Speaker 1: Today we're gonna be going over gastric disorders, so it's
going to be involving gastritis, peptic ulcer disease, and pyloric stenosis.
And I just want to mention really quick, if you
do like the podcast, it's helping you. Please, please, if
you wouldn't mind giving me a review on Apple Podcasts, Spotify,
just let me know that it's helping you. It kind
of also gets the word out about the podcast and
helps other people discovered as well. I'd really appreciate that.
So with that being said, let's go ahead and start
with aqte gastritis. So qute gastritis is an inflammation resulting
from gastric mucosal injury. It's important to note that there
is something else called gastropathy, which is going to be
a more superficial mucosal injury with no associated inflammation. So
that's another term that you need to know as well.
As far as eteologies, H pylori most common cause by
far H pylori. Remember this is going to be your
most common cause of acte gastritis.
Speaker 2: And H.
Speaker 1: Pylori is a GRAM negative bacteria that's very common. It's
actually found in about half of the world's population, So
not everybody gets symptoms from this though, So just because
it's part of your microbio doesn't mean you're gonna have symptoms,
but the people that do develop symptoms. H Pylori infects
the gastric mucosa. It releases certain enzymes and toxins, and
it injures the epithelial cells of the stomach, which leaves
the stomach more vulnerable to the acid that's present and
causes gastritis. It can cause peptic ulcers as well as
pain and a number of other symptoms. So that's how
H bilori causes that. Again, most common cause. That keep
repeating it because it's important. And then your second most
common cause is going to be from n seds and aspirin.
So the way n seds and aspirin and cause gastritis
one way is that it's just from a superficial irritation
of the epithelium of the gastric mucosa. So that can
happen if you take like eight hundred milligrams vibuprof and
you didn't any food with it, and you just have
this stomach pain for a couple hours. But the more
important factor is that n sets inhibit COX one production,
so COX one production is actually responsible for producing prostag landins.
So if you decrease COX one production, decrease production of
prostic landings. Well, why does that matter. It's because prostac
landins actually inhibit gastric acid secretion, so less prostac landins
means more gastric acid and more irritation like gastritis peptic ulcers.
So that's why n sets are really important as a
factor that can cause gastritis. And that's actually why n
sets like celebres, which is also known as celocoxid, were
created because celebres actually targets COX two rather than COX one,
So this leads to less gastric issues and they have
a number of other cardiovascular problems, but that's besides the point.
But that's why they were created because when you don't
target COX one, you don't affect the prostac landids in
the stomach and you have less gastric problems. So that's
why nc's are a big issue here. Some other less
important causes are going to be alcohol, trauma, acute stress,
radiation and things like that, but the ones you need
to know is going to be h pylori and n sets.
Do not forget those H pyloris You're most common and
says you're second most common costs.
Speaker 2: So remember those.
Speaker 1: As far as the patient presentation, some patients initially may
be asymptomatic, but as it progresses, you're going to have
these non specific symptoms. It's like epigastric discomfort also known
as dyspepsia. They may have some nausea, loss of appetite,
nothing really specific that you need to know that's gonna
stick out in a vignette, but just these non specific
epigastric symptoms. Diagnosing while your test of choice, although it
isn't necessarily going to be the first thing you do,
is going to be an upper endoscopy. This is going
to be your best test. But initially you're going to
do some testing for H pylori because these are things
that are non invasive. You can do a uria breath test,
a fecal antigen test to test for H pylori to
see if you need to treat that. I'll go over
those tests a little bit in pepticals or disease and
what they involve, but those so initially you probably test
for h uria breath test fecal antigen test, and then eventually,
if those tests come back negative, these patients are still
having symptoms, you may move on to an upper endoscopy,
which would be your best test. And this is going
to be patients that are refractory to PPIs, H two
blockers things like that. So some of the ways you
can diagnose test for H pylori, upper endoscopy, and treatment, well,
it all depends on the cause. So if these patients
have H pylori, your test came back positive, you're your
breath test or vecal antigen test came back positive. You're
going to treat H pylori. So how do you treat
H pyloria, whether it's quadruple therapy. Quadruple therapy is going
to be a combination of PPIs, bismuth, metronidazol, and tetracycling.
