Board Pearls

Chapter 1, Ep 1 of 3: Dysphagia: The Algorithm

Board Pearls — Fri, 03 Jul 2026 03:40:00 -0500

Dysphagia is the symptom that anchors the esophagus chapter, and the whole game is getting to the right test on the first move. Fix the vignette to one quadrant of a two-by-two, anatomy against mechanism, and the test selection falls out of the sort rather than being memorized. This episode builds that grid, then stress-tests it against the alarm-feature framework and the cases that break a careless read.

The case. A 55-year-old woman has twelve months of progressive dysphagia to solids and liquids, regurgitation of undigested food, nocturnal cough, and weight loss. EGD shows a dilated body with residue and a junction that passes with gentle pressure, no mass, biopsies unremarkable. The story is classic achalasia. Do you proceed to myotomy?

Topics covered

Two axes: oropharyngeal versus esophageal, mechanical narrowing versus motility
Localization: throat plus airway symptoms versus substernal sticking after the swallow
Oropharyngeal causes are neuromuscular: stroke, Parkinson, ALS, myasthenia, radiation
Modified barium swallow with a speech pathologist reads the swallow itself; EGD cannot
Solids-only progressive: ring, web, peptic stricture, EoE, malignancy
Solids-and-liquids from the start: achalasia, spasm, jackhammer, scleroderma
EGD with two-level biopsies even on normal-looking mucosa, because EoE is histologic
Barium esophagram and high-resolution manometry as the second-line motility tests
Alarm features raise malignancy pretest probability; they do not decide whether to scope
Zenker diverticulum: barium first so the scope does not perforate the pouch

Key decisions

New dysphagia is itself an alarm symptom: a 35-year-old with solid-food dysphagia still gets EGD; the over-50 cutoff is a dyspepsia rule, not a dysphagia rule
Throat plus cough, nasal regurgitation, or drooling routes to modified barium swallow, not EGD; EGD sees mucosa, not the swallowing maneuver
Solids-only that progresses over months with weight loss in an older patient is esophageal cancer until proven otherwise
A classic achalasia story still needs manometry before a myotomy: subtype changes the procedure, and pseudoachalasia from a cardia tumor mimics the picture
Borderline manometry (IRP just over cutoff, no pressurization) is inconclusive: FLIP or timed barium before the operating room, not a myotomy

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the two axes of dysphagia
(01:30) - Localization: where the patient points
(03:30) - Oropharyngeal dysphagia and the modified barium swallow
(06:00) - Esophageal dysphagia: reading the pattern
(08:30) - EGD with biopsies as the workhorse first test
(11:00) - The alarm-feature framework and the age-cutoff trap
(13:30) - Zenker diverticulum: why barium leads
(16:00) - The case that does not fit: manometry before myotomy
(19:00) - The algorithm in a handful of moves

Chapter 1, Ep 2 of 3: Globus, Rumination, and Odynophagia

Board Pearls — Fri, 03 Jul 2026 03:45:00 -0500

This episode takes the patients who arrive after a structural and reflux workup has already come back clean. Here the history leads and the test only confirms, so the whole skill is recognizing the phenotype on the story. PPI failure in someone who looks like GERD on the surface is the alert that the diagnosis is not GERD.

The case. A young woman regurgitates recognizable food ten to fifteen minutes after nearly every meal. It is effortless, without nausea or retching, and she has gained weight on twice-daily PPI. What is the diagnosis, what test confirms it, and why is more acid suppression the wrong move?

Topics covered

Globus: the sensation eases or is unchanged by swallowing, the inverse of true dysphagia
Globus workup is targeted; ENT exam and reassurance, not a default PPI
Rumination: effortless postprandial regurgitation of recognizable food, no retching
Rumination fingerprint on postprandial HRM-impedance: the abdominal-strain R-wave
Rumination treatment is diaphragmatic breathing, not acid suppression or fundoplication
Supragastric belching: learned air cycle, gone in sleep, retrained like rumination
Functional chest pain: visceral hypersensitivity treated with a neuromodulator, not more PPI
Odynophagia is mucosal injury until proven otherwise, sorted by exposure before EGD
Pill esophagitis: kissing ulcers at the aortic arch; doxycycline, KCl, bisphosphonates
Infectious esophagitis by host: Candida plaques, HSV volcano-edge, CMV deep serpiginous
Biopsy site separates the viruses: HSV from the ulcer edge, CMV from the ulcer base

