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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.
Today we're tackling what has to be one of the trickiest areas in day-to-day medicine, those chronic upper GI symptoms.
Yeah, the ones that just keep coming back.
Heartburn., that feeling of fullness, maybe pain, despite doing all the usual things.
Exactly.
So if you've got patients stuck in that cycle, this deep dive is definitely for you .
We're aiming to chart a clear path through it all.
We're really focusing on functional esophagogastric disorders, you know, what the RO for criteria called disorders of gut brain interaction or DGBI.
The goal is a clean triage pathway.
Right.
How do you, in the clinic, quickly sort out if it's something structural, like say severe GD or an ulcer?
Vers something functional, like functional heartburn or functional dyspepsia.
When do you scope?
When do you run tests?
And maybe most crucially.
When do you stop the acid blockers?
Precisely.
When is it time to treat the brain gut connection instead?
That's the map we're building today.
Okay, so our mission.
Yeah give you that framework.
Confidence in telling structural from functional.
And it all starts with a fundamental point, something you absolutely have to remember , a functional diagnosis.
It's always the last stop on the track, meaning, you can't just jump there.
You must systematically rule out the structural stuff, the organic diseases, the big motility problems first.
Only then can you confidently say, okay, this looks like a DGBI.
All right, let's start right at again.
Patient walks in, chronic upper GI complaints.
Yeah.
What's the very first step?
How do we categorize what we're hearing?
Well, you're listening for the main theme.
Broadly, it falls into two buckets.
Is it mostly heartburn, maybe regurgitation?
Okay, that sounds like the refflux spectrum.
Exactly.
Or is it more about epigashric pain, maybe burning, that feeling of fullness after meals getting full really quickly?
That puts the more in the dyspepsia camp.
Right.
Those are your two starting points. Reflex symptoms or dyspepsia symptoms.
But, okay, before we even think about treatment, there's that critical safety check, the alarm filter you call this sounds super important .
It's arguably the most important step right at the start.
These are the red flags that tell you something potentially serious might be going on, something that needs immediate investigation, usually with an EGD and endoscopy.
So what are these alarm features?
Let's list them out.
Okay, number one, dysphagia.
Any trouble swallowing.
Difficulty swallowing, right?
Then odonophia that's painful swallowing, any sign of GI bleeding, like vomiting blood, blood in the stool, or even just unexplained anemia showing up on labs.
Significant weight loss that the patient can't explain.
Yes, definitely.
Persistent vomiting is another big one, not just occasional nausea, but ongoing vomiting.
And age matters, too, right?
It does.
New onset of significant symptomptoms, especially dyspepsia, in someone over 60, that needs a look .
And finally, a strong family history of GI cancer, particularly esophal or stomach cancer.
Wow.
Okay, so if any of those are present.
Yeah.
Even just one.
Even just one.
The pathway pivots immediately.
You order the EGD.
Sometimes you'll add imaging too, like an ultrasound.
If you're worried about gallstones or bilary issues causing the pain , no waiting, no empiric trial first.
Got it.
Alarm features mean scope first, ask questions later.
But what if that filter is clear?
No red flags..
Okay, now we can consider empiric trial.
If it sounds like classic heartburn reflux, the standard approach is an eight-w trial of a proton pump inhibitor, a PPI.
And for the dysepsia picture, I assuming they're under 60 and no alarms.
There, you've got a couple of options, generally.
You could do an HPory test and treat strategy test for the benteria, treat if positive, or you could try an empiric trial of a PPI or maybe even a procketic agent, depending on the specific symptoms.
Let's follow that reflux patient.
So they did the eight weeks of PPI, maybe even doubled the dose like you sometimes see.
Yep.
Went to BG dosing.
And they're still having a significant heartburn or regurgitation.
Now what?
Now it's time for that EGD , the Empiric trial failed, so we need to look inside.
And what are we hoping to find or rule out with the scope?
The EGD gives us a major fork in the road.
If we see really clear severe damage specifically, LA grade C or D erosive esophagitis.
Those are the worst grades of inflammation.
Right.
Or if we see Barrettesophagus, which is a pre-canccerous change or a pepticure, a narrowing caused by acid damage.
If you see any of those, the diagnosis is locked in.
That's definite G. Conclusive GD.
No more testing needed for diagnosis there.
