– [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..