A Review of Liver Anatomy and Physiology

7/24/2019 A Review of Liver Anatomy and Physiology

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A Review of Liver Anatomy

and PhysiologyBy,

Dr. Arun Kumar B.S.

PG, Dept of Anesthesiology

!"

!oderator# Dr. !alli$ar%un


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&R'('A

Largest internal organ weighing appro) *.+*.-$g adult i.e + &B/, - in neonates.

Reddish 0rown triangular pyramid shaped, in

rt. 1ypo2hondrium and most of epigastrium. 1eld to pla2e 0y ligaments 3folds of

peritoneum4,hepatogastri2, hepatoduodenal,

lateral, fal2iform ligs, o0literated vessels li$e

ligamentum teres3um0ili2al vein4,ligamentum venosus3du2tus venosum4.


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!a2ro Anatomy

5or anatomi2ally divided into + left and rightlo0es with right 0eing 0igger.

5un2tionally divided into lo0es 0y the portal

vein into 6 lo0es. 7a2h lo0e having a portal vein, 0ran2h of

hepati2 artery and a 0ile 2anali2uli.

&he 0iliary system rt and lt hepati2 du2ts whi2h

2om0ine to form 2ommon hepati2 du2t drainsto the gall 0ladder 0y 2ysti2 du2ts.

Gall 82m in length, 2apa2ity of -9ml, 0ld supplyfrom 2ysti2 artery, 0ran2h of hepati2 artery.

Sphin2ter of :DD' is at the duodenal opening.


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5un2tional units !i2roAnatomy Des2ri0ed in 2lassi2 lo0ule stru2ture

0y Kiernan as early as *6;;. ashe)agonal str. /ith portal triads

forming angle %oints.

now its des2ri0ed as Rappaport


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!i2roanatomy 2ontd=.

5un2tionality is 0ased on the >ow of 0loodfrom the vessels towards the 2entrilo0ularveins.

&hree ?ones with ?one * high o)ygenationand ?one ; prone for hypo)i2 in%ury.

't is here all rea2tions in the liver ta$ingpla2e.

@one * periportal region, all rea2tions in0iotransformation is here esp. 2yt P-9en?yme 0ased.


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1epati2 ultrastru2ture

"ells li$e Kuppfer 2ells, >oatingma2rophages,

Stellate 2ells.


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1epati2 0lood supply

Dual supply of Portal vein and1epati2 artery.

Portal vein --9 of the total 0lood,- o)ygenation, hepati2 artery -9 of total 0lood 0ut 9o)ygenation.

1epati2 artery 0uCerresponse3hemire2ipro2al re>e)4.

!iddle, right and left hepati2 veins

ta$e the 0lood away from the liver


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1ABR

Also 2alled hemire2ipro2al response

Pressure >ow relationship 0etweenportal vein and hepati2 artery.

Portal venous >ow redu2ed thenthere is redu2tion in hepati2 arteryresistan2e.

But not vi2e versa.

Adenosine is suggested to 0e themediator of this response.


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5a2tors in2reasing hepati2 0lood >ow#feeding, glu2agon, hyper2apnia,re2um0ent position, hepato2ellular

en?yme indu2tion, a2. 1epatitis.

5a2tors de2reasing# Anestheti2agents, surgi2al trauma, 'PP(, P77P,

0et adrenergi2 0lo2$ade,1ypo2apnia, (asopressin.


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7Ce2t of regional Anesthesia#redu2tion in the 0lood >ow parallelsredu2tion in the systemi2 !AP.

Kennedy et al # &- 0lo2$ade redu2ed>ow 0y +; of the 2ontrol.

'nhalational# 1alothane greatestredu2tion in portal, arterial and totalhep 0lood >ow.

Attenuates 1ABR.

Des, sevo>urane maintained 0lood


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7Ce2t of intravenous agents#thiopentone, etomidate, propofolprodu2es dose dependant redu2tion

in the hepati2 0lood >ow.


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R7('7/ :5 AA&:! AD

P1S':L:G

5E"&':S :5 &17L'(7R#"ar0ohydrate

meta0olismGly2ogenesis

Gly2ogenolysis

Glu2oneogenesis

5at meta0olism $etogenesis

Protein meta0olismana0olism

deamination

urea formation

Secretion of bileDetoxication

Metabolism ofvitamins A,D,K,E

&Clotting factors,

esp prothrom0in

Storage

Blood store


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1eme meta0olism

!ain site.

1emoglo0in is heme and glo0ulin,with heme 2ontaining ferrous andporphyrin 'F.

+9 appro), heme synthesised in theliver.

Rate limiting step is synthesis of -aminolevulini2 a2id 2atalysed 0y ALAsynthetase.


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Biliru0in meta0olism

Sour2e is from the 1eme meta0olism.

Appro) ;99mg of 0iliru0in formed everyday.

69 0y the phagosytosis of s2ene2ent RB"s 0y

the R7 2ells. &he e)tra2ted heme is 2onverted to 0iliru0in, this

is the rate limiting step.

&his is then 0ound to al0umin and liver pro2essesthe mole2ules into 2on%ugated 0iliru0in in + steps,and then e)2reted.

7nterohepati2 2ir2ulation ensures some of theseprodu2ts to return to the liver.


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Feno0ioti2Biotransformation 't is divided into

Phase ' rea2tion.

Phase '' rea2tion. Phase ''' rea2tion.


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P1AS7 ' R7A"&':

't is o)idative, hydrolysis,

redu2tion rea2tions.

't is mainly mi2rosomal o)idases, "P

iso?ymes super family. &hese "P iso?ymes are 2on2entrated in the

2entrilo0ular ?one.