Exactly.
LCD is game over.
It's GD.
But what about the more common findings?
A totally normal scope, or maybe just mild inflammation, like LA grade A or B?
You mentioned this is where it gets tricky.
It gets very tricky Because while grade A or B erosions might be from GR, they're not specific enough.
Our sources highlight this up to 5% of completely healthy people walking around with no symptoms can have those minor breaks on an EGD.
Oh, wow.
So you can't hang your hat on grade A or B alone?
You really can't .
It's supportive, maybe suggestive, but absolutely not conclusive proof of GD, especially if symptoms are persisting despite PPIs.
So if the EGD is normal or inconclusive, A or B, and the patient failed PPIs, we need a tiebreaker test.
That's the ambientulatory reflux monitoring.
That's the gold standard.
Usually PH testing or combined imped PH monitoring.
And crucially, this test needs to be done off the PPI therapy.
Oh, off.
Because the whole point is to see if abnormal acid exposure is actually happening and causing the symptom .
If they're on a PPI, it might suppress the acid enough to make the test falsely negative, even if they do have, we need to know their baseline physiology.
Okay, it makes sense.
So off PPI, do the reflex monitoring.
What are the possible outcomes and what do they tell us?
Three main outcomes to find the path forward.
Outcome 1. .
The test shows abnormal acid exposure time AT usually defined as acid bathing the esophagus more than 6% of the time.
And if the AET is abnormal.
That confirms GD.
Even with a normal EGD, abnormal AT means they have nonusive reflex disease or ner.
They do have an acid problem.
Okay, Outcome.
Abnormal AT equals gerd.
What's outcome 2?
Outcome 2.
The AET is normal.
Acid exposure is within normal limits.
But the patient's symptoms correlate strongly with refl events detected by the monitor, even if those events aren't acidic, maybe just weakly acidic or nonacid gas reflux picked up by impedents. Normalormal amount of acid, but symptoms happen exactly when reflux occurs.
Precisely.
That's reflux hypersensitivity.
It's considered a functional disorder.
The esophagus is just overly sensitive. To normal or near-normal physiological events.
Got it.
Normal AT positive symptom link, reflux hypersensivity, and the third possibility.
Outcome three.
The AT is normal, and there's no correlation between their symptoms and any .
Symptoms seem completely random, unrelated to what's happening in the ophagus.
That sounds like.
Functional heartburn.
Pure functional, no link to ref at all.ity and functionalburnGBI under.
This distinction is huge.
Before we leave reflux, let's touch on something you flagged refractory and this potency trap .
Patients often get labeled PPI failures.
How do we know if it's true failure versus maybe this functional overlap?
This is such a critical point.
True refractory GRD isn't just, I still have symptoms on PPI.
It requires objective proof that the PPI, even at maximum dose, isn't adequately suppressing acid.
And how do you prove that?
You do the impedance PH monitoring study again, but this time, while the patient is taking their PPI, usually twice.
Ah, so an on PPI study?
Exactly.
If that study still shows abnormal AET, meaning significant acid is breaking through despiteite the PPI that is true refractory, GARD , the drug itself isn't doing the job sufficiently.
But what if the on-PPI study shows the AET is now normal?
The acid is controlled?
Then the ongoing symptoms aren't being driven by acid anymore.
They're likely due to that functional overlap reflex hypersitivity, perhaps.
The treatment isn't more acid suppression.
It's shifting gears to neuromodulation.
That's right. A massive treatment pivot.
And it highlights the potency trap, right?
Not all PPIs are created equal.
Absolutely not.
The sources are clear.
Pantrazol 40 milligram daily is generally considered the weakest in terms of a member'sal equivalent dose and duration of action.
So if a patient failed pantoprazole, maybe they just needed a stronger PPI.
It's very possible.
Before labeling someone refractory, you should ensure they've had a trial of a more potent option, like, 20 milligram, orMrizol 40 milligram, dosed properly, often twice daily before meals.
And now they're even newer options?
Yes, the potassium competitive acid blockers, or PCaves, like , these are a different mechan, generally faster acting and providing more profound,ustained acid suppression than traditional PPIs.
They're becoming important tools for those tr refractory cases where even potent PP aren't enough.
Okay, let's say the testing is done.
The diagnosis comes back .
It's functional Harper, or maybe reflux hypersensitivity.
