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I'm Dr. Joseph Kumka, Gastroenterology Fellow, educator, and creator of this podcasts. Whether you're a resident gearing up for the boards, a fellow diving deep into subspecialty topics, or a practicing clinician hungry for high-yield updates—you’re in the right place.
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Welcome to the Deep Dive.
We've got a really interesting set of sources today, covering some pretty complex stomach disorders.
We're going from these super rear conditions down to things you might actually see, you know, pretty often on endoscopy.
Yeah, it's quite a range.
And they can definitely be confusing.
Right.
So our mission today is to really cut through that confusion, find the key differences .
We want to get clear on, say, miniry disease versus Zer Ellison syndrome.
They sound similar sometimes, but are totally different beasts.
Absolutely.
One's about losing protein.
The other's about way too much acid getting that straight as, well, step one.
Exactly.
And then we'll pivot to those more common findings, like gastric polyps and intestinal metaplasia.
What's the real risk there?
When do you actually need to worry and do survey?illance? .
It's all about knowing what matters and what doesn't.
Okay, let's jump in.
So, like we said, the big contrast, the first major fork in the road, is protein loss versus acid overload.
Let's start with the weird one.
Minetria disease, the protein losing gastropathy.
The mechanism here, it kind of trips people up because it's all about cell growth, but not the cells you'd expect for stomach problems.
That's spot on.
Mini isn't about acid.
It's driven by too much signaling, specifically TGF alpha hitting the EGFR receptor.
This makes the mucus cells, the fuola cells, just grow like crazy , not the prietal cells that make acid.
So you get this massive overgrowth of mucus producing cells.
Right.
And that leads to the classic triad you need to know.
First, these giant, thick folds in the stomach lining, the rugge, mostly in the body and fundus.
Second, because the lining gets leaky from all that growth, patients lose protein, especially album into the stomach.
That causes low in the blood, hypobemia, and often edema, you know, swelling.
Okay.
Giant folds, protein loss leading to edema.
What's the third part?
And third, crucially low stomach acid.
Yeah.
Hypchlorydro.ria.
Because again, it's the mucous cells growing, not the acid ones.
Okay, so the stomach lining is thick and leaky, losing protein .
How do we actually prove the protein loss is coming from the gut?
You mentioned that's the diagnostic anchor.
Good question.
We use a test called stool Alpha 1 antitripsinance.
See, alen gets digested, so you can't just measure it in the stool easily.
But alpha 1 Antitripin is another protein from the blood that leaks into the gut if the lining damaged.
And it doesn't get broken down by digestion.
So if you measure how much of it is cleared into the stool and that level is high, it confirms you've got significant enteric protein loss.
That points strongly towards menetri in this context.
Got it.
And the sources mentioned the adult form is chronic and potentially premalignant.
Yes, that's key point for adults.
There's an increased risk of gastric cancer down the line, so surveillance endoscopy is needed .
For treatment, if it's severe and not responding to support supportive care, there's targeted therapy with sed that blocks the EGFR signaling, driving the growth.
Blocks the growth signal.
Makes sense.
And if things are really bad or cancer develops, then removing the stomach, the gastrectomy is the definitive option.
Okay, so that's minatri, thick folds, leaky protein loss, low acid .
Now, let's pivot hard to the complete opposite end of the spectrum.
Solinger Ellison syndrome, Z. Right.
ZS is the acid overdrive state.
It's caused by a tumor, a gastronoma that's a type of neuroendocrine tumor, or net.
These usually highly out in the dodenum or sometimes the pancreas.
And this tumor just pumps out gast.
Exactly.
Tons of gastron.
And gastron's job is to tell the bridal cells in the stomach to make acid.
So with the gastronoma, you get get massive bridal cell, hyperlasia overgrowth of the acid making cells, and just relentless overwhelming acid production.
And that insane amount of acid causes the classic signs we look for.
Precisely.
You see really stubborn, recurrent peptic ulcers.
Often they're at unusual places, like beyond the duod bulb further down.
