Continuing our discussion
of multiple myeloma.
Apart from serum protein electrophoresis,
what are the feature that
you’d expect to find?
Well, if you take a look at the skull,
you’ll find that you have
punched out lesions.
It’s a monoclonal gammopathy, you’d
expect there to be IgG or IgA,
but not IgM, and
these light chains.
Light chains are once again
either kappa or lambda.
And majority of them will be kappa.
And as the picture would show you,
oftentimes, actually almost on your
boards, they have to give you –
If they want you to
choose multiple myeloma,
they’ll give you lytic bone lesions
and these are punched out lesions,
not wide areas of complete
destruction of the bone.
The reason I bring that
to your attention is,
when we talk about Langerhans
there will be a subtype called
and that type is where you would
also find destruction of the bone,
but it’s quite chaotic.
It’s not so chaotic in plasma
cell multiple myeloma.
What I mean by that is
it’s punched out lesion,
almost looks as though that the skull was
shot by a bullet, going right through it.
I have to be careful as to how
I use the word chaotic though
because it is going to
cause chaos in your body.
So once you start having these lytic bone
lesions, the bone is very, very weak.
Your patient is now prone
to pathologic fractures.
the bone which is the major
reservoir for calcium,
the calcium is now being leaked
into circulation at great quantity.
You can expect your patient no
doubt to have hypercalcemia.
That calcium is going to
pass through the glomerulus.
You can absolutely expect your
patient to have hypercalciuria,
and with all this calcium
that’s now in your urine,
would you not expect there
to be calcium stones?
Everything’s a story.
Make sure you understand as to how the
disease initiates from the bone marrow.
with plasma cells, IgG and IgA,
and how it wreaks havoc
on the bone specifically.
A couple of other things
in terms of symptoms,
I’m giving you the fundamentals
of multiple myeloma,
there’ll be other things such as rouleaux
formation, but that is nonspecific,
and I’ll give you a little
bit of detail about that.
And there could be issues with the
kidney or Bence Jones protein.
But Bence Jones just
means light chains.
You can find light chains
in other diseases.
Lytic bone lesion, bone marrow.
Plasma cell, multiple myeloma, IgG,
IgA, gamma spike, nonspecific.
Is that enough information?
Get your question right.
The picture that you’re seeing here upon
histology would be from the bone marrow.
A bone marrow aspirate in which you
would then find tons of plasma cells.
How can you identify
these plasma cells?
Rows upon rows of rough
And if it’s multiple myeloma
specifically, from the bone marrow,
and what kind of immunoglobulins
are these then producing, please?
IgG or IgA.
With all these being produced, then
what wave is then going to be affected?
The gamma wave.
And now you have
created a gamma spike.
Signs and symptoms of multiple
myeloma, we’ll talk about that bone.
So here, you might have
osteoclastic activating factor.
Many times, interleukin 1
or 6 might be involved.
Remember that from immunology.
Interleukin 1 or 6.
All that osteoclastic activity
then causing bone infiltration.
There will be chronic pain.
The bone is now weakened.
Your patient is now susceptible
to pathologic fracture.
With all that bone being destroyed,
well, no doubt that the patient
is suffering hypercalcemia,
perhaps calcium stones.
The immunoglobulin that’s being
produced in great quantity.
You’re producing the light chains,
that then deposits on your glomerulus.
You’re going to have
And this amyloid then is stained with your
Congo red, which give you what color?
Apple green birefringence.
you have these Bence Jones proteins, but
then you also have Tamm, Horsfall, CAS,
and all of these is then going to
cause major damage to the tubules,
eventually leading into renal
failure, amyloid deposition.
What’s interesting about plasma
cell neoplasms or multiple myeloma?
You would think, you know, just by theory,
“Dr. Raj, you’re producing
all these immunoglobulins,
how is it possible that the patient
is susceptible to infection?”
You completely lose the
proper, proper protocol
for isotypes switching
of your immunoglobulin.
Remember, you have to have IgM 1.
You have to have isotype switching into the
type of immunoglobulin that’s necessary
to fend off the
antigen or infection.
In plasma cell multiple myeloma, my
goodness, you lose that isotype protocol.
So therefore, even though you might be
producing all these immunoglobulins,
it doesn’t mean that you’re hyper
immune, in fact, just the opposite.
Your immunity is
impaired or compromised.
Your patient is
susceptible to infection.
You’re producing the wrong –
You’ve lost the proper organization
of your immunoglobulin.
Clinically, who’s your patient?
Almost always older.
we don’t have proper methods of
controlling multiple myeloma, not yet.
The older the patient gets
with multiple myeloma,
I can almost say guaranteed
Incidence increases with
Prognosis is very poor.
Look at this, three
There are variants here, a little bit
more detailed than what’s necessary,
but understand there are variants.
I’ll have you focus on the one
that we have been discussing.
You have smoldering type,
your indolent type,
you have an osteosclerotic type even,
but then here’s your nonsecretory
that’s also quite rare.
But the one that we looked at by far,
would be one in which it’s a
classic, classic multiple myeloma
in which you’re going to produce
lots of immunoglobulin.
And it will be IgG
or it would be IgA.
However, just keep in
mind, I cannot guarantee
that that is only what they’ll ask.
So just to make sure that we’re
complete, here are variants.
You can actually have a
nonsecretory type of variant.
Has all other characteristics
of multiple myeloma,
but then your M protein, which represents
your IgG or IgA and such, it’s negative.