirubin (ID-D) and convert it to the
 Occur in: photo isomer form which is more soluble.
o Erythroblastosis fetalis BILIRUBIN TOXICITY :

o Hemolytic anemia  Very high bilirubin is danger and toxic it may cause
o Transfusion reaction brain damage effect on muscles, eyes and Leading
TYPE OF BILIRUBIN to death
JAUNDICE
 Indirect Bilirubin > Direct Bilirubin
CONFORMATIONAL TEST  Also known as “icterus”
 K+ ( High)  Yellowish pigmentation of the skin, mucous
 Hematology: CBC (low Hb) membrane and sclera of the eyes
HEPATIC JAUNDICE (HEPATO-CELLULAR JAUNDICE)  Due to accumulation of abnormal amounts of
either free or conjugated bilirubin or both
CAUSES
 It signifies hyperbilirubinemia and becomes
 Due to liver cell damage (cancer, cirrhosis or clinically evident when serum bilirubin exceed
hepatitis) 2mg/dL
 Conjugation of bilirubin decreased (ID.Bil. 🡩).  Normal concentration: 0.5-1.0 mg/dL
 Blilirubin that is conjugated is not efficiently  Jaundice: 2 mg/dL
secreted into bile but leaks to blood (D.Bil.) CLASSES OF JAUNDICE
 Occur in :
o Cirrhosis (scarring of the liver) PRE-HEPATIC JAUNDICE/PRE-HEPATIC
o Hepatitis HYPERBILIRUBINEMIA –HEMOLYTIC/RETENTION
o Gilbert's disease JAUNDICE
TYPE OF BILIRUBIN  Excessive production of bilirubin due to excessive
 D.Bil, ID.Bil, T.Bil all (High) destruction of RBCs
CONFORMATIONAL TEST  Free bilirubin is increased
 ALT, AST (High) o HDN/Malaria
POST-HEPATIC JAUNDICE (HAEMOLYTIC JAUNDICE) o Prolonged fasting, drug intake
CAUSES o Extrensive hematoma
 Due to obstruction of bile duct which prevents o Decreased activity of UDPG (neonatal
passage of bilirubin into intestine. jaundice)
 D.Bil will back to liver and then to circulation o Gilbert’ disease
elevating its level in blood and urine. o Crigler-Najjar syndrome
 Occur in:
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 HEPATIC JAUNDICE/ HEPATIC HYPERBILIRUBINEMIA–  Evelyn-Malloy Method
HEPATOCELLULAR OR INFECTIOUS JAUNDICE
 Jendrassik-Grof Assay
 Implies severe damage to hepatocytes INHERITED DISORDERS OF BILIRUBIN METABOLISM
 Both free and conjugated bilirubin is elevated GILBERT’S DISEASE
 Due to alcohol or microorganisms  Characterized by decreased conjugation and
 CAUSES: decreased uptake of bilirubin
1. RETENTION JAUNDICE OR INABILITY TO CONJUGATE AS SEEN IN:  Pre-conjugation failure
o Physiologic jaundice of the newborn  Increased B1
o Gilbert’s syndrome CRIGLER-NAJJAR SYNDROME
o Crigler-Najjar syndrome, Type I and II Type 1: autosomal recessive
2. HEPATOCYTE INJURY (HEPATOCELLULAR) AS SEEN IN:
o Absence of UDPGT
o Viral Hepatitis o Severe increase of B1 – death
o Cirrhosis and alcoholic hepatitis Type 2: autosomal dominant
o Toxic liver injury o Partial defect of the conjugating enzyme
o Parasitism o Increased B1 – survival to adulthood
3. IMPAIRED EXCRETION OF PRODUCTS FROM THE DUBIN-JOHNSON SYNDROME
HEPATOCYTES AS SEEN IN:
 Characterized by a decreased hepatic excretion of
o Dubin-Johnson syndrome bilirubin
o Rotor’s syndrome  Increased B2 with hepatic pigmentation (melanin)
o Viral hepatitis HEPATITIS
o cirrhosis  means inflammation of the liver, which may be
POST-HEPATIC JAUNDICE – REGURGITATIVE,
caused by viruses, bacteria, parasites, radiation,
OBSTRUCTIVE OR CHOLESTATIC JAUNDICE.
drugs, chemicals or toxins.
