Gastric Cancer is where we are next. In the
United States, there has been a dramatic decrease
in adenocarcinoma primarily because, well, we
have good proper screening methods in place.
Our diets, believe it or not, the society is becoming
better educated about not consuming nitrates,
smoked meats and such. Also, the fact that we
have proper regimen for H. pylori eradication.
Before we move on, there will be two major types of
primary gastric cancers or adenocarcinoma and there is
one of those lymphomas that we refer to with
H. pylori. Highest incidence however definitely Japan.
And to the point where the government itself is
getting involved to properly educate their society
so that they are not consuming large amounts of nitrates.
Or in other words, to manage and moderate how they
prepare their meat. In other words, smoked meat.
When you smoke the meat, you are then consuming
your nitrates. And the nitrate is extremely carcinogenic.
Who is your patient? Male over the age of 50.
Family history could be associated. And associated
with consumption of that smoked meat specifically
nitrate. And more likely low socio−economic status
as well. Remember, could it also occur in the US?
Sure it can. All depends on demographics, population
and history, usually the diet comes into play.
Adenocarcinoma. Here you’ll notice that apart
from what may look like a peptic ulcer disease.
Punched out lesion, but take a look at the margin
here. This is inflamed. This is adenocarcinoma.
You could tell that there is a major abnormal pathologic
growth taking place in the stomach and these are
rugal folds that you’re seeing more so in the periphery.
Adenocarcinoma of the stomach. There are two types.
The diffuse and the intestinal. H. pylori gives rise
to the intestinal and really doesn't metastasize.
Whereas if it is the diffuse type, it loves to
metastasize. You’ve heard of Virchow’s node.
Painless, left supraclavicular node involvement. You’ve
heard of Leser−Trelat sign, which is for example,
it literally looks like you’ve taken a piece of chocolate
out of your mouth like toffee, placing it on your skin,
and that's called Leser−Trelat sign. Seborrheic keratosis.
And you’ve heard of Krukenberg tumor of the ovary.
That is the diffuse type. And molecularly, we had a
discussion about E−Cadherin and that would be negative.
Risk Factors. The H. pylori that might be found
with type B chronic atrophic gastritis,
you have a phenomenon called Intestinal metaplasia.
From henceforth whenever you hear about H. pylori
and wherever it loves to live, the type of metaplasia
that it’s associated with that you need to know
clinically would be intestinal metaplasia. If it’s
smoked or salted food, that would be your carcinogen
that you’re consuming thus increasing risk of
primary gastric adenocarcinoma. Pernicious anemia.
If you’re thinking about increased pH of your gastric
lumen into luminal pH increasing in pernicious anemia,
primary atrophic gastric adenocarcinoma may be
associated. Post−gastrectomy. Smoking/tobacco use.
Any time that there is polyps. Now you'll find this
to be interesting as well. This is actually a pretty
major issue now. Polyps where? These are not polyps
in the colon. Is that clear? That is not our topic yet.
These are the polyps in the stomach. Okay, now that
you’ve understood where you are, why am I saying that
this is so important in our society now? Tell me
about PPIs. Proton pump inhibitors are available
over the counter. Prevacid, Prilosec, so on and so
forth.You take PPIs and patients do this quite a bit.
And the patient, if they are not able to properly
monitor how much PPI that they are taking
because their friends told them, "Oh, I’m
having heartburn, take PPI, take PPI, take PPI".
So we have now patients, many more of them, that
are taking PPIs. Okay, great. No, not really.
Because if acid is being diminished so very much
in these patients taking PPI, what’s the feedback
for acid? Gastrin. If the gastrin levels are low,
excuse me, acid levels are low, what’s my gastrin level?
High. Tell me about the physiology of gastrin.
Sure, it works on parietal cell. Sure, it is one of
the most important stimulators of acid secretion.
In addition, isn’t gastrin responsible for proper
development of the mucosa? And in fact if you have
too much gastrin, couldn't you result in hypertrophy?
And perhaps increased growth of your gastric tissue?
There you go. Therefore with PPIs, with the increased
growth that might be taking place due to gastrin, you
are developing or the patient is developing polyps
within the stomach. Any time that you have such
abnormal proliferation of cells and such, you’re always
increasing the risk of dysplasia. And with that dysplasia,
you’re worried about perhaps going on to adenocarcinoma.
That’s your full story for that second bullet point which
you should fully understand. It’s pharm, physio,
and here, the pathology. Familial polyposis.
Familial polyposis, we had that discussion
in neoplasia with Familial adenomatous polyposis.
And with familial adenomatous polyposis, we've talked
about APC gene mutation, beta catenin, Wnt. And you
could have polyposis up and down the alimentary canal.
Low consumption of fruit and vegetable. So we
have a high fat, low vegetable, low fiber diet.
All contributing to cancer in general, in the GI tract.
Not only colorectal cancer. Seing my risk factor there.
High fat, low fiber but then also gastric adenocarcinoma.
Let’s talk about your clinical presentation
of Gastric Cancer. Abdominal pain, weight loss, bleeding.
You’re causing damage. I showed you a picture
on gross examination of the wall of the stomach that
has now been compromised. Erosion, loss of blood,
iron deficiency anemia. Epigastric mass. The patient
will tell you, "Doc, I’m not hungry" or
"I eat food and I get satiated very quickly". And
weight loss and older patient and history of maybe
pernicious anemia, maybe smoked
meats or H. pylori, concerning.
If it is the gastric cancer that likes to spread,
it’s called diffuse. Where does it like to spread?
It loves to maybe perhaps spread to the left supraclavicular
lymph node. Left. This is called your Virchow’s node.
Maybe hematogenously. Hematogenenously, not seeding.
From your stomach and you then spread to the ovary.
These are called Krukenberg tumor and you would then
expect to find signet ring cells. This is all part
of your diffuse type of primary gastric adenocarcinoma.
A Krukenberg tumor in a 34-year-old woman in stomach
cancer you’ll notice that in the ovary you find
number of tumors and nodules representing metastasis
hematogenously from the stomach down into the ovaries.
And upon histologic examination, you would
expect to see a signet ring cell.
Management. What do you want to do? Endoscopy.
Remember, endoscopy not only do you check out the
esophagus, you do esophagogastroduodenoscopy.
The whole bit, upper. Endoscopy will show gastric mass
or an ulcer with heaped-up margin. Not punched-out
lesion. A clean punched-out lesion to you upon
description is peptic ulcer disease. The heaped-up
and I showed you a picture of exactly what I said,
around it there is increased proliferation. Total
gastrectomy to localized disease. Chemotherapy and
radiation, may be used for palliation. Responses not
good though. That's not good. The 5−year survival rate
drops from 90% for early gastric cancer to 10% for
lymph node involvement. So what the heck does that
mean to you? You want to make sure that you’re
extremely vigilant about who your patient is.
Surveillance programs in China and Japan for the exact
reason. Because if you catch your patient and then
the patient says, “Doc, I have a lump on my neck."
"Does it hurt?" "No." "Oh my goodness".
You see what I’m saying. You just drop from 90%
of survival 5-year, dropped to 10% because now
if there is lymph node involvement, that means
metastasis has now begun. Your patient,
high, high risk for mortality.