Key decisions

Rumination and functional chest pain both defeat escalating PPI because neither lesion is acid: retraining and neuromodulators are the answers
Globus with no alarm features (dysphagia, weight loss, hoarseness, neck mass, smoking) gets ENT exam and reassurance, not endoscopy
Pill esophagitis is a history diagnosis: sudden retrosternal odynophagia after a specific tablet taken with little water, kissing ulcers at the arch
HSV biopsies come from the ulcer edge (infected epithelium); CMV biopsies from the ulcer base (infected stroma). Forgetting this misses the organism
Candida host pattern (PPI plus inhaled steroid, CD4 under 200, transplant) supports empiric fluconazole; viral or pill features push straight to EGD

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the phenotype the history reveals
(01:30) - Globus: the inverse of dysphagia
(04:00) - Rumination syndrome and the abdominal-strain R-wave
(07:30) - Supragastric belching and functional chest pain
(10:30) - Functional heartburn and reflux hypersensitivity
(12:00) - Odynophagia: sort by exposure before the scope
(13:30) - Pill esophagitis: kissing ulcers at the arch
(16:00) - Infectious esophagitis: Candida, HSV, CMV by host and biopsy site

Chapter 1, Ep 3 of 3: Post-surgical and Systemic Dysphagia

Board Pearls — Fri, 03 Jul 2026 03:50:00 -0500

These patients carry a surgical or systemic history the EGD report was never built to surface. The connecting principle is simple: the diagnosis lives outside the scope findings, so the job is to ask the question that reveals it and to read post-surgical anatomy on a barium swallow before an endoscopy.

The case. A patient with severe reflux and dysphagia has absent contractility on nearly every swallow and a hypotensive lower esophageal sphincter. The reflux looks like the dominant problem. Should you offer an antireflux operation?

Topics covered

Post-fundoplication dysphagia: slipped, tight, and telescoped wraps each map to a next move
Barium swallow first after fundoplication: it shows wrap geometry the EGD cannot reconstruct
Sleeve gastrectomy: incisura stricture and worsened reflux, not relief
Roux-en-Y as the antireflux bariatric operation; anastomotic stricture and marginal ulcer
Scleroderma: absent distal contractility plus a hypotensive LES, the cleanest fingerprint
Scleroderma reflux is a pump failure, so fundoplication fails; aggressive PPI instead
Sjogren: dysphagia from lost salivary lubrication and a refractory-reflux clue
Amyloid: infiltrative fibrils, macroglossia as the AL hint, treat the underlying process
Neuromuscular dysphagia: ALS, myasthenia (fatigable), polymyositis and dermatomyositis
Dermatomyositis carries a malignancy association warranting age-appropriate screening
Chemoradiation: acute mucositis and late fibrotic stricture managed with dilation

Key decisions

Post-fundoplication or post-bariatric dysphagia is read first on a barium swallow, not an EGD: geometry drives the diagnosis
The tight wrap gets early pneumatic dilation; the slipped wrap gets PPI for its recurrent reflux, with revision for dilation failure
Scleroderma physiology (failed peristalsis plus open LES) means fundoplication fails: the pump cannot push a bolus past a wrap, so treat reflux medically
Sleeve gastrectomy worsens reflux, so Roux-en-Y is the antireflux bariatric operation in a patient with established GERD
New dysphagia plus macroglossia points to AL amyloid: send immunofixation, free light chains, and marrow biopsy; dermatomyositis triggers cancer screening

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the diagnosis outside the EGD report
(01:00) - Post-fundoplication dysphagia: three patterns
(03:30) - Post-bariatric dysphagia by operation
(05:30) - Scleroderma esophagus: the cleanest fingerprint
(07:30) - Sjogren and amyloid
(09:00) - The neuromuscular dysphagias
(10:00) - Chemoradiation injury and the through-line

Chapter 2, Ep 1 of 2: Manometry and Achalasia

Board Pearls — Sat, 04 Jul 2026 16:30:00 -0500

High-resolution manometry is the gateway physiologic test after a clean endoscopy in esophageal dysphagia or pre-fundoplication evaluation. The Chicago Classification version 4.0 reduces the report to four numbers read in a fixed hierarchy: relaxation first, propagation second. Once you hold that order, every diagnosis falls out. This episode walks the framework and applies it to achalasia, where elevated IRP plus body pressurization pattern picks the subtype and the therapy.

The case. A patient with progressive solids-and-liquids dysphagia. Manometry reports an IRP of 22, a DCI of 300, and a distal latency of 4.0 seconds. Which achalasia subtype, and which definitive therapy?

