Board Pearls

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

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

This episode reduces the entire dysphagia workup to two bedside questions, where food sticks and what sticks when, and shows why each answer selects its own test. It sorts oropharyngeal from esophageal dysphagia, maps the solids-versus-mixed and tempo patterns onto specific diagnoses, and clarifies why new dysphagia is itself an alarm symptom that mandates a scope regardless of age.

Topics covered

Oropharyngeal versus esophageal dysphagia
Modified barium swallow with speech therapy
Endoscopy with biopsies for solid dysphagia
Mechanical narrowing versus motility failure
Alarm features and dysphagia
Zenker diverticulum
Achalasia subtypes and manometry
Esophageal cancer red flags

Key decisions

Throat-level dysphagia with airway symptoms goes to modified barium swallow with a speech therapist, not endoscopy, because that study watches the swallow and tests airway protection.
Solids-first progressive dysphagia points to a narrowing and goes to endoscopy with biopsies; solids-and-liquids from day one points to a failed muscle wave.
Take esophageal biopsies high and low even when the mucosa looks normal, since eosinophilic esophagitis appears normal in up to a third of cases.
New dysphagia is itself an alarm symptom, so scope every patient regardless of age; the over-fifty cutoff belongs to dyspepsia, not dysphagia.
Suspect Zenker from regurgitation of old food, halitosis, and gurgling; diagnose with barium swallow and avoid leading with endoscopy to prevent pouch perforation.
Do not go to myotomy or dilation without manometry, because achalasia type (I, II, or III) decides the procedure and a junction tumor can mimic the picture.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The two bedside questions
(00:29) - Where does the food stick
(01:02) - What sticks and when
(01:55) - Oropharyngeal dysphagia and the swallow study
(03:34) - Esophageal dysphagia and endoscopy
(05:41) - Alarm features belong to dyspepsia
(07:07) - Zenker diverticulum
(08:19) - Achalasia: confirm before you cut

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

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

Episode two of the Esophageal Symptoms chapter covers the complaints that aren't classic dysphagia: globus, rumination, supragastric belching, functional chest pain, and painful swallowing. The unifying tell is a reflux-looking patient who fails real acid suppression, which means the problem was never acid. Diagnosis is made from the history and exposures; the test only confirms it.

Topics covered

Globus sensation
Rumination syndrome
Supragastric belching
Functional chest pain
Functional heartburn and reflux hypersensitivity
Odynophagia workup
Pill esophagitis
Infectious esophagitis

Key decisions

A reflux-looking patient who fails a real dose of PPI is telling you the problem is not acid; stop escalating and rethink the diagnosis.
Globus improves or stays unchanged with swallowing while true dysphagia worsens; workup stays narrow and reassurance is the treatment.
Rumination is effortless postprandial regurgitation of recognizable food with no retching, confirmed by postprandial impedance-manometry showing abdominal and esophageal pressure rising together; treat with diaphragmatic breathing, not more PPI or fundoplication.
Functional chest pain is treated with a low-dose tricyclic neuromodulator (imipramine or amitriptyline 25 to 50 mg at bedtime), not a higher PPI dose.
Pill esophagitis causes discrete, often kissing ulcers at the aortic arch level; classic offenders include doxycycline, potassium chloride, bisphosphonates, NSAIDs, and iron; treat by stopping the drug and correcting pill technique.
Herpes ulcers are shallow with volcano edges and viral cytopathic changes at the edge, so biopsy the edge; CMV ulcers are large, deep, and punched-out with owl-eye inclusions at the base, so biopsy the base.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Intro and the unifying tell
(01:05) - Globus
(02:13) - Rumination syndrome
(04:20) - Functional chest pain
(05:23) - Functional heartburn and reflux hypersensitivity
(06:08) - Odynophagia and the three exposures
(06:46) - Pill esophagitis
(08:28) - Infectious esophagitis

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

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

The dysphagias the standard scope-then-manometry workup misses: those after fundoplication and bariatric surgery, and those reaching the esophagus from systemic disease. The unifying skill is knowing which history question surfaces the surgical or systemic story the scope report cannot carry.

Topics covered

Post-fundoplication dysphagia patterns
Post-bariatric surgery dysphagia
Scleroderma esophagus
Sjogren and sicca-related dysphagia
Esophageal amyloidosis
Neuromuscular oropharyngeal dysphagia
Radiation esophageal injury
Barium swallow versus endoscopy

Key decisions

First test for post-fundoplication dysphagia is a barium swallow, not a scope, because it shows wrap shape and junction position; a too-tight wrap is dilated early to save revision surgery.
A slipped wrap gives both recurrent reflux and dysphagia because the wrap slides onto the stomach; telescoping produces the same combination with an intact wrap.
Sleeve gastrectomy worsens reflux by raising intragastric pressure and flattening the angle of His, so gastric bypass is the reflux-friendly bariatric operation; bypass dysphagia is anastomotic stricture treated with endoscopic dilation.
Scleroderma manometry shows failed contractions on nearly every swallow plus a weak lower sphincter, distinguishing it from achalasia where the sphincter fails to relax with high relaxation pressure.
Avoid fundoplication in scleroderma because a wrap needs a working peristaltic pump; wrapping an aperistaltic esophagus trades reflux for obstruction.
Macroglossia points to AL amyloid; work up with serum and urine immunofixation, free light chains, and marrow biopsy, and treat the underlying process rather than the esophagus.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: dysphagias the standard workup misses
(00:29) - The core idea: the answer is in the history
(00:52) - Post-fundoplication dysphagia patterns
(02:37) - Post-bariatric surgery dysphagia
(04:10) - Scleroderma esophagus
(05:34) - Sjogren and sicca-related dysphagia
(06:29) - Esophageal amyloidosis
(07:22) - Neuromuscular and radiation causes

Chapter 2, Ep 1 of 4: Manometry Principles

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

Manometry from first principles: every swallow the esophagus has two jobs, the sphincter must open and the body must squeeze in a top-to-bottom wave, and every number the test reports measures one of those two jobs. This episode teaches the order you read them in, sphincter first then body, because that sequence decides which half of the differential you are even in. Master the three numbers here and every motility diagnosis in the chapter becomes a specific pairing of two answers.

Topics covered

The two jobs of every swallow: sphincter opening and the peristaltic wave
Why you read the sphincter before the body, always
The manometry catheter and the standard ten supine, five upright protocol
IRP: how completely the sphincter relaxes, not resting tone
DCI bands: failed, weak, normal, and hypercontractile swallows
Distal latency and premature contraction as the signature of spasm
Fragmentation and ineffective motility
The recurring trap: same body tracing, two opposite diseases

Key decisions

A high IRP means the sphincter failed to open: think achalasia or outflow obstruction; a normal IRP moves the problem into the body of the esophagus
Normal IRP is under fifteen supine and under twelve upright, so a study that skips the upright swallows cannot finish the job
A totally silent body with normal IRP is absent contractility, but the same silent body with high IRP is achalasia: the sphincter you already checked is the only thing that separates them
DCI under 100 is a failed swallow, 100 to 450 weak, 450 to 8000 normal, over 8000 hypercontractile
Distal latency under four and a half seconds means the contraction fired too early, and that premature squeeze is spasm on the tracing
Fragmented contractions plus many weak or failed swallows is how you land on ineffective motility

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Two jobs per swallow: the whole test in one idea
(00:41) - Order of operations: sphincter before body
(01:02) - The catheter and the standard protocol
(01:48) - IRP: does the sphincter let go
(02:51) - DCI: the total force of the body's squeeze
(04:03) - Distal latency and fragmentation
(04:38) - The short version: two answers, in order
(05:32) - Next episode: building achalasia from mechanism

Chapter 2, Ep 2 of 4: Achalasia

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

Achalasia is where the manometry numbers point most often, and every strange feature of the disease falls out of one lesion: loss of the inhibitory nerves that relax the sphincter and time the wave. The sphincter clamps but never releases, the body loses its wave, and what the body does on those failed swallows names the subtype. Subtype picks treatment because it changes what the procedure has to accomplish.

