Dr GI Joe

Welcome to the deep dive.

Today, we're really digging into a vital piece of GI practice, handling helicobactter pori effectively, and maybe even trickier sorting out the those serious esophagal infections.

Exactly.

We've got some great source material, a synthesis of guidelines, and, you know, real clinical insights.

Yeah.

And the goal isn't just the basics.

We want to get into the weeds a bit.

Right.

It's about moving past just suspecting H.

P Laurie to navigating those diagnostic minefields, like why a negative text might not mean anything.

And then knowing the key differences when you see, say, a nasty esophagal ulcer.

So our mission for your listening is basically efficiency.

We want to give you that shortcut to feeling confident about the testing quirks, the treatment steps, and those critical core for esophagal infection signs.

Okay, let's jump in.

First off, H by L. Wind should testing absolutely bey on your radar?

What are those nonnegotiable clinical signs or lab findings?

Okay, yeah.

You're really looking for those h risk indicators.

First, definitely unexplain iron deficiency anemia.

That's a big one.

And of course, at peptic ulcer disease, whether it's gastric or dewatenal.

You so.

Then, if you're doing an anoscopy and anyway, and you see things like gastric intestinal metaplasia, those pre-cancerous changes, or just that nodular look of chronic gastritis, you test.

Okay.

And the last one , maybe less common, but important, is a strong family history of early onset stomach cancer, those really mandate testing.

So if we do decide to scope and we need biopsies, how do we make sure we actually find the bug if it's there?

You can't just grab one piece, right?

No, definitely not.

You've got to follow the protocol.

It's called the updated Sydney system.

Ah, yes, the Sydney system.

Right.

It means taking five or six biopsies total.

You need two from the interim, two from the body, and at least one, maybe two from the incicangularis.

That spots crucial.

Okay, multiple sites.

Yeah, and ideally, you run both histology maybe with silver stains to really highlight the bugs and a rapid u test, like the CO right there from the biopsy samples.

Doing both gives you the best shot.

Good redundancy.

Now, what if endoscopy isn't happening?

We're talking non-invasive tests .

You a breath test, UBT, or stool antigen is one better.

Honestly, both are really good.

UBT and stool and test testing, they both have excellent accuracy, usually over 90% sensitivity and specificity, that definitely the preferred non-invasive options.

And serology.

Blood tests.

Stay away from serology for diagnagnosing active infection or for checking if treatment worked .

It just shows exposure.

Those antibodies can stick around for ages, so it's useless telling you what's happening now.

Okay, crucial point.

Now, the big one.

The trap everyone needs to avoid.

Proton pump inhibitors, PPIs.

Why are they such a problem for HPR testing?

Oh, this is absolutely critical.

PPI's miss things up in a couple of ways.

First, they raise the stomach PH, which, you know, makes it less hospitable for the bacteria, so the overall number of organisms goes down.

Bridges is the load.

Exactly.

But maybe even more importantly, they caused the HHPy lory that are left to kind of scatter.

They migrate away from the anrim where we usually biopsy, up into the body or the funus.

Ah, so they're hiding.

Pretty much.

And that lower load plus the relocation means you can get false negatives on everything, UBT, stool, and gin, and the biopsyries test, even sometimes histology, if the pathologist isn't looking closely.

So there's a hard rule here for stopping them before testing.

Absolutely.

PPIs have to be stopped for at least two full weeks before any of those tests, UBT, stool, or biopsyries.

Two weeks.

Got it.

And if the patient's been on antibiotics or bismuth recently , you need even longer four weeks off those.

Four weeks, when?

Yeah.

The key takeaway is a negative test result within that two-w window after stopping a PPI.

It's just not reliable.

If you still suspect H.

P Laurie, you have to retest after they've been off the PPI long enough.

Okay, let me just jump in with a practical question.

What if someone's really sick , maybe actively bleeding, and you just can't safely stop their PPI for two weeks?

What do you do then?

That's a tough spot.

Definitely high stakes.