Topics covered

Catheter, sensors, and the Clouse plot: 36 solid-state sensors at 1 cm spacing; pressure topography by position vs time
The two-job reading: relaxation at the EGJ first, propagation along the body second
Standardized v4.0 protocol: 10 supine swallows, 5 upright, multiple rapid swallow, rapid drink challenge
Integrated relaxation pressure (IRP): catheter-specific thresholds, why upright matters
Distal contractile integral (DCI): failed, weak, normal, hypercontractile bins
Distal latency (DL) under 4.5 seconds defines premature contraction; CFV retired in v4.0
Contraction pattern and the v4.0 IEM definition: ≥70% ineffective or ≥50% failed
Achalasia phenotype: elevated IRP plus 100% failed peristalsis
Subtype assignment: type 1 silent body, type 2 panesophageal pressurization, type 3 premature spastic
Pseudoachalasia red flags: age over 55, symptom duration under 6 months, disproportionate weight loss, non-traversable junction
Achalasia therapies: pneumatic dilation, Heller with partial wrap, POEM, botulinum toxin for non-procedural patients
Subtype-driven therapy choice: type 1 to dilation, type 2 to any modality, type 3 preferentially to POEM

Key decisions

DCI of 300 with elevated IRP is failed peristalsis against a closed junction (achalasia); DCI of 300 with normal IRP is ineffective body peristalsis. Same number, different disease
Distal latency under 4.5 seconds identifies a premature contraction; contraction front velocity has been removed from v4.0 and is a board trap
Multiple rapid swallow augmentation vs no augmentation is the binary that decides full Nissen vs partial wrap pre-fundoplication
Pseudoachalasia red-flag cluster changes the next test from manometry to CT chest plus EUS, before any treatment
Subtype 2 has the best treatment response across modalities; subtype 3 preferentially responds to POEM because the myotomy can extend to cover the spastic segment
No therapy restores peristalsis. All therapies open the LES. Every intervention loses ground over time, so counsel patients up front that one in three need a second procedure

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the manometry framework as a hierarchy
(01:30) - What the catheter does and the Clouse plot
(03:30) - The two jobs and the Chicago algorithm order
(05:30) - IRP: the gate, with catheter-specific thresholds
(08:00) - DCI: contractile vigor and the four bins
(11:00) - Distal latency, contraction pattern, and IEM in v4.0
(13:30) - Walking the hierarchy: IRP first, peristalsis second
(16:00) - Achalasia phenotype and the three subtypes
(20:30) - Pseudoachalasia red flags
(23:00) - Achalasia therapy: dilation, Heller, POEM, botulinum
(30:00) - Subtype-driven therapy choice and durability
(33:00) - Synthesis and what's next

Chapter 2, Ep 2 of 2: Spasm, Scleroderma, and EGJOO

Board Pearls — Sat, 04 Jul 2026 16:35:00 -0500

The normal-IRP side of the Chicago algorithm covers everything that is not achalasia or EGJOO. The sphincter relaxes; the question shifts to what the body is doing. Distal esophageal spasm is a timing problem (premature contraction). Hypercontractile esophagus is a vigor problem (DCI above 8000). Ineffective motility and absent contractility sit at the failed end. Scleroderma is the one disorder that breaks the rule, presenting as absent contractility plus a hypotensive LES that lets reflux through. And EGJOO is the elevated-IRP-with-preserved-peristalsis bucket that v4.0 made harder to call on purpose, because v3.0 was overcalling it.

The case. A patient with chest pain and intermittent dysphagia. Cardiac workup is negative. Manometry shows a normal IRP, 30% of swallows with a distal latency of 3.8 seconds, and a normal DCI on the rest. What is the diagnosis, and what is the first treatment move?

Topics covered

IRP as the sorter: elevated IRP routes to achalasia or EGJOO; normal IRP opens the body branch
Distal esophageal spasm: ≥20% premature swallows (DL under 4.5s) on a normal IRP, in a symptomatic patient
Hypercontractile (jackhammer) esophagus: ≥20% of swallows with DCI above 8000, in a symptomatic patient
Why distal latency captures spasm and contraction front velocity does not: deglutitive inhibition vs raw wave speed
Spasm treatment ladder: address contributors first (opioids, GERD, EoE), then calcium channel blockers, nitrates, sildenafil, peppermint oil, neuromodulators
Type 3 achalasia vs spasm: same body pattern, different IRP, and POEM vs medical therapy follows
Scleroderma esophagus: absent contractility plus hypotensive LES as a dual hit; Nissen contraindicated, partial wrap or no wrap
Ineffective esophageal motility (IEM): more than 70% ineffective or at least 50% failed swallows; surgical implications for fundoplication planning
EGJ outflow obstruction: v4.0 requires both supine and upright IRP elevation, intrabolus pressurization, symptoms, and a confirmatory test
FLIP distensibility index below 2.0 mm²/mmHg or maximum diameter below 12 mm confirms reduced EGJ opening
Opioid-induced esophageal dysfunction: mimics type 3 achalasia, EGJOO, and spasm; reverses with taper before any therapy

