Liver Function Tests - an overview

Summary

本视频由Dr. Matt主讲，深入探讨了肝功能测试（LFTs）的基本概念、为何需要进行这些测试以及如何解读测试结果。视频首先定义了肝功能测试作为血液生物标志物，用以评估肝脏功能。接着，通过实例解释了可能需要进行肝功能测试的情况，如患者有肝病史、黄疸症状、药物中毒风险或家族肝病史。最后，视频通过图解详细说明了如何通过肝功能测试结果判断黄疸的原因，以及肝功能障碍的两大类别：胆汁淤积（胆固醇排泄问题）和肝细胞损伤（肝脏本身的问题）。

Takeaways

• 🧬 肝功能测试是通过血液生物标志物来评估肝脏是否正常工作的一种方法。
• 🩸 常见的肝功能测试包括酶类（如AST、ALT、ALP、GGT）和肝脏产生的产物（如白蛋白、凝血酶原时间、胆红素）。
• 📈 肝功能测试可能因为多种原因被要求进行，例如患者有肝病史、黄疸症状、药物或酒精使用史，或者属于高风险群体。
• 🔍 肝功能测试结果异常可能指示肝脏损伤或疾病，或者是肝脏功能不全。
• 🟠 黄疸是皮肤和黏膜出现黄色着色，通常是由于胆红素积累造成。
• 🩸 胆红素是红细胞分解的产物，主要在肝脏中被处理和排泄。
• 💡 通过肝功能测试可以区分黄疸的原因，如前肝源性（红细胞破坏增加）、肝内源性（排泄障碍）和后肝源性（胆汁排泄问题）。
• 📊 碱性磷酸酶（ALP）和γ-谷氨酰转移酶（GGT）的升高通常表明胆汁排泄受阻，即胆道阻塞。
• 🚨 AST和ALT的显著升高可能指示急性肝损伤，而轻微升高可能与慢性影响有关。
• 🍺 AST相对于ALT的升高可能与酒精性肝病有关，而两者比例的变化也可能指示肝硬化。
• 📉 肝脏功能不全时，白蛋白和凝血因子的产生会减少，同时胆红素的处理也会受到影响。

Q & A

肝脏功能测试是什么？

肝脏功能测试是血液参数，也称为血液生化标志物，用于指示肝脏可能没有正常工作。

AST和ALT的区别是什么？

AST（天门冬氨酸氨基转移酶）和ALT（丙氨酸氨基转移酶）都是指示肝脏损伤的酶。AST主要存在于线粒体中，而ALT主要存在于细胞质中。在血液中，这两种酶的比例大约是1:1。

为什么ALT比AST更特异于肝脏损伤？

ALT主要存在于肝细胞的细胞质中，因此当肝脏损伤时，ALT的水平会比AST更显著地升高，使其成为更特异于肝脏损伤的指标。

ALP和GGT在肝脏功能测试中的作用是什么？

ALP（碱性磷酸酶）和GGT（γ-谷氨酰转移酶）在肝脏功能测试中用于指示胆道阻塞或胆汁淤积。ALP的增加可能与肝脏外部的骨组织有关，而GGT的增加则更特异地指示肝脏问题。

黄疸是如何产生的？

黄疸是由于血液中胆红素积累导致的，表现为皮肤和黏膜的黄染。胆红素是红细胞分解的产物，在肝脏中被代谢和排泄。

如何区分黄疸的前肝性和后肝性原因？

前肝性黄疸通常与红细胞破坏增加有关，导致间接胆红素（未结合胆红素）水平升高。后肝性黄疸则与胆汁排泄障碍有关，导致直接胆红素（结合胆红素）水平升高。

肝脏功能测试中的凝血因子和白蛋白有什么意义？

凝血因子和白蛋白是肝脏产生的产品，它们的水平可以反映肝脏的合成功能。如果这些水平低于正常范围，可能表明肝脏功能受损。

肝脏功能测试可能因为哪些原因被要求进行？

肝脏功能测试可能因为患者有肝病史、黄疸、药物或毒物暴露史、家族肝病史、高风险群体筛查（如血液透析、病毒性肝炎暴露、药物滥用史）或疑似肝脏损伤的其他原因而被要求进行。