If stopping the PPI is truly impossible, endoscopy with biopsies is still probably your best best, but you have to tell the pathologist the situation and take extra biopsies, especially from the body and funus thinking about that migration.

Right.

Targeting the hiding spots.

Exactly.

Some might use serology just to see if there's ever been exposure, kind of as a placeholder, knowing it doesn't confirm active infection.

But really, the gold standard is testing when they can be off the PPI.

That real world angle is helpful.

Okay, let's tivotet to treatment.

We've confirmed H.

Pori.

What are the go-to reliable 14 day regim now?

Right, Treatment.

Given resistance issues, the number one choice, the real workhorse first line, isism quadruple therapy .

That's a PPI plus bism, plus mronol, plus tetycling, all for 14 days.

Bismuth quad.

Yeah.

Especially if you don't know the local resistance rates or if the patients had macroles like chloromycin before, it's just the most robust option out there.

If it's the best, why do we still hear about other options like concomin therapy?

That's a fair question.

Bismuth Quad involves, well, a lot of pills, and sometimes side effects like GI Upset or Black stools can be an issue for compliance.

Concomitin therapy, that's PPI, amoxicillin, chomycin, and metronitis is maybe a bit simpler.

But there's a catch.

Big catch.

You should only really consider concomitin therapy.

If you're in an area where you know chlorromycin resistance is very low, like under 15%.

And honestly, in most places in the U.S. And Europe now, that's not the case.

Chlorromycin resistance is widespread, which is why older triple therapies are pretty much obsolete.

Okay, so Bismismuth Quad is generally safer from a resistance perspective.

What about penicillin allergies?

That's where bismuth Quad really shines again, since it uses tetrycline and metronid dole.

There's no amoxicillin or any penicillincl drug involved.

So it's the perfect choice, the safety net for someone with a true penicillin allergy.

Good to know.

We're also seeing some newer combination pills, like Telicia.

Where does that fit?

It's It's got Rutin, right?

Yes, Telines a zol, amoxicillin, and Rutin in one capsule.

It's convenient and very effective.

The FDA did approve it as a first line option.

But I sense abut.

But yeah, the major GI guidelines, like from the ACG and the Toronto group, strongly recommend reserving Rabutin-based therapies like Talicia for salvage situuations , meaning you use it only after a standard regimen like Bismuth Quad has failed.

Why hold back such an effective drug if it's FDA approved first line?

It really comes down to antibiotic stards.ardship.

Riffibutin is incredibly important for treating tough infections like tuberculosis and MA, especially in immunocompromised patients.

Oh, okay.

If we start using it routinely for something as common as H pilot, we risk driving resistance to Rutin and then we might lose it for those much more serious infections where we have fewer options.

So it's about preserving its effectiveness long term.

That makes perfect sense.

Strategic use.

Can we circle back to bismitz for a second?

What's it actually doing in that quadruple therapy?

It's not just coating the stomach, is it?

No, it's much more active than that.

Bismuth actually has direct antimicrobial effects.

It messes with the H cell, inhibits some of its crucial enzymes, like, which it needs to survive in acid.

Interesting.

Plus, it seems to workgically with the antibiotics, and helping to resistance .

It's really hitting the bug from multiple angles.

Okay, so the patient finishes their 14 days of, say, bismuth quad.

Are we done?

Absolutely not.

This is maybe one of the most missteps.

You must confirm that the treatment worked.

You need a test of cure.

Always.

Always.

No exceptions.

And you use UBT orool antigen, again, never ser .

The timing is also critical.

You have to wait at least four weeks after the last antibiotic dose and at least two weeks after stopping the PPI.

Same wash-up periods as for diagnosis.

Exactly the same.

Gotta let the bug recover if it's still there.

And if the test is positive, meaning treatment failed, you absolutely switch antibiotic classes.

Don't just repeat the same regimen hoping for a different result.

Right.

Switch it up.

Any other follow-up needed after treatment?

One key thing.

If the reason for treatment was a gastric ulcer, specifically, you need to repeat the Indoccopy after treatment is done and they've healed up a bit.

Why repeat the scope?

