liver function مهم - copy

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Liver function testsLiver function tests



• Liver plays many important functions inLiver plays many important functions inthe body as regard carbohydrate, lipid andthe body as regard carbohydrate, lipid and

protein metabolism. Liver is the site ofprotein metabolism. Liver is the site ofsynthesis of albumin, all clotting factorssynthesis of albumin, all clotting factors(except factor VIII), carrier proteins (As(except factor VIII), carrier proteins (Asceruloplasmin, transferrin), cholesterol,ceruloplasmin, transferrin), cholesterol,

bile salts and urea. It also has abile salts and urea. It also has adetoxication function (removal ofdetoxication function (removal ofammonia and other toxic substances)ammonia and other toxic substances)



LIVER FUNCTION

• rotein synthesis (most plasma proteins)• !olubility of lipid compounds (e.g., bili)

• !ynthesi"es glucose, lipids, lipoproteins

• roduces bile acids

• !ite of hormone synthesis• #emoves Ag$Ab complexes from blood.

• %xtensive reserve capacity & function normal in many'ith liver disease

• !ynthetic functions dependent on liver mass, ra'

materials from portal venous blood often abnormal inportal *+

• etabolic functions more dependent on liver mass-excretion also depends on bile drainage.



efining *ermsefining *erms

• Inflammation that lasts long enough 'illInflammation that lasts long enough 'ill

create fibrosiscreate fibrosis

• %xtreme fibrosis is called cirrhosis%xtreme fibrosis is called cirrhosis

• /irrhosis can be either compensated or/irrhosis can be either compensated or

decompensateddecompensated

• /ompensated cirrhosis can be subtle/ompensated cirrhosis can be subtle

• ecompensated cirrhosis is more obviousecompensated cirrhosis is more obvious



/hronic hepatitis can lead to fatal/hronic hepatitis can lead to fatal

complications (cirrhosis, //)complications (cirrhosis, //) /irrhosis 0th or 12th cause of death %xpected/irrhosis 0th or 12th cause of death %xpected

to increase 3x by 4252to increase 3x by 4252

// rare, but increasing in incidence in 6!.// rare, but increasing in incidence in 6!.Laboratory tests 7ey to recognition of chronicLaboratory tests 7ey to recognition of chronic

hepatitis and many cases of acute hepatitishepatitis and many cases of acute hepatitis

Laboratory tests also used for monitoring,Laboratory tests also used for monitoring,

prognosis in both acute and chronic liverprognosis in both acute and chronic liver

disease.disease.



Liver 8unction testsLiver 8unction tests

Liver function tests include manyLiver function tests include many

laboratory tests. *he most important testslaboratory tests. *he most important tests

are9are9

• 11 Synthetic function :Synthetic function : Albumin and Albumin and

immunoglobulins.immunoglobulins.

• 44*ests of liver in:ury (Liver en"ymes).Liver en"ymes).

• 55 CholestasisCholestasis 9;ilirubin (total and9;ilirubin (total and

direct)direct) , ALP, GGT, ALP, GGT

• 3rothrombin time3rothrombin time



1 Albumin and immunoglobulins1 Albumin and immunoglobulins

• I Albumin9I Albumin9 Is the most important serum proteinIs the most important serum proteinsynthesi"ed by the liver. It has a long half life(41synthesi"ed by the liver. It has a long half life(41days) and is therefore not a good indicator ofdays) and is therefore not a good indicator of

acute liver in:ury. 8urthermore, there is a highacute liver in:ury. 8urthermore, there is a highreserve of hepatic albumin synthesis and thusreserve of hepatic albumin synthesis and thusalbumin isalbumin is decreased only in chronic liver decreased only in chronic liver diseasesdiseases 'ith severe cells destruction.'ith severe cells destruction.

#eduction of serum albumin provide an#eduction of serum albumin provide anexcellent indicator of severity and prognosis ofexcellent indicator of severity and prognosis ofchronic liver disease.chronic liver disease.



y!oal"u#ine#iay!oal"u#ine#ia

$lo"ulin chol%TG "

1.decrease synthesis

protein malnutritionchronic liver disease

chronic inflammation

4.increase loss

L%+!

