Liver Function Tests - an overview
Summary
TLDR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
🧬 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。
💛 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。
📈 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。
🦠 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。
📊 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。
Mindmap
Keywords
💡肝功能测试
💡酶
💡肝脏产物
💡胆红素
💡肝细胞损伤
💡胆汁淤积
💡黄疸
💡酶活性
💡肝脏小叶
💡肝脏疾病
💡溶血性贫血
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
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