Key decisions

Type 3 achalasia and distal esophageal spasm share the body pattern; the IRP separates them. The therapy follows: tailored myotomy for type 3, medical ladder for spasm
Distal latency under 4.5 seconds identifies spasm; DCI above 8000 identifies jackhammer. Both require symptoms before they become a clinical diagnosis
Severe IEM and absent contractility separate at 70% vs 100% failed swallows; absent contractility plus hypotensive LES is the scleroderma fingerprint
EGJOO requires confirmatory imaging, FLIP or timed barium, before invasive intervention. v4.0 deliberately raised the bar
Any tracing that mimics type 3 achalasia in an opioid-using patient triggers an opioid taper and a repeat manometry before any procedure
Scleroderma esophagus contraindicates a full 360-degree Nissen; partial wrap or no wrap is the rule because the dysmotility cannot overcome a tight wrap

Related episodes

esophageal-motility/ep-1

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: IRP sorts everything
(02:00) - Spasm and jackhammer share preserved relaxation
(05:00) - Distal latency and why CFV was retired
(08:30) - Spasm clinical picture and workup
(11:30) - Spasm treatment ladder
(16:00) - Hypercontractile esophagus and the symptom rule
(19:30) - Scleroderma esophagus and the partial-wrap rule
(23:00) - Ineffective and absent contractility
(26:00) - EGJOO and the v4.0 bar
(30:00) - FLIP and timed barium as the rescue
(33:00) - Synthesis and what's next

Chapter 3, Ep 1 of 2: Mechanisms, Grading, and the Acid-Suppression Ladder

Board Pearls — Sun, 05 Jul 2026 21:57:16 -0500

The most useful move at the start of a GERD vignette is to ask what is wrong with the barrier, not how much acid the patient makes. Acid output is usually normal; what fails is the apparatus that keeps acid in the stomach. Hold that frame and the chapter falls into a sequence: barrier anatomy, then grading, then the acid-suppression ladder.

The case. A patient with classic heartburn has been on a once-daily PPI taken at bedtime with incomplete relief. Endoscopy shows LA grade B esophagitis. Before escalating the dose, what single change to the regimen is most likely to fix it?

Topics covered

The antireflux barrier: intrinsic LES and crural diaphragm in series, angle of His, intra-abdominal segment
Most GERD patients have a normal resting LES; a hypotensive LES marks severe disease
Transient LES relaxations (TLESRs) as the dominant reflux mechanism
Sliding hiatal hernia as the structural amplifier; size cutoffs drive procedure choice
American Foregut Society flap-valve grading in retroflexion
LA classification A through D: grading erosive esophagitis
LA grade stratifies treatment intensity and Barrett surveillance risk
PPI pharmacology: pre-meal dosing, why timing decides efficacy
The acid-suppression ladder: once-daily, twice-daily, and the role of P-CABs
When endoscopy is confirmatory versus when reflux monitoring is needed

Key decisions

PPIs need a meal to work: take 30 to 60 minutes before the first meal, not at bedtime. A mistimed PPI is the commonest reason for apparent failure before any dose escalation
A normal resting LES does not exclude GERD: transient LES relaxations carry the reflux, so manometry is not the diagnostic test for reflux
LA grade C or D confirms GERD outright and mandates a follow-up scope to assess Barrett after healing; grade A is nonspecific and needs objective reflux testing
Hiatal hernia size gates the operation: under 2 cm allows TIF, larger hernias need a formal hiatal repair
Escalate to twice-daily PPI or a P-CAB before calling reflux truly refractory, but only after confirming timing and adherence

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: GERD is a barrier problem
(01:30) - The antireflux barrier anatomy
(04:30) - Normal LES and transient relaxations
(08:00) - Hiatal hernia and the flap valve
(12:00) - LA classification of erosive esophagitis
(16:00) - The acid-suppression ladder and PPI timing
(22:00) - P-CABs and when to escalate

Chapter 3, Ep 2 of 2: Refractory Reflux, Lyon, Surgery, and Functional Heartburn

Board Pearls — Sun, 05 Jul 2026 21:57:25 -0500

The patient who anchors this episode is on twice-daily PPI and still symptomatic. The question is not how to escalate, it is what they actually have. Most PPI-refractory patients do not have refractory acid reflux; they have reflux hypersensitivity or functional heartburn, and each has its own treatment that acid suppression and surgery do not touch.