5increase Vd (ascites, overhydration)

3.increase turnover (catabolic state, steroid)



• II Immunoglobulins9II Immunoglobulins9

*here is a*here is a polyclonal increasepolyclonal increase of gamma globulinof gamma globulin

( due to( due to &clea'ance o' (synthesis)&clea'ance o' (synthesis) in ch'onicin ch'onic li*e' +iseaseli*e' +isease ith 'e*e'se+ al"u#in%$lo"ulinith 'e*e'se+ al"u#in%$lo"ulin

'atio -In li*e' ci''hosis I$A is #ainly (an+ to a'atio -In li*e' ci''hosis I$A is #ainly (an+ to a

less e.tent othe' i##uno$o"ulins- In ch'onicless e.tent othe' i##uno$o"ulins- In ch'onic

he!atitis the'e is a #ain ( in I$G-he!atitis the'e is a #ain ( in I$G-Total !'otein in ch'onic li*e' +iseases is not ofTotal !'otein in ch'onic li*e' +iseases is not of

+ia$nostic *alue /#ay "e( o' & o' no'#al)+ia$nostic *alue /#ay "e( o' & o' no'#al)



4 Liver en"ymes4 Liver en"ymes• I AminotransferasesI Aminotransferases99

• Aspartate aminotransferase (A!*, also sometimestermed !<=*) and alanine aminotransferase (AL*,also sometimes termed !<*) are 'idelydistributed in cells throughout the body. A!* isfound primarily in heart, liver, s7eletal muscle, and

7idney, 'hile AL* is found primarily in liver and 7idney,'ith lesser amounts in heart and s7eletal muscle.

• A!* and AL* activity in liver are about >,222 and5,222 times serum activities, respectively . AL* is

exclusively cytoplasmic- both mitochondrial andcytoplasmic forms of A!* are found in all cells.

• *he halflife of total A!* is 1> ? @ hours, 'hile thatof AL* is 3> ? 12 hours . *he halflife ofmitochondrial A!* averages > hours .



Aminotransferases contin.. Aminotransferases contin..

• In adults, A!* and AL* activities are significantlyhigher in males than in females, and referenceintervals vary 'ith age.

• 6ntil about age 1@, A!* activity is slightly higher than

that of AL*, 'ith the pattern reversing by age 1@ inmales but persisting till age 42 in females . In adults, A!* activity tends to be lo'er than that of AL* untilapproximately age B2, 'hen they become roughlyeCual.

• Liver disease is the most important cause ofincreased AL* activity and a common cause ofincreased A!* activity. A number of factors otherthan liver disease affect A!* and AL* activities.



Aminotransferases contin.. Aminotransferases contin..

• In hepatocytesIn hepatocytes AL* AL* is found exclusively inis found exclusively incytoplasmcytoplasm 'hile'hile A!* A!* exists inexists in bothbothcytoplasmcytoplasm and mitochondriaand mitochondria..

• In acute viral hepatitis ,there is mar7edIn acute viral hepatitis ,there is mar7edelevation of AL* and A!*elevation of AL* and A!* (12122 times).(12122 times). *he rise of AL* is usually more than*he rise of AL* is usually more than

A!*(AL*$A!* ratioD1)because more A!*(AL*$A!* ratioD1)because moredamage of cytoplasmdamage of cytoplasm .. oe*e' se'u#oe*e' se'u#AST has a sho'te' half life /01 hou')AST has a sho'te' half life /01 hou')than ALT/21 hou') an+ thus AST isthan ALT/21 hou') an+ thus AST isuse+ in follo u! an+ to assessuse+ in follo u! an+ to assess'eco*e'y of acute *i'al he!atitis-'eco*e'y of acute *i'al he!atitis-



Aminotransferases /ontin,, Aminotransferases /ontin,,

• In liver cirrhosis ,there is mild to moderateIn liver cirrhosis ,there is mild to moderate

elevation of AL* and A!*elevation of AL* and A!* (4@ folds).(4@ folds). *he rise of*he rise of

A!* is more than AL*(AL*$A!* ratio is E1) A!* is more than AL*(AL*$A!* ratio is E1)because the damage affecting the mitochondriabecause the damage affecting the mitochondria

of liver cells 'ith release of more A!*.of liver cells 'ith release of more A!*.