And the other big clue is that combination, ulcers plus chronic diarrhea, often fatty diarrhea,arhea.
Why the diarrhea?
I always found that part interesting.
It's a direct consequence of the acid flood .
The sheer volume of acid pouring into the duodenum just overwhelms the pancreas's ability to neutralize it.
The environment becomes too acidic for pancreatic lip, the main enzyme for fat digestion, to work properly.
N, so the fat doesn't get digested.
Right.
Malabsorbed fat leads to ceteria, and contributes to the diarrhea.
Okay, so let's just recap that contrast one more time, because it's so fundamental.
Menitria.
Mucus cell overgrowth, low acid, protein loss, edema, Petal cellg driven by, high acid, uc, and diarrhe from fat malabsorption.
Couldn't have said it better.
Totally a different physiology, totally different workout needs. .
All right, let's dig into that ZS.
The sources really hammer home that the diagnostic sequence here is critical, especially because common meds can mess things up.
What's the absolute first thing you have to deal with?
You have to think about proton pump inhibitors, PPIs, drugs like omeprazol, pantrazol, they're incredibly common.
And they block acid, which sounds good, but...
But they cause a major problem for diagnosis.
By blocking acid so effectively, they cause the body to reactively increase gastro production.
So if your patient is on a PPI, their gastro level will be falsely high, sometimes very high, and you won't know if it's the drug or a tumor.
Plus, it makes the PH test useless.
So you have to stop the PPI.
How do you do that safely if they need acid suppression?
You stop the PPI, usually for at least a week or two, but you can bridge the patient with an H2 receptor blocker, like fomododine.
H2 blockers aren't as potent and don't screw up the gas levels nearly as much, so they're safe to use while you're doing the diagnostic tests .
Okay, PPIs off may be bridged with an H2 blocker, then what?
We measure.
Then you get the core biochemical tests, fasting serum gastron level, and a measurement of gastric pH, usually during an endoscopy.
And how do those numbers tell us if it's ZES?
We don't need exact cutoffs, but what's the pattern?
You're looking for the extreme combination .
If the gastron level is really high, the sources often use a benchmark, like over 1,000 pGML.
And the stomach pH is very low, meaning very acidic, typically less than two.
That combination pretty much seals the diagnosis of ZES .
High gast plus high acid.
But what if it's not that clear cut?
Like, the gastrine is high ish, maybe 500, but the pH is low, that gray zone.
Exactly.
That's where the secretin stimulation test comes in.
It's the tiebreaker.
Right.
And the physiology behind this test is the key, isn't it?
How it separates a tumor from normal stomach function.
Precisely.
Normally, if you give someone secret intravenously , it tells the normal gast producing cells, G cells in the stomach to stop making gastro.
It's a negative feedback signal.
Okay, normal response is suppression.
But the gastronoma tumor cells.
They don't play by the rules.
They react paradoxically.
When you get secretin to a ZS patient, their gastron level doesn't drop.
It actually spikes up significantly, usually by more than 120 PGML from the baseline.
That paradoxical rise is diagnostic gold for ZES.
Fascinating.
Okay, so we've confirmed ZES biochemically.
Now we need to find the tumor.
What's the best way to look for these castronomas?
They can be small and tricky to find, right?
They can be .
The modern approach really prioritizes functional imaging first.
Because these are neurocrine tumors, they often express some metatin receptors on their surface.
Ah, so we use something that binds to those receptors.
Exactly.
The best test now is usually a Gallium 68 Dotate PE CT scan.
It's incredibly sensitive, often finding over 90% of these tumors, including the primary one, and any spread like to the liver or lift n , it lights up the tun based on its function.
O in an older version can be used if pitchy isn't.
So functional imaging first, then do we still need regular CT or MRI?
Yes, you typically follow up with anatomic imaging CT or MRI for staging to see the exact size, location relative to other structures, especially things like liver mets, where MRI might be a bit better.
And what if even the Dotate scan is negative, but you're sure the patient has EES biochemically?