To confirm the ulcer is fully healed and crucially to make sure there wasn't an underlying malignancy, like a cancer, hiding in or under that ul.

Doal ulc generally don't need that scope, but gastric ones do.

Okay, great point.

So bottom line for H pori . Meticulous attention to those washout periods for testing and cure confirmation is key.

All right, let's shift gears now.

Moving from the stomach down to the esophagus.

Infectious esophagitis, especially in folks who are amocompromised, like HIV patients,, this is where things can get really tricky.

Before we dive into the Core 4, maybe the toughest pair to separate is HV and CMV ulcers.

Do you have like, a quick mental hook for telling them apart?

I do, actually.

It all comes down to where the virus likes to hang out, and that dictates where you need to biopsy to find it.

Think.

Edge versus bass.

Edge versus bass.

Okay, I like that.

HSV infects the surface epithelial cells, right at the rim or edge of the ul.

CMV goes deeper, it infects the endothelial cells in the blood vessels andom cells at the base of the ulcer crater.

Perfect.

Edge versus base.

Let's use that.

So walk us through the core for differentiators.

Appearance, biopsy site, histology.

Start with the most common one, Candida.

Okay.

Canda .

Endoscopically, it's usually pretty classic.

You see those thick, white kind of cottage cheesy plaques stuck to the esophagal wall..

Treatment wise, the big pearl is you need systemic fuconisol, orally, just swishing and spitting nestatin like you might for oral thrush.

That's not enough for ophageitis.

It's an invasive infection.

Just to make treatment.

Got it.

What if they don't get better?

Good question .

If someone has thrush, trouble swallowing, you treat empirically for candidita, but if they don't improve quickly onucanol, you absolutely need to rescope them.

You have to look for resistant candita.

Or maybe it wasn't candy at all.

Maybe it's HSV or CMV hiding underneath.

Okay, now for the viral twins.

Using our hook .

HV.

All right, HSV.

Appearance wise, think multiple, usually small, well defined, almost punched out our volcano like, shallow ulcers.

Volcano likeike.

Okay.

Unbbiopsy site.

Remember the hook?

HSV is superficial, so you biopsy the EdG of the ulcer.

That's where the infected epithelial cells are.

Edge for HSV.

And histology.

Histology shows those classic viral changes in the Squamous cells, multiucleated giant cells, and pathologists talk about the 3Ms molding of nuclei, margination of chromatin, and multiucleus..

Treatment is a cyclovir, or Velacycllovir.

Got it.

Now, CMV, how's that different?

CMV is usually quite different visually.

Often it's one or maybe just a few large, linear, and typically much deeper ulcers compared to HSV.

Large linear deep.

And the biopsy side.

It's deeper, infecting intoothelial and stromal cells.

So you need to biopsy the base of the ulcer crater.

That's where you'll find the diagnosticstic cells.

Space for CMV makes sense.

Histology.

The classic finding for CMV is the owl'sye inclusion body, that large, purplish, intranuclear inclusion surrounded by a clear halo, you usually within an endothelial or .

Cheatment here is Glover, orglover.

Ed versus B really helps lock that in.

Okay, what about the last one?

The tricky one?

Idiopathic HV ulcer?

Yeah, the idiopathic orphis ulcer in HIV.

These can look a lot like CMV ulcers, often large and deep.

So how do you know it's not CMV or something else?

The key is the workup.

You biopsy it, maybe multiple times, from the base, from the edge, and all the stains and cultures for CMV, for HSV, for fungi, for bacteria, everything comes back negative.

Consistently negative, despite looking like an infection.

It's a diagnosis of exclusion.

Exactly.

It's thought to be related to immune dgulation in advanced HIV.

And because it's not infectious, the treatment is an antiviral or antifungal.

It's immune modulation.

Usually starts with systemic steroids.

And if steroids don't work...

If it's refractory , the classic sort of high yield treatment to know is thalidomide.

It's a potent anti-inflammatory, works partly by inhibiting TN alpha, used carefully, of course, due to its history.

Wow, phaladomide.

Okay, that's a really clear breakdown of those critical four.