• In chronic active hepatitis ,there is also mild toIn chronic active hepatitis ,there is also mild to

moderate elevation of AL* and A!* 'ithmoderate elevation of AL* and A!* 'ith AL*$A!* ratio D1. AL*$A!* ratio D1.



AST ALT

cataly3e t'ansfe' a#ino$'ou!s to fo'# !y'u*ate

cataly3e t'ansfe' a#ino$'ou!s to fo'# o.aloacetate

cytosol /456) an+

#itochon+'ia /756)

cytosol

T0%4 01 h'- /cytosol)

71 h'- /#itochon+'ia)

T0%4 21 h'-

li*e', ca'+iac #uscle,

s8eletal #uscle, 8i+neys,"'ain, !anc'eas, lun$s,leucocytes, an+ R9C

lo concent'ation in othe'

tissues



AST%ALT 'atioAST%ALT 'atio

• 0 : #a;o'ity of li*e' +isease 0 : #a;o'ity of li*e' +isease

• <4<4

& e.t'ahe!atic sou'cee.t'ahe!atic sou'ce & alcoholic he!atitisalcoholic he!atitis & ische#ic an+ to.inische#ic an+ to.in & acute =ilson>s +isease : he#olysisacute =ilson>s +isease : he#olysis

& ci''hosisci''hosis• <2 : ful#inant =ilson>s +isease<2 : ful#inant =ilson>s +isease



IIAl7aline phosphatase (AL) andIIAl7aline phosphatase (AL) and

gammaglutamyl transferase(<<*)gammaglutamyl transferase(<<*)

• *hese en"ymes are found in biliary tract*hese en"ymes are found in biliary tract

epithelium. In cholestasis (obstructiveepithelium. In cholestasis (obstructive

:aundice) and space occupying lesions in :aundice) and space occupying lesions inliver (As in cancer) there is mar7edliver (As in cancer) there is mar7ed

elevation of these en"ymeselevation of these en"ymes (more than 5(more than 5

folds).folds). *his mar7ed rise is due to increase*his mar7ed rise is due to increaseen"yme synthesis by cells lining biliaryen"yme synthesis by cells lining biliary

canaliculi. AL activity decreased aftercanaliculi. AL activity decreased after

blood transfusions (chelation of g, Fn)blood transfusions (chelation of g, Fn)



AL and <<* contin AL and <<* continGG

• !light to moderate elevation!light to moderate elevation (14 fold)(14 fold) occur inoccur inpatients 'ith parenchymal liver diseases such aspatients 'ith parenchymal liver diseases such ashepatitis and cirrhosis.hepatitis and cirrhosis.

• <<* is<<* is more specificmore specific for liver disease than AL.for liver disease than AL.*he latter is also increase in non hepatic*he latter is also increase in non hepaticdisorders as bone diseases (ric7etsdisorders as bone diseases (ric7ets,osteomalacia). <<* also provides a,osteomalacia). <<* also provides a moremore sensitive indexsensitive index of cholestasis than AL.of cholestasis than AL.%levated levels of <<* are also seen in%levated levels of <<* are also seen in

alcoholic even 'ith normal liver.alcoholic even 'ith normal liver.• Another en"yme called @Hnucleotidase is Another en"yme called @Hnucleotidase is moremore specific for cholestasis than ALspecific for cholestasis than AL but its use isbut its use isnot popular.not popular.