Topics covered

One lesion: inhibitory nerve loss, excitatory nerves spared
Dysphagia to solids and liquids from the start
Three subtypes as three ways a wave-less body behaves
EGD first as a rule-out, not a rule-in
Bird-beak on barium, IRP and subtype on manometry
No treatment fixes the muscle: all lower sphincter pressure
Botox, dilation, Heller, POEM tradeoffs
Opioids and pseudoachalasia as framework-breaking traps

Key decisions

Dysphagia to solids AND liquids from onset points to a failed wave, not a physical narrowing
A normal-looking endoscopy does not exclude achalasia: up to 40 percent look clean
Type two (pan-esophageal pressurization) has the best prognosis and responds to every treatment
Type three needs a long myotomy reaching the spastic segment, so POEM; pneumatic dilation is the wrong answer
Never Botox a healthy young surgical candidate: it scars the plane and raises later myotomy perforation risk
Avoid a full fundoplication after Heller: a wave-less esophagus cannot push through a complete wrap
Chronic opioids can mimic type three or spasm; stop the drug and repeat manometry before any procedure
Age over 60, short history, and disproportionate weight loss mean rule out pseudoachalasia with EUS and cross-sectional imaging

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

Questions or feedback: hello@boardpearls.com.

(00:00) - One lesion, one disease
(00:30) - The nerve lesion and the three subtypes
(01:11) - Presentation as mechanism
(02:23) - Workup: endoscopy, barium, manometry
(03:15) - Type one: the silent body
(03:38) - Type two: the pressurizing body
(04:27) - Type three: the spastic body
(05:08) - Treatments: nothing fixes the muscle
(09:07) - Two traps: opioids and pseudoachalasia

Chapter 3, Ep 1 of 3: Mechanisms and Endoscopy

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

GERD is a failure of the antireflux barrier, not acid overproduction. Most patients have a normal resting sphincter, so transient lower esophageal sphincter relaxations are the dominant mechanism, and a sliding hiatal hernia amplifies every failure mode at once. Endoscopy grades the erosive damage, sizes the hernia, and decides treatment intensity, surveillance, and surgical candidacy from one look.

Topics covered

Barrier failure, not acid excess
LES plus crural diaphragm stacked as one valve
Transient LES relaxations as the main mechanism
Sliding hiatal hernia amplifies every failure mode
Postprandial acid pocket and the alginate raft
Failed acid clearance: supine, saliva loss, weak swallow
Obesity, visceral pressure, and Barrett risk
LA-grade erosive esophagitis and its consequences

Key decisions

A resting sphincter under 10 mmHg is the exception, seen only in severe disease
Baclofen stimulates GABA-B to cut transient LES relaxations and reduce reflux
Hiatal hernia over 3 cm mandates formal diaphragm repair plus laparoscopic fundoplication
Alginate forms a raft that sinks the acid pocket, helping postprandial breakthrough even on a PPI
LA grades C and D are unambiguous proof of reflux and require repeat endoscopy after healing to unmask Barrett's
Gastric bypass is reflux-friendly, sleeve gastrectomy worsens reflux and is the wrong bariatric choice

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Reflux as barrier failure
(00:27) - What fails: the two-muscle valve
(01:21) - Transient relaxations, the main mechanism
(02:33) - Sliding hiatal hernia amplifies everything
(03:23) - Hernia size and valve grade as decision points
(04:27) - The acid pocket and why alginate works
(05:17) - Failed clearance and obesity
(07:20) - Endoscopy: grading erosions and complications

Chapter 3, Ep 2 of 3: Acid Suppression Drugs

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

Acid-suppressing drugs work only when their mechanism and timing line up. This episode explains why proton pump inhibitors heal erosive disease when histamine blockers fade, why wrong meal timing is the top cause of apparent PPI failure, and where vonoprazan changes the game.

Topics covered

One pump, three switches: gastrin, histamine, acetylcholine
H2 blockers fade as the cell ramps up
PPIs are prodrugs that need meal-timed acid
PPI potency ranking and escalation logic
Nocturnal acid breakthrough on twice-daily dosing
Vonoprazan as a mechanistically different acid blocker
Long-term safety associations versus randomized data
Clopidogrel and PPI interaction

Key decisions

First move in apparent PPI failure is confirming dosing 30 to 60 minutes before a meal
Dexlansoprazole is the one PPI that does not need strict meal timing
Pantoprazole is weakest, rabeprazole strongest; switch agents before adding a second dose
Vonoprazan is the answer for true breakthrough after correctly taken twice-daily PPI, especially severe disease
Do not stop a PPI for safety worry in severe erosive disease, stricture, or Barrett's; use lowest effective dose
For dual-antiplatelet patients needing acid suppression, choose low-interaction pantoprazole or rabeprazole, do not withhold

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction
(00:24) - One pump, three switches
(00:52) - Histamine blockers fade
(01:31) - PPIs: prodrug, timing, and onset
(03:12) - PPI potency and dosing strategy
(04:02) - Nocturnal acid breakthrough
(04:24) - Vonoprazan, a different class
(05:36) - Long-term safety and clopidogrel

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

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

Episode one of the Barrett Esophagus and Esophageal Cancer chapter covers how to diagnose Barrett's, why the metaplasia climbs toward cancer, and how the dysplasia grade sets the surveillance interval. The organizing idea: the worse the cells look, the faster they progress, and that speed dictates how often you scope. American definition, sampling protocol, screening criteria, and grade-based intervals throughout.

Topics covered

Barrett's definition and the gastroesophageal junction
Goblet-cell requirement and American versus British criteria
Prague C and M measurement
Seattle-style biopsy protocol and nodule resection
Screening criteria and non-endoscopic tools
Metaplasia-dysplasia-carcinoma sequence
Dysplasia grading and expert confirmation
Grade-based surveillance intervals

Key decisions

Barrett's requires salmon columnar lining at least one centimeter above the junction PLUS intestinal metaplasia with goblet cells; use the American definition on exams.
Any visible nodule or irregularity is resected, not forceps-biopsied, because resection also stages it; flat segment gets four-quadrant biopsies every two centimeters, tightened to every centimeter when dysplasia is present.
Every dysplasia call must be confirmed by a second pathologist with GI expertise before management changes; most community low-grade reads are downgraded on expert review.
Non-dysplastic Barrett is scoped every five years for short segments and every three for long ones, but the first surveillance after a new diagnosis is at one year.
Indefinite dysplasia and surveillance-path low-grade are managed with twice-daily acid suppression and repeat biopsy; confirmed low-grade in fit patients and essentially all high-grade go to endoscopic eradication.
Mucosal cancer carries little nodal risk and stays endoscopic; submucosal invasion raises node risk steeply and brings surgery into play.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the organizing idea
(00:30) - Defining Barrett's: segment plus goblet cells
(02:59) - Sampling protocol and resecting nodules
(04:35) - Who to screen and non-endoscopic tools
(05:45) - Why the tissue becomes cancer
(09:34) - Surveillance intervals by grade
(10:54) - Low-grade dysplasia: the decision point

Chapter 4, Ep 2 of 3: Endoscopic Eradication Therapy

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

Endoscopic eradication of Barrett esophagus rests on one principle: the segment holds two kinds of tissue that demand two treatments in a fixed order. Resect visible disease first for a staging specimen, then ablate the flat metaplastic field. This episode covers EMR versus ESD, radiofrequency ablation, cryotherapy salvage, and the intensive post-eradication surveillance that recurrence at the junction and buried glands demands.

Topics covered

Resect-first, ablate-second principle
Endoscopic mucosal resection technique and staging value
Endoscopic submucosal dissection indications
Radiofrequency ablation of the flat field
Cryotherapy and salvage modalities
Complete eradication of intestinal metaplasia
Post-eradication surveillance and buried glands
Eradication failure and complications

Key decisions

Always resect a visible nodule before ablating; ablating first destroys the specimen that decides endoscopic versus surgical management
EMR is the staging step because the fuller specimen re-grades forceps biopsies in both directions, most often downgrading high-grade dysplasia
En bloc single-piece resection works up to 1.5 to 2 cm; larger lesions or depressed morphology warrant ESD to preserve margins
Radiofrequency ablation is the default for the flat field; ablation for low-grade dysplasia requires expert-pathologist confirmation
Cryotherapy is the salvage option after RFA fails and suits strictures, very long segments, and burn-intolerant patients
Post-eradication surveillance is more intensive than before treatment, front-loaded in the first year, biopsying the junction and healed squamous lining for buried glands under twice-daily 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) - Episode overview: two tissues, two treatments
(00:24) - The core principle: resect first, ablate second
(01:19) - Endoscopic mucosal resection technique
(01:54) - Why resection is the staging step
(02:35) - Endoscopic submucosal dissection for larger lesions
(03:30) - Radiofrequency ablation of the flat field
(04:44) - Cryotherapy and other ablation modalities
(05:25) - Complete eradication, surveillance, and buried glands

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

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

Esophageal cancer from histology through staging to treatment, built around the one depth boundary that decides endoscopic versus surgical care. Covers adenocarcinoma versus squamous cell, T-stage depth categories, the mucosa-to-submucosa node-risk jump, the fixed staging workup, and the regimens for locally advanced and metastatic disease.