The case. A patient on twice-daily PPI for months still has heartburn. Off-PPI pH testing shows an acid exposure time of 3 percent with a positive symptom association. What is the diagnosis, and why is more acid suppression or surgery the wrong next move?

Topics covered

Reflux monitoring as the test that assigns the diagnostic bucket
Lyon Consensus 2.0: acid exposure time thresholds and supportive metrics
The on-PPI versus off-PPI decision, driven by what you are trying to prove
The four buckets: confirmed GERD, reflux hypersensitivity, functional heartburn, and no reflux
Reflux hypersensitivity: normal acid exposure, positive symptom association
Functional heartburn: normal acid exposure, negative symptom association, neuromodulator treatment
Objective reflux documentation required before antireflux surgery
Matching the operation to the anatomy: fundoplication, magnetic sphincter augmentation, TIF
Why most PPI-refractory patients are not refractory acid reflux

Key decisions

PPI-refractory heartburn is a sorting problem, not an escalation problem: run the Lyon framework before adding acid suppression or referring for surgery
Off-PPI testing proves whether the patient has GERD at all; on-PPI testing evaluates a known-GERD patient with breakthrough symptoms. The question you are asking picks the protocol
Functional heartburn (normal AET, negative symptom association) is treated with a neuromodulator, not more PPI and not surgery
Antireflux surgery requires documented objective reflux first: operating on functional heartburn reliably fails
Reflux hypersensitivity (normal AET, positive symptom association) gets combined neuromodulator plus acid suppression

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the PPI-refractory patient
(01:30) - Reflux monitoring and the Lyon framework
(05:00) - On-PPI versus off-PPI testing
(08:00) - The four diagnostic buckets
(12:00) - Antireflux surgery: matching operation to anatomy
(18:00) - Functional heartburn and reflux hypersensitivity

Chapter 4, Ep 1 of 3: Barrett: Diagnosis, Pathogenesis, and Surveillance

Board Pearls — Sun, 05 Jul 2026 21:57:35 -0500

Every piece of a Barrett vignette is downstream of the definition, so this episode starts there and holds it precisely: a visible columnar segment above the gastroesophageal junction plus intestinal metaplasia on biopsy. From that anchor the Prague criteria, the goblet-cell debate, and the dysplasia-driven surveillance intervals all follow.

The case. Endoscopy shows salmon-colored mucosa extending 2 cm above the top of the gastric folds, and biopsies return columnar mucosa without goblet cells. Is this Barrett esophagus by the American definition, and what do you do next?

Topics covered

The two-part American definition: columnar mucosa >=1 cm above the GEJ plus intestinal metaplasia
Locating the gastroesophageal junction: top of the gastric folds as the anchor
The 1 cm floor: shorter salmon mucosa is intestinal metaplasia of the cardia
American (goblet cells required) versus British (columnar alone) definitions
Prague C and M criteria for describing segment length
Pathogenesis: metaplastic response to chronic acid and bile injury
The dysplasia ladder: no dysplasia, indefinite, low-grade, high-grade
Surveillance intervals keyed to segment length and dysplasia grade
Seattle protocol biopsies and the role of expert pathology confirmation
Chemoprevention: PPI and the AspECT trial signal for aspirin

Key decisions

No goblet cells on a <1 cm salmon segment is intestinal metaplasia of the cardia, not Barrett by the American definition: do not enroll in Barrett surveillance
Low-grade and high-grade dysplasia both require confirmation by a second expert GI pathologist before acting, because interobserver variability is high
Confirmed low-grade dysplasia favors endoscopic eradication over surveillance in most patients; high-grade dysplasia mandates eradication
Surveillance interval is set by segment length and the highest dysplasia grade, not by symptoms
Nondysplastic Barrett is surveilled, not ablated by default, and every patient stays on a PPI

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the definition drives everything
(01:30) - Locating the gastroesophageal junction
(04:00) - The 1 cm floor and cardia metaplasia
(06:00) - American versus British goblet-cell debate
(09:00) - Prague criteria and segment description
(12:00) - The dysplasia ladder
(15:00) - Surveillance intervals and the Seattle protocol
(18:00) - PPI and chemoprevention

Chapter 4, Ep 2 of 3: Endoscopic Eradication Therapy

Board Pearls — Sun, 05 Jul 2026 21:57:42 -0500

Endoscopic eradication rests on a single organizing principle: the Barrett segment holds two kinds of tissue that need two different treatments. Visible disease is resected first because the resection specimen is the staging test, and the flat field is ablated second. Reverse that order and you destroy the information the whole plan depends on.

