Ja R a MD MPH

These enzymes B Colerialefrom normal

when the liver is neat functioning
property

• A pa a e Amino an fe a e AST
• L ca ed ch d a
Enzymesfoundin the liver that
• Ac h ch d a transfer nitrogengroupsbetween
• AST ALT a c h c he a aminoacids
will
a
BITboth
beelevated • Alanine Amino an fe a e ALT The level of these enzymes
9when there is damage to
• L ca ed c a the liver
• ALT AST e f he a h ce a da age
 These enzymes B Colerialefrom normal
when the liver is neat functioning
properly

• Alkaline pho pha a e Alk Pho

• E ef e b e GI ac
• P ec e f c
• he h b c ed b e ch e a
• Se e e e h ch e a 2
when there is obstruction
• Le e e a e c d to bile flow bile duct
more
epithelium will develop
• P eg a c ace a
of this enzyme it serum
• Th d d ea e levelswill rise
• B e d ea e
 Helps us identifywhether
alk pros has 9 due to
• Gamma gl am l an pep ida e GGT hepatic
a hepatic er extra
problem
• S a a h b e e a ed b e d ea e
is in that it 4 incholestasis
• U ed de e e g fa h ee a
• A Ph GGT he a b a ca e f A Ph
• A e e a ed af e hea alcohol con mp ion But
I If 9 Alk pnos g
• N cleo ida e used todetermine
f whetherpatients normal a at then
similarto • B have beendrinking the p in Alk pnos
att this
b a d ec d ec is due to a bone
enzyme can problem
be usedto determine
the source of an AK
Phoselevation
 The tests measure how well the
liver is functioning
they measure something the
liver is supposed to produce
normally
Te fS he c F c

• Ab Albumin levelsfail if the liver is failing because its

the liver'sjob to produce albumin
• PT PTT c ag a fac 2
prothrombin time will
increase if the
• G c e liver is failingbecause its the
liver's
Jobto producecoagulationfactors
• Need e f g c ge b ea d a dg c e ge e
• Ab a e e e e e d ea e 2
so if the liver failsthen
glucose levels will fall

Abnormality in these testsuggests

that the liver isfailing
• Th ee a ac h e ha ca da age e
• A c h c fa e d ea e
• Ac e he a
• C h occurs due to
chronic consumption

W ed a P b c D a
 • Acc a f fa acid fa f a f e
• U a a a ca g hea d e
• Ma ca e he a ega e a
• Ab a LFT AST ALT Because alcohol is a mitochondrial
toxin AST is a mitochondrial enzyme
alcohol pathologies
• Of e e e b e h ce a f a c h only cause a greaterincrease
M AST
• fc h

Alcoholconsumption
leads to the
Ifat deposition
the hepatocytes
accumilationof fatty ywituin
acids

T NT N W ed a
 portal triad

cenmaf
Vien

Re a W ed a
Re a W ed a
 Fa infil a ion in
literal Alcoholic Li e Di ea e
begin he e
IEEE first al o fib o i in ci ho i

Zone I Zone II Zone III

most liver pathologiesaffect Pe ipo al Mid Zone Cen ilob la

Zone 3 Except viralnep it
tends to affect zone 1first
N a c h c Fa L e D ea e

• Fa f a f e d e ac h
• NAFL Fa e Non ALCOHOLICFAITH LIVER
• NASH S ea he a fa a d f a a Hepatitis
NON ALCOHOLIC STEATO
• Of e a a c
• Ab a LFT ALT AST
• Ma ge c h
• A c a ed h obe i
• Ma e h e gh
Acutehepatitis

• Ca ca cc af e hea b ge d g f
gh fac h c
• T c effec f ace aldeh de
2
• S acetaldehyde will accumilatein the
liverdue toheavyalcoholconsumption
• Fe e
• Ja d ce
• RUQ a e de e

Ae a d eN a d F
 Alcoholic liverdisease causes the
formation of Mallory bodies

• Ca ch a h g f d g a c h c e d ea e
• C a c c in the hepatocytes
2
• Da aged in e media e filamen he a c e

Mallory body

Ne h W ed a
 • Th b f he a c e blood cannot drain from the
liver the liver swells
• Abd a a a c e he a ega
due to back up of blood into the portalsystem which
• Zone c ge ec he hage leadsleakageof
fluid into the abdomen
• C ca e Polycythemia
Vera
p chronicmyelogenous
• M e fe a e d de P e a ET CML leukemia
• He a ce a ca c a essential
2
f thrombocythemia
the tumor
compresses
• OCP GP eg a c
use
the hepatic •
Vienspreventing
H oralecontraceptive
c ag ab e a e
blood flow
 back up of blood from the right heart into the
I
due
vena Cava will lead to swellingof the liver
• Ca d ac c h to the accumilation of blood 2