肝脏细胞损伤时，AST和ALT水平的变化意味着什么？

如果AST和ALT水平显著升高（超过正常值的10倍），通常意味着有急性严重的肝脏炎症。如果水平升高较轻（约5倍），则可能表明是慢性肝脏损伤。

肝脏功能测试中的胆红素水平变化指示了什么？

胆红素水平的变化可以指示肝脏在处理和排泄胆红素方面是否存在问题。胆红素水平的升高可能与肝脏损伤、胆道阻塞或红细胞破坏增加有关。

如何通过肝脏功能测试判断是否存在胆汁淤积？

如果ALP和GGT水平升高，且直接胆红素水平也升高，这可能表明存在胆汁淤积。胆汁淤积可能是由于胆道阻塞或其他影响胆汁排泄的因素导致的。

Outlines

00:00

🧬 肝脏功能测试概述

本段介绍了肝脏功能测试（LFTs）的基本定义，它们是血液参数或生物标志物，用于评估肝脏是否正常工作。主要讨论了两类指标：一是肝脏释放的酶类，如AST、ALT、ALP、GGT，它们若显著升高可能表明肝脏受损；二是肝脏产生的物质，如白蛋白、凝血酶原时间和胆红素，它们若超出正常范围则可能表明肝脏功能异常。此外，还探讨了进行LFTs的原因，包括患者有肝病史、黄疸症状、药物或酒精使用史、家族肝病史、高风险人群筛查等。

05:01

💛 黄疸与胆红素

这段内容详细解释了黄疸的原因，即皮肤和黏膜出现黄色着色，这是由于胆红素积累造成的。胆红素是红细胞分解的产物，主要在肝脏中被处理和排泄。介绍了胆红素的生成、运输和代谢过程，以及如何通过LFTs中的胆红素水平来判断黄疸的原因。还讨论了肝脏的微观结构，即肝小叶，以及胆红素如何在肝细胞中被代谢和排泄。

10:02

📈 胆红素水平的异常原因

本段讨论了胆红素水平异常的不同原因，包括红细胞破坏增加（前肝源性）、肝脏排泄功能受阻（肝内源性）和胆汁排泄障碍（后肝源性）。详细解释了如何通过LFTs中的直接和间接胆红素比例来区分黄疸的类型，并探讨了可能导致胆红素水平升高的具体疾病和情况，如溶血性贫血、Gilbert综合症、胆道阻塞等。

15:05

🦠 肝细胞损伤与胆汁淤积

这部分内容聚焦于肝细胞损伤和胆汁淤积的问题。肝细胞损伤时，AST和ALT水平会上升，而胆汁淤积时，ALP和GGT水平会升高。解释了ALP和GGT在肝细胞膜上的活性增加的原因，以及如何通过这些指标来判断胆汁淤积。同时，讨论了肝细胞损伤的两种情况：急性损伤（如药物中毒、病毒感染）和慢性损伤（如脂肪肝、慢性肝炎）。还提到了肝细胞功能不全时其他参数的变化，如白蛋白和凝血因子的产生减少，以及胆红素处理和排泄问题。

20:05

📊 肝脏功能测试的综合理解

最后一段总结了肝脏功能测试的目的和意义，以及如何通过LFTs的结果来理解肝脏健康状况。强调了LFTs在诊断肝脏疾病、监测肝脏功能和指导治疗决策中的重要性。通过图表和示意图，帮助观众更直观地理解LFTs的各个方面，以及它们如何反映肝脏的生理和病理状态。