The case. A patient with a visible 1 cm nodule in a Barrett segment is referred for ablation. Why is radiofrequency ablation the wrong first move, and what must happen before any of the flat segment is touched?

Topics covered

Two tissues, two treatments: resect visible disease, ablate the flat field
Why resection precedes ablation: the specimen is the staging test
EMR technique: suck-and-cut and cap-band methods
EMR upstages the histology in a third to a half of cases
ESD for larger or bulky lesions where en bloc margins matter
Radiofrequency ablation as the workhorse for the flat segment
Cryotherapy as an alternative and for RFA-refractory disease
Complete eradication of intestinal metaplasia as the endpoint
Post-eradication surveillance and recurrence at the neosquamous junction
Buried Barrett and stricture as the main complications

Key decisions

Resect any visible nodule before ablating: ablating it destroys the specimen and the depth-of-invasion information that decides endoscopic versus surgical management
EMR is a staging step, not just therapy: it changes the histologic diagnosis in roughly one third to one half of nodular cases
Radiofrequency ablation treats the flat field, not visible lesions; the endpoint is complete eradication of intestinal metaplasia
Post-eradication patients still need surveillance: recurrence at the gastroesophageal junction is the reason
T1a mucosal cancer is endoscopically curable; T1b submucosal invasion generally moves the patient toward surgical or multimodal therapy

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: two tissues, two treatments
(01:30) - Resect first, ablate second, and why
(04:30) - EMR technique and its role as staging
(08:00) - ESD for larger lesions
(10:00) - Radiofrequency ablation and cryotherapy
(13:00) - Endpoint and post-eradication surveillance

Chapter 4, Ep 3 of 3: Esophageal Cancer: Staging and Treatment

Board Pearls — Sun, 05 Jul 2026 21:57:51 -0500

The cancer side picks up where eradication ends: the patient whose EMR specimen shows invasion past the mucosa, or who presents with cancer outside a known Barrett field. The histology split, the TNM T categories, and the T1a-versus-T1b line organize everything that follows, because depth of invasion is what selects the treatment lane.

The case. An EMR done for a Barrett nodule returns adenocarcinoma invading the submucosa (T1b). The patient assumed endoscopic cure. Why does the depth change the plan, and what is the next step?

Topics covered

Two histologies: adenocarcinoma (rising, distal, Barrett-linked) and squamous cell (proximal, different risks)
Squamous risk factors: smoking, alcohol, achalasia, caustic injury, tylosis (RHBDF2)
TNM staging: Tis is high-grade dysplasia, T1a mucosa, T1b submucosa
The T1a-versus-T1b boundary as the endoscopic-eligibility line
EUS for T and N staging; PET-CT for distant disease
Node risk climbs sharply once tumor reaches the submucosa
CROSS neoadjuvant chemoradiation for locally advanced disease
Esophagectomy and the role of definitive chemoradiation in squamous cell
Palliative stenting and the management of malignant dysphagia

Key decisions

T1a mucosal cancer is endoscopically curable; T1b submucosal invasion carries enough nodal risk to move most patients to esophagectomy or multimodal therapy
An EMR that upstages to T1b changes the plan from endoscopic cure to surgical or neoadjuvant treatment: depth, not the initial biopsy, decides
Locally advanced disease (T3 or node-positive) gets CROSS neoadjuvant chemoradiation before surgery, not surgery alone
Squamous cell carcinoma is more radiosensitive: definitive chemoradiation is a curative-intent option, unlike for most adenocarcinoma
Staging sequence is EUS then PET-CT: local depth and nodes first, distant disease before committing to a curative plan

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: two histologies, different lives
(02:00) - Squamous risk factors and tylosis
(04:00) - TNM staging and the T categories
(07:00) - The T1a versus T1b boundary
(09:30) - EUS and PET-CT workup
(12:00) - CROSS neoadjuvant chemoradiation and esophagectomy

Chapter 5, Ep 1 of 2: Eosinophilic Esophagitis: Diagnosis Through Refractory Disease

Board Pearls — Mon, 06 Jul 2026 09:00:00 -0500

Every diagnostic criterion and every drug in the EoE ladder is downstream of one mechanism: a Th2 allergic response to food allergen in a susceptible host that ends in fibrosis, rings, and impaction if untreated. Hold the cytokine story and the 15-eosinophil threshold, and the diagnosis, the EREFS score, and the treatment ladder follow.