What is the absolute first thing we need to do?
Stop the PPI, especially for functional heartburn, where acid is clearly not the issue.
Continuing, it offers no benefit and potentially some long term risks.
And definitely no surgery, right?
Absolutely not.
Anti-reflex surgery, like a Nissan fund application , targets a mechanical problem.
These functional conditions aren't mechanical, surgery won't help and could even make things worse.
The treatment focus has to shift completely.
Towards what?
Towards neuromodulation and behavioral therapies.
We need to address the heightened sensitivity, the brain gutis communication .
Okay, the neuromodulator ladder.
This can seem daunting using antidepressants for gut issues.
Can you walk us through the approach?
We're not training depression heroes, are we?
Not primarily, no.
We're using these medications at much lower doses than for psychiatric indications, specifically leveraging their effects on nerve signaling and pain perception within the gut.
So first line .
First line is usually a low dose tricyclic antidepressant, a TCA.
The mor is start low, go slow.
You're aiming for gut symptom relief, not a full antidepress effect.
What kind of doses are we talking?
Specs.
Typically, amatryptylline or nort, start really low, like 10 milligrams, maybe 25 milligrams, taken at bedtime.
Why those two?
Any preference.
Nortryptoline is often preferred.
It tends to have fewer side effects, particularly less sed and less of the dry mouth, those anticolergic effects compared to amatrypt.
Okay, start low with a DCA, preferably noryptine.
Yeah.
What if a patient can'tlerate TCAs, even at low doses?
Side effects are still too much.
Then you move to second line options.
These are often the SSRIs, selective serotonin reuptake inhibitors, or the SNRIs, serotonoraern reuptakehibitors..
For an SNRI,axine is commonly used, maybe starting at 37.5 milligrams and going up to 75 milligrams .
For SRIs,op or acid are frequent choices, again, starting at low doses like 10 milligram.
Are there other options beyond TCAs and SSRI SNRIs?
Yes, there are adjuncts or alternatives.id, soapentin can be very helpful, particularly if or hypersivity is a major feature .
They work by damerve.
Interesting.
Anything else?
Don't underestimateatin.
Taking to milligrams at bedtime seems to have some good evidence for visceral pain relief, possibly antiflamm.
And non-rug.
Critically important and often behavioral therapitive behavioral therapy, CBT, or gut hypotherapy, can be incredibly effective.
They directly target that brain gutulation. Take time and commitment, the results can be All right, let's shift focus downstream now to the stomach and do item.
We have patients with that chronic upper abdominal pain or bothersomeness after eating dyspia.
We've done the EGD.
It's normal, no ulcer, no cancer.
What's next?
There's a rule here right?
Yes.
Before you can firmly diagnose functional dyspepsia, you have to apply the functional triad rule.
Basically, three things must be actively ruled out.
Okay, what are three?
One, structural disease.
The normal EGD takes care of the big ones like ulcers and malign.
Okay, EGD normal.
Check.
Two.
Helicobact py infection, you have to test for py and treat it if it's present, because eradicating it can sometimes resolve dyspepsia symptoms.
Test and treat H pilory.
Got it.
And number three.
Number three.
Celiac disease.
This one is often is a crucial organic mic.
Celiac.
Even if the main symptom is stomach pain or , not diarrhe.
Absolutely.
Celiac disease can present primarily with dyseptic symptoms.
You need to check series, specifically the IGA tissue translutamine antibody, IGATT.
And there's a catch there, right, with the IGA?
Yes.
You also need to check the total serum IA level.
Some people are IGA deficient, meaning IAT will bealy negative, even if they have celac.
IA is low , you need to rely on IG based proceed to biopsy based on suspicion.
So duadal biopsies during that initial EGD might be important even if the stomach looks fine.
Highly recommended, especially if celiac is on the differential at all.
Only once you've excluded structural disease, H py and celiac, can you confidently land on a functional dyspepsia diagnosis?
Okay, fine functional triad rules satisfied.
Now, within functional dyssia itself, there are subty, and this seems really important for treatment.
It's critical.
We divide it mainly into epigastric Pain syndrome, EPS, and postbrandial distress syndrome, PD.
What's the difference in symptoms?
EPS is primarily about pain or burning felt in the epigastrum, the upper central abdomen.