Keywords

💡肝功能测试

肝功能测试，也称为肝脏生化指标，是通过血液参数来评估肝脏是否正常工作的医学检测。视频主要介绍了这些测试的定义、为何需要进行这些测试以及如何解读测试结果。

💡酶

酶是生物体内催化化学反应的蛋白质，肝功能测试中的酶如AST、ALT、ALP（碱性磷酸酶）和GGT（γ-谷氨酰转移酶）的升高，可能指示肝脏损伤或疾病。

💡肝脏产物

肝脏产物指的是肝脏合成并释放到血液中的物质，如白蛋白和凝血因子。这些产物的水平可以反映肝脏的功能状态。

💡胆红素

胆红素是红细胞分解产生的一种黄色物质，肝脏负责将其结合并排出体外。胆红素水平的异常升高可能指示肝脏处理胆红素的能力受损。

💡肝细胞损伤

肝细胞损伤指的是肝脏细胞由于各种原因（如药物、病毒、酒精等）受到损害。AST和ALT的显著增加通常与肝细胞损伤有关。

💡胆汁淤积

胆汁淤积是指胆汁流出肝脏和被排出体外的过程中出现问题，导致胆汁在肝内积聚。ALP和GGT的升高通常与胆汁淤积有关。

💡黄疸

黄疸是一种由于胆红素水平升高导致皮肤和黏膜出现黄色的症状。它可能是肝脏功能障碍或胆红素代谢异常的表现。

💡酶活性

酶活性是指酶催化化学反应的能力。在肝功能测试中，特定酶的活性增加可能表明肝脏细胞损伤或胆汁流动受阻。

💡肝脏小叶

肝脏小叶是肝脏的基本结构单位，由肝细胞围绕中心静脉排列形成的六角形结构。肝脏小叶的结构和功能对于理解肝脏的生理和病理状态至关重要。

💡肝脏疾病

肝脏疾病是指影响肝脏功能的一系列病理状态，包括肝炎、肝硬化、肝脏肿瘤等。肝功能测试是评估肝脏疾病的重要手段。

💡溶血性贫血

溶血性贫血是一种由于红细胞过度破坏导致的贫血类型，这会增加肝脏处理胆红素的负担，可能导致胆红素水平升高。

Highlights

定义了肝功能测试（LFTs）为血液参数，用于指示肝脏可能功能不佳。

介绍了常见的肝脏酶，如AST、ALT、ALP、GGT，它们在肝脏损伤时会显著增加。

解释了肝脏产生的产品，如白蛋白、凝血酶原时间和胆红素，它们在肝功能异常时会表现出异常。

讨论了肝功能测试可能被要求的原因，如患者有肝病史或怀疑存在问题。

提到了药物可能导致的肝损伤，如对乙酰氨基酚（扑热息痛）和酒精使用。

强调了高风险群体的筛查，如输血、病毒性肝炎暴露或使用非法药物。

解释了黄疸作为肝功能测试的一个关键指标，是由于胆红素积累导致的皮肤黄染。

描述了胆红素的来源和在肝脏中的代谢过程。

讨论了肝功能测试结果异常的两大原因：胆汁淤积（胆汁排泄问题）和肝细胞损伤（肝脏本身的问题）。

解释了如何通过LFTs区分黄疸的前肝源性和后肝源性原因。

强调了ALP和GGT在诊断胆汁淤积中的重要性，因为它们在胆汁排泄受阻时会上升。

讨论了AST和ALT在诊断肝细胞损伤中的作用，以及它们在急性和慢性肝损伤中的不同表现。

指出了白蛋白和凝血酶原时间在肝功能不全时的下降，以及胆红素处理问题的指标。

解释了肝脏的解剖结构，如肝小叶和中央静脉，以及它们在肝功能中的作用。

讨论了胆红素在肝脏中的代谢过程，包括其在肝细胞中的结合和排泄。

描述了肝细胞损伤时，AST和ALT的释放和它们在血液中的比例。

解释了ALP和GGT在胆汁淤积中的升高，以及如何通过这些指标判断肝脏问题。

Transcripts

hi i'm dr matt and welcome to this video

on liver function tests also known as

your liver chemistries in this video

we'll firstly define what these tests

are

secondly we'll look at some examples of

why they may be ordered and then thirdly

we'll go through a schematic drawing to

try to categorize and make sense why

these may be deranged

so starting with the definition so the

liver function tests are basically blood

parameters blood biomarkers that give an

indication that liver may not be

functioning as well as it should be so

some examples that we'll go through

firstly these are enzymes that are

released from the liver

number one in no order we have one

that's called ast

so that's aspartate transaminase

alanine transaminase

a lp

alkaline phosphatase

ggt

gamma gluta transferase now these are

all enzymes so that will give an

indication if these are markedly

increased there could be a possibility

that liver is injured and releasing

these as a result the next three are

actually products that are produced by

the liver so we have albumin

which is a protein

we have prothrombin thyme which is an

indication of the clotting factors that

are released from the liver

and then lastly we have bilirubin

which is

something that's made outside the liver

but the liver conjugates it to allow it

to be excreted so these four first four

are enzymes these are more to do with

how the liver is functioning or working

because albumin is made there the

clotting proteins are made in the liver

and the bilirubin is processed and

conjugated in the liver so if these are

outside their range it indicates that

the liver isn't functioning whereas

these enzymes indicate it might be

diseased or injured

so moving on to why

may they be ordered firstly

to look at maybe the patient has a

history of liver disease or you are

concerned that there might be a problem

so for instance if the patient comes

with jaundice this is a yellow

discoloration you may want to have an

exploration to figure out why it's

caused so you might have a look at this

panel

you may be concerned that they've taken

a medication so they've taken a poison

or something that could cause liver

injury hepatotoxic medications such as

paracetamol

in america this is acetaminophen or

tylenol but in australia we call it

paracetamol

the patient may have a history of

alcohol use

or they may have a positive family

history of so a known family history of

something that may cause damage to the

liver an example is

hematochromatosis which is basically the

way that iron is stored in the liver or

elsewhere in the body and that can cause

damage and disease to the liver

next we might look at groups that are

high risk so it's a screening tool for

patients that may be in a high risk

category this could be if they've had a

transfusion

a blood transfusion

they've been exposed to

viral hepatitis let's say

or maybe they

have used illicit drugs

now moving to another cause this could

be extra hepatic so this big certain

things that are outside the liver that

could impact the liver so examples here

would be malignancy

so this is cancer so cancer a common a

place where the cancer can spread as

secondary so this is metastasizing it

can go to the liver which then would

suggest that the liver will start to

become dysfunctional and these may start

to increase another example if the liver

has been

hypoxic so a low level of oxygen low

level of blood flow so

let's say shock a patient has a history

of shock