So H pylori positive treat the H pylori with quadruple therapy.
You want to discontinue n SAID use if that's what's
causing it, and you can also use PPIs and H
two blockers, particularly in patients who require the continued use
of n SET. So whether it's a cardiovascular patient that
requires daily aspirin patient with chronic pain that has to
take their ND sets but they develop gastritis, then you
can use PPIs and H two blockers as well for
the treatment. So treatment depends on the cause H pylori.
Treat the H pylori discontinue n said use if they're
using it, and PPIs and H two blockers are going
to be your main.
Speaker 2: Ways to treat qute gastritis.
Speaker 1: As something else that I'm going to go over, it's
definitely not very high yield, but you need to know
that it exists because it is on the blueprint. It's
something called autoimmune metaplastic atrophic gastritis, so again not high yield,
but be aware that it exists. It's a chronic form
of gastritis. It's an inherited autoimmune disease, so unlike a
cute gastritis, this isn't going to be from N sets
or it's pylori use. It's going to be an autoimmune process.
So the immune system is actually attacking the parietal cells,
an intrinsic factor in the body. This can lead to
B twelve deficiency as well as this gastritis that these
patients have. These patients are also at a high risk
of gastric carcinoma.
Speaker 2: And one other important thing.
Speaker 1: That you need to know is that while acute gastritis
most commonly affects the antrum of the stomach, chronic or
autoimmune gastritis spares the antrum and most commonly affects the
fundus or the body. So for real life maybe not
so important, but for a vin yet they may mention that.
So remember a QT gastritis affects the antrum, chronic autoimmune
is going to most commonly affect the fundus in the
body and spares the andantrum. That's really all you need
to know for that. Don't go crazy again, not very
high yield.
Speaker 2: Now moving on.
Speaker 1: To something that is high yield is peptic ulcer disease.
So there's a lot of stuff you need to know
on this. Let's go over that. There's going to be
some overlap two with gastritis as well. So peptic ulcer
disease encompasses both duodenal ulcers and gastric ulcers. So some
things that two have in common, some things that help
differentiate them. So we'll go over the different things. So
let's start with duoden ulcers so duoden ulcers are going
to be an area of erosion obviously in the duodenum.
It's going to be your most common type, so much
more common, about four times more common than gastric ulcers,
and usually it's benign. Gastric Ulcers are going to be
an area of erosion in the stomach, and these are
less prevalent than duodenal ulcers and more commonly associated with
gastric edinal carcinoma. So remember that duodenal ulcers usually benign.
Gastric ulcers are more commonly associated with gastric adino carcinoma,
and duoden ulcers are your more common type as far
as eteologies, a lot of overlap here with gastritis. Again
h pylori most common cause overall, nothing new that you
need to know there, Second most common cause, N SAIDs
an aspirin really easy. You already know this for gastritis,
So again hpylori most common. N says an aspirin second
most common. And then another odd bowl that you need
to know of that's not very common about you know,
like less than one percent of patients. It's something called
Zollinger Ellison syndrome and This is a disease that produces
high levels of gastrin from a neuroendocrine tumor, and gastrin
leads to high levels of acid in the stomach, which
can lead to ulcers and gastritis as well as another
a few other things. So again not a very common cause,
but something that you do need to know because it
may come up in the boards, and just a small
factor that you need to know as well. So hpylori
is your most common cause overall, but it's going to
be more associated with duodeno ulcers, where n sets an asper,
your second most common cause overall is going to be
more commonly associated with gaster cultures, So just know that,
but again same overlap with gastritis. Hpylori most common, and
sayd as an aspirin second most common, and then just
know about zolinger ellison just as that oddball that may
come up, as well as some of the other factors
you know that can lead to pepic ulcers as well.
Increased alcohol use, smoking also more common and elderly. Those
are the less less important things that you need to know.
But of course hpilor and SAIDs know those. Don't forget
that as far as the history and exam, these patients
are going to have some again non specific epigastric pain, burning, nausea,
they may have early satiety.
Speaker 2: Those things aren't that important.