 Due to obstruction of the biliary flow STAGES OF ALCOHOLIC LIVER DISEASE
o Dubin-Johnson syndrome
 Steatosis
o Rotor syndrome
o Triglycerides deposits in the liver
o Intra-hepatic cholestasis
 Steatonecrosis
 Obstruction in the extra-hepatic biliary tree
o Further fat accumulation
o Gallstone (cholelithiasis)
o Inflammation
o Strictures
o Fibrosis
o Spasms
o Necrosis
o Atresia
 Cirrhosis
o Parasite or bacteria
o Extensive fibrosis
o Cancer of the pancreas
o Further inflammation
CHOLESTASIS
o Hepatocellular carcinoma
 Hyperbilirubinemia with bilirubinuria HEPATIC PROFILE TEST
 Elevation of ALP, GGT, 5’-nucleotidase and LAP
 Hypercholesterolemia Hepatic enzymes Clinical utility in liver disorders
 High serum bile salts (cholate and chenodeoxycholate) Alkaline phosphatase Elevated primarily in
DIFFERENTIAL DIAGNOSIS OF PRE-HEPATIC AND POST- obstructive process
HEPATIC JAUNDICE Aminotransferases Elevated in variety of liver
(ALT/AST) disease; ALT – more sensitive
PRE-HEPATIC JAUNDICE POST-HEPATIC JAUNDICE indicator of cellular destruction
 Elevated free bilirubin  Elevated conjugated
Gamma-glutamyl Some increase in liver disease
 Negative urine bilirubin bilirubin
Transferase Sensitive indicator of ethanol
 Elevated urine  Positive urine bilirubin
urobilinogen  Decreased urine
intake
 Darkly-colored stool urobilinogen Cholinesterase Normally quite high: values
 Kernicterus (deposition  Clay-colored (acholic or decrease in liver disorders
of bilirubin in brain putty) stool Lactate Elevated in wide variety of
tissues) may occur  Steatorrhea dehydrogenase (L5) situations
 Increased ALP and 5’-  ALT and AST – reliable monitor for hepatitis
nucleotidase  Infective stage – quite high
 Recovery stage – gradual decline
BILIRUBIN DETERMINATION
 Chronic disease – continued high values
 Van den Bergh Reaction/Diazotization Reaction  Recurrence – decline and subsequent increase.

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 BILIRUBIN MEASUREMENT  The difference between the total bilirubin and the
direct bilirubin is the direct bilirubin.
HOW TO PREPARE FOR THE TEST
 WHERE AS : TB – DB = IB
 You should not eat or drink for at least 4 hours  ERLICH’S DIAZO REAGENT:
before the test. o DIAZO A – 0.1% sulfanilic acid
 Your health care provider may instruct you to stop o DIAZO B – 0.5 % sodium nitrite
taking drugs that affect the test. o DIAZO blank- 1.5 % Hydrochloric acid
 Many drugs may change the bilirubin levels in your CONVERSION FACTOR: 17.1
blood. Make sure your doctor knows which JENDRASSIK AND GROF METHOD
medications you are taking. PRINCIPLE:
 Tell your doctor if you have allergy  Plasma or serum is added to a solution of sodium
WHY THE TEST IS PERFORMED
acetate (buffer) and caffeine sodium benzoate
 Large amounts of bilirubin in the blood can lead to (coupling accelerator).
jaundice. Jaundice is a yellow color in the skin,  The Diazotization is terminated by the addition of
mucus membranes, or eyes. ascorbic acid.
 Jaundice is the most common reason to check  With the use of a strong alkaline tartarate solution,
bilirubin levels. the pink azobilirubin is then converted to a blue
 Most newborns have some jaundice. The doctor or azobilirubin.
nurse will often check the newborn's bilirubin DELTA BILIRUBIN
level. See: Newborn jaundice  It is bilirubin tightly bound to albumin
 The test may also be done in older infants,  It has a longer half-life than other forms of bilirubin
children, and adults who develop jaundice.  It is formed due to prolonged elevation of
 A bilirubin test will also be done if your doctor conjugated bilirubin in biliary obstruction.