• Ra e ca e f e fa e this can lead to

aimnosis
• Ch c e ede a c h
• Re n meg li e
Fuseesto
• M ed e ea eg
Jta'S JEFF
the liver to be chronically
• A ee B dd Ch a swollen

Da d M a W ed a
• Ra e ca e f li e fail e a d encephalopa h
• Ch d e h a fec h a ea
• Ca ca ch c e a icella o e a d infl en a B
• Ra d e e e e fa e
• E de ce ha a pi in inhibi be a o ida ion
• M ch d a da age ee
• Fa cha ge e he a ega
• V g c a dea h
• A da ch d e e ce Ka a a
d
rare vasculitis that
responds well to aspirin
its a dangerous condition so the
benefit out ways the risk of
gettingReye'ssyndrome
 • I he ed a a co dominan
• Dec ea ed d f c a AAT
• AAT ba a ce a a cc g ea e

P ea e
destroytissues
A P ea e
f e g AAT
counteract the action
of proteases so that
they do NIT completely
destroy our tissues
 2
leads to auto digestion
• L g of the tissue
• Emph ema AAT will lead to early onset in someone who is a
smoker
• I ba a ce be non
ee e h e a a e de ea a d
ea a e hb AAT ec e a
a
• L e involvement is less common leads to the destruction of
than the liver the wing parachyme emphysema
• Ci ho i
• Ab a b d e e d a c e c it paymenses
in the ER
• Pa h g c pol me i a ion f AAT
leads to death
• Occ e d a c e c f he a c e of hepatocytes
 AAT e ain i h PAS I they stain purple
Re e i dige ion b dia a e AATis NOT brokendownbydiastase
e g c ge glycogenalso stain purple with
PAS stain glycogenstoragediseases
But
diastase will breakdown
the glycogen the purple
stains will go away
UNLIKE AAT

purpledeposites
within the hepatocytes
are pathological
polymers of AAT

Je ad M Ga d e MD
 • Wa ed ff fec f he e
• I he US a bac e a
E can travel to the
I • Bac e e a bacteria in the blood stream
8 liver potentiallyform an abscess
8 • Ch a g GN R d K eb e a f e de f ed a

1 EEEEEEEI.EE iEaniiFee
• En ameba hi ol ica a
• C c a a ed a e b d d a hea d e e
• A ce d he b a ee
• Echinococc he h
• Feca a ge f egg
• Ma e e c
O
He e h ff W ed a
• He a A B C D E
• Ve h gh AST ALT
• Of e a
• H e b b e a a d a d ce
• If e e e a ee ab a he c f c
• H g ce a e e a ed PT PTT ab
• D ag ed a a a b d e
 • A e fa a f he e
• M c a g e
• Ra ge f
• A a c ac e e d ea e c h
• A c ea a b de ANA
• M c a b d ab a

I
• Se e ec f c
if1 • An i moo h m
sina.mn iotienoaouYoimmaEeaEnnoaimtioahs
cle an ibodie ASMA
• M e ec f c f AHA
autoimmune hep
• T ea e e d a d e a
Ace a he Pa ace a APAP N ace aaa he

• Ma ec e ded d e ga e h
• O e d e ca e ac e e fa e he a c ec
wa
• E e e h gh AST ALT dueto

Tviral hep shock liver

paracetamoloverdose
causesuch
a significantP

Ka Wa e W ed a
T ea e

• Ac a ed cha c a a e e ab
• N ace lc eine ea e f ch ce
• U ed e e hg a h e
• U a g e a a e h e d e

N ace c e e C e e G ah e

it replenishes the levels

of glutathione in the liver
 Glutathione needs to be
replenished because it is
T ea e necessary for the metabolism
of acetaminophen
• Th ee e ab e f ace a he
• NAPQI c e If there is enough glutathione
it can be metabolised to
• N ace be e e a non toxic smocture
• Me ab ed b g ah e

non toxic
metabolites of
acetaminophen

one toxic
metabolite

in the presence ofsufficient

glutathione
W the
ed a P b cD toxic
a metabolite can be metabolised
to a non toxic metabolite
I che c He a

• D ff e e f h pope f ion
• Of e ee ICU a e h h c f a ca e
• Ma ed e e a ed AST ALT
• U a ef ed
• Pa h g one nec o i ea ce a e