However, let's get into actual cancer. The
way that this is divided into clinical lung
cancer is the following. Let's take a look
at our first family and this then includes
our bronchogenic carcinoma. 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. 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. 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? Because we know
that number one cause of death in both the
men and women mortality is lung cancer. Of
all the lung cancers, it is one of the non-small
cell lung cancer. And what is that? Adenocarcinoma.
So, that’s where our focus shall be. But
before we get there though, a couple of things
that you want to keep in mind as we go through.
Small cell lung cancer. It’s also called
oat, oat cell. Location. This is a primary
lung cancer. This means it will be one nodule
first. 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. Now
usually, if it’s benign in nature, it would
then be, well, let's say within 3 cm.
Keep that in mind.
Now, where is this nodule located? If it’s
a small cell lung cancer? Well, this would
be by the mediastinum. Hence we call this,
take a look, pay attention, what is significant
here is the word 'centrally located'.
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.
That’s what’s meant by central.
Characteristics, there’s a bunch. Let's
walk through this. First, let's get into
our patients and then I’ll walk you through
the verbiage, just like I’ve been doing.
Otherwise, I mean, what’s the point of me
reading this to you, you could do that on
your own. So, the small cell lung cancer,
say that your patient comes in, then they
have a broomstick appearance of the extremities.
The arms, the extremities down by the legs.
They have truncal obesity, they have moon faceies.
Well, it kind of looks like you, Dr. Raj.
No, it’s not, I don’t have moon facies.
Maybe I do. But, I definitely, and I do
have truncal obesity, I’ll give you that.
Broomstick appearance, oh, now, I’m kind
of doubting myself, huh? What am I referring
to? Good. Cushing’s syndrome. What’s causing
this Cushing’s syndrome in a patient that
has small cell lung cancer? The hormone. Is
the lung cancer producing too much cortisol
or is it producing too much ACTH? You tell
me. You stick to letter A. ACTH, clear? Now
you tell me two major places or origin or
sources where ACTH would be produced in excess,
resulting in excess cortisol. Good. One would
be the anterior pituitary. You call that Cushing
a disease, right? And then second one would
be the lung and this would be small cell lung
Now, if you want, I might want take a look
at the A in small cell and use it to your
advantage. You have ACTH. Let me give you another
patient. This patient is one in which, well,
they’re not urinating a whole lot, they’re
really not. It’s not polyuria, it’s oliguria.
The urine that they are producing is extremely
concentrated. Maybe the urine osmolarity is
up to 900. Take a look at the plasma osmolarity
and it’s at 250. Diagnosis, SIADH. Syndrome
of inappropriate ADH. ADH, another hormone
that also begins with letter A. So now you
tell me a couple of places where ADH might
be released in excess. Good, maybe from the
hypothalamus, maybe from the posterior pituitary,
centrally or maybe you’re releasing it paraneoplastically.
You see your patients, too much ADH, concentrated
urine, plasma osmolarity decreased. Move on.
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.
As the day progresses, I get stronger, get
stronger, get stronger. Wow, I feel great
in the afternoon. This is how I feel.” What
am I referring to? This is Lambert-Eaton myasthenic
syndrome. Right? What is this? This is associated
with small cell lung cancer. It is an auto
antibody disease, completely opposite of myasthenic
So, myasthenia gravis is one in which your
female patient, most likely. She wakes up
in the morning and what happens? She’s feeling
good. In Lambert-Eaton, you wake up in the
morning and maybe not so good. 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. 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. Do you have any problem of acetylcholine
supply? In Lambert-Eaton, no. 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. That
is your voltage-gated calcium channel. You
see that? So, your voltage-gated calcium channel
are then being destroyed or targeted by the
auto antibodies that may be produced paraneoplastically
by small cell lung cancer. Amazingly complicated,
but once you get it all down, it all makes
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. The body will find a way in
which it will release the acetylcholine from
the neuromuscular junction. Once that acetylcholine
comes out of the presynaptic terminal, it’s
gonna cross the cleft. Where does it bind
to? Yes, it will continue. 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. Move on.
What else might you have? Antibodies against
neurons in Paraneoplastic myelitis. Keep that
in mind. So, every once in a while, you might
have issues with the nerves. It’s called
Paraneoplastic myelitis. Maybe encephalitis.
There could be subacute cerebellar degeneration.
Amplification of MYC oncogenes, is the big one.
Management with chemotherapy, chemotherapy,
chemotherapy and that then becomes your pharmacology.
So, small cell, a lot of stuff going on here
in bronchogenic. And then as I told you earlier,
our next set of cancer we’ll take a look
at will be non-small cell.
Histology becomes important for us. We have
neuroendocrine. Lot of paraneoplastic. Take
a look at this. Paraneoplastic myelitis, encephalitis.
So, whenever you have CNS issues within the
cancer, you can expect there to be neuroendocrine,
okay? So, neoplasm, neuroendocrine, Kulchitsky
cells appear – small dark blue cells.
Okay. What else might you find? You want to
be specific here. By that I mean, neuron-specific
enolase positive. That’s important. And
you want to know chromogranin A. And many of
these you actually find in many of your neuroendocrine
type of cancers, including carcinoids.
We’ll talk about that later. Welcome to
Let's continue our discussion of bronchogenic
carcinoma. 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.