Topics covered

Adenocarcinoma vs squamous cell carcinoma
Squamous risk factors and named associations
T-stage depth categories and nodal staging
Mucosal vs submucosal node-risk boundary
Endoscopic vs surgical treatment selection
Staging workup sequence
Neoadjuvant and perioperative regimens
Metastatic palliation and biomarker-directed therapy

Key decisions

Mucosal disease stays endoscopic because node risk is near zero; submucosal invasion crosses to surgery as node risk climbs steeply.
Favorable superficial-submucosal exception: invasion under half a millimeter, well or moderately differentiated, no lymphovascular or perineural invasion, clean en-bloc margins, and a real reason to avoid surgery.
Staging order is endoscopy, then CT, then PET, then endoscopic ultrasound, with endoscopic resection of any visible early lesion as the depth test.
Carboplatin and paclitaxel with concurrent radiation is the neoadjuvant standard for both histologies; a four-drug perioperative chemotherapy is the alternative for junction and gastric adenocarcinoma.
Residual cancer in the specimen after neoadjuvant chemoradiation and surgery earns a year of adjuvant checkpoint-inhibitor therapy.
Cervical and very high esophageal squamous tumors get definitive chemoradiation, not chemoradiation then esophagectomy, to spare the larynx.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction
(00:30) - Two histologies: adenocarcinoma vs squamous
(01:29) - Named squamous risk associations
(02:10) - Staging by depth and nodes
(02:54) - The mucosa-to-submucosa boundary
(04:50) - The staging workup sequence
(06:08) - Regimens for locally advanced disease
(08:01) - Palliation in metastatic disease

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

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

Eosinophilic esophagitis explained from a single mechanism: IL-4 and IL-13 drive eotaxin, eosinophils flood the lining, and chronic inflammation lays down scar. This episode walks the diagnostic criteria, the inflammatory-versus-fibrotic endoscopy split, and the three drugs plus diet, then closes on refractory disease and the dupilumab-plus-dilation combined approach.

Topics covered

EoE pathophysiology and eotaxin signaling
Diagnostic criteria and biopsy protocol
Dropping the PPI diagnostic trial
Endoscopic inflammatory vs scarring features
PPI, topical steroids, and elimination diet
Step-up empiric food elimination
Refractory fibrostenotic disease
Dupilumab dosing and esophageal dilation

Key decisions

Diagnose EoE with at least fifteen eosinophils per high-power field plus symptoms, after excluding other causes; no PPI trial needed because a PPI response is treatment, not a rule-out.
Take at least six biopsies from at least two levels (upper and lower) because disease is patchy and distal-only sampling reads falsely negative.
Any adult with a food impaction gets esophageal biopsies at the first endoscopy even if the mucosa looks normal.
Endoscopy splits into inflammatory features (edema, exudates, furrows) that reverse with drugs and scarring features (rings, strictures) that need mechanical dilation.
Fluticasone is sprayed into the mouth and swallowed, never inhaled, with no food or drink for thirty minutes; budesonide is a viscous slurry with the same rule.
Refractory fibrostenotic disease is treated with dupilumab dosed weekly (less frequent dosing clears eosinophils but fails to improve dysphagia) plus graduated dilation.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The cytokine engine
(01:30) - The typical patient
(02:17) - Food impaction and the biopsy rule
(02:47) - Diagnostic criteria and sampling
(03:33) - Dropping the PPI trial
(04:23) - Endoscopy: inflammatory vs scarring
(05:35) - Drugs and diet
(09:54) - Refractory disease

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

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

Episode two of two on eosinophilic and infectious esophagitis, covering the infections and direct chemical injuries of the esophagus. One principle links them all: the lining got hurt by something that touched it, and immune status, ulcer shape, and biopsy site tell you the agent. Candida, herpes, CMV, pill esophagitis, and caustic ingestion, each read from contact time, anatomy, and host defenses.

Topics covered

Candida esophagitis
Herpes esophagitis
CMV esophagitis
Pill esophagitis
Caustic and corrosive ingestion
Biopsy targeting by organism
Zargar injury grading
Immune status and organism prediction

Key decisions

Candida: non-washable plaques, fluconazole 200 to 400 mg daily for 14 to 21 days; echinocandin for azole failure, critically ill, or Candida glabrata; ART is the durable prevention in HIV.
Herpes makes shallow volcano-edge ulcers, biopsy the edge for multinucleated giant cells with Cowdry inclusions, treat with acyclovir; CMV makes deep geographic ulcers low in the esophagus, biopsy the base for owl-eye inclusions, treat with ganciclovir then valganciclovir.
Pill esophagitis: discrete shallow kissing ulcers at the aortic arch with normal lining between; stop the drug, sucralfate, and prevent by taking pills upright with a full glass of water staying up 30 minutes.
Caustic injury: alkali causes liquefactive necrosis and damages the esophagus, acid causes coagulative necrosis and biases toward the stomach; airway first, and never give emetics, neutralizing agents, or a blind early nasogastric tube.
Grade caustic injury with the Zargar scale at endoscopy within a day or two; do not scope the unstable patient or one with perforation or airway necrosis, image with CT and consult surgery instead.
A significant caustic ingestion is a lifelong premalignant condition: strictures heal with fibrosis and squamous cell carcinoma risk warrants surveillance endoscopy starting 15 to 20 years later.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: the injured lining and its agent
(00:45) - Candida esophagitis
(03:11) - The white esophagus differential
(03:52) - Viral infections: herpes versus CMV mechanism
(04:43) - Herpes esophagitis
(05:44) - CMV esophagitis
(07:49) - Pill esophagitis
(09:29) - Caustic and corrosive injury

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

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

H. pylori from biology through eradication and salvage, driven by a handful of load-bearing mechanisms. Urease survival explains both diagnosis and why acid suppression causes false negatives, infection location decides gastric versus duodenal disease, and rising clarithromycin resistance has reshaped first-line therapy toward optimized bismuth quadruple and vonoprazan-based regimens.

Topics covered

Urease biology and diagnostic tests
Infection location and ulcer physiology
Suppression rule and false negatives
Serology limits and test of cure
Expanded testing indications
Clarithromycin resistance and first-line therapy
Vonoprazan-based regimens
Salvage and susceptibility testing

Key decisions

Hold acid blockers 1 to 2 weeks and antibiotics or bismuth 4 weeks before active testing; histology on a body biopsy is the most resilient test when the acid blocker cannot be stopped.
Serology cannot distinguish active from past infection and is never the test of cure; retest everyone at least 4 weeks post-antibiotic with breath or stool antigen.
Clarithromycin triple is wrong empirically once local resistance exceeds 15 percent or with any prior macrolide exposure, including azithromycin.
Optimized bismuth quadruple for 14 days is the strong first-line choice because it avoids clarithromycin and leans on the low-resistance trio.
Clarithromycin and levofloxacin are one-way streets after failure; amoxicillin, tetracycline, and rifabutin stay reusable.
After two failures, get culture or molecular susceptibility testing and treat with full-dose 14-day therapy rather than guessing; de-label weak penicillin allergies first.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Urease and how the organism survives
(01:20) - Virulence factors and prevalence
(01:58) - Location decides the disease
(03:14) - The suppression rule and the four active tests
(04:30) - Serology and mandatory test of cure
(05:26) - Testing indications
(06:46) - First-line therapy and clarithromycin resistance
(11:26) - Salvage and susceptibility testing

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

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

Episode two of the Peptic Ulcer Disease and H. pylori chapter covers the ulcers that are not driven by H. pylori. It works through NSAID and aspirin injury and its prevention, the sequential exclusion behind refractory and idiopathic ulcers, and the perforation and penetration emergencies that split on whether the leak is free or contained.

