LPU – ST. CABRINI SCHOOL OF HEALTH SCIENCES, INC.

COLLEGE OF ALLIED MEDICINE – BSMLS BATCH 2025

LIVER FUNCTION
CLINICAL CHEMISTRY 1 – MICHAEL VINCENT O. ALGOZO, RMT, MSHSM
ADAPTED FROM: POWERPOINT/LECTURE

COURSE OUTLINE: FINALS

1. Liver Function 3. synthesis
2. Bilirubin legproteinFatiyacias
ecarrieanyvin
LIVER FUNCTION
ANATOMY skin largestorganinthe body emanation energy
nay mm
 approximately weighs 1.2 to 1.5 kilograms engram
[Link]
[Link]

 responsible for most major metabolic functions in the body mostortheproteinsaremadenytheliver hindilanssaner proteins
except
for immunoglobulin ran ginagawaenatueiiaiiens
[Link]
 reddish brown and located under the diaphragm in the upper
right quadrant of the abdomen
 1,500 mL/ min blood supply
 major vessles:
o when carbohydrates are ingested and absorbed, the liver
o hepatic artery
can do three things:
 for oxygen and nutrients Fromarteryandvein riverisextremely
vascular 1. use glucose for its own cellular energy requirements
 contributes 20% of blood supply
2. circulate glucose for use at the peripheral tissues
3. store glucose as glycogen
o portal vein comesfromtheextract spleen
and
 drains GI tract and spleen
o lipids are synthesized in the liver under normal
 contributes 80%
circumstances when nutrition is adequate and the
 first-pass phenomenon ilanatngkinarainaydaaaanrativer
demand for glucose is being met 70% of the daily
Forprocessing detoxify production of cholesterol is produced by the liver
 functional unit: Lobule
o almost all serum proteins are synthesized by the liver
o six-sided structure with a central vein and one portal triad at
each corner Bresseisineaucomer
4. storage
Components of Lobule vein
portal
i
hepaticartery leauts
o vitamins both
water and
soluble insoluble
1. branches of the hepatic portal vein and hepatic artery
o glycogen
2. central vein
3. sinusoids branchesinside
taunter o iron
nonunion
4. hepatocytes and Kupffer cells
5. metabolism
5. bileliverans
macrophage
canaliculi
6. bile ducts bothpapuntaanapalabassaliver

 cell composition:
o hepatocytes (80%)slivercentuatareakaparenanymalans
o Kupffer cells (20%)
o stellate cells fibroblastsrim
for
esponsible fibrosis

i tototallyabolishLivertunction starringours
whatisthe
got sirainangiverant
resultD eathw ithin
r umours
FUNCTIONS b ecause
ofHypoglycemia
proteinaminoacids BILIRUBIN
1. detoxification
o drugs and foreign compounds ammonia  major waste product of heme catabolism
o ammonia wienie
o uric acid
by
detoxified
the
liver ammoniawin  approximately 200-300 mg of bilirubin produced per day
overturnintourea
o first pass phenomenon: every substance absorbed by the
me
iiiin
GIT must first pass through the liver
o phagocytosis by Kupffer cells imname i Eniana
mmmm

i
o the drug metabolizing system of the liver takes place [Link]
mean
mostly in the liver microsomes via the cytochrome p450
isoenzymes
unanimaraninnina
mmmm
camerainmantase

ing
ummmm
tamiami
[Link]
inanimate
2. secretion/excretion awesternamniversonorestiniwinneprimaryinbidia caimanaman animanaminnina
B
warm
o bile acid/bile salts imaicacia
menaeoxymolic
Do
masamune
amminman
i i
minimum
[Link]
amainmammonism
air
 formed from cholesterol [Link] mmonanwnnia
uniugarewith
 important in increasing absorption of dietary fats glycine [Link]
a.m mn aaamaiamronia
name I
starrints [Link]
gallbladder

i
o bile pigments smarties

i
mumenanmaninnin
 heme waste products (bilirubin and porphyrin products) [Link]
[Link]
sewnaancabieavid insane
river deoxymolicacid large
intestine
manana anuria
 LPU – ST. CABRINI SCHOOL OF HEALTH SCIENCES, INC.
COLLEGE OF ALLIED MEDICINE – BSMLS BATCH 2025
LIVER FUNCTION
CLINICAL CHEMISTRY 1 – MICHAEL VINCENT O. ALGOZO, RMT, MSHSM
ADAPTED FROM: POWERPOINT/LECTURE