Now, segment four, the Z zebras , those less common GI infections that can trip people up, maybe show up on exams, why are they important to keep in mind?

They're important because missing them can have serious consequences or they require a very specific, sometimes unusual next step.

And yeah, they often get tested using kind of a buzzword association.

Give us an example.

Think stoloids.

The buzzword clue is finding larvavae on a biopsy, usually datal or maybe gastric , the context is often an immunosuppressed patient, especially someone on chronic steroids.

Seroids plus larvae equals strongoloids.

That's the mental shortcut, yeah.

And you need to treat it with imectin because if you miss it, especially in someone amosuppressed, they can get this devastating hyper infectant syndrome.

So recognizing those larvae is critical.

Okay, what's another key zebra?

Maybe one related to food.

Ah, yes.

Enisis.

The story here is almost always.

Patient develops sudden, severe upper abdominal pain shortly after eating raw fish.

Sushi, sashimi, ceiche, often associated with travel to places like Japan or Northern Europe where it's more common.

Raw fish.

Severe pain.

What's the diagnostic step?

Endoscopy is key.

You scope them and you might actually see the thin little Enisaki's worm burrowing into the gastric or duodenal wall.

You see the worm . And the treatment.

This is the really unique part.

The definitive treatment isn't a drug.

It's endoscopic removal.

The gastroerologist literally has to grab the worm with forceps and pull it out.

So the endoscopist becomes a worm hunter.

Huh.

Yeah, pretty much.

It's quite memorable, I imagine.

Definitely a unique management step to know.

Absolutely.

Okay, one last really important area you touched on earlier infections that look like stomach cancer.

Yeah.

This sounds like a nightmare scenario.

It really can be.

You see something on imaging or endoscopy, maybe lumpy thickened folds, a discret mass, a big non-healing ul, even a narrowedure.

And your first thought is, understandably, cancer, aococarcinoma or lymphoma.

But it might not be.

Exactly.

There are specific infections that are ratorious mimics you absolutely have to consider tuberculosis, GITB , Biopsies might show those KCating granulom.

Okay,TB.

What else?yphilis Tertiaryyphilis can cause, which are masses in the stomach special stains to see.

Syphilis, wow.

Any others?

Certain deep fungal infections can do it too.

Things like histoplasmosis,uccosis, sometimes cryptococcus can form mass like lesions or ulcers that look malignant.

So the absolute key is.

Biopsy, biopsy, biopsy.

And talk to your pathologist.

You cannot reliably tell these infections apart from cancer just by looking.

You need tissue confirmation to make the right diagnos and avoid you, disastrously wrong treatment.

That's a critical point.

Okay, we have covered a ton of ground .

From holding PPIs for HPlo testing to the nuances of treatment like Bismuth Quad versus Tal, the mandatory test of Cure, and then differentiating candita, HSV, CMV and idiopathic ulcers, using that edge versus base.

Plus the zebras.

Let's try to wrap this up.

Yeah, I think the main threads are for HP Laurie, it's all about protocol adherents , the washout rules, the right first line therapy, like Bism Quad, and Confirming Cure.

Get those steps right, you'll succeed mostly the time.

And for the esophagus.

For the esophagus, particularly in complex patients, it's pattern recognition, the visual look of the ulcers combined knowing exactly where to biopsy.

Edge for HSV, , for CMV, get the tissue from the right spot, get the right stains, and you can usually sort it out.

So what's the big picture takeaway here?

I think it's about having a solid framework.

Knowing these details allows you to move quickly and accurately when faced with these high stakes GI situations, whether it's Hy or rare, potentially dangerous, esophageal ulcer, or even something mimicking cancer.

Right.

It gives you confidence in those differential diagnoses.

Okay, so final thought for you, our listener, to chew on.

We talked about infections, micking cancer, syphilis fungi presenting his gastric masses .

Beyond just checking immune status, what specific clues from a patient's history, maybe their travel or background should make you pause and really push for infectious work before jumping to a cancer diagnosis when you see an unusual stomachion.

Something to think about next time you encounter that scenario