Topics covered

NSAID and aspirin ulcer mechanism
Multiplicative NSAID risk factors and tiers
Acid-blocker co-prescription and misoprostol
Celecoxib, the aspirin trap, and dual antiplatelet therapy
Refractory ulcer sequential exclusion
Gastric cancer and repeat biopsy rule
Zollinger-Ellison and fasting gastrin pitfalls
Free perforation versus contained penetration

Key decisions

NSAID mucosal injury is primarily systemic COX-1 prostaglandin depletion, so suppositories and injections cause ulcers as readily as pills.
High-risk patients (prior complicated ulcer or more than two factors) need a PPI with any non-selective NSAID; standard-dose H2 blockers are inadequate for prevention.
Celecoxib plus aspirin loses most of the COX-2 GI advantage, so add a PPI when a further risk factor is present; give a PPI alongside dual antiplatelet therapy without fear of clopidogrel interaction.
A negative H. pylori test on a patient still taking a PPI is a deferred test; retest off acid suppression for one to two weeks and off antibiotics or bismuth for four.
Every gastric ulcer gets a follow-up scope at eight to twelve weeks and every non-healing one gets many repeat biopsies from rim and base; duodenal ulcers do not need routine follow-up.
Fasting gastrin is confounded by PPIs (feedback rise) and by atrophic gastritis; gastric pH under two with high gastrin confirms gastrinoma, pH above four points to atrophic gastritis.
Free perforation goes to a Graham omental patch without added vagotomy; posterior duodenal penetration into the pancreas is managed medically with high-dose 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) - Introduction: the non-H. pylori ulcers
(00:35) - NSAID and aspirin injury mechanism
(01:18) - Multiplicative risk factors and tiers
(02:51) - Acid-blocker co-prescription for prevention
(03:36) - COX-2 drugs, the aspirin trap, and dual antiplatelet cases
(05:39) - The refractory ulcer: what was missed
(08:51) - Zollinger-Ellison and the gastrin workup
(10:51) - Perforation: free versus contained

Chapter 2, Ep 3 of 4: Spasm and Hypercontractile

Board Pearls — Fri, 10 Jul 2026 18:25:38 -0500

Once achalasia is off the table, a normal IRP sends you into the body of the esophagus, which can only fail two ways: too much or too little. This episode is the too-much side: distal esophageal spasm and hypercontractile jackhammer. Both hinge on a normal IRP, both require symptoms to count, and both must clear secondary causes before earning the word diagnosis.

Topics covered

Normal IRP moves the problem into the esophageal body
Distal esophageal spasm: short distal latency under 4.5 seconds
Jackhammer: DCI over 8000 on a fifth of swallows
Symptoms required or the pattern is inconclusive
Type three achalasia as the mirror-image trap
Secondary mimics: opioids, reflux, EoE, mechanical obstruction
Stepwise treatment: smooth muscle relaxants then neuromodulators

Key decisions

A normal IRP keeps you out of achalasia and points into the body
Distal latency under 4.5 seconds on a fifth of swallows defines spasm
DCI over 8000 on a fifth of swallows defines the hypercontractile jackhammer pattern
Premature contraction with an elevated IRP is type three achalasia, not spasm
Opioids raise DCI and shorten latency, so stop the drug and restudy before any procedure
Endoscopy with biopsies comes first to exclude EoE and mechanical obstruction

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The too-much body
(00:47) - Same costume, check the IRP
(01:24) - Spasm and distal latency
(02:04) - Jackhammer and the DCI bar
(02:44) - Symptoms required to count
(03:20) - The type three achalasia trap
(04:20) - Clear the secondary mimics
(05:29) - Stepwise treatment logic

Chapter 2, Ep 4 of 4: Weak Pump Scleroderma Obstruction

Board Pearls — Fri, 10 Jul 2026 18:25:46 -0500

The fourth and final Esophageal Motility episode covers the weak-body disorders on a normal IRP: ineffective motility, absent contractility, and scleroderma, then the one diagnosis you are required to distrust, outflow obstruction with an elevated IRP but peristalsis still firing. The weak-body tracings resolve into three different diseases depending on two numbers: what the body is doing and what the LES is doing. Obstruction is never a manometry diagnosis alone; it needs pattern, symptoms, and a confirmatory test.

Topics covered

Ineffective esophageal motility: strict criteria, common pattern, rare disease
Multiple rapid swallows: probing pump reserve before fundoplication
Absent contractility versus type one achalasia on the IRP
Scleroderma esophagus: failed pump plus hypotensive LES together
Twice-daily PPI, not a Nissen, in scleroderma reflux
Elevated IRP outflow obstruction and its defensive criteria
FLIP distensibility index and the Dallas Consensus line of 2.0
Impostor differential: opioids, EoE, hernia, malignancy, obesity

Key decisions

The only decision ineffective motility changes is whether the esophagus can survive a full fundoplication
A flat multiple-rapid-swallow response predicts post-op dysphagia and sends you to a partial wrap (Toupet or Dor)
Absent contractility on a normal IRP means the pump is guilty and the sphincter is innocent; on an elevated IRP suspect type one achalasia
Scleroderma is the paired hit: absent contractility plus a resting LES below ten, driving Barrett in five to thirty-five percent
Outflow obstruction requires the IRP elevated both supine and upright (upright cutoff twelve) plus elevated intrabolus pressure
On manometry alone, junction outflow obstruction is always inconclusive; it needs symptoms and a confirmatory timed barium or FLIP

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The weak pump on a normal IRP
(00:44) - Ineffective motility and the fundoplication question
(02:42) - Absent contractility and the systemic hunt
(03:56) - Scleroderma esophagus: two hits at once
(07:04) - Outflow obstruction: the diagnosis to distrust
(11:17) - The imaging probe and distensibility
(14:09) - The whole weak-body and obstruction picture

Chapter 3, Ep 3 of 3: Refractory Lyon Surgery Functional

Board Pearls — Fri, 10 Jul 2026 18:25:54 -0500

Drug failure on twice-daily acid suppression is not refractory reflux, it is a reason to work the patient up, and the workup usually turns up something other than reflux. The Lyon Consensus framework, with its acid-exposure cutoffs and symptom-association tests, sorts persistent symptoms into confirmed reflux, borderline, reflux hypersensitivity, and functional heartburn. Antireflux surgery is matched to proven reflux and to motility, and it is reserved for the small group left standing after the mimics are excluded.

Topics covered

PPI failure is a different diagnosis, not breakthrough reflux
Lyon Consensus: proof, support, and evidence against
Testing on-drug versus off-drug depends on what you must prove
Four buckets: confirmed, borderline, hypersensitivity, functional heartburn
Matching wrap type to esophageal motility
Magnetic device, incisionless fundoplication, and bariatric options
The ordered refractory workup and its mimics
Atypical presentations and weak reflux linkage

Key decisions

Acid exposure time above six percent is proof-level reflux; under four percent is evidence against; four to six is borderline and leans on supporting measures
Test off-drug (hold about a week) to prove reflux exists; test on-drug with impedance to characterize breakthrough when reflux is already known
Functional heartburn gets a neuromodulator alone; reflux hypersensitivity gets a neuromodulator plus acid suppression; the most common cause of fundoplication failure is operating on functional heartburn
Full 360-degree wrap for normal motility, partial two-thirds wrap for weak or scleroderma esophagus; a full wrap on a weak esophagus causes dysphagia
Magnetic bead device is excluded by hernia over three centimeters, BMI over thirty-five, Barrett's, severe esophagitis, or absent peristalsis; incisionless fundoplication needs a hernia under two centimeters
Gastric bypass is the antireflux operation of choice in the obese refluxer; avoid the sleeve, and BMI over thirty-five independently predicts fundoplication failure
PPIs are prodrugs: dose thirty to sixty minutes before meals, and confirm timing before calling a patient refractory
Take high and low biopsies even on a normal-looking scope; eosinophilic esophagitis is fifteen or more eosinophils per high-power field

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The patient whose reflux drug has failed
(00:57) - The Lyon Consensus framework
(02:25) - Testing on-drug versus off-drug
(03:15) - The four diagnostic buckets
(04:16) - Proving reflux before surgery
(05:22) - Matching wrap type to motility
(07:57) - The obese refluxer and bariatric surgery
(10:03) - The ordered refractory workup and its mimics

Chapter 7, Ep 1 of 2: Atrophic Correa ZES

Board Pearls — Sun, 12 Jul 2026 15:45:53 -0500

Covers the chronic gastritides and precursor lesions of the stomach for boards, unified by what each disease does to gastrin. Teaches autoimmune atrophic gastritis, the H. pylori Correa cascade toward intestinal-type cancer, Menetrier disease, and Zollinger-Ellison syndrome. Emphasizes the two high-yield differentials: high gastrin sorted by gastric pH, and giant gastric folds sorted by acid output and biopsy.