That's where endoscopic ultrasound, or ES, can be really helpful , especially for those tiny tumors, sometimes hidden in the wall of the duodum, which is actually the most common spot, but easy to miss on other scans.
E can get right up close.
Okay, diagnostics covered.
Now, management, this seems critically important.
What is the absolute number one lifeaving priority as soon as you confirm ZES?
Acid control.
No question.
Before you even think too hard about finding or removing the tumor, you have to get that massive acid production under control.
High dose PPIs are essential, often needing much higher doses than usual, sometimes twice a day or even more.
Why is that so urgent?
Because the complications of uncontrolled acid and ZS are severe and potentially fatal massive bleing from ulc .
Perforation of the stomachuad esid strictures, you have to shut down the acid immediately to prevent disaster while you plan the next steps.
Make sense.
Control the immediate danger first.
Then you think about cure.
Then you think about cure, yes, Cative surgery removing the astronoma is the goal, but it's really only feasible if the tumor is localized, no spread, and it's sporadic, meaning not associated with MEN1 syndrome.
Oh, right.
Multiple endocrine neoplasia typeype 1.
How does that change things?
Z.E and MEN is different.
These patients often have multiple tiny gastronomas, usually in the duod .
Trying to find and remove them all surg is often impossible and rarely curative.
So for ME1 associatedE, the management is primarily long term medical therapy, high dose PPIs to control the acid, sometimes combined with someatin analogues like octotide orriotide, which can help control symptoms and potentially slow tumor growth, surge is less common.
Okay, we've wrestled with the rare but dangerous ZES.
Let's shift gears now to things you're much more likely to encounter during a routine GGD, managing those potentially precancerous changes, gastric polyps and intestin metaplasia.
Starting with polyps, how do we sort them out?
Polyp management really comes down to figuring out what type of polyp it is.
And you often get clues from where it is in the stomach and what else is going on, like medication use or background inflammation.
The sources highlight three main types to know.
Let's take them one by one.
First up, Fundit gland polyps, FGPs.
Right?
FGPs.
Usually find these in the fundus and body of the stomach, the area with the acid producing chal cells .
They're strongly associated with long-term PPI use, very common nowadays.
Are they dangerous?
Generally, no.
If they're sporadic, meaning not part of a genetic syndrome like FAP, and they're small, say less than a centimeter, the risk of cancer is minimal.
The standard practice is often just a biopsy one or two to confirm they are FGPs, and then you can usually leave the rest alone .
No routine surveillance needed for small sporadic ones.
Okay, FGPs, common, PPI related, low risk if small.
What's next?
Hyperplastic polyps.
Hyperplastic polyps.
These tend to show up more in the anrim, the lower part of the stomach.
Their big association is with chronic inflammation, chronic gritis, and usually that inflammation is caused by H bil infection.
So look for H pyri with these .
Do they carry cancer risk?
The risk is low, but it does go up a bit if they get larger.
Usually the cutoff mention is a over one centimeter.
So the approach is twofold.
Definitely remove the larger ones over one centimeter.
But crucially, you always test for and treaty if it's .
Eradicating the H pilori can actually make these polyps shrink or even disappear.
Interesting.
So treat the underlying cause.
Okay, Third type, adonomas.
These sound more concerning.
They are.
Gastric adomas are true premalignant lesions.
They have definite potential to turn into cancer.
Like hyperplastic polyps, they're often found in the anm and are associated with underlying damage specifically, a trophical. Gastritis and intestinal metaplasia.
So what's the rule for adonomas?
The rule is simple and absolute.
Always reset them completely, regardless of their size, every adonoma needs to come out, and you need to ensure the removal is complete.
Okay.
Always remove adonomas.
And you mentioned they' link to atrophy and intestinal metoplasia, which brings up a really key point from the sources.
Always biopsy the surrounding Eucosa when you find these results.kier polyps, right?
Yes, absolutely critical.
When you find a hyperplastic polyp, especially a large one, or an adonoma, you need to take separate biopsies from the nearby stomach lining, even if it looks normal.
You're looking for those background changes atrophy and especially gastric intestinal metaplasia, or Jim.