5;ilirubin5;ilirubin

• ;ilirubin is the end product of heme degradation;ilirubin is the end product of heme degradation

• eme oxygenase oxidi"es heme to biliverdin,eme oxygenase oxidi"es heme to biliverdin,

and biliverdin reductase reduce biliverdin toand biliverdin reductase reduce biliverdin tobilirubinbilirubin

• epatocellular processing of bilirubin involvesepatocellular processing of bilirubin involves

/arrier mediated /arrier mediated upta7eupta7e by hepatic cellsby hepatic cells

/on:ugation/on:ugation 'ith 6<* (uridine diphosphate'ith 6<* (uridine diphosphate

glucuronosyltransferase)glucuronosyltransferase)

%xcretion%xcretion into bileinto bile



;ilirubin contin,,,;ilirubin contin,,,

• *he gut bacterial ;glucuronidases decon:ugate*he gut bacterial ;glucuronidases decon:ugatemost bilirubin to colorless urobilinogenmost bilirubin to colorless urobilinogen

• *he urobilinogen are largely excreted in feces as*he urobilinogen are largely excreted in feces asstercobilinogen and stercobilin.stercobilinogen and stercobilin.

• 42 of urobilinogen are reabsorbed in the ileum42 of urobilinogen are reabsorbed in the ileumand colon and escape enterohepatic circulationand colon and escape enterohepatic circulationand pass to the 7idney to be excreted in urineand pass to the 7idney to be excreted in urine

• ;ile acids (cholicJchenodeoxy cholic acids) are;ile acids (cholicJchenodeoxy cholic acids) arederived from cholesterol and secreted in bile.derived from cholesterol and secreted in bile.ost of them are reabsorbed, especially in theost of them are reabsorbed, especially in theileum and returned to the liver for resecretionileum and returned to the liver for resecretionagain (enterohepatic circulation)again (enterohepatic circulation)

• *he focal loss of bile acids is 2.4 to 2.B gm$day*he focal loss of bile acids is 2.4 to 2.B gm$day



• 6ncon:ugated bilirubin6ncon:ugated bilirubin is insoluble in 'ater andis insoluble in 'ater andis tightly complexed to serum albumin andis tightly complexed to serum albumin and notnot

excreted in urineexcreted in urine• /on:ugated bilirubin/on:ugated bilirubin is 'ater soluble, non toxic,is 'ater soluble, non toxic,and only loosely bound to albumin andand only loosely bound to albumin and excretedexcreted in urine.in urine.

• *he rate of systemic bilirubin production eCual to*he rate of systemic bilirubin production eCual tothe rate of hepatic upta7e, con:ugation andthe rate of hepatic upta7e, con:ugation andbiliary excretionbiliary excretion

• Kaundice occur 'hen the eCuilibrium bet'eenKaundice occur 'hen the eCuilibrium bet'eenproduction and clearance is disturbed e.g.production and clearance is disturbed e.g.

excessive production, reduced hepatic upta7e,excessive production, reduced hepatic upta7e,impaired con:ugation, decreased hepatocellularimpaired con:ugation, decreased hepatocellularexcretion and impaired bile flo'excretion and impaired bile flo'

• *he most common causes are uncon:ugated*he most common causes are uncon:ugated

hyperbilirubinemia, con:ugatedhyperbilirubinemia, con:ugatedhyperbilirubinemia and mixed hyperbilirubinemiahyperbilirubinemia and mixed hyperbilirubinemia



1 6ncon:ugated hyperbilirubinemia1 6ncon:ugated hyperbilirubinemia

• A? O*e'!'o+uctionA? O*e'!'o+uction

e#olytic anae#iae#olytic anae#ia

Ineffecti*e e'yth'o!oiesisIneffecti*e e'yth'o!oiesis• 9? @ec'eases u!ta8e9? @ec'eases u!ta8e

• <ilbert syndrome<ilbert syndrome

#elatively common& ;enign course#elatively common& ;enign course /ongenital defect of en"ymes or binding/ongenital defect of en"ymes or binding

proteins ( no evidence of hemolysis)proteins ( no evidence of hemolysis)



1 6ncon:ugated hyperbilirubinemia1 6ncon:ugated hyperbilirubinemia

• C? +ec'ease con;u$ationC? +ec'ease con;u$ation

hysiologic :aundice (+eonatal :aundice)hysiologic :aundice (+eonatal :aundice)

/rigler+a::ar syndrome type 1. /omplete/rigler+a::ar syndrome type 1. /ompleteabsence of 6<*. 8atal 'ithin 1 months ofabsence of 6<*. 8atal 'ithin 1 months of

birth. ;ilirubin more than 42 mg$dl.birth. ;ilirubin more than 42 mg$dl.

