What if the uric acid accumulates
in soft tissue?
We call that tophi, or tophaceous gout.
Take a look at the pictures here.
Immediately show you the toe.
You see that toe? Inflamed like crazy, huh?
You call that, what, podagra.
You'd find in there uric acid crystals.
Let's identify these uric acid crystals
just to get ahead a little bit.
Once you possibly using polarized
light, let me ask you a question.
That polarized light that you're trying
to identify the uric acid,
you think you'd find it to be negative
or positive for birefringent?
That we'll talk about in a little bit.
Okay? Keep that in mind.
What if the uric acid accumulating
in soft tissue?
We no longer call that podagra, for example.
Think that maybe you might be
accumulating in the elbow,
or maybe as we see here, in
the hands and such.
Do not confuse this with osteoarthritis.
Remind me, in osteoarthritis,
what was it called when you had
inflammation to the DIP?
Oh, Heberden nodes, correct? Had
nothing to do with uric acid.
What about in PIP? It's called Bouchard,
and maybe the thumb.
However, osteoarthritis was non-inflammatory.
You did not have an inflammatory
So, as you move through rheumatology here,
you're going to categorize
the different arthritis,
and what it comes under so that
you can clearly understand
how to deal with and identify each patient.
Recurrent episodes of the gout could
eventually result into chronic.
By definition, though, is that
what chronic means?
Chronic usually means recurrent, recurrent,
recurrent, acute, correct?
There we have it. When you have recurrent
issues, then may turn into chronic.
When it turns into chronic, oftentimes, maybe,
it might be affecting your knees and such.
Keep that in mind. These flares.
Do you find a toe here?
Well, let me tell you, the one
on the left is your hand.
That's your fingers, all right?
So therefore, you can't call that podagra.
Is that your toe? Uh, no. I think
that's you're index finger.
Yeah, correct. So that is your tophi.
Or periauricular, around the ear.
It's the tophaceous gout or tophi.
Accumulation of what? Uric acid.
Remind me, on polarized light, what
are we going to look for?
So now, let me tell you, it's negative
But what does that mean? Well, I'll
walk you through that in a bit.
Diagnosis. We're going to
In the synovial fluid, we're going
to find…here it is.
The uric acid crystals. It's needle-
shaped. It's needle-shaped.
Needle. If you don't know what rhomboid or…
Rhomboid looks a little bit more like
a square, a little bit larger.
If you want, look it up.
That's some geometry, but needle
is what we're looking at here.
It's a negative birefringent.
So, if it's negative birefringent, what
does that even mean?
First know that you're going to be
looking for polarized light.
With polarized light,
it is the parallel nature of these needles
that you're going to be looking for.
If you know that these negative
crystals are negative
for polarized light,
is that mean that the color is
blue or yellow, please?
Now, what does that mean?
That means that you're going to be looking
for yellow, needle-like crystals
that are parallel.
That a parallel, I repeat.
So we have polarized light, we have parallel,
and it's negative, which means
that it will be yellow.
Which means if it's perpendicular
type of light, then it'd be blue.
That is the definition of
Most important thing, the needles,
polarized light, negative,
yellow, parallel. Is that understood?
We're going to compare this with
what goes on with CPPD,
which is calcium pyrophosphate
deposition disease as we shall see next.
Well, you want to take a look
at the underlying issue.
And, in fact, we know that
uric acid levels could…
seen during flares, most of the time.
So, usually, it can be immeasurable,
so be careful with these flares
Only 10% of hyperuricemia patients
truly develop gout.
That's another point that you
want to keep in mind.
But, trust me, if the boards want you to know
that this is gout, they're going to
give you the classic symptoms
in which you'd be able to identify.
However, you do need to make sure that
you understand the difference between
acute and chronic, especially, when
we get into management.
So let's attack the acute gout
in this patient.
What's that acute gout patient
So much though, they can't even
place a feather on their toe.
So therefore, NSAIDs,
colchicine. Now, be careful colchicine, though.
Colchicine literally, is going to inhibit
the migration of neutrophils
towards that crystal.
In other words, it's like you're
kind of creating
If you're with me, you're great.
If not, no worries.
At this point, colchicine inhibits
of neutrophils towards your crystal.
So if you don't have the migration,
you don't have phagocytosis, you don't
have inlfammasome, oh, guess what?
You don't have the pain. Nice job.
But with colchicine,
the side effect profile is devastating,
could be extremely severe.
and also as bad as pancytopenia.
Keep that in mind, please. The side effect
profile is quite bad for colchicine.
Now, apart from that,
oral steroids for patients
who cannot tolerate
NSAIDs or colchicine
because now you're worried about a patient
who comes in with kidney disease.
And on top of that, you're going
to give colchine? Be careful.
Or even NSAIDs, for that matter, correct?
Let's divide this into chronic.
In chronic, you may not even find
high levels of uric acid.
So uric acid level might be low.
And then with chronic gouty attack,
now at this point,
you're not so much worried about
the pain in the patient
but it's the fact that you want to try to
stop the synthesis of uric acid.
The drugs we have here is
allopurinol or febuxostat.
In other words, you're going to
stop the growth or stop,
more or less, the enzymatic conversion,
known as your xanthine oxidase.
So, if you inhibit that enzyme, now obviously,
that takes a lot longer, right?
So therefore you can't use allopurinol
and febuxostat with acute gout.
Is that clear?
As we're dealing with chronic.
Now, especially if you're overproducers.
I gave you 1 example for overproducers
and that was…?
Good. That was the fact that I gave
you tumor lysis syndrome.
Increase chemotherapy, increase destruction,
increase release of uric acid,
that's one. Number 2,
what if you had a patient that was young
and had hypoglycemia, had hepatomegaly.
Also had hypertriglyceridemia,
and also had gout formation,
and also had gout formation,
did not have proper gluconeogenesis
Put all that together for me and
you're going to tell me about
a particular condition that you
know as being a type 1
glycogen storage disease, we call von Gierke.
There you might have overproduction.
So when you have over production,
it's nice to have a tool,
such as allopurinol,
to inhibit that enzyme.
The goal is to bring your uric
acid < 6 mg/dL.
If urinary uric acid > 1000 mg/day,
patient at risk for acute obstructive
uropathy, so be careful.
Should be started until several weeks
after the acute gouty attack.
So, in other words, remember, you want to wait,
and you want to take care of the pain first.
And then you want to try to
inhibit the enzyme
that will produce your uric acid.
Several weeks, please, is key there.
You'll need dose adjustment
for chronic kidney disease.
Now, anytime that you have issues there,
you're worried about allopurinol.
What about your allopurinol
and, at this point, you still have
high levels of uric acid?
Now, these become quite interesting.
So now what you're going to do
inspite increased excretion
of your uric acid.
So, these are then known as uricosuric drugs.
These include your loop diuretics,
such as probenecid and sulfunpyrazone.
Maybe uricase treatment,
and there's a particular…
keep this in mind, IL-1 β antagonist