thinks you may have liver or gallbladder problems  It helps in monitoring the decline of serum bilirubin
PROCEDURE MEASURING SERUM BILIRUBIN LEVEL
following surgical removal of gallstones
Principle:  It reacts with diazo reagents in the direct bilirubin
assay
 It is computed by using this formula: TB-DB+IB= DELTA
 BILIRUBIN
 It is not calculated on neonatal patients (< 14 days)
 Kit components
 Reference values : < 0.2mg/dL (<3umol/L)
o Sulfanalic acid reagent METHODS OF BILIRUBIN DETERMINATION
o Sodium nitrate reagent
 EVELYN-MALLOY
o Methanol reagent
 MICROBILIRUBIN
o Bilirubinequavalent standard (5mg/dl
 THANNHAUSER AND ANDERSON
T.bil; 2.5 mg/dl D.bil)
METHODS OF DETERMINATION  ANINO,WATSON AND DUCCI
 GENERAL REACTION:  JENDRASSIK AND GROF
VAN DEN BERG REACTION  MICHEALSON
Principle:  STONER AND WEISB
 Bilirubin + diazo reagent → azobilirubin (red; acid  ALKALINE METHANOLYSIS
ph; blue: alkaline pH)  DIRECT READING BILIRUBINOMETER
 * Diazo reagent – diazotized sulfanilic acid to form NOTE: 1-4 FOLLOW THE PRINCIPLE OF EVELYN MALLOY
pink to purple azobilirubin which is measured 5-9 FOLLOW THE PRINCIPLE OF JENDRASSIK AND GROF
spectrophotometrically. PROCEDURE:
MALLOY-EVELYN METHOD
Principle:
 Bilirubin is coupled with diazotized sulfanilic acid
(Ehrlich’s DiazoReagent) forming a purple
azobilirubin.
 The bilirubin that has reacted with the diazo rgt.
After standing for 1 minute is the prompt or
conjugated bilirubin.
 Fifteen minutes after addition of methanol
(coupling accelerator) total bilirubin is measured.
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 CALCULATIONS:  In normal individuals, <5% of the dye is retained at
 Conc. of Bilirubin equavelant is 5mg/dl for T.bil, the end of 45 min.
and 2.5 mg/dl for D.bil  Any impairment in liver function causes an
Direct Bilirubin: increased retention of the dye.
 Abs (test) - Abs (test blank) X 2.5 mg/dl  This test is quite sensitive to assess liver
Abs of bilirubin equivalent abnormality with particular reference to excretory
Total Bilirubin: function.
2. SERUM ENZYMES
 Abs (test) - Abs (test blank) X 5 mg/dl
Abs of Bilirubin equivalent  A large number of enzyme estimations are
To convert to μmol/L multiply by 17.1 available which are used to ascertain liver
NORMAL RESULTS function.
 It is normal to have some bilirubin in your blood.  They are be divided into two groups:
 Normal levels are:  Most commonly & routinely done in the
o Direct (also called conjugated) bilirubin: 0 laboratory.
to 0.5 mg/dL  AST & ALT
o Total bilirubin: 0.3 to 1.9 mg/dL  Not routinely done in the laboratory
ASPARTATE TRANSAMINASE (AST/SGOT)
 Note: mg/dL = milligrams per deciliter
 Normal value ranges may vary slightly among  AST or SGOT (serum glutamate oxaloacetate
different laboratories. transaminase)
ICTERUS INDEX
 This is a measurement of the amount or degree of
icteresia or yellowishness of the serum or plasma
in cases of jaundice.
 Principle: serum or plasma is diluted with NSS or
sodium citrate solution until the color of the
specimen matches with that of a reference
 Normal range: 10-45 U/L.
standard.
 AST is found in both cytoplasm & mitochondria
 The standard of used is a 1:10,000 dilution or
 AST/GOT also reflects damage to the hepatic cells
0.01% potassium dichromate.
& is less specific for liver disease.
 METHODS:
 It can also be released with heart, muscle & brain
1. Muellengracht – 0.85 – 0.90 % saline as
disorders.
diluent
 AST help diagnose various heart, muscle or brain
2. Newberger – sodium citrate as diluent
BILIRUBIN IN URINE disorders, such as a myocardial infarct (heart
 The conjugated bilirubin is water soluble & is attack).