Kim, the sources call it the stomach's version of Barrett's esophagus.
That's a great analogy.
Jim is basically the stomach lining, changing his character in response to chronic injury, most often from long term H pylor infection, but also autoimmune gastrit is.
The normal gastric cells get replacedaced by cells that look like they belong in the intestine.
This is part of that Korea cascade, the stepwise progression towards gastric cancer.
And not all gym is created equal in terms of risk, right?
There's a distinction.
Correct.
Histologically, pathologists classify gym into two main types , complete and incomplete.
Complete IM looks more like small intestinal lining is considered more stable, lower risk. Incomplete IM looks more like colonic lining.
It's less differentiated, considered more unstable, and carries a significantly higher risk of progressing to dysplasia and eventually cancer .
Knowing the type is really important for risk stratification.
So if someone has Jim, especially the higher risk incomplete type, does everyone need surveillance endoscopy every few years?
The guidelines seem a bit nuanced here, particularly in the U.S. They are nuanced.
Routine surveillance, like an EGD every three years, is not recommended for all patients with Jim in the U.S. It's really reserved for those deemed high risk.
What puts someone in that high risk bucket for surveillance?
Several factors.
Hav incomplete IM is one major flag .
Another really important one is the extent of the metaplasia.
If it's extensive or multifocal meaning, it's found in the anm and the stomach bodyus that significantly increases risk and warrant surveillance.
Other factors include having a strong family history of gastric cancer in a close relative or having underlying autoimmune gastritis.
So the trap to avoid is thinking any gym automatically means years of surveillance .
A small patch of even incomplete gym, just in the intrim, without those other risk factors, might not require it.
That seems to be the current thinking based on U.S. Guidelines.
The risk is really driven by the type, incomplete being worse, and the extent more widespread being worse, plus those other clinical factors .
Focal ent metaplasia alone is often lower risk.
Okay.
And regardless of surveillance, what's the one action you always take if Jim is found?
Always test for an eradadicate each pilori if present.
It's the most common cause, and getting rid of it is the only intervention we have that might potentially slow or halt further progression along that cascade.
Makes sense.
And if during surveillance, you actually find dysplasia the step before cancer.
If dysplasia is found, that's a clear indication for intervention .
The standard of care is endoscopicction techniques like EMR, endoscopic mosal rection, or ESD endoscopic subosal dissection, to remove the displastic area completely.
Hashtagagoutro.
Okay, this has been a really helpful deep diet.
We've definitely clarified those crucial distinctions.
First, realizing thatatria and ZS are polar opposites, physiologically protein loss and low acid, versus massive acid and ulcers that really guides the initial approach.
Absolutely.
And second, for ZES, remembering the critical diagnostic sequence deal with PPIs first , confirm with gast pH orin image functionally, and immediately control the acid before anything else.
That's lifing.
Yeah.
And third, shifting to the more common stuff, knowing how to tri polyps based on type and location, and understanding that for intestinal metaplasia, surveillance isn't automatic.
It's really focused on features , the incomplete type, involve other factors like family history.
Exactly.
It reflects a broader shift in GI, I think.
Moving beyond just managing acute crises like a bleeding ZS ulcer towards more proactive, long-term management, and risk stratification of these premalignant conditions we find on noscopy.
That's a great point.
You know, we focused entirely on these structural or se secretary problems today, but the original source list you also touched on purely functional gut disorders, things like rumination syndrome or cyclic vomiting syndrome, CVS.
Which brings up a really interesting final thought for you, the listener, to chew on.
If you know a patient's severe vomiting is due to CV, a functional disorder treated mainly with neuromodors and behavioral therapy.
How fundamentally different is that entire approach compared to working of ZS or minat?
Right.
And why is making that distinction structural versus functional so incredibly important early on ?
Think about how it prevents potentially unnecessary, invasive, and expensive tests looking for a structural cause that just isn't there.
Something to definitely ponder.
Yeah.
It highlights the importance of a broad, differential, but also knowing when to shift diagnostic gears entirely until the next deep dive