/rigler+a::ar syndrome type 11. artial/rigler+a::ar syndrome type 11. artial

deficiency of 6<*.;ilirubin less than 42 mg$dl.deficiency of 6<*.;ilirubin less than 42 mg$dl.



4 /on:ugated hyperbilirubinemia4 /on:ugated hyperbilirubinemia

• A? I#!ai'e+ sec'etion:A? I#!ai'e+ sec'etion: @efect of@efect of"ili'u"in t'ansfe' into "ile-"ili'u"in t'ansfe' into "ile-

@o"in onson syn+'o#e@o"in onson syn+'o#e: he'e+ita'y: he'e+ita'y+iso'+e' of "ili'u"in sec'etion- Li*e' is+iso'+e' of "ili'u"in sec'etion- Li*e' is+a'8ly !i$#ente+-+a'8ly !i$#ente+-

Roto' Syn+'o#eRoto' Syn+'o#e: usually: usuallyasy#!to#atic- Li*e' is not !i$#ente+-asy#!to#atic- Li*e' is not !i$#ente+-



4 /on:ugated hyperbilirubinemia4 /on:ugated hyperbilirubinemia

• 9? Cholestasis:9? Cholestasis: due todue to int'ahe!aticint'ahe!atic oror

e.t'ahe!atice.t'ahe!atic obstructionobstruction

• Int'ahe!atic +ue to :Int'ahe!atic +ue to : hepatic malignancy orhepatic malignancy orinfiltration, primary biliary cirrhosis, biliaryinfiltration, primary biliary cirrhosis, biliary

atresia, cholangitis and drugs (chloroproma"ineatresia, cholangitis and drugs (chloroproma"ine

and some steroids)and some steroids)

• E.t'ahe!atic:E.t'ahe!atic: inclu+einclu+e gallstones and cancergallstones and cancerhead of pancreas and external pressure byhead of pancreas and external pressure by

lymph nodes or tumorslymph nodes or tumors



5 /on:ugated and uncon:ugated5 /on:ugated and uncon:ugated

hyperbilirubinemia (hepatic :aundice)hyperbilirubinemia (hepatic :aundice)

• ue to hepatocellular diseasesue to hepatocellular diseases

acute viral hepatitis,acute viral hepatitis,

cirrhosis,cirrhosis,

hepatic failure,hepatic failure,

toxix hepatitis due to some drugstoxix hepatitis due to some drugs

(halothan and paracetamol)(halothan and paracetamol)



3 rothrombin time(*)3 rothrombin time(*)

• *he liver is the ma:or site of synthesis of*he liver is the ma:or site of synthesis ofcoagulation factors. * is dependent oncoagulation factors. * is dependent on

normal hepatic synthesis of coagulationnormal hepatic synthesis of coagulationfactors (I, II,V,VII and M). any of thesefactors (I, II,V,VII and M). any of thesefactors are vitamin N dependant.factors are vitamin N dependant.rolongation of * in liver disease may berolongation of * in liver disease may be

due to impaired synthesis of clottingdue to impaired synthesis of clottingfactors or impaired absorption of vitaminfactors or impaired absorption of vitaminN.N.



* contin,G* contin,G

• 1 Impaired synthesis of clotting factors91 Impaired synthesis of clotting factors9 As in chronic liver diseases (cirrhosis). ;ecause As in chronic liver diseases (cirrhosis). ;ecause

these factors have a shorter half life thanthese factors have a shorter half life thanalbumin * may be an earlier indicator of severealbumin * may be an earlier indicator of severeliver in:ury than albumin and is useful to assessliver in:ury than albumin and is useful to assessseverity and prognosis of chronic liver disorders.severity and prognosis of chronic liver disorders.

