00:01
So the clinical presentation.
00:04
In cirrhosis that is no longer
being adapted to
and compensated,
patients will have
fatigue and weight loss.
00:13
They'll clearly be jaundice.
00:15
Because of the increased bile
salts peripherally in the skin,
they will develop pruritus
that is pretty intense.
00:22
Asterixis can be one
of the manifestations
that you see involved
in the encephalopathy.
00:28
And if you don't know
what asterixis is,
you would have your
patient close their eyes,
hold up their hand as if
they're stopping traffic.
00:36
Now for me because I
don't have cirrhosis,
not that I know of,
my hand stays up.
00:41
But if a patient
has CNS effects,
secondary to cirrhosis,
they will do this.
00:49
And not be aware that they
are flapping their hands,
that's asterixis.
00:54
Patients can get
Dupuytren's contractures.
00:57
So abnormal fibrosis
typically of the ring finger.
01:00
For reasons that are
not entirely clear,
it's just one of
those associations.
01:04
We'll see a hepatomegaly.
01:06
End stage, the liver
tends to be smaller,
but in earlier stages
of cirrhotic injury,
you may have an enlarged liver.
01:12
And because of
that hypersplenism,
and the impact on
the portal circulation,
you may have splenomegaly.
01:19
And then hyperestrogenism.
01:21
And that can present as increased
vascular ectasia or telangiectasia,
and even gynecomastia,
in patients who have severely
elevated levels of estrogen.
01:32
This is just
showing you ascites,
remember ascites is going to
because of the portal hypertension,
but also the hypoalbuminemia.
01:39
And this is going to be
largely a serous effusion,
so it's going to be water and
electrolyte relatively protein poor.
01:46
On the right hand side,
we're demonstrating
esophageal varices.
01:49
So these very dilated Porto
esophageal connections
with very minimal
epithelium over them.
01:56
And you can imagine a
potato chip going down there
and eroding the epithelium and now
you would have a massive bleed.
02:03
How are we going to
make the diagnosis?
Well, we're going to look at a
variety of laboratory studies.
02:09
But also it's going to
be based on history,
obesity, or alcohol,
or hepatitis,
in most cases is going to
be our underlying etiology.
02:19
Early findings in cirrhosis
in the laboratory
diminished platelet count.
02:23
Some of this is due
to hypersplenism.
02:25
But the other part of it is
the liver,
is the source of thrombopoietin.
02:31
And if liver doesn't make that,
you don't make
adequate platelets.
02:37
The AST and the ALT are
going to be elevated.
02:41
So these are going to be
markers of hepatocyte injury,
those are transaminases that are
involved in normal liver metabolism
as hepatocytes die, they
release those enzymes
and we can detect
them in the blood.
02:55
Now, in the later
stages of cirrhosis,
when the patient is going
to be more symptomatic
with other things that
we've already talked about.
03:03
You may actually have normal
or even low levels of AST/ALT.
03:07
That means that we've
pretty much killed
all the liver parenchyma
that we can or that we will
and so we don't see
release of those enzymes.
03:17
We will see that the
partial thromboplastin time
and the prothrombin time,
so PTT and PT are elevated.
03:25
That means that the international
normalization ratio,
the INR will also be up
and that's because of the
inability to synthesize the
normal coagulation factors.
03:34
Bilirubin will be up and it may
be both direct and indirect.
03:38
Glucose will be down
because we don't have the
ability to store glycogen
and albumin will be way down.
03:45
We can also do some imaging.
03:46
So typically on
ultrasound or CT,
we will see a small
granular or smaller
more granular looking liver.
03:54
And what's been demonstrated
here is actually an angiogram
showing the formation
of a Caput medusae.
04:00
The arrow is pointing
to this dilation
of the systemic vasculature
around the umbilicus.
04:07
Cirrhosis is shown in a
intact liver from an autopsy
on the left hand side.
04:14
You see nodules of
regenerating hepatocytes
and intervening zones with
depression that's the scarring.
04:22
We can see on histology,
the correlation to that.
04:25
This is not your typical H and E
stain, this is a trichrome stain.
04:30
And in the stain, the
fibrosis, the scarring is blue.
04:34
So you can see that there are
numerous regenerating nodules
throughout those are kind
of pink with more white,
the whiteness there
is actually steatosis
because this was a
drinker who kept drinking,
so ended up with
alcoholic steatosis.
04:48
But then you have outside
the regenerating nodules,
all this bridging fibrosis.
04:53
And by seeing this image,
hopefully you can appreciate
why there would be abnormal
flow into this liver,
blood supply wise,
and abnormal flow out of the
liver in terms of say bilirubin,
but also why we have
diminished synthetic function.
05:07
So what are we going
to do about this?
I've already said a
couple of different times
that this is end stage,
there is no going back,
the liver will not ever
get back to normal,
and we're stuck with
whatever level of cirrhosis
is already present.
05:20
We want to minimize
accumulating any more.
05:23
And we want to avoid
things that will injure
whatever residual
hepatocytes are present.
05:28
So we're going
hepatotoxic substances,
alcohol, acetaminophen,
things that can potentially
injure the liver.
05:35
For the secondary manifestation,
the varices, were
going to band those,
basically put a rubber
band around them,
and then they will thrombose.
05:44
Or, if necessary, we
can do vascular shunts.
05:47
So there's a procedure
by which we can put in
by interventional
radiology, a shunt,
that takes blood
from the portal vein
and goes right into
the inferior vena cava.
05:58
In that way, we reduce
the portal hypertension,
of course that shunts,
the materials coming
out of the GI tract
directly into the brain.
06:08
So encephalopathy
may be exacerbated.
06:12
For severe ascites, we'll give
diuretics and salt restriction
and paracentesis literally
pull off the fluid.
06:17
For the encephalopathy,
it turns out if we reduce the
amount of protein in their diet,
so we reduce the ammonia
that we can reduce
the encephalopathy.
06:27
However, since patients with cirrhosis are often malnourished,
protein intake restriction is no longer recommended.
06:34
One of the other ways we can do
it is a laxative called lactulose,
which causes increased quicker
transit time through the GI tract
so we don't get as
much absorption.
06:48
And it also will reduce
the bacterial content
because they're clearly
also a source of protein.
06:54
Coagulopathies are
treated with vitamin K,
we give as much
support as we can
for whatever the
liver can synthesize.
07:03
And in end stage disease,
we will do liver transplant.
07:07
Now you won't transplant someone
if they continue
to be a drinker,
you won't transplant someone
if they won't lose weight
because then the same disease
will recur in the new liver.
07:20
And the liver
transplant is expensive,
limited resources
and requires constant
then surveillance
for the possibility
of rejection.
07:29
So we won't treat with
a liver transplant
unless the patient is
willing to play fair with us
and to be a good citizen.
07:41
how do we decide whether
or not we want to
who's going to get
a liver transplant.
07:46
So there is a Child-Pugh score,
it's based on various
biomarkers and signs.
07:51
Not important that you be
able to rattle this off
on the tip of your tongue
but just be aware that
we do have these criteria
upon which we can
decide life expectancy
and the need for
liver transplant.
08:09
With that, we will conclude
and you've learned quite a bit in
just about 10 minutes on cirrhosis.