Speaker 1: It's not going to help you differentiate on of it and yet,
But what you do need to know with this on
the history and exam is the different presentation. Do oddinal
ulcers are going to get better with food? Gastric ulcers
are going to get worse with food. So why does
that happen? Well, gastric cultures. When you eat, acids obviously
released to help break down the food, and so the
ulcers in the stomach you have pain right away. So
as soon as you eat, immediately these patients start having pain,
whereas duadinal ulcers obviously a little bit further down the
GI tract. As you're eating, the food's kind of shut down,
it's clamped off, it's churning up in there trying to
break down the food. So all the acids in the stomach,
but it's not until about two to five hours later
that the food starts to be released from the stomach
enters the duodom. Now these patients start to have pain.
So while these patients are eating and they have a
duodin ulcer. They have some relief for about two to
five hours while the acids still sitting in the stomach.
Speaker 2: Once it starts to come out, then they have pain.
Speaker 1: So duodenal ulcers they're gonna have, They're gonna have relief
with food. They're gonna see their symptoms improved. Duadinals are
going to be better with food. Gastric is gonna be
worse with food. The way I remember that duodenal ulcers.
Du I remember, dude, give me food?
Speaker 2: Do you do?
Speaker 1: Just like in dude and duodenal? Dude give me food?
So better with food, duodonal ulcers and gastric.
Speaker 2: Is worse with food.
Speaker 1: And that's why patients with gastric ulcers that the pain
gets worse with eating. A lot of times you'll see
weight loss in these individuals compared to duaden ulcers. You
may see weight gain because their symptoms get better with food,
so they tend to eat more, So it makes sense.
Speaker 2: One other thing to be.
Speaker 1: Mindful of is that peptic ulcers can bleed and they
can also perforate, So you need to know that peptic
ulcers are actually peptic ulcer disease is the most common
cause of an upper GI bleed. Peptic Ulcer disease most
common cause of an upper GI bleed. And in the
case that they do perforate, these patients are going to
go from this kind of vague epigastric pain pepsia blah
blah blah, to this sudden onset of this sharp, acute
abdominal pain. They may have signs of peritonitis like rebound
tenderness guarding. So know that these peptic ulcers can perforate,
they can bleed, and the presentation is going to be
much different. It's obviously a much more serious situation as
far as diagnosing. Ultimately, your most sensitive and specific test
is going to be in an endoscopy, But there's a
few things you want to do before you get to
an endoscopy. But remember, if an endoscopy is on the
answer listen it says what is your best test endoscopy,
it's always going to be the endoscopy. But in real life,
there's a few things that you're going to do first
and a few other tests. So if it says what's
your initial test, you may go with some other things.
So let's go over that Initially you're probably going to
test for H. Pylori, So you can do that a
couple of different ways. You can do a urrea breath
test or an H. Pylori stool antigen H pylori testing.
When you do a uria breath test, what you need
to know about this is is that H. Pylori produces
an enzyme called urease, which breaks down urrea into ammonia
and carbon dioxide. So the way this test works is
that during the test, the patient is given a pill
containing urea and then they blow into this bag. They
blow into the bag, they close off the bag, it's
sent to a lab, and then they test for the
amount of exhaled carbon dioxide. And remember again they were
given urea, and as I said before, H pylori turns
urea into carbon dioxide and ammonia. So if there's an
increase in all this carbon dioxide that's in this bag,
then obviously this is gonna be a positive test for H.
Speaker 2: Pylori.
Speaker 1: So that's how a urrea breath test works. H Pylori
stool intogen is straightforward. It's literally just checking for a
stool antigen of H.
Speaker 2: Pylori.
Speaker 1: So that's another test that you can do as well.
And then ultimately, like I said before, the gold standard
test is going to be your endoscopy. That's going to
be to diagnose. You can visualize the ulcer and you
can take biopsies if needed, and then treatment depends on
the cause. So let's start with H pylori. If this
patient is H pylori positive, again, just like in guesstritis,
you're going to do quadruple therapy. The way I remember
quadruple therapy for an hpylori positive patient is I remember
these patients have belly pain. They want you to treat
their belly pain so they can get better. So they
say to you, treat my belly, please, treat my belly please.
TMBP that stands for tetracycling, metronideisol, bismyth subseliciy, and PPIs
treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,
and P. Those are for your H. Pylori positive patients. Now,
if these patients are hpylori negative, how do you treat
their peptic ulcer disease? Well, first, treat the underlying cause.