• 4 Impaired absorption of Vit N 94 Impaired absorption of Vit N 9 due todue toobstructive :aundice and thus there is failure ofobstructive :aundice and thus there is failure ofvit N absorption. *his condition can bevit N absorption. *his condition can be

distinguished from impaired hepatic synthesis bydistinguished from impaired hepatic synthesis byreassay of * after parenteral in:ection of Vit N,ifreassay of * after parenteral in:ection of Vit N,ifit is normali"e this indicate cholestasis and notit is normali"e this indicate cholestasis and notdecrease liver synthesisdecrease liver synthesis



A=+IA A=+IA

• ItHs a metabolite of nitrogen containingItHs a metabolite of nitrogen containing

products.products.

• Its metabolised to urea in liver via Nrebs cycle.Its metabolised to urea in liver via Nrebs cycle.• Increased 'ith liver failure, portal *+Increased 'ith liver failure, portal *+

• Increased in brain in hepatic encephalopathyIncreased in brain in hepatic encephalopathy

• Very high levels are seen in fulminant liverVery high levels are seen in fulminant liver

failure, signifying poor prognosis.failure, signifying poor prognosis.



Laboratory changes in some liver diseasesLaboratory changes in some liver diseases

• Acute viral hepatitis9 Acute viral hepatitis9

1 reicteric stage91 reicteric stage9

AL* is increase early in is more sensitive and AL* is increase early in is more sensitive andspecific than A!*. ;ilirubin is still normal.specific than A!*. ;ilirubin is still normal.

4 Icteric stage94 Icteric stage9 ar7ed elevation of AL* and A!* and AL*$A!*ar7ed elevation of AL* and A!* and AL*$A!*ratioD1.ratioD1.

Increase both direct and indirect bilirubin (fe'Increase both direct and indirect bilirubin (fe'cases are Anicteric and bilirubin is normal).cases are Anicteric and bilirubin is normal).

AL and <<* sho'ed mild increase. AL and <<* sho'ed mild increase.

Albumin is normal Albumin is normal

* is prolonged only in severe fulminated* is prolonged only in severe fulminated

cases.cases.

6rine 9 is dar7 bro'n ositive for bilirubin and bile6rine 9 is dar7 bro'n ositive for bilirubin and bile



Acute viral hepatitis contin,,, Acute viral hepatitis contin,,,

• 5#ecvery95#ecvery9 increase urine urobilinogen.increase urine urobilinogen.

• Liver en"ymes start to decline and follo' up isLiver en"ymes start to decline and follo' up isbetter done by A!* because of shorter half lifebetter done by A!* because of shorter half life

• Immunological iagnosis9Immunological iagnosis9• acute viral hepatitis is mainly due toacute viral hepatitis is mainly due to AVAV (self(self

limited and not proceed to chronicity) orlimited and not proceed to chronicity) or;V;V( may lead to chronicity). =ther viruses may( may lead to chronicity). =ther viruses may

be also responsible as /V ,%V,..be also responsible as /V ,%V,..• AV Ig ( mar7er of recent infection)AV Ig ( mar7er of recent infection)

• ;sAg, bcAb Ig (mar7ers of recent;sAg, bcAb Ig (mar7ers of recentinfection)infection)



Acute Hepatitis B Virus Infection with Recovery

Typical Serologic Course of HBV

Weeks after Exposure

Titer

Sy#!to#s

9eA$ anti?9e

Total anti?9c

I$B anti?9c anti?9s9sA$

5 2 7 04 0 45 42 47 D4 D 4 055



UNUSUAL CAUSES OF ACUTEUNUSUAL CAUSES OF ACUTE

EPATITISEPATITIS

O Autoimmune hepatitis & up to 4@ have

acute presentation- clues include more

prolonged A!*$AL* elevation, lo' albumin,high total protein

O PilsonHs disaese & often fulminant 'hen

acute- clues include acute renal failure,

hemolytic anemia, lo' al7aline phosphatase

(Neyser8leischer rings usually absent)



/hronic active hepatitis/hronic active hepatitis

• It may be due to viral infection (;V orIt may be due to viral infection (;V or

/V) or autoimmune./V) or autoimmune.