ELEVATED LEVELS OF AST MAY INDICATE
excreted in urine.
 Acute hemolytic anemia
 The unconjugated bilirubin is not excreted.
 Cirrhosis of the liver
 Bilirubin in urine can be detected by Fouchet's test
 Hepatitis
or Gmelin's test
 Acute pancreatitis or inflammation of pancreas
 Major liver function tests may be classified as
follows  Acute renal failure or loss of kidney function.
 Tests based on excretory function Measurement  Heart attack
of bile pigments, bile salts. bromosulphthalein.  Primary muscle disease
 Tests based on serum enzymes derived from liver  Recent surgery
ALANINE TRANSAMINASE (ALT/SGPT)
- Determination of transaminases. alkaline
phosphatase, s'-nucleotidase. Y -  ALT or SGPT (serum glutamate pyruvate
glutamyltranspeptidase transaminase)
1. BROMOSULPHTHALEIN (BSP) TEST  ALT is a cytoplasmic enzyme.
 Bromosulphthalein is a dye used to assess the  Normal Range: 5-40 U/L.
excretory function of liver.
 It is a non-toxic compound & almost exclusively
excreted by the liver (through bile).
 BSP is administered intravenously (5 mg/kg body
weight) & its serum concentration is measured at
45 min & at 2 hrs.
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 ELEVATED LEVELS OF ALT/SGPT MAY INDICATE  Prothrombin time is prolonged in patients with
 Alcoholic liver disease liver damage, compared to normal.
 Cancer of liver  It generally falls 10 - 15 seconds
 Hepatitis or inflammation of the liver 5. DETOXIFICATION
 Noncancerous tumor of the liver  The liver is the major site for the metabolism of
 Use of medicines or drugs toxic to the liver xenobiotics (detoxification).
 Cirrhosis or scarring of the liver  Measurement of hippuric acid synthesis is an ideal
 Death of liver tissue. test for assessing the detoxification function of
ALKALINE PHOSPHATASE (ALP) liver.
 ALP occurs in in all tissues, especially liver, bone.  Hippuric acid is produced in the liver when benzoic
bile duct, kidney & the placenta. acid combines with glycine
 The ALP used to help diagnose certain liver  About 6 g of sodium benzoate (dissolved in about
diseases and bone disorders. 250 ml water) is orally given to the subject, after a
 Normal range: 30-95 IU/L (3-13 kings unit) light breakfast (usually 2 hrs later) & after
 ALP is a hydrolase enzyme responsible for emptying the bladder.
removing phosphate groups from many types of  Urine collections are made for the next 4 hours &
molecules, including nucleotides & proteins. the amount of hippuric acid excreted is estimated.
 Most effective in an alkaline environment.  A reduction in hippuric acid excretion (particularly
 Levels are significantly higher in growing children < 3g) indicates hepatic damage.
3. METABOLIC CAPACITY
GALACTOSE TOLERANCE:
 Galactose is almost exclusively metabolized by the
liver.
 The liver function can be assessed by measuring
the utilization of galactose.
 The subject is given intravenous administration of
galactose (about 300 mg/kg body weight).
 Blood is drawn at 10 minute intervals for the next
2 hours & galactose estimated.
 In the normal individuals, the half-life of galactose
is about 10-15 minutes.
 This is markedly elevated in hepatocellular
damage (infective hepatitis, cirrhosis)
4. SYNTHETIC FUNCTION
SERUM ALBUMIN:
 Albumin is solely synthesized by the liver.
 It has a half-life of about 20-25 days.
 It is a good marker to assess chronic (& not acute)
liver damage.
 Low serum albumin is commonly observed in
patients with severe liver damage.
 Albumin is also decreased in malnutrition.
 Functional impairment of liver is frequently
associated with increased synthesis of globulins.
 Cirrhosis of the liver causes a reversal of
albumin/globulin ratio (A/G ratio).
 Serum electrophoresis of proteins reveals
increased albumin & decreased y -globulin
concentrations
PROTHROMBIN TIME
 The liver synthesizes all the factors concerned with
blood clotting.
 A decrease in the concentration of plasma clotting
factors is found in the impairment of liver function.

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