If they're taking nsids, they're smokers, they drink a bunch
of alcohol. You're going to discontinue all those things obviously,
and then you're going to give them PPIs as well.
You can also use H two blockers, but realistically, anytime
you have an option of a PPI or an H
two blocker, unless there's some contraindication of PPIs, always use PPIs.
Why is that PPIs are much more effective, and that's because,
I mean, just really quickly break down the way these
work and just to give you a little bit about
the may of the mets. So you have a parietal
cell in the stomach. The parietal cell has a proton pump.
That's what shoots out all the hydrochloric acid into the stomach.
That's where all of your acid in the stomach comes from.
So how is your prietal cell activated. Well, acetylcholine, histamine,
and gastrin all activate the prietal cell to pump out
this acid. An H CH two blocker obviously blocks H
two and that's histamine, So that's a histamine blocker, So
it blocks just histamine, but you still have acetocholine and
gastrine that can activate the parietal cell. So while it
helps because you stop the histamine from activating the paryal cell.
Stylcholine and gastrine are still working there to pump out acid,
so there's still some acid production, Whereas a proton pump
inhibitor actually completely shuts off the proton pump, so it
doesn't matter how much is stylcholine, how much histamine, how
much gastrine is activating that parietal cell. The pump is
shut off, so no acids coming out. So PPIs are
much more effective. So remember, if you have an option
of a PPI or hto blocker, use the PPI. So
again H pylor negative, treat the underlying cause, give them PPIs.
That's the treatment. If they're H pylori positive, treat the
H pylori very easy treatment. And then there's one other
treatment option that you should probably know. For refractory patients.
The PPIs aren't working, you discontinued all the ensis, et cetera,
and they're still having SIN, you can do something called
the parietal cell veagotomy, which is where they sever the
vagual nerve, which essentially shuts down the portion of the
stomach where the parietal cells are located. And this obviously
leads to decreased acid by about seventy five percent, So
pretty effective procedure, but it's invasive. Obviously, there's a lot
of things you want to try before you get to
a parietal cell vegotamin. This is just going to be
for your refractory patients. So those are the treatments. Let's
move on to the home stretch here. The last thing
we're going to go over, and that's going to be
pyloric stenosis. So this is going to be a condition
commonly in newborns. About three to six weeks is going
to be your most common age range, and it's a
thickening hypertrophy, a thickening or hypertrophy of the pyloris, which
is the sphincter, the muscular valve between the stomach and
the duodenum, so it prevents gastric emptying. Risk factors are
going to be males four times more common in male,
so definitely know that males are going to be much
more common. Look at your vignette. If it's a female,
you know for a vignette probably and that's so common
that it's going to be pylar scinosis. Three to six
weeks is going to be your most common age of presentation.
Sometimes they'll say three to twelve, but generally three to
six is the most common. And then first born patients
are also going to be at a higher risk. And
then the last thing too, not as you know, not
as big of a risk as the other ones, but
macrolide antibiotics, in particular erythromycin within the first two weeks
of birth can also lead to pyloric stenosis. And this
is the way it's explained, is most likely due to
the increased gastric motility with macrolight antibiotics. Erythromycin, even a
zythromycin can cause this. So the increased gastric motility in
these drugs can lead to hypertrophy from the pyloris basically
just being overworked. And it's the same reason that we
use erythromycin and gastroparesis because it increases the gimotility. So
if you have a patient under two weeks they give
them a erythromycin, this may lead to pyloric stenosis. So
risks again males first born three to six weeks of
life and macrolide antibiotics in particular erythromycin. All right, So
as far as the history and the exam. They may
have some non specific symptoms weight loss, dehydration doesn't matter.
You don't care about that stuff because it's not going
to help you differentiate it in Yet, what you need
to know for pylor ex stenosis, there's two really big
things you cannot forget. So pilar stenosis non bilious projectile
vomiting after feeding. That is going to be your vignette
right there. You can just go ahead and circle pilar stenosis.
That's gonna be your answer. So you see non bilious
projectile vomiting after feeding pilar stenosis. So why is it
non bilious? Well, remember this is an obstruction at the stomach.