• Albumin is lo' and gamma globulin is high Albumin is lo' and gamma globulin is high(Ig< mainly).(Ig< mainly).

• ild elevation of AL* and A!* (AL*DA!*)ild elevation of AL* and A!* (AL*DA!*)

• Auto antibodies may be found particularly Auto antibodies may be found particularlyin autoimmune type.(A+A.A!A,LN2in autoimmune type.(A+A.A!A,LN2



*ype 19 A+A, antismooth muscle$antiactin

*ype 49 antiliver 7idney microsome (LN1)-rare in 6!, usually teens$young 'omen

*ype 59 antisoluble liver antigen liver

pancreas, !LA)- rare in 6!



=ILSON>S @ISEASE

Autosomal recessive mutations in A*ase

(copper attachment)- multiple mutations,usually compound hetero"ygotes

O 6sually liver and$or neuropsychiatric

presentations- often in teens or youngadults, rarely older

O /eruloplasmin best screening test (lo')-

may be lo' 'ith cirrhosis regardless of cause, acute phase response protein so

falsely normal 'ith acute inflammation

e'en a on e een e'en y!es oe'en a on e een e'en y!es o



e'en a on e een e'en y!es oe'en a on e een e'en y!es o

ch'onic he!atitisch'onic he!atitis Fin+in$sFin+in$s Autoi##uneAutoi##une 9V9V CVCV

Se.Se. fe#alefe#ale #ale#ale eualeual

A$eA$e 0?40?4 ol+e' ol+e' allall

9sA$9sA$ ?*e?*e *e*e ?*e?*e

CV A"CV A" ?*e?*e ?*e?*e *e*e

Autoi##uneAutoi##une+iseases+iseases

f'euentf'euent 'a'e'a'e occasionaloccasional

Autoanti"o+ieAutoanti"o+ies /ANA,ASBA,s /ANA,ASBA,

LHBLHB

i$h tit'ei$h tit'e Lo o'Lo o'a"senta"sent

Lo o'Lo o'a"senta"sent

Ris8 of cance' Ris8 of cance' lolo hi$hhi$h hi$hhi$h



/irrhosis/irrhosis

• Albumin is lo' and gamma globulin is high 'ith Albumin is lo' and gamma globulin is high 'ithreversed A$< ratio. *otal protein is variablereversed A$< ratio. *otal protein is variable

• !%9 polyclonal increase of gamma globulin 'ith!%9 polyclonal increase of gamma globulin 'ithbeta gamma bridgebeta gamma bridge (due to increase of IgA(due to increase of IgA

mainly).mainly).• ild to moderate elevation of A!* and AL*ild to moderate elevation of A!* and AL*

(A!*DAL*).(A!*DAL*).

• AL is normal or mild increase. AL is normal or mild increase.

• <<* is mild increased (specially alcoholic).<<* is mild increased (specially alcoholic).• ;ilirubin is usually normal or;ilirubin is usually normal or (in late sta$es(in late sta$es..

• Pt is !'olon$e+ ant not co''ecte+ "y Vit HPt is !'olon$e+ ant not co''ecte+ "y Vit H



epatic failureepatic failure

• =ccur in severe decompensated cirrhosis 'ith=ccur in severe decompensated cirrhosis 'ith

the follo'ing findings are usually found-the follo'ing findings are usually found-

• Kaundice 'ith moreKaundice 'ith more QQ of bilirubin (both types).of bilirubin (both types).• ore rise of transaminases (AL*,A!*)ore rise of transaminases (AL*,A!*)

• ar7ed prolongation of *.ar7ed prolongation of *.

• ecrease urea, glucose, potassium ,andecrease urea, glucose, potassium ,andcholesterol 'ith mar7edcholesterol 'ith mar7ed &of al"u#in&of al"u#in..

• Inc'ease a##onia /!o'toca*al anasto#osis)Inc'ease a##onia /!o'toca*al anasto#osis)



epatic infiltrationsepatic infiltrations

• ue to space occupying lesions as in tumors,ue to space occupying lesions as in tumors,primary or secondaries, cysts, lymph nodes andprimary or secondaries, cysts, lymph nodes andothers.others.

