00:02
However,
let's get into actual cancer.
00:05
The way that this is divided into
clinical lung cancer is the following.
00:09
We'll take a look
at our first family
and this then includes our
bronchogenic carcinoma.
00:14
Under bronchogenic carcinoma,
the way that this is then worded,
if you take up any,
if you pick up any medical journal,
New England, Lancet, whatever.
00:23
On the first few pages, often times,
you have this huge plastered advertisements
and it’s dealing with how to treat with
what’s known as non-small cell lung cancer.
00:35
Why do they choose,
and as we walk through here,
things that you want
to keep in mind,
why do they choose on every single
magazine to be talking about
a non-small cell lung cancer?
This is because lung cancer is the
leading cause of mortality from cancer
and the 6th leading cause
of mortality overall,
according to the World
Health Organization.
00:54
Of all the lung cancers, it is one
of the non-small cell lung cancer.
00:59
And what is that?
Adenocarcinoma.
01:01
So, that’s where
our focus shall be.
01:02
But before we get there though,
a couple of things that you want
to keep in mind as we go through.
01:06
Small cell lung cancer.
01:08
It’s also called oat, oat cell.
01:11
Location.
01:12
This is a primary lung cancer.
01:15
This means it will
be one nodule first.
01:19
Understood?
So, the fact that you found a solitary
nodule in a previous discussion
could be concerning because
if it’s a primary lung cancer,
it would be one nodule.
01:28
Now usually, if it’s benign in nature, it
would then be, well, let's say within 3 cm.
01:34
Keep that in mind.
01:36
Now,
where is this nodule located?
If it’s a small
cell lung cancer?
Well, this would be
by the mediastinum.
01:42
Hence we call this,
take a look, pay attention,
what is significant here is
the word 'centrally located'.
01:49
And by centrally located, we mean
that you will find on a chest X-ray
(CXR) a primary nodule, one,
dark calcific by the mediastinum.
02:00
That’s what’s meant by central.
02:03
Characteristics,
there’s a bunch.
02:04
Let's walk through this.
02:06
First, let's get into our patients and
then I’ll walk you through the verbiage,
just like I’ve been doing.
02:11
Otherwise, I mean, what’s the
point of me reading this to you,
you could do that on your own.
02:14
So, the small cell lung cancer,
say that your patient comes in,
then they have a broomstick
appearance of the extremities.
02:21
The arms,
the extremities down by the legs.
02:26
They have truncal obesity,
they have moon faceies.
02:28
Well, it kind of looks like
you, Dr. Raj.
02:30
No, it’s not, I don’t have moon facies.
Maybe I do.
02:33
But, I definitely, and I do have
truncal obesity, I’ll give you that.
02:36
Broomstick appearance, oh, now,
I’m kind of doubting myself, huh?
What am I referring to?
Good. Cushing’s syndrome.
02:42
What’s causing this Cushing’s syndrome in
a patient that has small cell lung cancer?
The hormone.
02:48
Is the lung cancer producing too much
cortisol or is it producing too much ACTH?
You tell me.
02:54
You stick to letter A.
02:56
ACTH, clear?
Now you tell me two major places
or origin or sources where ACTH
would be produced in excess,
resulting in excess cortisol.
03:10
Good.
03:10
One would be the
anterior pituitary.
03:12
You call that Cushing a
disease, right?
And then second one would be the lung
and this would be small cell lung cancer.
03:20
Now, if you want,
I might want take a look at the A in
small cell and use it to your advantage.
03:26
You have ACTH.
03:28
Let me give you another patient.
03:29
This patient is one in which,
well, they’re not urinating a whole
lot, they’re really not.
03:33
It’s not polyuria,
it’s oliguria.
03:36
The urine that they are producing
is extremely concentrated.
03:39
Maybe the urine
osmolarity is up to 900.
03:44
Take a look at the plasma
osmolarity and it’s at 250.
03:47
Diagnosis, SIADH.
03:51
Syndrome of inappropriate ADH.
03:54
ADH, another hormone that
also begins with letter A.
03:59
So now you tell me a couple of places
where ADH might be released in excess.
04:03
Good, maybe from the hypothalamus, maybe
from the posterior pituitary, centrally,
or maybe you’re releasing
it paraneoplastically.
