Our topic now brings us into Peptic Ulcer Disease.
With 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
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 or 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, your
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 says, 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 is 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 we 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 will take the urea and they will create
a force field for itself. That force field that the
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 cortisol. Hypercortisolism, is then knocking
out your phospholipase A2. You don’t have the
necessary prostaglandin to protect the lining of
the stomach and 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
damage to the lining. Whereas if it is pathogenesis
for peptic ulcer disease of the duodenum, then in
fact there 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 all that acid.
Mucosal ischemia is always a possibility whenever
there is infarction that’s taking place. And then at some
point in time you might then be hurting or injuring
the 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, with peptic ulcer disease in the stomach
you would not find and the patient would not be
complaining of 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
out lesion in the stomach. And a 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 is perforation that’s taking place
especially of the duodenal 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 to 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, then the perforation then causes
damage to the gastroduodenal artery. Gastric outlet
obstruction due to peri-pyloric scar formation is an
important complication. At some point in time when
there is enough damage that has taken 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 a scar formation
and therefore decreasing the emptying of the stomach.
Gastric ulcers may be malignant while duodenal 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, there's possibility
of a primary gastric cancer developing and duodenal
almost never. On the left, the peptic ulcer disease
is in the duodenum. You’ll notice that you have a
clean, punched-out lesion. Whereas in gastric
ulcer, you also have a clean, punched-out lesion.
Endoscopy, Esophagogastroduodenoscopy, would be
your 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. Antacids.
Because of the burning sensation that’s taking place,
magnesium and aluminum cause long-term toxicity.
Be careful with antacids, magnesium and aluminum.
Milk alkali syndrome due to prolonged use of calcium.
A symptom that you want to keep in mind with antacids.
Once again, milk alkali syndrome due to prolonged
use of calcium. H2 Blockers. Here once again,
you block your receptors on histamine for H2 and
decrease acid production if in fact that is one of
your concerns with peptic ulcer disease. H2 blockers,
however, does inhibit the cytochrome P450 system
in the liver so therefore may then cause decreased
metabolism with certain drugs. So drug-drug
interactions become a important side effect. An
interaction that you want to keep in mind for H2 blockers.
Proton pump inhibitors. Extremely effective in terms
of decreasing the amount of hydrogen that you’re
pumping into the stomach. Irreversible blockage of
your hydrogen-potassium pump. However, if you are
using this, keep in mind that because you're
decreasing acidity within the stomach, here once again,
you might then cause interference of absorption of
other drugs. Drug-drug interactions become incredibly
important here. Sucralfate. It stimulates endogenous
prostaglandin productions so that it helps to then
protect the lining of the stomach. Avoid in
renal insufficiency 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. Duration of
therapy if it’s duodenal ulcer being the most common
type of presentation in the US, 4 to 6 weeks of
duration. If it's gastric ulcer, then it's 6 to 8 weeks
with repeated esophagogastroduodenoscopy to document
the healing. The management, remember, H. pylori
highly associated with both of these issues.
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 treatment. So you want to
either think quadruple bismuth. And the quadruple
therapy would inlcude 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.