• ar7ed elevation of <<* and AL.ar7ed elevation of <<* and AL.

• ;ilirubin may be normal;ilirubin may be normal (partial obstruction allo'(partial obstruction allo'passage of bilirubin and stimulates synthesis ofpassage of bilirubin and stimulates synthesis of AL and <<*). AL and <<*).

• +ormal or slight increase of A!* and AL*+ormal or slight increase of A!* and AL*(A!*DAL*)(A!*DAL*)

• *umor mar7ers9*umor mar7ers9QQ A8 in //, A8 in //,(CEA in GIT(CEA in GITcance' ith li*e' secon+a'iescance' ith li*e' secon+a'ies



/holestasis (obstructive :aundice)/holestasis (obstructive :aundice)

• Increase bilirubin (mainlyIncrease bilirubin (mainly direct or con:ugateddirect or con:ugated))

• ar7ed rise of <<* and ALar7ed rise of <<* and AL

• +ormal AL* and A!* except in late stages 'ith+ormal AL* and A!* except in late stages 'ith

secondary liver cell damage from bile.secondary liver cell damage from bile.• 6rine9 dar7 (positive for bilirubin and bile salts6rine9 dar7 (positive for bilirubin and bile salts

and negative urobilinogen).!tool is clay color.and negative urobilinogen).!tool is clay color.

• * is prolonged and can be corrected by Vit N* is prolonged and can be corrected by Vit N

in:ection. (mal absorption of fat soluble Vit)in:ection. (mal absorption of fat soluble Vit)• Increase cholesterol and ; lipoproteins.Increase cholesterol and ; lipoproteins.

• ruritis, itching and s7in xanthoma are commonruritis, itching and s7in xanthoma are common



emolytic :aundiceemolytic :aundice

• Increase bilirubin (Increase bilirubin ( indirect or uncon:ugatedindirect or uncon:ugated type)type)

• Increase urobilinogen in urine.Increase urobilinogen in urine.• 6rine is normal in color (absent bilirubin,6rine is normal in color (absent bilirubin,because indirect type is not excreted in urine)because indirect type is not excreted in urine)

• !tool is dar7 (increase stercobilin)!tool is dar7 (increase stercobilin)

• No'#al li*e' en3y#es o' only sli$ht ( of ASTNo'#al li*e' en3y#es o' only sli$ht ( of AST/!'esent in R9Cs)/!'esent in R9Cs)

• E*i+ence of he#olysis: ('eticulocytesE*i+ence of he#olysis: ('eticulocytes,..,..



epatic :aundiceepatic :aundice

• *he laboratory findings are similar to that*he laboratory findings are similar to that

mentioned in viral hepatitis 'ith increasementioned in viral hepatitis 'ith increase

of both types of bilirubinof both types of bilirubin (direct and(direct and indirect)indirect)

• ar7 urine (positive for bilirubin)ar7 urine (positive for bilirubin)

Fin+in$sFin+in$s e#olytice#olytic O"st'ucti*O"st'ucti* e!atice!atic



Fin+in$sFin+in$s e#olytice#olytic ;aun+ice ;aun+ice

O"st'ucti*O"st'ucti*e ;aun+icee ;aun+ice

e!atice!atic ;aun+ice ;aun+ice

S- 9ili'u"inS- 9ili'u"in (( in+i'ectin+i'ect (( +i'ect+i'ect (( "oth"oth

U'o"ilino$eU'o"ilino$enn

(( && (( in ea'lyin ea'lysta$es,sta$es,then &then &

U'ineU'ine"ili'u"in"ili'u"in

a"senta"sent P'esentP'esent !'esent!'esent

U'ine "ileU'ine "ilesaltssalts

a"senta"sent P'esentP'esent P'esentP'esent

U'ine colo' U'ine colo'

Stool colo' Stool colo'

No'#alNo'#al

+a'8+a'8

@a'8@a'8

clayclay

@a'8@a'8

clayclay

liver function مهم - copy

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