and therefore you're concerned that

liver might be damaged through ischemia

or hypoxic

finally medication there might be

certain medications that might cause

injury so you want to get a baseline

before you prescribe this medication

examples could be methotrexate as i said

paracetamol or vaporate so these are

some examples so there you have it there

are there are some reasons why a

clinician might order lft is to get an

idea of what is happening at the liver

now we're going to have a look at that

schematic

diagram to again to break this down and

make sense of them

now we move to the third part of this

video which is trying to make sense of

why these numbers why the liver function

tests may be out of range what i want to

look at is if your patient has jaundice

how can we figure out what is the cause

of the jaundice by looking at the lfts

and then finally the two biggest causes

of the derangement of lfts cholestasis

which means a problem with the way the

bile is leaving the liver and being

excreted or hepatic cellular injury

which means there's a problem intrinsic

to the liver itself

so let's start with jaundice jaundice is

a yellow discoloration of the skin the

sclera the mucous membranes which is due

to a buildup of bilirubin so the lft

we're going to look for here is

bilirubin

okay and basically anything above 1.2

milligrams per deciliter or per 100 ml

now before we go on we just got to

quickly make sense of where does

bilirubin come from

so bilirubin is the breakdown product of

red blood cells red blood cells will

last approximately 120 days once they

get to that age they get destructed and

killed within certain organs like the

spleen the bone marrow or the liver

themselves now when the red blood cell

is broken down

a lot of the parts will be recycled the

iron gets taken back to the liver to be

reformed into other constituents

the protein the globulins will get made

into amino acid pools but the heme

component will get broken down

phagocytosed by macrophages and

essentially be made into bilirubin

now i'm not going to go through all the

steps

mike has done a video on this so i

encourage you to have a quick look at

that if you haven't covered this before

but the bilirubin in this case will what

we call b

unconjugated bilirubin which means it

has to be carried

with a protein called albumin so that's

a complex that will get transported in

the blood and taken to the liver

before i get to the more detail what i

want to draw your attention to is this

histological unit of the liver there's

about a million of these and these are

called the liver lobules the liver

lobules are these kind of hexagonal

shaped

sections of the liver that has in the

center what we call a central vein which

is the accumulation of blood that has

diffused or percolated through all the

hepatocytes and then all of this central

vein blood will eventually accumulate

and then leave the liver via the

inferior vena cava

but what blood does it receive well it

gets arterial blood so about 20 percent

of arterial blood

is what goes through this lobule and the

70 to 80 of blood is through the portal

vein so those two bloods merge together

as the sinusoid kind of go through these

plates of cells called the parasite and

what goes the opposite direction is the

bile cannuculi which is like a river of

bile that goes out towards the outer

part of the lobule and all of these bile

ducts will start to come together

form the hepatic ducts which then become

the common hepatic duct meets the cystic

duct of the gallbladder and then we have

the common bile duct that goes down to

the duodenum

so it's this unit that i want to refer

you to specifically just one hepatocyte

so just one of those black dots will

focus in here now so this is one

hepatocyte

on the outside so this is the sinusoid

so this is the combination of portal

blood and

arterial blood fuse in through

the hepatocyte will grab things

and metabolize and filter and

do all the different functions that the

liver cells does and everything it

doesn't want it gets put into the bile

conuculide to be excreted out of the

liver but we're focusing on bilirubin

here so bilirubin will be coming along

in the systemic blood remember it's

unconjugated so it's got albumin

attached to it it gets transported

across into the hepatocyte where the

abdomen detaches and then this

unconjugated bilirubin gets taken to an

enzyme called uridine diphosphate

glucosyl transferase or ugt what this

enzyme essentially does it will add a

group to it to make it lipid sorry to

make it water-soluble this now makes it

a conjugated bilirubin

also known as

direct bilirubin so we'll focus on db

direct bilirubin from here this

conjugated bilirubin can get

excreted via a protein called mrp2 and

be put into the bile where it gets

excreted

eventually leaving the liver

