00:01
Our topic now brings us to paraneoplastic syndromes and
the different times in which you would expect to see
certain syndromes and the associated cancer. Our first
paraneoplastic syndrome will be acanthosis nigricans.
00:16
Acanthosis nigricans means thickening of the keratinocyte
giving it thus a dark colour. You might find this
underneath the armpit or maybe the back of the neck and you
should be thinking about maybe pancreatic or gastric adenocarcinoma.
00:31
A topic here, this patient "Hey Doc, wake up in the mornning
and I feel a little tired. Takes me a while to get going.
00:44
5, 6 o'clock in the evening I feel great. I wish my work
day actually started at 5pm." In this patient,
as the day wears on, he or she gets stronger. Not myasthenia
gravis, the opposite. This is Eaton-Lambert myasthenic syndrome.
01:06
Associations, small cell lung cancer. With small cell, we
will take a look at 3 different associations.
01:12
This is one of them. So what is Eaton-Lambert and what does
it do? If you remember correctly from your Immunology,
that you would have your immunoglobulin and autoantibodies.
That are then attacking instead of acetylcholine receptors,
they are attacking the calcium channels. Now I need you to
picture this. Picture neuromuscular junction. Are you picturing it?
Neuromuscular junction. Normally you would release what from the
pre-synaptic terminal. Acetylcholine. What does it then bind to
the post-synaptic terminal? Acetylcholine receptors. No problem
there. What caused the fusion of your vesicle to the membrane in
the pre-synaptic terminal. A trigger would be voltage gated calcium
channels. Voltage gated calcium channels. These are the channels
that are then being attacked by auto antibodies. So if the voltage
gated calcium channels are dead, the patient wakes up in the morning,
does'nt feel that great. Dr. Raj but how are your patient getting
better? How is your patient getting stronger? The body will find a way.
02:18
The body will find a way in which it releases acetylcholine from
the neuromuscular junction or from the pre-synaptic terminal.
02:23
You have any problem with your receptors in Eaton-Lambert? So
therefore your patient is then going to present with?
well you will have your end plate potential then have action
potential and then down it goes to the T-tubules,
skeletal muscles and contraction. Right. Small cell lung
cancer's paraneoplastic syndrome. Hypertrophic osteoarthropathy.
02:47
What does it look like? Take a look at the fingers here. Those
fingers are clubbed. It looks like it's clubbed. But this is
the bone underneath the nail that is undergoing hypertrophy. Your
differential, bronchogenic carcinoma. Hypertrophic osteoarthropathy.
03:05
Why? We don't know exactly. Then you have NBTE. Stands for
non bacterial thrombotic endocarditis. And for this
you should be thinking about mucous secreting cancers and these
include examples such as pancreatic and colorectal cancer.
03:21
Where are you by the way? Endocarditis. Most likely on the valves
of your heart. Non bacterial, sterile. Think about where you are
and know it's interesting associations. Seborrheic keratosis.
The picture here on the right that you are seing,
and know it's interesting associations. Seborrheic keratosis.
The picture here on the right that you are seing,
the first picture will be that of your Leser-Trelat sign. This
to you should also indicate adenocarcinoma, and usually
it will be the diffuse type in which the E-cadherin will be
negative. Another name for Leser-Trelet is called
seborrheic keratosis. And on your boards, do not confuse this
with, good, actinic keratosis. One has nothing to do with the other.
04:04
The picture here on the right is a seborrheic
keratosis or brown scaly spot on the skin
commonly found anywhere on the body.
04:12
Although seborrheic keratosis are a benign skin
finding in many people,
an abrupt development of multiple seborrheic
keratosis can be a cutaneous
neoplastic indicator of internal malignancy.
04:23
This is called the Leser-Trelat sign.
04:26
It's a fairly rare pair neoplastic syndrome,
but it's been associated with GI adenocarcinoma.
04:31
The path of physiology,
of the sign of lesser Chilla
Syndrome is unknown, but it's suspected
to be related to the release of cytokines
and epidermal growth factors
from the neoplasm.
04:41
The last pair in Neoplastic syndrome
we're going to discuss
is a cutaneous finding called necrolytic
migratory erythema.
04:48
This is a transient weeping exhibit,
this rash that is seen in about 70%
of patients with glucagon secreting
pancreatic islet cell tumors or glucagon
comas.
04:58
The rash primarily occurs around the mouth
or genitals and includes inflammatory,
scaly plaques with an appearance similar
to eczema or psoriasis.
05:06
In summary, paraneoplastic syndromes
are due to chemical signaling molecules
produced by tumor cells or by an immune
response against the tumor.
05:15
They can manifest with cutaneous findings.
05:17
Neurologic syndromes, hypercalcemia
endocrinopathies or hematologic abnormalities.