Topics covered

Autoimmune atrophic gastritis
B12 and iron deficiency
Type 1 gastric neuroendocrine tumors
H. pylori Correa cascade
Intestinal metaplasia staging and surveillance
Menetrier disease
Zollinger-Ellison syndrome
MEN1 and gastrinoma triangle

Key decisions

Autoimmune atrophic gastritis destroys body/fundus parietal cells with antral sparing, causing achlorhydria, failed B12 and iron absorption, and reflex hypergastrinemia driving ECL hyperplasia into type 1 NETs.
Never give folate for unexplained macrocytic anemia without checking B12; folate corrects the anemia while dorsal column and corticospinal neurologic disease keeps progressing.
High gastrin sorts on gastric pH: pH under 2 with gastrin over 1000 is gastrinoma; gastrin over 1000 with pH above 2 is atrophic gastritis. Intermediate gastrin (100 to 1000) needs secretin, positive being a paradoxical rise over 120 within 10 to 15 minutes.
Giant gastric folds sort on acid and protein: Menetrier is low acid with protein loss (foveolar hyperplasia via EGFR, treat with anti-EGFR antibody); ZES is high acid without protein loss; lymphoma and linitis-plastica adenocarcinoma need deep biopsy.
Eradicate H. pylori at every cascade stage, but eradication lowers risk without erasing it once metaplasia appears; high-stage atrophy/metaplasia gets surveillance endoscopy about every 3 years, escalated by ancestry, first-degree relative, incomplete-type metaplasia, and both-region involvement.
In MEN1 gastrinoma (multiple, duodenal, rarely cured surgically), treat hyperparathyroidism first with parathyroidectomy because lowering calcium reduces gastrin and acid; localize with DOTATATE PET, control acid to under about 10 mEq/hr.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: gastrin ties it together
(00:30) - Autoimmune atrophic gastritis: one anatomic lesion
(02:56) - Endoscopy, biopsy, and serology
(04:46) - The H. pylori cancer cascade
(05:49) - Staging atrophy and metaplasia for surveillance
(07:07) - Menetrier disease and giant folds
(09:18) - Zollinger-Ellison syndrome

Chapter 7, Ep 2 of 2: Gastric Tumors MALT NET GIST

Board Pearls — Sun, 12 Jul 2026 15:46:10 -0500

Episode two of the Gastritis and Gastric Cancers chapter works through the four gastric tumor families where histology and molecular driver are the discriminator: adenocarcinoma by Lauren type, MALT versus large B-cell lymphoma, the three gastric neuroendocrine tumors, and GIST as the model targeted-therapy cancer. Each tumor's biology drives its staging and its drug. Board-relevant triggers, molecular markers, and treatment sequences throughout.

Topics covered

Gastric adenocarcinoma and the Lauren classification
Hereditary diffuse gastric cancer and CDH1
Adenocarcinoma staging and molecular profiling
MALT versus large B-cell gastric lymphoma
Three types of gastric neuroendocrine tumor
GIST molecular biology and risk stratification
Targeted therapy sequences (FLOT, R-CHOP, TKIs)

Key decisions

Intestinal-type adenocarcinoma arises from the H. pylori atrophy cascade; diffuse type comes from E-cadherin/CDH1 loss, signet-ring cells, and worse prognosis. Signet-ring histology in a 30s-40s patient with a first-degree relative triggers germline CDH1 testing and prophylactic total gastrectomy.
Linitis plastica gives a rigid non-distensible leather-bottle stomach; superficial forceps biopsies miss it because cells sit deep, so non-diagnostic superficial biopsies mandate deeper sampling. Resectable disease gets perioperative FLOT plus D2 dissection; metastatic disease is profiled for HER2, PD-L1, MMR/MSI, and claudin 18.2.
MALT lymphoma is H. pylori-driven and eradication is curative in most early stomach-confined cases, but t(11;18) marks non-responders needing radiation or rituximab. Large B-cell lymphoma gets R-CHOP, never antibiotics alone.
Gastric NETs sort by gastrin: type 1 from atrophic gastritis (high gastrin, high pH), type 2 from ZES/MEN1 (high gastrin, low pH), both low-risk; type 3 is gastrin-independent on normal mucosa with normal gastrin and is the dangerous one, resected like adenocarcinoma. A normal gastrin flags the highest-risk NET.
GIST arises from interstitial cells of Cajal as a fourth-layer (muscle) hypoechoic mass, CD117/DOG1 positive, with no nodal spread so no lymphadenectomy. Rule of fives (size and mitotic count) plus small-bowel site and rupture stratify risk; resect gastric GISTs over 2 cm.
GIST drug follows the mutation: KIT-mutant responds to imatinib (exon 11 best, exon 9 higher dose), PDGFRA D842V needs avapritinib, and resistance sequence is imatinib then sunitinib then regorafenib then ripretinib.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: histology and driver as discriminator
(00:33) - Adenocarcinoma and the Lauren split
(03:58) - Staging and molecular profiling to therapy
(06:12) - Gastric lymphoma: MALT versus large B-cell
(09:31) - Neuroendocrine tumors sorted by gastrin
(12:25) - GIST: molecular biology, ultrasound, and drugs
(16:11) - Recap by histology and driver

Chapter 8, Ep 1 of 2: Gastroparesis

Board Pearls — Sun, 12 Jul 2026 15:46:21 -0500

Gastroparesis is one phenotype with three failure points: the vagus for accommodation and coordination, the interstitial cells of Cajal for rhythm, and smooth muscle for force. Diabetes hits two of the three, surgery hits the vagus, idiopathic disease hits the pacemaker, and drugs mimic the whole picture by slowing the antrum. Four-hour scintigraphy with strict drug holds and controlled glucose anchors the diagnosis, and the favored move is often to stop a drug rather than confirm a disease.

Topics covered

Three-system model of gastric emptying
Diabetic and idiopathic gastroparesis
GLP-1 agonists and drug-induced delay
Four-hour gastric emptying scintigraphy
Pre-test drug holds and glucose control
Prokinetic drugs by mechanism
Antiemetics and refractory interventions
Emptying-symptom mismatch

Key decisions

Diagnose delayed emptying only with four-hour scintigraphy: more than 10 percent retained at four hours is diagnostic; grade severity as mild 10-15, moderate 15-35, severe over 35 percent.
Confirm glucose under 200 before testing, hold prokinetics 2-3 days (false negatives), hold opioids, anticholinergics, cannabinoids, and tobacco (false positives); for delayed emptying on a GLP-1 agonist, stop the drug and repeat only if symptoms persist.
Scope first to exclude obstruction, bezoar, or pyloric stenosis before ordering the emptying study, especially in a diabetic with vomiting.
Metoclopramide is the only approved prokinetic, first-line, capped near 12 weeks for tardive dyskinesia risk; prolactin elevation makes it the favored cause of secondary amenorrhea in a young woman.
Domperidone needs a baseline ECG and QTc below 450 in men, 470 in women; IV erythromycin is the most effective agent for an acute inpatient flare but oral form fails long-term via tachyphylaxis.
Intrapyloric botulinum toxin is recommended against and is the favored wrong answer; gastric electrical stimulation helps diabetics with severe vomiting, and G-POEM suits selected refractory patients with real baseline retention.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Three failure points
(01:24) - Diabetic gastroparesis
(02:14) - Idiopathic and post-surgical causes
(03:02) - Drug causes and GLP-1 agonists
(05:03) - Diagnostic workup and scintigraphy
(08:35) - Treatment foundation and diet
(09:55) - Prokinetic drugs by mechanism
(14:49) - Refractory options and next episode

Chapter 8, Ep 2 of 2: CVS Pseudo FD

Board Pearls — Sun, 12 Jul 2026 15:46:31 -0500

Episode two of the Gastric and Small Bowel Motility chapter covers the episodic and functional presentations where the structural workup comes back clean and the pattern carries the diagnosis: cyclic vomiting syndrome, cannabinoid hyperemesis, chronic intestinal pseudo-obstruction, and functional dyspepsia. Reading dilated bowel or delayed emptying as mechanical disease misleads you every time. Each condition is answered by naming the pattern, not by another motility drug.