as the bile duct goes down into the

intestines where a lot of it will be

metabolized by bacteria

some of it metabolized in a way that it

can be reabsorbed in the bowel with some

of it coming back

absorbed it back across and it does this

big long loop

the rest of it will get taken and put

out into the faeces that's what gives

the brown coloring some of it will

continue on as conjugated bilirubin

which can then get

urinated out and then that can be

cleared as well and the rest will just

go in this cycle

so now with that basis we need to figure

out well what could cause the bilirubin

to be increased

so this first part if your patient comes

to you with that yellowness you don't

really know what the cause and if you

were to do

some of the lfts and just find that

their bilirubin is high you still don't

know what's causing it so let's try to

figure some of this out

the first category of causes is

something that's causing an increasing

amount of red blood cell destruction and

this is what we call pre-hepatic

so if you were to have a patient that

has high amounts of red blood cell

destruction so they've got some kind of

anemia hemolytic anemia or some kind of

problem with their um hemoglobin that

could cause an increase in destruction

that would increase the amount of

hemoglobin coming for bilirubin coming

to the liver or they may have a lot of

hemorrhage hematoma that would also

increase it but another thing that could

increase it is this enzyme could be

slightly

sluggish it's not working as quickly as

it could

the common condition that that could

lead to or could lead to that decrease

in activity is gilbert syndrome so if

you have that syndrome the patient has

that syndrome this is not working so

well so therefore the conjugation speed

is going to be decreased and then you'll

have a up in the uncon unconjugated so

if you want to figure out whether

they've got a pre-hepatic cause

of their jaundice what you will do is

you do a blood test and if you see that

their total bilirubin is proportionally

higher

than their direct

so these two should be in a ratio but if

this one goes much higher to this one it

would suggest that

there's a problem pre-hepatically so it

could be increased destruction or a

problem with this enzyme

now

the other option

now there is intra-hepatic causes but

i'm going to leave it to kind of this

part so

if there's a problem with his excretion

okay that would mean that

the same the right amount of bilirubins

come to the liver the liver is doing

everything it's supposed to do it

conjugates it spits it out into the into

the bio caniculide but there's a problem

downstream there's a blockage for some

reason which means we go backwards so

the bile builds back up that means the

conjugated bilirubin comes back across

and spills across into the blood and

then we see it in the blood okay but

with this post-hepatic cause

in comparison to the pre-hepatic cause

what we actually see is an increase in

the direct

proportionally to the total

so it switches

with the pre so the post hepatic so if

it's a post hepatic cause

you'll actually see a much higher amount

or percentage of the direct

in the total because you've conjugated

it you've gotten rid of it but it's come

back and then it's gone across into the

blood okay so this is one way you can

figure out

what is leading to the jaundice

and so as we said this is a post-hepatic

cause which is essentially going to be

the collostasis which we're going to go

through now so the the remaining part of

your lfts

is to try to figure out is the cause due

to a cholestasis so a problem with the

excretion or a problem with the cell

itself

so let's have a look at this one to

start with

so let's assume that there is a blockage

so there could be a stone

in the bar duct or there could be a

structure so it's narrowed or there

could be a tumor down in the head of the

pancreas

causing the flow to be disrupted in any

case the bi will come backwards so it

will come back up and what you'll see is

the bile acid will come across

back into the hepatocyte

now

on the membrane the bile the biconicular

side of the hepatocyte so this side of

the membrane there is an enzyme here

that can produce

a number of other

and

what this is going to be

is

alp so that's the alkaline phosphatase

and this is generated by that enzyme on

that membrane so when it's exposed to

increased amount of bile acid this

enzyme will become more active which

increases the alp which then is pushed

across into the sinusoid which then goes

into the central vein and the ivc and

then in your blood so if you start to

see an increase in alp

so let's say you do your alp levels and

you've got a big increase or two two

arrows up of alp

you have a suspicion that it's due to a

cholestasis cause

but an important point here is alp

is not specific to the liver it's also