It's at the pylorus, so we're not into the area
where the bile is coming from the common bioduct. It's
not evolves. It's an unomal rotation of the small bowel,
so we're not in the area where the bile is
being excreted. So it's gonna be non bilious. It's in
the stomach, So non bilious projectile vomiting after feeding that
is going to be pathonomoonic, almost as pathonomonic as The
second thing you need to know for the exam and
that's going to be an olive shaped mass. So on
physical exam, we talked about the the pyloris being hypertropheed.
It's enlarged, and on physical exam, normally you're not gonna
be able to feel the pylorus. But these patients, because
it's hypertrop feed, you're actually going to feel this olive
shaped mass in the epigastric area and it's going to
feel like a small round mass and it's described as
an olive shaped mass. If you see this on a vignette,
you see this or you feel this in real life,
this is really pathdomonic for the disease. And actually, years ago,
before ultrasound was around, this would be the only way
you would diagnose it. If you felt this olive shaped mass,
they would go right to surgery, you know, after you
treated them with fluids and things like that. So physical
exam no non bilious projectile vomiting and no olive shaped mass.
So those are the two things you need to know
as far as diagnosing. Ultrasound is going to be your
test of choice. It's ninety seven to ninety nine percent
sensitive no radiation.
Speaker 2: These are newborns.
Speaker 1: You really don't want to radiate them if you don't
have to. And then on the ultrasound, you're going to
see some pyloric muscle thickness over four millimeters and the
pyloric canal length will be over seven eighteen millimeters. Don't
worry about those numbers, but I just want to throw
that out there so you know that's how you actually
have a positive ultrasound.
Speaker 2: But ultra sound is gonna be your test of choice.
Speaker 1: The only reason I'm even going to mention an upper
GI series not so much that you're going to use
it in real life. It's really only going to be
if ultrasounds inconclusive, the physical exam is inconclusive. But you
need to know for the exam because on an upper
GI series, there's a couple of key terms.
Speaker 2: There's one called a string sign.
Speaker 1: It's not specific only to pyloxynosis, but if you do
see it in this vignette, this is going to be
a narrowed area of barium flow. It's literally going to
look like a string of barium because that hypertro feed
area only allowing a small amount of barium through. So
that's a string sign and upper GI. And there's another
one called a railroad track sign, and this is due
to the pyloric mucosa compressing and pushing causing this double
canal where you're going to see two small tracks of
barium flowing through. It kind of looks like a railroad
and that's a railroad sign on upper GI. So again
in real life, probably not going to do an UPPERGI,
but you do need to know for the exams because
they like to throw out these key terms of string
sign and railroad track sign on what you'll see on UPPERGI.
And then as far as labs, they're vomiting up all
the stomach acids, so you may have this hypochloromic metabolic acidosis.
They may also have hypokalmia, and this is just because
the kidney's compensating and flushing out all of the renal
potassium excretion. So hypochloromic metabolic acidosis may be seen. And
then they also may have hypokalemia on labs. But your
key for diagnosis is going to be your ultrasound. But
know these things as well. So as far as treatment,
initially these patients can be kind of sick. They're volume depleted,
so before you get to any intervention, you need to
start with some fluids. You want to do electrolyte replacement.
Remember again I said they may be HYPOKLEMICX you want
to replace the potassium, may give them some dextros IV
fluids and things like that. Once they're euvulymic, then you
get to the actual procedure that needs to be done
in these patients. And this is called the pyloral miotomy
is the name of the procedure that you want to
do once they're stable their euvolemic and this is normally
done laparoscopically. The surgeon makes this longitudinal incision into the
pylorus and once they make this longitudinal incision, that hypertrophied
muscle kind of pops out through this incision that they made.
And once it pops up through this area of the incision,
now beneath the area of the incision, there's this canal
that opened up this new space because all the muscle
kind of tunneled up through this incision, and they actually
have this area where the stomach contents can flow through
this area, so that again it's called a pyloromiotomy. Pyloromotomy
is going to be the treatment of choice once these
patients are stable and euvolemic, so that's what you need
to know. Those are the main things. I feel like
I kind of touched on all the high yield stuff.
I hope that was helpful. And as always, good luck
on your pants, your panry, your ear, and good luck
in PA school and