Topics covered

Cyclic vomiting syndrome and migraine biology
Cannabinoid hyperemesis and hot-water bathing
Rumination and chronic nausea/vomiting syndrome
Acute colonic pseudo-obstruction (Ogilvie)
Chronic intestinal pseudo-obstruction
Neuropathic vs myopathic manometry
Paraneoplastic pseudo-obstruction (anti-Hu, SCLC)
Functional dyspepsia subtypes and alarm features

Key decisions

Stereotyped four-phase episodic vomiting with well intervals and migraine history: bedtime low-dose tricyclic to prevent, triptan to abort.
Same cycle with daily cannabis and compulsive hot-water bathing: stop cannabis; capsaicin, haloperidol, benzodiazepine for active episodes, not a tricyclic.
Chronic pseudo-obstruction manometry: neuropathic shows normal-strength disorganized contractions; myopathic shows low-amplitude contractions with pattern preserved; late scleroderma and amyloid read myopathic.
Older smoker with rapidly progressive dysmotility and weight loss out of proportion: chest CT and oncologic workup for anti-Hu paraneoplastic small cell lung cancer, PET if chest CT unrevealing.
Functional dyspepsia under sixty with no alarm features: H. pylori test-and-treat then empiric acid trial; sixty or older or any alarm feature, scope first.
Normal emptying with impaired accommodation and fullness-type dyspepsia: buspirone; thin patient with early satiety and weight loss: mirtazapine.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: the clean structural workup
(00:32) - Cyclic vomiting syndrome: stereotyped four-phase attacks
(01:50) - CVS treatment: prevent and abort
(02:22) - Cannabinoid hyperemesis: the cannabis look-alike
(04:36) - Pseudo-obstruction: dilated bowel, no transition point
(05:21) - Chronic intestinal pseudo-obstruction and secondary causes
(07:25) - Paraneoplastic pseudo-obstruction: the older smoker
(10:42) - Functional dyspepsia: subtypes and alarm features

Chapter 9, Ep 1 of 2: Nonvariceal UGIB

Board Pearls — Sun, 12 Jul 2026 15:46:41 -0500

Nonvariceal upper GI bleeding worked as a fixed sequence: perfusion first, diagnosis second, endoscopy third. The first hour moves mortality more than the scope does. Covers resuscitation, transfusion thresholds, pre-endoscopy pharmacology, risk scores, anticoagulant reversal, Forrest-directed endoscopic therapy, and post-hemostasis medical management.

Topics covered

Resuscitation and airway in massive UGIB
Restrictive transfusion threshold
Pre-endoscopy PPI and erythromycin
Glasgow-Blatchford risk stratification
Timing of endoscopy within 24 hours
Anticoagulant and antiplatelet management
Forrest classification and dual therapy
H. pylori eradication and secondary prevention

Key decisions

Transfuse red cells at hemoglobin 7 in most patients; aim 8 to 10 only in acute coronary syndrome; the stable cirrhotic variceal bleeder does worse with a liberal target.
High-dose IV PPI targets intragastric pH above 6 to stop clot lysis; give 72 hours after hemostasis of a high-risk lesion, then oral taper.
Glasgow-Blatchford 0 or 1 identifies the very-low-risk patient for outpatient endoscopy; Rockall needs the scope and AIMS65 predicts ICU need, not the go-home patient.
Non-variceal endoscopy within 24 hours with no benefit before 6; tranexamic acid is not used in acute UGIB.
Reverse warfarin with 4-factor PCC plus IV vitamin K, dabigatran with idarucizumab, Xa inhibitors with andexanet alfa reserved for life-threatening bleeding; resume early because late risk is thrombotic.
High-risk Forrest stigmata (spurting, oozing, non-bleeding visible vessel) get dual therapy: epinephrine plus a thermal method or clip; epinephrine alone is inadequate; over-the-scope clip rescues the recurrent bleeder.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The fixed sequence: perfusion, diagnosis, endoscopy
(00:39) - Resuscitation and airway
(01:08) - Restrictive transfusion threshold
(02:09) - Pre-endoscopy acid suppression and erythromycin
(03:35) - Risk stratification and disposition
(04:21) - Timing of endoscopy
(05:01) - Anticoagulant and antiplatelet management
(07:58) - Forrest classification and endoscopic therapy

Chapter 9, Ep 2 of 2: Variceal and Unusual

Board Pearls — Sun, 12 Jul 2026 15:46:51 -0500

Episode two of the Upper GI Bleeding chapter covers acute variceal hemorrhage and the unusual non-variceal causes a routine scope misses. It anchors on the variceal bundle delivered before endoscopy, early TIPS for the high-risk cirrhotic, and the Sarin split for gastric varices. The second half is a recognition drill: each rare lesion is easy to treat once its history cue is named.

Topics covered

Variceal bundle: octreotide, ceftriaxone, band ligation
Restrictive transfusion and selective coagulopathy correction
Balloon tamponade and covered esophageal stent bridges
Early pre-emptive TIPS in high-risk cirrhotics
Sarin classification and gastric varices
Dieulafoy, Mallory-Weiss, GAVE, Cameron lesions
Angiodysplasia, Heyde syndrome, and HHT
Hemobilia, hemosuccus, aortoenteric fistula

Key decisions

Start octreotide, ceftriaxone, and band ligation reflexively the moment variceal bleeding is suspected, before endoscopic confirmation; octreotide runs five days, ceftriaxone seven.
Transfuse restrictively to hemoglobin of seven in cirrhotics; liberal transfusion raises portal pressure and worsens rebleeding.
Choose early pre-emptive TIPS within seventy-two hours for Child-Pugh C, or Child-Pugh B with active bleeding on the index endoscopy.
An isolated fundal gastric varix without esophageal involvement always triggers a splenic vein thrombosis workup.
GAVE (distal antral stripes) does not respond to TIPS and is treated with argon plasma coagulation; portal hypertensive gastropathy (proximal snake-skin) responds to beta-blockade and TIPS.
A herald bleed after prior aortic aneurysm graft surgery is aortoenteric fistula until proven otherwise; get CT angiography and go to emergent repair.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction
(00:23) - The variceal bundle before endoscopy
(02:30) - Resuscitation modifiers in cirrhosis
(03:33) - Balloon tamponade as a bridge
(04:09) - Early TIPS in the high-risk patient
(05:07) - Gastric varices and the Sarin classification
(06:46) - Unusual non-variceal causes
(07:03) - Dieulafoy and the recognition cues

Chapter 10, Ep 1 of 2: Celiac Diagnosis and Treatment

Board Pearls — Sun, 12 Jul 2026 15:47:01 -0500

Celiac disease built from mechanism through monitoring: modified gluten peptides bind HLA-DQ2/DQ8, drive T-cell inflammation, and trigger lymphocyte-mediated villous atrophy. The modern adult presents like IBS, iron deficiency, or an extraintestinal finding, so the threshold to test is broad. Diagnosis is serology-anchored and biopsy-confirmed while the patient still eats gluten, treated by a strict lifelong gluten-free diet with structured monitoring.

Topics covered

Pathogenesis and HLA-DQ2/DQ8
Extraintestinal and IBS-like presentations
Silent, potential, and seronegative phenotypes
Dermatitis herpetiformis
tTG-IgA serology and total IgA
Duodenal biopsy and Marsh classification
Gluten-free diet and nutritional repletion
Serologic and histologic monitoring

Key decisions

Order tTG-IgA plus a total IgA as first-line serology while the patient is still eating gluten; pivot to deamidated gliadin peptide IgG if IgA deficient.
Use HLA-DQ2/DQ8 to exclude, never to confirm; it is not part of the initial algorithm.
Confirm with at least four distal duodenal biopsies plus one or two bulb biopsies, since a minority have bulb-only atrophy.
No-biopsy adult diagnosis needs tTG greater than 10x upper limit plus a positive endomysial antibody on a second sample, but biopsy remains the adult default.
A persistently positive antibody after one year means ongoing gluten exposure and prompts a dietitian re-evaluation, not a refractory workup.
Confirm mucosal healing with a repeat duodenal biopsy at about two years, because negative serology can dissociate from persistent atrophy.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Mechanism: gluten to villous atrophy
(00:00) - Monitoring and confirming mucosal healing
(01:22) - HLA as an exclusion tool
(01:58) - Epidemiology and autoimmune comorbidity
(02:42) - Modern presentations: IBS and iron deficiency
(04:14) - Phenotypes and dermatitis herpetiformis
(05:55) - Serology-anchored, biopsy-confirmed diagnosis
(13:22) - Treatment: gluten-free diet and repletion

Chapter 10, Ep 2 of 2: Refractory Celiac and Complications

Board Pearls — Sun, 12 Jul 2026 15:47:11 -0500

Most celiac patients failing a gluten-free diet are not refractory; they are eating hidden gluten or have a coexisting condition, so a structured non-responsive differential precedes any refractory workup. When refractory disease is genuine, the type one versus type two split on intraepithelial lymphocyte phenotype separates a steroid-responsive disease with good survival from a pre-lymphoma syndrome. The malignancy spectrum, enteropathy-associated T-cell lymphoma, ulcerative jejunitis, and small-bowel adenocarcinoma, is the payoff of getting that distinction right.