found in the placenta it's also found in

bone tissue so you need to be sure that

it is actually from the liver so there's

another enzyme that kind of works on

that membrane as well and that's the g

g t that's the gamma gluta transferase

so you want to also look for that one

and if that is also up which is kind of

the same mechanism you'll see that one

up as well and if you see ggt up with

alp you are confident that it's

a cholestasis cause particularly if your

direct bilirubin is up as well okay now

for whatever reason let's just say your

alp was up but this was normal and there

was nothing here

you need to suspect that it's coming

from somewhere else outside the liver

for instance

bone is a big one so osteoblasts when

they're highly active they're releasing

this enzyme so this could be recent

fractures or certain conditions where

there's maybe tumors in the bone or

pages disease causing an increase in ap

levels

finally we're going to have a look at

hepatocellular injury so i'll just clear

this off quickly

and the two big enzymes that you need to

be aware of with a paracellular injury

is ast

and a l t

an important thing just to remember

the s here

even though these are found in the liver

the s

the way i remember is also striated

muscle so this can be found in cardiac

muscle and skeletal muscles so it's not

specific to the liver so sometimes

problems with heart or or spleeder

muscles could also increase ast so just

be aware of that but the alt-l is

specific l to liver so this is much more

specific to liver

in terms of asp

asd the majority that 80 is found in the

mitochondria

whereas the majority of alt is found out

in the cytoplasm just to reiterate that

ast 80 is found in the mitochondria 20

in the cytoplasm whereas the majority of

the alts in the actual hepatocyte

cytoplasm itself in terms of the ratio

there's more ast in the cell than alt

but this is

diffused out quicker which means in the

blood these two are about a one to one

ratio so if you would a

normal person and normal

levels of these two they're about a one

to one ratio

okay so we've understood that ast and

alt is more specific to the hepatocyte

injury okay but how do we distinguish

with what kind of injury well if the

numbers are kind of above

10 times what they normally are that's

an indication that there is an acute

injury

and it's

severe

so this is inflammatory based so

anything that's kind of causing

hepatocell inflammation acutely and

quite severely is going to raise the

amount of these two

significantly this could be due to

paracetamol so the toxic effects a viral

acute viral infection like hepatitis or

hypoxic injury like there's not enough

blood coming to the liver which is going

to cause extreme inflammation causing

these levels to go up a significant

amount so this is more acute

causes of liver injury if the number is

only let's say five

times increased it's more suggestive

that it's a chronic effect

okay so chronic effects this could be

things like

fatty liver which could be

alcohol-based or non-alcohol based fatty

liver a chronic viral hepatitis

or certain medications over time

it's important to distinguish though

that ast

seems to be more sensitive to alcohol

the reason well the theory for why that

could be

is a combination of ethanol

causes irritation to the mitochondria

which causes it to spill out and go into

the blood at a higher amount so the

ast like we said it should be one to one

it's a higher ratio with alcohol-induced

injury so the ast could be higher or the

other cause of ast being increased

relative to alt is through more chronic

fibrosis or cirrhosis that causes the

flow the blood flow through the liver to

be sluggish which then reduces the

amount of ast that normally leaves which

then increases its buildup so

ast

increased relative to alt in ratio is

usually due to cirrhosis

and alcohol

finally

because the hepatocyte in the

hepatocellular injury they're not it's

not functioning as well you're going to

see those certain parameters like

albumin album has been isn't being

produced to its normal level same with

the clotting proteins and also the way

that the

bi the way that the bilirubin is

processed through the hepatocyte it's

going to be diminished and they're going

to see the changes a reduction in

abdomen problems with clotting time so

the clotting time increases and we see

problems with the bilirubin processing

that's outside pre-hepatic and

post-hepatic if there's a problem

intrinsic to the cell with the enzymes

and the transport proteins that's going

to play around with bilirubin secretion

excretion as well

so hopefully today you've seen

what liver enzymes are what are the

indications of why they will be ordered

and then we've schematically moved

through to try to make sense why each

one of them may be increased or deranged

outside their normal values