The case. A 32-year-old atopic man presents with a food bolus impaction. After it is cleared, what biopsies do you take, how many, and what threshold makes the diagnosis?

Topics covered

Th2 mechanism: IL-5 and IL-13 driving eosinophil recruitment and remodeling
The diagnostic threshold: at least 15 eosinophils per high-power field
Biopsy strategy: multiple levels, proximal and distal, even on normal-looking mucosa
EREFS endoscopic score: edema, rings, exudates, furrows, strictures
Demographics: atopic men in the third and fourth decades, food impaction as the presentation
PPI as first-line therapy (PPI-responsive EoE folded into the disease)
Topical swallowed steroids: budesonide and fluticasone formulations
Dietary elimination: empiric six-food and step-up approaches
Dupilumab for refractory or steroid-dependent disease
Dilation for fibrostenotic strictures once inflammation is controlled

Key decisions

Any adult food bolus impaction gets esophageal biopsies at that endoscopy, even if the mucosa looks normal, because EoE is a histologic diagnosis
Take biopsies at multiple levels (proximal and distal): EoE is patchy and a single-site sample misses it
PPIs are now first-line EoE therapy, not a rule-out step: PPI-responsive eosinophilia is EoE, not a separate entity
Treat the inflammation before dilating a stricture: dilation addresses fibrosis but does not treat the disease
Refractory or steroid-dependent EoE escalates to dupilumab rather than open-ended steroid escalation

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the Th2 mechanism drives everything
(02:00) - The 15-eosinophil diagnostic threshold
(04:30) - Biopsy strategy and the food impaction presentation
(07:00) - EREFS endoscopic score
(09:30) - The treatment ladder: PPI, steroids, diet
(14:00) - Dupilumab for refractory disease
(17:00) - Dilation for fibrostenotic strictures

Chapter 5, Ep 2 of 2: Infectious and Direct-Injury Esophagitis

Board Pearls — Mon, 06 Jul 2026 09:05:00 -0500

These patients share one principle: the mucosa was injured by something that touched it, whether an organism the host could not keep down, a tablet that lodged where the lumen narrows, or a swallowed corrosive. Depth reflects contact time, site reflects local anatomy, and host status reflects who is vulnerable. That framework sorts the differential before the scope.

The case. An HIV patient with a CD4 count of 40 has odynophagia and one large, deep, serpiginous distal ulcer on endoscopy. Where do you biopsy, and what organism are you looking for?

Topics covered

Candida: the most common infectious esophagitis, white adherent plaques
The host spine: HIV with CD4 under 200, inhaled steroids, transplant, antibiotics
HSV: shallow volcano-edge ulcers, epithelial inclusions at the ulcer edge
CMV: large deep serpiginous ulcers, stromal inclusions at the ulcer base
The biopsy-site rule: HSV from the edge, CMV from the base
Treatment: fluconazole, acyclovir, ganciclovir by organism
Pill esophagitis: kissing ulcers at the aortic arch, offending drugs and technique
Caustic injury: acid versus alkali, the role and timing of endoscopy
When to biopsy versus treat empirically for Candida

Key decisions

Host status sorts the infectious differential before biopsy: Candida with inhaled steroids or CD4 under 200, CMV with CD4 under 50
Biopsy site is the exam trap: HSV lives in the epithelium at the ulcer edge, CMV in the stroma at the ulcer base
A classic Candida host with typical plaques can be treated empirically with fluconazole; viral or pill features push to biopsy first
Pill esophagitis is a history diagnosis (a specific tablet taken with little water); stop the drug and coach technique
Caustic ingestion is graded endoscopically within the first 24 to 48 hours; avoid blind instrumentation of a deeply injured esophagus

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: injured by something that touched it
(01:30) - Candida and the immunocompromise workup
(05:00) - HSV: edge ulcers and epithelial inclusions
(07:30) - CMV: base ulcers and stromal inclusions
(09:30) - The biopsy-site rule and treatment by organism
(12:00) - Pill esophagitis and caustic injury

Chapter 6, Ep 1 of 2: H. pylori: Biology, Eradication, and Salvage

Board Pearls — Mon, 06 Jul 2026 10:00:00 -0500

Every H. pylori diagnostic and every regimen is downstream of one fact: the organism survives in gastric mucus by producing urease in industrial quantities. Hold that, and the breath test, the stool antigen, the off-PPI timing rule, and the shift away from clarithromycin triple all follow.