It often feels sort of ulcer-ike, even though there's no ulcer.
Okay, Pain predominant is EPS .
And PD.
PD is more about symptoms triggered by eating.
Specifically, bothersome fullness after a normal sized meal or getting full weight too quickly known as early satiety.
Bating can be part of it, too.
It suggests a problem with how the stomach is handling food.
And this subtying directly guides treatment.
Directly.
If the patient fits the EPS profile, that ulcer like pain , what's the first thing you might try?
Well, if it feels like an ulcer, maybe a PPI.
Exactly.
For EPS, a trial of a PPI is a reasonable first step.
If that doesn't work, what did we use for functional esophage pain?
Low-dose TCAs.
Right again.
Low-dose TCAs are the next step for refractory EPS.
Okay, so EPS Path, PPI, then maybe TCA.
What about PTS, the fullness and early Sid?
PPOs probably don't work well there.
Generally, no.
PPIs are often pretty ineffective for PTS because the underlying issue is an acid .
It seems to be more about gastric accommodation, the stomach not relaxing properly to receive food or perhaps delayed emptying.
So what do we use for PDS?
You target the presumed mechanism.
Procanetics, agents that help move things through, like metalopermide or dumpyridone, though, access bries.
Or increasingly, we use drugs that help the top part of the stomach, the fundus relax.
Fundic relaxants.
Like what?
Musperone, often used for anxiety, actually works well here at 10 mills three times a day before meals.
Another good option is myzine, an antidepressant, typically at 15 milligrams nightly.
It helps with fundundic relaxations and can also improve appetite and reduce nausea.
Interesting uses for those drugs.
Now, one last clarification.
If we suspect PD involves poor stomach motility, do we need to jump to specialized testing, like monometry?
Generally, no.
Especially not esophageal monometry that's completely the wrong test.
It looks at swallowing.
For PDS, we usually treat empirically based on the symptoms subtype.
So no routine motility test for PDTS .
Not routinely.
However, if a patient has really severe refractory symptoms, particularly significant nausea and vomiting that isn't responding, then you might consider more specialized testing, like a gastric emptying study, to measure how quickly the stomach empties, or maybe even a wireless motility capsule, smart pill, which assesses transit through the whole gut .
But that's reserved for complex, refractory cases, not standard PDashtag.
Wow, okay.
We've covered a huge amount of ground there, essentially mapping out these two critical pathways for upper GI symptoms.
Yeah, I think we distilled it down.
The reflex path really hinges on that EGD result, Conclusive.
It's GRD, inconclusive .
Then you need that objective off PPIPH or impedance testing to sort out nerd from the functional conditions like reflex hypersensitivity or functional heartburn.
And the dyspepsia path is all about that functional triad rule first.
Normal scope, ruleout Hory, ruleout celiac.
Only then do you diagnose functional dysepsia?
And then you subtype it.
EPS gets treated kind of like an alter, maybe with a PPI or TCA.
PTS needs prochonetics or Fundic relaxants like busperone or mercertazepine targeted therapy based on the symptom profile.
So here's the final thought.
Something really provocative that ties us all together.
Consider the patient who definitely had GRD, maybe severe sophophagitis that healed on PPIs.
Or they had that positive off PPI PH study initially.
Okay, Proven GRD history.
But now they're on maximum PPI therapy, maybe even is Brazal, twice a day, and they still have significant heartburn or chest pain.
Right.
So according to our earlier discussion, if we did an on PPI PEH study, what would we likely find?
We likely find the acid is actually wellcrolled, the AET would be normal.
Exactly.
So they don't have true refractory GRD by definition, because the acid isn't the driver anymore.
What's causing their symptoms?
It must be that functional overlap developing on top, reflux hypersitivity.
That's the key insight.
Even in patients with documented structural disease like GRR, once you've optimized the acid suppression , the remaining symptoms are very often functional.
The next step isn't a PCAB or surgery necessarily.
It's adding a neuromodulator.
So the functional approach isn't just for purely functional diagnoses.
It's essential for managing those really difficult, lingering symptoms, even when there was an underlying structural issue.
It absolutely is.
It highlights that you always need to consider the brain gut axis, especially in patients who aren't getting fully better.
It's often the missing piece.
A powerful reminder , always in brain gut.
Thank you for joining us on this deep dive.
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