Topics covered

Non-responsive celiac differential
Refractory celiac type 1 vs type 2
Intraepithelial lymphocyte phenotyping
Enteropathy-associated T-cell lymphoma
Ulcerative jejunitis
Small-bowel adenocarcinoma
Small-bowel imaging and surveillance

Key decisions

Persistent symptoms on a gluten-free diet are most often ongoing gluten exposure; the first step is a dietitian reviewing the diet line by line, not a refractory workup or steroids.
Work the non-responsive differential in order: incomplete gluten avoidance, incorrect original diagnosis, coexisting condition (microscopic colitis, pancreatic insufficiency, overgrowth, IBS), then drug-induced enteropathy (olmesartan, NSAIDs, mycophenolate) before invoking refractory disease.
Send duodenal biopsies for flow cytometry in saline or tissue medium, not formalin, because formalin destroys the surface markers; take extra samples for histology and T-cell clonality.
Type 1: polyclonal, surface CD3 and CD8 retained, abnormal fraction under 20 percent, treated with open-capsule budesonide, good prognosis; check TPMT before a thiopurine.
Type 2: over 20 percent abnormal clonal lymphocytes with loss of surface CD3 and CD8 but retained cytoplasmic CD3, monoclonal clonality, a pre-lymphoma diagnosis treated with cladribine and autologous transplant at a tertiary center.
Worsening of a stable celiac course on a verified diet, even with negative transglutaminase, mandates capsule endoscopy plus CT or MR enterography and device-assisted enteroscopy to find lymphoma, ulcerative jejunitis, or adenocarcinoma.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The non-responsive celiac differential
(00:51) - Working the differential in order
(02:21) - When it is truly refractory: type 1 vs type 2
(03:04) - Phenotyping the lymphocytes on flow cytometry
(05:26) - The malignancy spectrum
(05:56) - T-cell lymphoma and ulcerative jejunitis
(08:44) - Small-bowel adenocarcinoma
(09:40) - Surveillance and pulling it together

Chapter 11, Ep 1 of 1: Small Bowel Mucosal

Board Pearls — Sun, 12 Jul 2026 15:47:23 -0500

What to think about when a small-bowel biopsy shows enteropathy and celiac has already been excluded on a gluten-containing diet. Walks the non-celiac differential mechanistically: wheat-related symptom syndromes, autoimmune enteropathy, Whipple disease, drug-induced enteropathies, checkpoint inhibitor enteritis, bacterial overgrowth, and tropical sprue. The histology, the medication list, and the exposure history read in parallel resolve the fork.

Topics covered

Non-celiac gluten sensitivity and FODMAPs
IgE-mediated wheat allergy
Autoimmune enteropathy and IPEX
Whipple disease
Drug-induced enteropathy (olmesartan, NSAID)
Checkpoint inhibitor enteritis
Small intestinal bacterial overgrowth
Tropical sprue

Key decisions

Celiac must be excluded on a gluten-containing diet first; a gluten-free patient needs a gluten challenge or HLA testing, where a negative haplotype excludes celiac.
Villous atrophy with depleted goblet and Paneth cells plus deep crypt apoptosis in a celiac-negative diet-failure points to autoimmune enteropathy; test anti-enterocyte antibodies and treat with open-capsule budesonide.
Whipple is diagnosed on distal duodenal/jejunal biopsy showing foamy PAS-positive macrophages that are acid-fast-negative; treat with IV ceftriaxone then a year of oral trimethoprim-sulfamethoxazole for CNS coverage.
Older patient on olmesartan with severe diarrhea, weight loss, negative celiac serology, and villous atrophy: stop the drug, not start a gluten-free diet or steroids.
Checkpoint inhibitor enteritis: hold the drug, rule out infection including C. diff and CMV, start steroids ~1 mg/kg, escalate to infliximab or vedolizumab if refractory within a few days.
SIBO gives low B12 with high folate; diagnose by breath testing (rise of at least 20 ppm within 90 minutes) and treat with rifaximin plus correcting the cause; tropical sprue gives combined low folate AND B12 and is treated with tetracycline plus folate.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - When celiac is excluded
(01:03) - The wheat-related trio
(03:06) - The FODMAP framework
(04:08) - Autoimmune enteropathy
(07:13) - Whipple disease
(10:20) - Drug-induced enteropathy
(12:30) - Checkpoint enteritis and SIBO
(15:23) - Tropical sprue and synthesis

Chapter 12, Ep 1 of 2: Framework and Mechanism Workup

Board Pearls — Sun, 12 Jul 2026 15:47:35 -0500

Chronic diarrhea is too much stool water, and because normal absorptive efficiency runs near ninety-nine percent, small physiologic insults produce large clinical phenotypes. Episode one builds the four-mechanism framework, osmotic, secretory, fatty, and inflammatory, and lets that mechanism drive a staged workup. History, basic labs, stool studies, and endoscopy sort most patients within a few tests toward a targeted second-stage evaluation.

Topics covered

Four mechanism categories of chronic diarrhea
Stool osmotic gap calculation and cutoffs
History, medication, and surgical review
Basic labs and celiac serology with total IgA
Stool studies: calprotectin, elastase, fecal fat
IBS-D overlap traps
Secretory workup and neuroendocrine tumors
Fatty diarrhea: maldigestion versus malabsorption

Key decisions

Osmotic gap is 290 minus twice the sum of stool sodium and potassium; under 50 is secretory, over 100 is osmotic, in between is mixed.
Order total IgA with celiac serology because IgA deficiency invalidates the IgA-based test, the single most common workup error.
Collect a formed stool for fecal elastase because a watery sample falsely lowers it; a low value supports pancreatic insufficiency.
Hold acid blockers for a week before gastrin and chromogranin A because PPIs raise both and cause false positives.
Random biopsies of normal-looking colon are mandatory in older patients with chronic watery diarrhea to catch microscopic colitis.
After cholecystectomy or ileal resection, an empiric cholestyramine trial for bile acid malabsorption is diagnostic and therapeutic in one step.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Framework and why mechanism drives the workup
(00:21) - Too much stool water and the four-week cutoff
(02:08) - The osmotic gap and category signatures
(05:32) - History, medications, and surgical mapping
(08:01) - Stool studies do the mechanism assignment
(10:31) - Secretory workup and neuroendocrine tumors
(14:56) - Fatty diarrhea: maldigestion versus malabsorption
(16:51) - Inflammatory diarrhea and the endoscopic patterns

Chapter 12, Ep 2 of 2: BAM Microscopic Obscure

Board Pearls — Sun, 12 Jul 2026 15:47:45 -0500

Episode two of the Chronic Diarrhea and Malabsorption chapter works the patient who arrives after a clean standard workup. Three entities account for most of what the first pass missed: bile acid malabsorption, microscopic colitis, and a structured algorithm for obscure chronic diarrhea. Board-tested reasoning on typing, testing, and the trials that are diagnostic and therapeutic in one step.

Topics covered

Bile acid malabsorption
Camilleri classification
Hundred-centimeter ileal resection rule
Post-cholecystectomy diarrhea
Microscopic colitis
Lymphocytic vs collagenous colitis
Obscure chronic diarrhea algorithm
IBS-D overlap

Key decisions

Under 100 cm of resected ileum, cholestyramine fixes bile acid diarrhea; over 100 cm the picture flips to steatorrhea and cholestyramine worsens it, so use medium-chain triglycerides plus a low-fat diet.
Idiopathic (type 2) bile acid diarrhea hides inside the IBS-D label; low fasting FGF19 and elevated C4 are the serum surrogates, and an empiric sequestrant trial responding within a week or two confirms it in the US where the SeHCAT scan is unavailable.
Microscopic colitis is diagnosed only on random biopsies from at least the right and left colon; lymphocytic colitis needs more than 20 intraepithelial lymphocytes per 100 surface cells, collagenous colitis a subepithelial band over 10 microns, both with preserved crypt architecture.
First therapeutic move in microscopic colitis is removing the offending drug (NSAIDs, PPIs especially lansoprazole, SSRIs) and smoking cessation; budesonide six to eight weeks is first-line for moderate to severe disease.
A celiac patient with persistent watery diarrhea on a strict gluten-free diet needs colonoscopy with random biopsies, not a repeat duodenal biopsy, because microscopic colitis is far more common in celiac.
Obscure diarrhea is worked in prevalence order: sequestrant, then rifaximin, then lactose-free, then low-FODMAP, then pancreatic enzymes, with HLA testing to exclude celiac before committing to lifelong gluten avoidance.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Three commonly missed causes after a clean workup
(00:38) - Bile acid malabsorption: mechanism and phenotype
(01:26) - Camilleri types and the hundred-centimeter rule
(03:32) - Diagnostic testing: SeHCAT, C4, FGF19, empiric trial
(05:08) - Microscopic colitis: the biopsy-only diagnosis
(06:36) - Random biopsies, histology, and severity-based treatment
(08:17) - The obscure chronic diarrhea algorithm
(09:19) - Sequential empiric trials and the IBS-D endpoint

Chapter 13, Ep 1 of 2: ROME IV Pathophys IBS C

Board Pearls — Sun, 12 Jul 2026 15:47:58 -0500

Episode one of two on Irritable Bowel Syndrome and functional bowel, covering positive diagnosis, Rome IV criteria, and subtyping. It maps the brain-gut model and its five mechanisms onto the drug classes. It closes with the mechanism-targeted pharmacology of constipation-predominant IBS.