Graystool mayappearwhenBaisnotexcreted a. pre-haptic jaundice

no urobilinogen
nosterwhilinogen  also known as hemolytic or retention jaundice
lawand tin
 increased amounts of bilirubin are being presented to
nostenobi
stool
Aaronic
union color
g ives the liver
MB1
mefeces  causes:
1. excessive destruction of RBC
2. hepatic uptake decreased

b. hepatic jaundice
 also known as hepatocellular of infectious jaundice
 primary complication in the liver
indirectBilirubin nirectBilirubin
 causes:
1. severe damage to the hepatocytes due to
microorganisms or alcohol
foreign
2. starvation and certain medications
man
armadamian
3. hepatitis and a rias
cirrhosis
4. parasitism as guidesit
itlascarisstrong
5. conjugation defects/deficit
6. impairment of hepatic excretion (acquired disorder)
detect
excretion
 Dubin-Johnson: removal of conjugated bilirubin from
the liver cell and the excretion into the bile are defective

if
 Rotor Syndrome: hypothesized to be due to a
ALTERATIONS DURING DISEASES reduction in the concentration or activity of intracellular
binding proteins; liver biopsy does not show dark
pigmented granules (lipofuscin) transports uptake
d etect

BI
liver

Disease
[Link] crigler
hasam
najjar

ni liver
cancer
prison
way
detect
inhibition
circulating
b rown
normal reddish
insomecases it
wanna intermsofexcretion
metastasizes

HEPATITIS
o may be acute/chronic, in which there is damage to liver cells
I carexit
cannot
insonnson
amateur
be
can via
confirmed aversion
roman
pigment
rotorsyndrome on
CIRRHOSIS same son
memanismwimmin
except mat
mean
o process in which death of liver cells with regeneration leads in
aversion

to fibrosis, scarring and destruction of the normal liver

awomanpigment

structure
o most common causes include chronic alcoholism and chronic
asymptomatic most
inmeliver
detect
common
 Gilbert’s Disease: lower production of UDPGT due to
hepatitis C infection a genetic lesion and overall enzymatic activity; an
additional defect related to a transport deficit in the
LIVER TUMORS
sinusoidal membrane of the hepatocyte may be present;
o metastatic liver cancers are more common than primary liver

É
decreased uptake
cancers
 Crigler-Najjar Syndrome: more serious disorder,
o hepatocellular carcinoma is the most common malignant
multiple mutations in the gene coding for UDPFT results
tumor of the liver
in the production of mildly dysfunctional to completely
PRIMARY BILIARY CIRRHOSIS nonfunctional UDPGT
o progressive disease characterized by destruction of  Lucey-Driscoll: circulating inhibitor
intrahepatic bile ducts, presence of antimitochondrial
antibodies in the plasma c. post-hepatic jaundice
 also known as regurgitative, obstructive, or cholestatic
JAUNDICE/ICTERUS itis asignbecause itisobservable jaundice
o yellow pigment of the skin, mucous membrane and sclera of  major cause:
the eyes due to increased bilirubin (hyperbilirubinemia) 1. obstruction of biliary flow s may
baraornarrowing
o not apparent until the bilirubin reaches >3.0 mg/dL  minor causes:
1. intrahepatic cholestasis
 LPU – ST. CABRINI SCHOOL OF HEALTH SCIENCES, INC.
COLLEGE OF ALLIED MEDICINE – BSMLS BATCH 2025
LIVER FUNCTION
CLINICAL CHEMISTRY 1 – MICHAEL VINCENT O. ALGOZO, RMT, MSHSM
ADAPTED FROM: POWERPOINT/LECTURE

2. obstruction of the extra-hepatic biliary tree

3. Cholelithiasis or gallstones
4. stricture, spasms, atresia, and microorganisms narrowing
5. cancer of the head of the pancreas swelling
of
thepain
6. Ascaris lumbricoides, etc. infection

note Bacanbeexameainurinebutonceitnina
ammineitcannotbe nearer
excreted
Disease liverdisease REYE’S SYNDROME
shield negatingHemolytic namingianaanepanasies
o non-inflammatory hepatic encephalopathy and fatty liver
Data
Bilirubin
am
many
s
mansion
ancamorbeaneria
maringitinanana
degeneration
lawman i measeacuseara
am o hepatic destruction following recovery from viral infection

ii
fiIII1f
ramenammeminarm
[Link]
and aspirin ingestion in children, wherein the patient
Lya develops neurologic abnormalities due to accumulation of
miantbina ammonia in the CNS
win Ba Baunbilinogen o almost exclusively seen in children
Be I'd Hemonstanisease
in normal a
nt
o mild bilirubinemia; threefold changes in ammonia and
rivernisease
r ar aminotransferases (AST and ALT)
a an torment
Bilianoramation

