Continuing our discussion in rheumatology.
This time we'll take a look at
Now, you've commonly probably
come to encounter
gout versus pseudogout.
But we need to be more technical.
So, pseudogout, referred to, as we shall see,
calcium pyrophosphate deposition disease,
and prior to going into
or diving into detail,
we'll take a look at gout, first.
So, what is gout, by definition?
By definition, gout is uric acid
accumulating in your body.
How did it accumulate?
90% of your patients with gout
have a hard time excreting the
uric acid from the kidney.
90% of the time.
Now, with that 90%, most of your
patients will be idiopathic.
Now, could renal failure result
in lack of excretion?
Sure. It could contribute.
Next, we'll take gout
and then we'll divide it into acute
and chronic, that's important.
And by acute and chronic, remember,
we begun begin the discussion
by discussing the timeline.
And then we said that 6 weeks
was the magic number.
You start getting into greater than 6 weeks,
then you're getting into chronic
category, aren't you?
So, gout is acute.
It's inflammatory, no doubt, all
right? So, this is inflammatory.
Then you're going to accumulate
these monosodium urate crystals.
That's the operative word. You see that? MSU,
monosodium urate crystals. That's
what you're focusing on.
Where is it accumulating? In
different parts of the body.
For example, commonly here, the patient,
who's usually a male,
is going to be complaining of pain, where?
Let's say watching a football game
and then having a beer,
and all of a sudden, complains
of pain in the big toe,
Acute, inflammatory, monoarticular.
What's that mean? One joint, asymmetric.
Not both big toes, one big toe.
"Oh, my goodness, Doc.
It's my right toe that's in excruciating pain."
I'll give you alcohol there on purpose.
I'll tell you why as we move forward.
Welcome to gout.
What exactly are we accumulating?
What we're accumulating in
this picture showing is
monosodium urate crystals.
This may then accumulate in the big toe,
called the metatarsophalangeal joint.
Or maybe perhaps it accumulates
in your tissue.
When it accumulates in your
tissue, let me tell you,
it's then called tophaceous gout.
Or you've heard of tophi.
But the point is, it's accumulating
That's the genesis. So what then happens?
What's causing that pain?
Well, let's say that the
is unable to properly get rid
of uric acid, right?
So now these monosodium urate crystals
are accumulating in your joint.
Now it's an antigen.
So then what are you going to do?
Well, just like any antigen, you're
going to immediately, then,
respond with an inflammatory response.
The phagycitic cells,
the neutrophils and such, are
going to try to come in and
at these wonderful crystals.
Not too successful,
because now these neutrophils are then
going to release cytokines and such.
And these cytokines are then going to
cause quite a bit of pain,
as you can imagine.
what you're focusing upon
is the fact that the activation
will not necessarily be asked about,
but understand it will contribute
to the pain. So ultimately,
what does that mean to you? In acute
gout, what are you trying to do?
You're trying to lessen the pain in
this patient, aren't you?
You lessen the pain by giving anti-
inflammatory drugs, don't you?
For example, NSAIDs or maybe colchicine.
What do they have in common?
Both are acute anti-inflammatory agents.
Something that you want to keep in mind
because you're trying to prevent
the cytokines from causing
pain in your patient.
Pathogenesis, we said that
90% of your patients
are accumulating uric acid. Hyperuricemia.
uric acid of < 7 mg/dL.
Highlight that. Keep that in mind.
Disorders of uric acid, as I told you,
could be the overproducers,
but 90% will be the under-excreters.
You understand the definition?
The kidneys are unable to properly
get rid of the uric acid.
What about the overproduction?
Important? Oh, yeah.
What if you have a patient that has
cancer receiving chemotherapy?
What do you know about cancer? Neoplasia,
increased proliferation of these cells.
And these cells are still made
up of DNA, are they not?
Because what is uric acid,
It is a breakdown product of purine.
And so, therefore, if the patient
you are then causing lysis of the tumor,
therefore releasing quite a bit of uric
acid called tumor lysis syndrome.
That would come under which category?
Talk a little bit more.
As I told you, under-excreters will
be 90% of your patients.
or the patient could have
renal failure and such.
Or what if the patient was drinking alcohol,
as I gave you with the initial patient
with the presentation?
Please know that alcohol metabolites
will compete with uric acid,
so that uric acid can no longer
be secreted into the urine.
Is that understood?
Once again, let me repeat.
These alcohol metabolites are going
to compete with uric acid
so that uric acid can no longer be secreted.
So therefore, a patient is not
able to excrete uric acid.
Welcome to Hyperuricemia,
compliments of alcohol.
What kind of associations do
you want to keep in mind?
Well, chronic kidney disease,
type 2 Diabetes, dyslipidemias.
You have a long little list.
Transplant patients, especially cardiac,
related to cyclosporine. Keep that in mind.
All due to accumulation of what?
The uric acid.
What's the cardinal signs of acute gout?
It's a sudden onset of pain.
This pain, as I told you, is so, so severe
that the affected joint, for
example, the big toe,
even if you were place a bed sheet,
as light as it may be.
I don't mean a whopping comforter,
and definitely not a brick,
just saying a bed sheet.
A light, white bed sheet made out of cotton
on that toe…ouch. That hurts.
That's the kind of pain we're talking about.
The joint is inflamed,
inflammatory, red, hot, swollen.
Most common joint to be
affected, the big toe.
It's called the metatarsophalangeal joint.
We call this podagra, right?