Our topic of End stage liver disease,
and we're going to further
detail of cirrhosis,
the final common pathway
resulting in pretty severe sequelae.
I will be every once in a while
and making sure that we focus on
certain concepts that students tend
to miss because they overlook it.
Final common pathway, progression
injury due to severe fibrosis
which means you are going to find
tons of collagen
you've heard of trichome stain maybe
even reticular stain,
and this is specifically for finding
We'll talk about the clinical
consequences in great detail.
Lots to come.
When you hear stigmata of cirrhosis
we'll walk in each one of these.
Palmer erythema due to
spider angiomata, you've heared *Tangiactasia
due to increased estrogen.
paper money skin, extremely thin.
bilateral parotid enlargement
in addition to other complications
we will walk through.
*gland often associated.
Here, we have a cirrhotic liver.
You've noticed that there
is a complete loss of that fleshy
almost like a pink-like appearance
the liver should have.
In cirrhosis, there will be increase
in fibrotic nodules.
Either micro or macro nodules.
With all this fibrosis,
and the nodules, it looks like,
Extremely rough on top.
The nodules here represent
either micro or macro nodules.
With extensive fibrosis and a shrunken
So, imagine now that the
liver is dead.
What kind of sequelae are
we looking for?
Let's begin with synthetic dysfunction.
Remember that the liver
is responsible for producing
the most abundant protein in
our body, albumin.
You lose that albumin,
due to the lack of synthesis,
you lose your oncotic pressure
what your patient look like?
protruding stomach, what's going
on with that?
Edema, right? Edema.
is the albumin synthesis been
as is your coagulation factors.
What are they again?
Give me the pro coagulant factors
the liver produces.
II, VII, IX and X.
The anti-coagulant factors include
protein c and protein s.
Of all of these,
II, VII, IX and X which are vitamin K,
the test that you are going
to use clinically,
to find out as to whether or not the function
of the liver has been compromised,
once again is prothrombin time.
Once again, please tell me what
the time is for prothrombin time.
What time is it?
Time for you to take your
what kind of issues are you
going to have with
cirrhosis and endocrine pathology?
The liver is often responsible for
If you don't have the liver and it is
your estrogen levels arise.
Estrogen levels arise especially
on a male,
hypogonadism, testicular atrophy
you put them all together and
what hormone am I referring to?
This estrogen is going to do what
to your blood vessels?
It will cause ectasia. What does
And what if the pattern of that ectasia
looks like spiderlegs?
It's called spider angiomata.
That estorgen is going to cause
erythema of the palm.
My topic: Dead liver
is Cirrhotic liver.
Important sequelae that you are
if you are going to find
a common pathway. Remember,
many of these sequelae may or
may not be present
in a patient that took a bottle
and swallowed a bunch
Let's talk about Cardiopulmonary.
Students get this confused all the time.
There's one type
and massive hypotension.
in a cirrhotic patient.
I guess maybe you've got through
and you just forget
that you have two
circulations in your body.
Well, actually, technically,
you want to probably
want to start thinking about it as three.
We have our systemic circulation,
our pulmonary circulation,
and then we have our portal
That is how you need to approach this
In cirrhosis, which we haven't talked
about it yet,
the portal hypertension we are referring
to is esophagal varices.
I like to use the word "head".
You'll see why.
And they you have hemorrhoids
and that is the butt.
Head, butt and then around the
ambilicus we have our kaput.
Head, butt, kaput,
that's portal hypertension.
That is not our topic yet, but we will
come to it.
I will hit it hard.
No such thing as portal
So you will have portal hypertension
in cirrhosis but overall,
the patient globally,
is suffering from hypotension.
We'll talk about that in great detail.
Is this clear?
I haven't talked about pathogenesis
but understand your patient
will be most likely hypotensive.
There will be what is known as
and we'll talk about this.
we'll talk about another issue
called hepato renal syndrome.
Let's begin by looking at portal hypertension.
As I said earlier this will be head, butt, kaput.
If there is portal hypertension,
this will be what kind of force in excess?
Dr. Raj, you said that there is
decrease in oncotic pressure?
So, were you wrong?
No, I wasn't.
If you're losing albumin,
that is decreased oncotic
If you are having portal hypertension,
that is increase hydrostatic pressure.
The combination of the two,
what is the stomach that I made?
that is ascites.
Of all the three, head, butt, kaput,
which one is the emergency?
No, it is not.
I'm sorry, I had to do that.
It's the esophagial that you are paying
This is the emergency.
We talked about teh esophagus in
I showed you a number of
I showed you esophageal varices
in the esophagus.
You saw that there is dilation
of the esophageal veins,
raptures, my goodness, you are going
to have hematemesis
and there might be choking.
Meaning to say, the patient is
suffocating on his or her own blood.
That is an emergency. No joke.
porto-systemic encephalopathy. I'll talk
about that in greater detail.
I will separately,
take out. spontaneous bacterial peritonitis.
Warrants its own discussion.
And splenomegaly with
because their liver gets knocked out,
guess what happens to the spleen?
I will talk about in greater detail
known as hepato-renal syndrome.