DRUG AND ALCOHOL-RELATED D/O

o drugs causes injury most commonly via immune-mediated
injury to the hepatocytes
o ethanol: most important drug which can cause liver damage;
can lead to alcohol cirrhosis
o acetaminophen can cause fatal hepatic necrosis
or paracetamol
TESTS

BILIRUBIN DETERMINATION
d. neonatal jaundice o specimen: serum or plasma
 buildup of unconjugated bilirubin nindipamaturedan liver o very sensitive and is protected from light (light decreases
toprocesssum
 noted 2-3 days of neonatal life, rarely rises greater than bilirubin by 30-50%/hour)
5 mg/dL (peaks at 4-5 days)  should be in dark room, test for 2-3 hours (if possible,
 most common cause of HDN Hemolytic immediately)
ofthenewborn
Disease
 exchange transfusion: napsinBilirubinmetabolism
sunlight  storage: room temp (2 days), 4C (1 week), -20C (indefinite)
 to remove bilirubin from the circulation of the baby
 indicated when neonatal bilirubin approaches 20 Considerations:
mg/dL despite UV phototherapy hemolysis: falsely decreased
babyisjaundice
enthe lipemia: falsely increased
to
expose sunlight
NajarDisease ne
suititdidn'twork I builds a. colorimetric method
Br up carrion principle: Van den Berg Reaction (Diazo reaction)
appwaontouriign [Link]
siframes
theBrainnighaffinity o diazotization of bilirubin to produce azobilirubin
roman itis called
kerniciens
o initially done on urine
acommon
more
inchild
Diazo reagent:
o 0.1% silfanilic acid + HCl
o 0.5% sodium nitrite jumposition

Unconjugated bilirubin (B1) – reacts to albumin with an

accelerator indirect solubizer accelerator
Conjugated bilirubin (B2) – reacts directly with diazo reagent
 LPU – ST. CABRINI SCHOOL OF HEALTH SCIENCES, INC.
COLLEGE OF ALLIED MEDICINE – BSMLS BATCH 2025
LIVER FUNCTION
CLINICAL CHEMISTRY 1 – MICHAEL VINCENT O. ALGOZO, RMT, MSHSM
ADAPTED FROM: POWERPOINT/LECTURE

Delta bilirubin ithasa characteristicofbeingdirectlyreacted wdiazoreagent ENZYME STUDIES

o B2 bound to albumin and behaves like B2 o aminotransferases
o seen only when there is significant hepatic obstruction o phosphatases
Act Ast
Alr t s nucleotidase n
o third fraction of bilirubin o gamma-glutamyltransferase
eat aver
2 types:
hit min o LDH

Direct method 8Q [Link]

No coupling accelerator is added to initially convert B1

to B2 before the reaction, therefore only direct bilirubin is
determined

Indirect method:
A coupling accelerator of reaction is added to make
both B1 and B2 react with the reagent
appliespiano
reactioninpirectly

moresensitive

on
transy
exchange
photothera

a ffected
severely the many n eeds
intervention
b. direct spectrophotometry
o uses bilirubinometer
o determine bilirubin concentration by measuring affected
moderately thebabyneeds
aremonitoring
absorbance at 450-455 nm
o this method is applicable only in measuring total bilirubin
o used in neonatal populations; cannot be done in adult
populations due to positive interference by carotinoid
compounds Bilirubin
omens
o principle: Reflectance photometry t inmates if whatistherelationshipor
the
Mfg M of
concentration reelection
in
bilirubinometry
Bilirubin
raw
bilirubin
urobilinogen test in urine and feces aconcentration
preflection
a concentration
areflection
o uses Erlich’s reagent: p-dimethylaminobenzaldehyde pear
o red color nonspecific
ai langsauroniinogen italso with
reacts other
compounds
Watsonsonwarts enionreactingcompounds
thespecificcompound
usedtoidentify urominogen
porphoniinogen
other tests for liver function indole
skatole
PT (Prothrombin Time) aHaa
o sensitive marker for impaired hepatic synthetic function
m
y
o also used for determining intrahepatic vs extrahepatic cause
timecan
fam ing

pi
of jaundice beactiva
o to differentiation prolonged PT due to cholestasis or impaired
vitamin K absorption, administer parenteral vitamin K f vitamin
dependentfactors
TOTAL PROTEIN AND ALBUMIN TESTS
pagwalang tax
ax andnag ng
o tests for hepatic synthetic function ingest vitaminK
hindinaman
a ctivate
any prothrombintime
GAMMA GLOBULINS
o autoimmune hepatitis: increased polyclonal IgG
o primary biliary cirrhosis: increased polyclonal IgM
o A/G ratio in liver disease is <1.0