- [Voiceover] So gout is a joint disease
that actually doesn't have much to do with the joint
in the sense that the joint is fine.
But it's a deposition of something
that doesn't belong in the joint
that causes all our problems.
I'm drawing it on the big toe here
because that's where gout is most commonly located.
And it's been described as one of the worst kinds of pain.
An acute gout inflammation, this person probably can't walk,
and their big toe will be swollen like this.
The culprit here, the little crystals
are called monosodium urate.
Monosodium urate.
And it's a crystallized form of uric acid,
which is something that is normally in our body
as a byproduct, a breakdown product
of our DNA and RNA.
But when for some reason there's too much of this,
it crystallizes and as it goes throughout our body,
it gets stuck in this joint.
And whatever joint it's stuck in
is gonna be painful and cause gout.
But more often than not it's here.
And by the way, gout in the big toe is so common
it actually has its own name called podegra.
Podegra.
The group of people that most often get gout,
if we're trying to look at statistics,
it's gonna be males and usually a little older,
on the older side.
So I will say 50 plus.
Some people say it has to do with lifestyle.
And one of the treatments for gout is lifestyle changes.
They're on a path of physiology level.
Anything that increases uric acid
is likely to lead to the symptoms of gout.
So in terms of symptoms, we have a lot of pain.
Especially in an acute flare.
And if we look at it, it will look red,
which we call erythema.
It's red and swollen.
Any way that we think of it as a joint disease,
this metatarsal joint,
but the deposition is actually also
in the surrounding tissues as well.
And this intense inflammation here
will also cause the area to feel hot to the touch.
So the symptoms and the history
should give a lot of good clues for diagnosis.
But to formally diagnose it,
we have a gold standard test.
We can take some of the fluid
in the joint space and analyze it.
And the diagnostic of gout is to find these needles.
When we look at it under polarized light,
they're gonna be negatively birefringent.
Birefringent.
So that's a lot physics that I don't understand.
But I know that what they mean by a negative birefringence
is that if they're laying flat,
the needles aren't laying flat.
It's gonna be a yellow color.
And this will be helpful later on
when we talk about distinguishing gout from pseudogout.
These particular needles made of monosodium urate will,
as a rule, when laid flat with the polarized light on it,
it's gonna look yellow.
So that's the synovial joint fluid.
But we can also take some blood.
And in people who have chronic gout
or even just more likely to get gout,
we might, we'll probably see hyperuricemia.
Uricemia, which is gonna lead to more uric acid.
This is a direct evaluation of uric acid.
It can not only tell us this person has
or is likely to get gout,
but as we treat them, we can use this to track
how effective the treatment is.
We can also get a white blood cell count
and a erythrocyte sedimentation rate,
which is measuring how fast
the red blood cells become sediment.
But these are really inflammation markers.
This one is a marker of inflammation,
and this one is a marker of how active our immune system is.
So both of these can actually go up
even without an infection.
White blood cell we think of as a marker for an infection.
Even though this is not an infection
because these crystals are not bacteria,
they're not pathogen,
but the immune system it elicits,
can make these numbers go up as well.
So even though the history
can be very characteristic of gout,
we want to do these tests to distinguish it
from other things it could be,
like infectious arthritis or the auto-immune things
that you really don't want to miss,
because the treatment for gout can be very specific.
First, there's gonna be the non-specific treatments.
We want to deal with the pain, so NSAIDs,
which also will actually decrease the inflammation.
So NSAIDs and possibly stronger things,
if they cannot tolerate NSAIDs or if the pain is too great.
And then we want to decrease the inflammation.
These are not specific.
You can use these in a lot of auto-immune type diseases.
And in here we can use steroid injections,
among other things.
But in gout, actually, the first thing they should do
is to have a lifestyle change.
There is a genetic component to gout,
but there's also a lifestyle component.
It is actually hard to separate
the genetic from the lifestyle.
But thinking of the uric acid,
we want to help them do things
that decrease the uric acid to begin with.
So eating less meat,
not drinking alcohol,
organic things to help them produce less uric acid.
And on top of that we can use drugs to do the same thing,
decrease the uric acid.
And these can be taken during a flare.
But also perhaps more importantly,
we can take them as prophylaxis.
So even if the patient is not having symptoms at the moment,
or they just have a history of gout,
we can give them a steady, long-term dose.
And the prophylaxis has to do with the pathway
that leads to the production of uric acid.
And we can slow these down
to chemically decrease uric acid in the blood.
But of course, lifestyle is still very important.
And we shouldn't just rely on the drugs.
So patients really need good counseling,
in addition to having the drugs
that just treat the symptoms.
And lastly, we want to talk about pseudogout.
It's named because it looks very much like a gout,
but it is not because of the deposition
of the crystals in the joint.
So first of all, instead of being in the big toe,
we actually think of gout
as more likely to happen in the knee.
So instead of being in the toe,
we have all the same symptoms in the knee.
You have the pain, the redness, the swelling,
the temperature, that's why it looks like gout.
But the thing that's deposited
is actually completely different.
Instead of monosodium urate,
we have calcium pyrophosphate.
Let's see if I can fit this whole word here.
Pyrophosphate dihydrate.
Dihydrate.
But most people probably just wanna use the acronym,
and that's why you'll probably see it as CPPD.
So it has nothing to do, so it's a very different pathway,
different deposition of crystals.
And for the diagnosis, we actually
go through the same system to distinguish the two.
And instead of needles,
when we look at this fluid under the same light,
there are gonna be rhomboid shaped crystals
instead of a thin needle.
And it's gonna be weakly positive birefringence.
So this is the whole reason that we care about it
because they birefringence tells us
whether it's pseudogout or gout
and also the shape of the crystals.
And treatment also will actually follow the same themes.
So we treat the symptoms, the pain,
and the anti-inflammatory things are the same.
And by the way, steroids,
instead of taking oral steroids for both of these,
you can inject into the joint space
right to where the pain is.
May provide faster and more stronger relief.
But since in the pseudogout
we're not dealing with uric acid,
the prophylaxis here obviously doesn't apply.
Pseudogout is somewhat less common than gout.
And so for the purpose of having
the correct specific treatment
and also for following the disease in the long run,
we really want to distinguish between gout and pseudogout
before we proceed with drugs like the uric acid prophylaxis.