It is important that you understand
My topic for all of these four is
Oncologic. Remember please that anytime,
anything that causes cirrhosis,
the increase of risk for hepatocellular
On your boards, you are looking for
Ascites is our topic.
Remember if there is liver damage in
is definitely taking place.
We'd have to go to the
just make sure that you are clear
and there's more.
in terms of a particular ratio called
As we all shall take a look at.
So, what is ascites, it is
excess fluid of
in the peritoneal cavity.
Two major causes once again;
elevated hydrostatic pressure.
Due to decrease
albumin may result in
decrease of oncotic pressure.
Both of these will contribute to therefore
of fluid in the peritoneal cavity.
Back to physiology.
Where is our fluid right now?
In the peritoneal cavity.
Do you know of any blood vessel
or vascular system
a vascular system at the
So now, you have all these fluid
which is not all.
A lot of it is fluid.
which escaped the blood vessel
and has entered
How much profusion is taking
place down to the kidney.
Not a whole a lot.
Or never that you find
the * apparatus
that then senses the decrease
amount of fluid through the arterial
what are you going to release?
If you have not corrected the liver issue,
you continue to having ascites.
More fluid in the peritoneal cavity,
thus you are going to have
increase aldesterone which does what?
reabsorb more sodium or water.
You've put this all together.
I've done this for you
Right sided heart failure.
Nephrotic syndrome and cirrhosis.
You tell me, what is the common
denominator for those three.
fluid in intertisium
decreased in profusion in kidney.
If you do not the underlying cause,
you're going to continue accumulating,
fluid in the interstitium.
In this case, the peritoneal cavity.
Ascites, clinical presentation,
I have that even without
Shifting dullness and fluid wave
indicate >500cc. What does that mean?
You stand up here, you push the side
of their flank,
you walk to the other side,
and watch the wave come towards you.
I'm joking. That doesn't actually
Shifting dullness. You get the point?
Because of their fluid,
Quite a bit, look at this,
greater than 500cc, where?
in the peritoneal cavity. Next.
You think it's possible.
you think that you might actually
accumulating fluid elsewhere
on some other cavities?
especially the pleural activity.
And we talked about the pleural
cavity being an interesting place of developing,
You have to refer to this as being,
Hepatic hydrothorax. Why?
Because you can have malignant
hydrothorax. Secondary to
You can have something like
So, a lot of interesting about
We spent time with pleural effusion.
Investigating transti date
versus exit date.
This is hepatic hydrothorax.
I'll walk you through
But before we get there,
At least for now,
Memorize the following.
SAAG. I'll tell you what that stands for.
Serum Albumin Ascites Gradient
But you find it to be greater than
Don't worry. If you didn't catch that,
not to worry. I have a table upcoming
that goes to greater detail.
New Entry 192
For now, if you find that your SAAG
is greater than 1.1,
this to you should indicate portal
hypertension. It is that clear.
The diagnostic evaluation
well, if you are thinking
and it is not portal hypertension,
wouldn't it be good to recommend
Why specifically Spironolactone
because in a patient
What do you expect their
aldesterone levels to be?
What do you know about
It blocks aldesterone.
you have this fluid,
remember when you had
a pulmonary edema?
What kind of loop diuretic did
you use to get rid of that fluid?
Beginning with 100mg.
A little bit more detail here.
Monitor electrolytes constantly.
That is huge.
And can cause painful gynecomastia
as you remember.
Remember the side effects that may
Gynecomastia is a possibility.
Why do you want to monitor
Because you are using it
And using a aldesterone blocker
so therefore, you might have,
excess sodium being removed and such.
Large volume paracentesis with
What does basically means is once
upon a time, you open up a window,
so that you can then remove some of the
Here is an important concept.
It used to be a more
high level type of question
but you can expect this on your basics.
It is called transjugular.
Intrahepatic Porto-Systemic Shunt. New Entry 224
Your main focus here should be,
that you are bypassing the liver
which is dead.
Here is my problem:
So, you are bypassing the liver
with a cirrhosis.
Because you are waiting for
a liver transplant.
So, you're kind of stuck.
You have to do something
in the meantime,
to bypass the liver circulation.
If you bypass the liver circulation,
And go straight in to systemic
There is every possibility of tips.
You'd probably seen the
It's the fact that when you are
bypassing your liver,
that you would actually
up into the head.
And you migh facilitate,
or exacerbate hepatic
But one of those things where you have
to take a look at
risks vs benefits.
Because your patient is already cirrhotic.
Here we have the prognostic scoring
One is called
and the other one
is called your MELD.
At this point,
just understand the concept.
The liver is dead.
Your arterial pH is less than
And you have Ascites, encephalopathy,
bilirubin, albumin levels being decreased,
Elevated PT and bilirubin will
All the concepts that we talked
I won't sit here and memorize
Because you already know all of these.
On the other side, something
Model for end stage
And for this, you find the PT
to be quite elevated.
You might have renal damage
called hepato-renal syndrome,
which we'll talk about.
Creatinine will be elevated and
PT will be elevated with INR.