't needs ADP1 for its rea2tions and hen2eformation of supero)ides and rea2tive freeradi2als, more 2han2e of in%ury to these2ells, ne2rosis.


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"P -9 inhi0itors

Grapefruit %ui2e.

erythromy2in,

isonia?id, sulfonamides,

$eto2ona?ole


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P1AS7 '' R7A"&':

"on%ugation with the endogenoushydrophili2 mole2ules.

't involves several pro2esses su2h asglu2uronidation, sulphation,methylation, a2etylation.

Glu2uronidation is the 2ommon type.

1epati2 mi2rosomal uridinediphosphate glu2uronyl transferasemediates the rea2tion.


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P1AS7 '' 2ontd=

&hese are sus2epti0le to en?yme indu2tion.

1eavy smo$ing, phenytoin admistrationseen to in2rease glu2uronidation in humans.

'n some drugs the 2on%ugation ends up witha meta0olite more potent than the parentdrug. 7g# morphine 0e2omes morpine glu2uronide a potent 0yprodu2t whi2h is

responsi0le for some of the analgesiaprodu2ed 0y morphine.


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P1AS7 ''' R7A"&':

't is a energy mediated transportH elimination.

0y A&P 0inding 2assette transport proteins.

5a2ilitates e)2retion of )eno0ioti2s and

endogenous 2ompounds. &hese proteins use A&P hydrolysis to drive

mole2ular transport.

&hese resides on the 2anali2ular surfa2es of

hepato2ytes and ena0les 0iliary e)2retion of2ationi2 2ompounds, in2luding anti2an2er

drugs.


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Factors affecting Drug

BiotransformationGenetic factors

Diet

Environment

Age

Enzyme Induction/Inhibition

Liver disease

Cardiac disease


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1epati2 drug 2learan2e

5a2tors # rate of hepati2 0lood >ow, protein0inding, hepati2 intrinsi2 2learan2e.

7)tra2tion ratio374# amt of drug removed

from the 0lood during a simple pass throughthe liver.

Anestheti2s signiI2antly alter e)tra2tion 0yredu2ing hepati2 0lood >ow. 7sp inhalational

agents. Also inhi0ition of "P and Phase ii rea2tions.


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L'(7R 5E"&': &7S&S

A'!# to identify hepati2 a0normality

to diCerentiate hepati2

o0sH2holestati2 disease. Assess the severity of hepati2

a0normality.

'dentify the spe2iI2 2ause. 'nvestigate the possi0le

2ompli2ations.


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L5& 2ontd=

&his group of tests in2lude serum0iliru0in, SG:&, SGP&, Al$P:, totalprotiens in2luding Al0umin, glo0ulin

and AHG ratio.

&hese are the 0io2hemi2al

mar$ers.


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Serum Biliru0in

't 2omprises of total 0iliru0in, indire2t0iliru0in and dire2t 0iliru0in.

'ndire2t is also un2on%ugated 0iliru0in

normal value is# 9.*9.-mgHdl Dire2t is 2on%ugated or water solu0le

0iliru0in, normal value# 9.*9.-mgHdl

&otal 0iliru0in normal value#9.+*.+mgHdl

't is in2reased more rapidly in primary 0iliarydisease than hepati2 disease32irrhosis4.


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Al0umin

Produ2ed in the liver.

Plasma half life is + wee$s.

1en2e may not 0e seen in a2ute liverfailure 0ut deInitely seen in 2hroni2liver failure.

ormal value# ;.+-gHdl


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SGP&HSG:&3AS&HALP4

&hese are the en?ymes in the hepati22ells mainly the mito2hondria.

1en2e when these en?ymes are seenin the 2ir2ulation they denotehepato2ellular damage.

ormal value J9.


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Al$aline phosphate

&his is a 2olle2tion of en?ymes whi2h 2leavephosphate esters in the al$aline environment.

't is present in liver, 0ones, G'& et2..

Endergo post trans2riptional modiI2ations in theliver.

Present in the 0iliary 2anali2uli and 2ellmem0ranes of hepati2 sinusoids.

1en2e the raise indi2ates pathology in theintraHe)tra hepati2 0iliary o0s., and sinusoid o0s.

ormal value# 9*+9mgHdl


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'&7RPR7&A&':

SGOT/SGT !"#"$%!" A#KO'

B'L'AR :BS

17PA&'&'S

AL":1:LHDREGS

H


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:ther tests

"B" 10 may show anemia esp with thetarget 2ells in %aundi2ed patients due toma2ro2ytosis.

Leu2openia 2ompli2ates portal 1& andhypersplenism.

Leu2o2ytosis in hepati2 a0s2ess, al2oholi2hepatitis, 2holangitis.

&hrom0o2ytopenia in 2irrhosis, due to de2in throm0opoetin in liver, andhypersplenism.


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:ther tests= 2ontd=

"oagulation# K dependent fa2tors.

ormal half life is -+ hrs, hen2e2an 0e seen in 2hr.liver diseases,prothrom0in time, 'R raised.


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&a$e home msg

Liver is a important organ, whi2h asan anesthesiologist should $now as awhole.

Epto ;9 normal liver is essential fornormal fun2tion.

Dual 0lood supply, upto +l of 0lood

pumped into it. umerous fun2tions, whi2h 2an 0e

hampered 0y various pro2esses,

drugs.


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&ests to 2onIrm these disordersshould 0e as$ed for in patients with2hroni2 diseases, and ha0its.

And 0ased on whi2h the anestheti2drugs should 0e titrated, eitherredu2e the dosage or in2rease the

time interval of adminstration.


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GRA&'&ED7

!illers Anesthesia thedition vol *.

Prys Ro0erts te)t0oo$ of Anesthesia+ndedition.

Davidson


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&1AK :E

A Review of Liver Anatomy and Physiology

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