The case. A patient treated for a duodenal ulcer returns after clarithromycin triple therapy with a positive urea breath test. Which salvage regimen do you choose, and what must you avoid repeating?

Topics covered

Biology: a urease-producing spiral gram-negative living in gastric mucus
Virulence: the cag pathogenicity island and vacA
Urea breath test and stool antigen as active-infection tests
The off-PPI rule: hold PPI 2 weeks and antibiotics/bismuth 4 weeks before testing
Serology cannot distinguish active from past infection
First-line has shifted: bismuth quadruple and vonoprazan-based dual/triple over clarithromycin triple
Penicillin allergy and local resistance as regimen drivers
Salvage: never repeat a failed macrolide or levofloxacin regimen
Confirming eradication with a breath test or stool antigen after therapy
Indications to test and treat: ulcer, MALT lymphoma, early gastric cancer resection, unexplained iron deficiency

Key decisions

Test for active infection off acid suppression: hold the PPI 2 weeks and any antibiotics/bismuth 4 weeks, or the breath test and stool antigen turn falsely negative
Clarithromycin triple is no longer first-line where resistance exceeds 15 percent: use bismuth quadruple or a vonoprazan-based regimen
Salvage never reuses the antibiotic class that just failed: a failed clarithromycin regimen goes to bismuth quadruple or levofloxacin-based therapy, not another macrolide
Always confirm eradication after treatment, at least 4 weeks out and off PPI, with a breath test or stool antigen, not serology
Every H. pylori-positive peptic ulcer gets eradication plus confirmation, because it changes recurrence risk

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: urease is load-bearing
(02:00) - Biology and virulence factors
(05:00) - Diagnostics and the off-PPI rule
(09:00) - First-line: bismuth quadruple and vonoprazan regimens
(13:00) - Salvage: do not repeat a failed class
(16:00) - Confirming eradication and test-and-treat indications

Chapter 6, Ep 2 of 2: NSAID Ulcers, Refractory Disease, and Perforation

Board Pearls — Mon, 06 Jul 2026 10:05:00 -0500

NSAIDs damage the gastroduodenal mucosa by two mechanisms, and the systemic COX-1 mechanism is the one that matters for prevention: no topical avoidance protects the mucosa. The risk factors are the teaching point because they do not add, they multiply, and the H. pylori interaction compounds them.

The case. A 70-year-old on daily NSAIDs and low-dose aspirin with a prior ulcer presents with a new gastric ulcer. Beyond stopping the NSAID, what does the risk-factor stack tell you about prevention going forward?

Topics covered

NSAID mechanism: systemic COX-1 inhibition strips prostaglandin-driven mucosal defense
Why the systemic mechanism means enteric coating does not protect
Multiplicative risk factors: age over 65, prior ulcer, high-dose or multiple NSAIDs, anticoagulation, steroids
The H. pylori and NSAID interaction: two pathways that compound
PPI co-prescription as the primary prevention strategy in high-risk patients
COX-2 selective agents: GI benefit versus cardiovascular cost
Refractory ulcers: exclude persistent H. pylori, occult NSAID use, ZES, and malignancy
Zollinger-Ellison: fasting gastrin, secretin stimulation, and the off-PPI caveat
Gastric ulcers require follow-up to confirm healing and exclude cancer
Complications: bleeding, perforation, and gastric outlet obstruction

Key decisions

Every high-risk patient who must stay on an NSAID gets a co-prescribed PPI: risk factors multiply, so a stacked patient is high-risk even without a prior ulcer
Enteric coating and rectal or IV routes do not protect the stomach: NSAID injury is systemic through COX-1, not topical
A refractory ulcer triggers a specific checklist: confirm H. pylori eradication, hunt occult NSAID/aspirin use, check fasting gastrin for ZES, and biopsy to exclude malignancy
Gastric ulcers get a follow-up endoscopy to document healing and rule out cancer; duodenal ulcers usually do not
Fasting gastrin for suspected ZES must be interpreted off PPI, because acid suppression itself raises gastrin

For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening: the systemic NSAID mechanism
(02:30) - Multiplicative risk factors
(05:30) - PPI co-prescription and COX-2 tradeoffs
(08:30) - Refractory ulcers and the exclusion checklist
(12:00) - Zollinger-Ellison and fasting gastrin
(15:00) - Complications: bleeding, perforation, obstruction