04:12
You see your patients,
too much ADH,
concentrated urine,
plasma osmolarity decreased.
04:19
Move on.
04:20
What else might you find?
Well,
this is a patient in which,
“Hey doc,
when I wake up in the morning
and I’m not feeling that great,
I’m kind of tired and fatigued.
04:28
As the day progresses, I get
stronger, get stronger, get stronger.
04:32
Wow,
I feel great in the afternoon.
04:34
This is how I feel.”
What am I referring to?
This is Lambert-Eaton
myasthenic syndrome.
04:40
Right?
What is this?
This is associated with
small cell lung cancer.
04:45
It is an autoantibody disease,
completely opposite of myasthenic syndrome.
04:51
So, myasthenia gravis is one in which
your female patient, most likely.
04:57
She wakes up in the
morning and what happens?
She’s feeling good.
05:02
In Lambert-Eaton, you wake up in
the morning and maybe not so good.
05:06
In myasthenia gravis, as the day
progresses, maybe at noon time,
she’s working in front of a
computer and she can’t see too well
because of the eye drooping.
05:15
And by 3 or 4 o’clock,
she rolls around, she tells you,
“I can barely get
out of my chair.”
Whereas with Lambert-Eaton,
what happens?
Do you have any problem with
your acetylcholine receptors?
In Lambert-Eaton, no.
05:29
Do you have any problem
of acetylcholine supply?
In Lambert-Eaton, no.
05:33
Where is my problem?
The problem lies in the fact that
you’re having a hard time releasing
your acetylcholine at the
neuromuscular junction, aren’t you?
What is it that allows for acetylcholine to
be released from the presynaptic terminal
at the neuromuscular junction?
Good.
05:49
That is your voltage-gated
calcium channel.
05:51
You see that?
So, your voltage-gated calcium
channel are then being destroyed
or targeted by the autoantibodies that
may be produced paraneoplastically
by small cell lung cancer.
06:02
Amazingly complicated,
but once you get it all
down, it all makes sense.
06:07
So, Dr. Raj, how is the
individual getting stronger?
If you can’t even
release acetylcholine,
you sure you know what
you’re talking about?
I do, trust me.
06:15
The body will find a way in which
it will release the acetylcholine
from the neuromuscular junction.
06:22
Once that acetylcholine comes
out of the presynaptic terminal,
it’s gonna cross the cleft.
06:27
Where does it bind to?
Yes, it will continue.
06:29
It binds to acetylcholine receptors,
open up the sodium channel,
you have an amplified potential,
end up hitting threshold,
action potential, welcome
to, increase contraction.
06:41
Let's move on.
06:42
What else might you have?
Antibodies against neurons
in Paraneoplastic myelitis.
06:48
Keep that in mind.
06:49
So, every once in a while,
you might have issues with the nerves.
06:53
It’s called
Paraneoplastic myelitis.
06:55
Maybe encephalitis.
06:57
There could be subacute
cerebellar degeneration.
07:01
Amplification of MYC
oncogenes, is the big one.
07:04
Management with chemotherapy,
chemotherapy, chemotherapy
and that then becomes
your pharmacology.
07:09
So, small cell, a lot of stuff
going on here in bronchogenic.
07:12
And then as I told you earlier,
our next set of cancer we’ll take
a look at will be non-small cell.
07:17
Histology becomes
important for us.
07:20
We have neuroendocrine.
07:21
Lot of paraneoplastic.
07:22
Take a look at this.
07:23
Paraneoplastic
myelitis, encephalitis.
07:26
So, whenever you have CNS
issues within the cancer,
you can expect there
to be neuroendocrine.
07:31
Okay.
07:31
So, neoplasm, neuroendocrine, Kulchitsky
cells appear – small dark blue cells.
07:39
Okay.
07:40
What else might you find?
You want to be specific here.
07:43
By that I mean,
neuron-specific enolase positive.
07:46
That’s important.
07:47
And you want to
know chromogranin A.
07:49
And many of these you actually find in many
of your neuroendocrine type of cancers,
including carcinoids.
07:55
We’ll talk about that later.
07:57
Welcome to small cell.
07:59
Let's continue our discussion
of bronchogenic carcinoma.
08:02
Now, we’ll take a
look at non-small cell
and these are the ones that are much
more common as we go through this.