Our topic now brings us
into, “Peptic ulcer disease.”
A peptic ulcer disease you
divide this into that disease,
or erosion that's taking place in the stomach,
versus that type of erosion that
might be taking place in duodenum.
By far in the US,
the most type of most common
type of peptic ulcer disease,
would be the type that's
taking place in the duodenum,
however, for learning purposes,
we need to make sure that we cover
both sets of peptic ulcer disease,
and then, importantly,
we will go through the symptoms of your patient,
so that you're able to
distinguish one from the other.
Mechanism of injury:
If there's direct mucosal
damage due to toxins (ethanol),
NSAIDS, bile, H. pylori.
Now, for the most part,
you can think of peptic ulcer
disease taking place in the stomach,
as really not due to increased acid production,
remember that, the stomach is extremely effective,
with protecting the lining
of the stomach from the acid.
And due to all that bicarbonate,
prostaglandins and such,
so therefore, protecting the
stomach from all that acid.
However, if the lining of the
stomach has been compromised,
where it could take place
due to, let's say, NSAIDS,
which is then inhibiting your COX pathway,
then you might then inhibit the
formation of the prostaglandin
necessary to properly protect,
or contribute to the protection of the stomach,
or if there's actual chemical damage
taking place to the lining of the stomach,
due to bile, that might then
regurgitate back into the stomach,
remember bile, is being released
or secreted from your gallbladder,
into the second part of the duodenum,
so therefore, there must be some kind of method,
by which the bile is,
retrograde flow back in
the stomach causing damage.
H. pylori in the stomach would be residing where?
In the antrum of the stomach and from henceforth,
whenever you deal with H. pylori,
you should be thinking either
the distal end of the stomach,
or the first part of the duodenum,
as being its place of residence.
In the stomach the H. pylori
if you remember from micro,
then has an enzyme called urease.
Therefore, it'll take the urea and it
will create a force field for itself,
that force field that H. pylori then
creates in the antrum of the stomach,
is then made up of ammonia, amazing isn't it.
At some point in time, it could then
burrow into the lining of the stomach,
and so therefore weakening the lining,
resulting in peptic ulcer disease.
H. pylori, bile, NSAIDS, alcohol.
Prostaglandin inhibition, like we
just said with NSAIDS or steroids,
even with pathologies such as, Cushing,
in which you would have excess
is then knocking out your phospholipase A2,
you don't have the necessary prostaglandin,
to protect the lining of the
stomach as such, against the acid.
Increased acid production could be a cause,
but more importantly the
most important pathogenesis
for peptic ulcer disease of the stomach,
would be damaged to the lining.
Whereas if it is pathogenesis peptic
ulcer disease of the duodenum,
then in fact it would be increased acid.
For example, if you do Zollinger-Ellison syndrome,
and with the gastrinoma,
with all that acid which is then
coming out like a huge wave,
out of the stomach and into the duodenum,
there is no way that the duodenum
can properly protect itself
against the all that acid.
Mucosal ischemia, is always a possibility,
whenever there is a infarction
that's taking place,
then at some point in time,
you might then be hurting or
injuring lining of the stomach.
Peptic ulcer disease,
if it is in the stomach, the patient here,
is going to be complaining of epigastric pain,
however, this time around,
the peptic ulcer disease in the stomach,
you would not find, and the patient
would not be complaining a pain,
that's radiating to the back, is that clear?
On your step, and on your wards,
if the pain is radiating to the back,
then this gives you the high suspicion
and differential of pancreatic damage,
however, if it's not,
then you're thinking about peptic ulcer disease.
Also, with this erosion
that's taking place, remember,
you have not perforated,
ulceration means ulceration,
it's a clean punched up lesion in the stomach,
and the clean punched out lesion here,
with bleeding taking place,
may result in hematemesis.
With all this blood that's now being released,
either from the stomach or
maybe perhaps the duodenum,
you can only imagine that, as I told you earlier,
that the stool has an opportunity to
completely saturate itself with blood.
So, therefore by the time it's evacuated,
here the stool, in fact is
going to look black and tarry.
Hematemesis, hematochezia, iron deficiency anemia,
all these, well, all part of bleeding.
Next, if there's perforation that's taking place,
especially of the duodenum
type of peptic ulcer disease,
it will then perforate and then it
will then affect different organs
or blood vessels.
If it is peptic ulcer disease of the stomach,
which is usually found in the
lesser antrum of the stomach,
and if it is the perforate,
then you are then going to,
or the perforation is going to
affect the left gastric artery.
Whereas if the perforation takes
place down in the duodenum,
and then the perforation,
then causes damage to the gastroduodenal artery.
Gastric obstruction due to
peri-pyloric scar formation,
is an important complication.
At some point in time,
when there is enough damage that's taking place,
any type of damage at some point,
the body wishes to respond
with the repair process.
This repair process that you're looking for,
at some point with fibrosis taking place,
may actually then cause, gastric outlet problems,
because of the more or less think of
it as being a stricture formation,
or scar formation,
and therefore, decreasing
the emptying of the stomach.
Gastric ulcers may be malignant,
while duodenum ulcers are basically never.
Once again, peptic ulcer disease,
keep in mind that if it's the stomach,
you should be monitoring or should be thinking,
“The possibility of a primary
gastric cancer developing”
in duodenal, almost never.
On the left, peptic ulcer
disease is in the duodenum,
you'll notice that you have
a clean punched out lesion,
whereas a gastric ulcer,
you also have a clean punched out lesion.
would be your guest best measure
or best method of diagnosis.
With this ulceration, at some point remember,
keep your ulceration and
perforation completely separate.
Management of peptic ulcer disease.
Because of the burning
sensation that's taking place,
magnesium and aluminum cause long-term toxicity,
be careful with antacids.
Magnesium and aluminium.
Milk alkali syndrome due to
prolonged use of calcium,
is something that you want to
keep in mind with antacids.
Once again, milk alkali syndrome
due to prolonged use of calcium.
PPIs are first line treatment for a PUD,
and they're also used in combination
with antibiotics to treat H. pylori.
It stimulates endogenous prostaglandin
production so that it helps to then,
protect the lining of the stomach.
Avoiding renal insufficiency,
so, and that's a big deal.
So, the drugs that I've given here for management,
I've given you as to what it does objectively,
and then things that you want to
keep in mind, as side effects,
because these patients will be on these drugs
for quite a bit of time.
Peptic ulcer disease.
We have two types,
the duration of therapy if it's duodenal ulcer,
being the most common type
of presentation in the US,
4-6 six weeks of duration.
If it's a gastric ulcer,
then at 6-8 weeks with repeated,
to document the healing.
The management remember H.
pylori highly associated with,
both of these issues,
so therefore, the importance
of eradicating H. pylori,
cannot be understated,
responsible for developing lymphomas perhaps,
and maybe even our intestinal type
of gastric primary adenocarcinoma.
Now, we have two types of treatments,
so, you want to either think quadruple bismuth,
and the quadruple therapy would
include bismuth metronidazole,
tetracycline and proton pump inhibitor,
or you could have clarithromycin
based triple therapy,
which would then consist of,
amoxicillin, clarithromycin and your PPI.