Topics covered

Rome IV positive diagnosis
IBS subtyping by Bristol form
Alarm features and targeted testing
IBS-D differential and mimics
Brain-gut five-mechanism model
Visceral hypersensitivity
IBS-C secretagogues
Prucalopride prokinetic

Key decisions

IBS is a positive clinical diagnosis, not exclusion: apply after a brief targeted screen for celiac (tTG plus total IgA), IBD (CRP and calprotectin), and Giardia, not a full rule-out workup.
Rome criterion is pain related to defecation (not necessarily improved by it), at least one day a week over three months; subtype by Bristol form on abnormal-BM days only.
Abnormal screening tests suspend the IBS label: elevated calprotectin, high CRP, or anemia demands colonoscopy with ileal biopsy and small-bowel imaging; positive tTG with normal IgA is celiac until proven otherwise.
Lubiprostone dose split is tested: 8 mcg BID for IBS-C (women), versus 24 mcg BID for chronic idiopathic constipation; give with food to blunt nausea.
Linaclotide 290 mcg once daily on an empty stomach at least 30 minutes before the first meal; plecanatide 3 mg with or without food; interchangeable, both boxed warning for dehydration in young children.
Prucalopride is a selective 5-HT4 prokinetic (2 mg daily, 1 mg in renal impairment) approved for chronic idiopathic constipation, not IBS-C; designed for cardiac selectivity, the answer for refractory slow-transit constipation after secretagogue failure.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Intro: diagnosis, mechanisms, and IBS-C drugs
(00:21) - IBS is a positive diagnosis, not exclusion
(01:05) - Rome criteria and Bristol-based subtyping
(02:19) - Alarm features and targeted testing
(04:17) - IBS-D differential and treatable mimics
(05:39) - Brain-gut model and five mechanisms
(11:01) - IBS-C general measures and fiber
(12:09) - Prescription secretagogues and the prokinetic

Chapter 13, Ep 2 of 2: IBS D Neuromod Bloating

Board Pearls — Sun, 12 Jul 2026 15:48:10 -0500

Episode two of the IBS and Functional Bowel chapter covers the diarrhea-predominant subtype, the neuromodulators and behavioral therapies that work across subtypes, and the mechanistic workup of bloating. Drug selection is mechanism-matched to the dominant symptom and driver, not subtype-matched in the abstract. Carry mechanism, subtype indication, and contraindication together to pick the right answer.

Topics covered

IBS-D pharmacology
Loperamide, rifaximin, eluxadoline
Bile acid sequestrants and alosetron
Neuromodulators by side-effect match
Antispasmodics and peppermint oil
Behavioral and mind-body therapy
Bloating versus distension
Low-FODMAP diet and fiber

Key decisions

Loperamide controls stool frequency and urgency but never abdominal pain; for crampy IBS-D add a low-dose tricyclic or rifaximin, not more loperamide.
Rifaximin responders who relapse can be retreated with the same 14-day course, up to two retreatments for three courses total; never lock the patient out.
Eluxadoline is absolutely contraindicated after cholecystectomy (sphincter of Oddi spasm causing pancreatitis), and with biliary obstruction, heavy alcohol use, pancreatitis history, or severe constipation.
Alosetron is restricted to women with severe refractory IBS-D, carries ischemic colitis and severe constipation boxed warnings, and is contraindicated in the mixed subtype; obstipation means stop and evaluate, not titrate.
For IBS-D neuromodulation, low-dose tricyclics are favored because the anticholinergic transit slowing is therapeutic; switch amitriptyline to nortriptyline or desipramine for side effects, and SSRIs do not help IBS-D pain.
Abdomino-phrenic dyssynergia is the answer for visible distension out of proportion to luminal content, with daytime progression, overnight resolution, and no excess gas on CT, treated with diaphragmatic breathing retraining.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: IBS-D, cross-subtype therapy, bloating
(00:46) - Loperamide: frequency, not pain
(01:28) - Rifaximin and the retreatment rule
(02:27) - Eluxadoline: the contraindication list
(07:35) - Neuromodulators by side-effect match
(09:17) - Behavioral and mind-body therapies
(10:19) - Bloating versus distension and its workup
(12:33) - Low-FODMAP diet and fiber

Chapter 14, Ep 1 of 3: UC Complete

Board Pearls — Sun, 12 Jul 2026 15:48:23 -0500

Episode one of three on inflammatory bowel disease, covering ulcerative colitis from classification through full medical management. Walks the UC-versus-Crohn distinction, the Mayo score driving severity-tiered therapy, the acute severe UC inpatient script with its day-three salvage rule, mesalamine for mild-to-moderate disease, and mechanism-based positioning of biologics and small molecules. Board-focused framework for choosing therapy by matching drug mechanism to patient phenotype.

Topics covered

UC vs Crohn distinction
Montreal extent classification
Mayo score and severity
Acute severe UC management
Mesalamine formulations and delivery
Biologics and small molecules
JAK and S1P modulators
Mechanism-to-patient drug selection

Key decisions

Smoking is protective in UC but harmful in Crohn's; a quiescent UC patient who quits can flare within months.
Day three is the salvage trigger in acute severe UC: Oxford rule is more than eight stools daily, or three to eight stools with CRP above forty-five.
Salvage is a single shot: no response to infliximab or cyclosporine within five to seven days means colectomy, not sequential salvage.
Antimotility agents are contraindicated in acute severe UC because they precipitate toxic megacolon; anticoagulate despite rectal bleeding.
Combined oral plus topical mesalamine beats either alone for distal and left-sided disease; oral induction dose is 4.8 g/day.
Sulfasalazine wins in the UC patient with peripheral inflammatory arthritis; give mandatory folic acid, and mesalamine paradoxical worsening means stop the drug.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - One immune problem, two faces
(01:16) - Sorting UC from Crohn's
(02:35) - Diagnosis and Montreal extent
(03:56) - Mayo score and mucosal healing
(04:52) - The acute severe UC script
(08:45) - Mesalamine for mild-to-moderate disease
(12:26) - Biologics and small molecules by mechanism
(17:28) - Matching mechanism to patient

Chapter 14, Ep 2 of 3: Crohn Complete

Board Pearls — Sun, 12 Jul 2026 15:48:44 -0500

Episode two of the IBD chapter takes Crohn disease from phenotype through complete medical management. It runs the Montreal classification into risk stratification and the top-down versus step-up decision, then walks Crohn-specific induction, immunomodulators, and biologic positioning. It closes with the phenotype-specific algorithms for perianal disease, strictures, and post-operative recurrence.

Topics covered

Montreal classification and phenotype drift
Top-down versus step-up risk stratification
Crohn-specific induction and steroids
Thiopurines and methotrexate
Biologics by mechanism and safety
Perianal Crohn algorithm
Stricturing disease and bowel preservation
Post-operative recurrence and Rutgeerts score

Key decisions

Budesonide 9 mg is induction for mild-to-moderate ileal or right-colonic disease but fails as maintenance beyond six months and does not treat left-sided colonic disease.
The high-risk stacked phenotype (young age, deep ulcers, perianal fistula, steroid requirement, smoking) starts biologic plus immunomodulator combination, not step-up.
TPMT genotype or activity is mandatory before thiopurines, with NUDT15 testing added in Asian, Hispanic, and Native American patients; hepatosplenic T-cell lymphoma clusters in young men on thiopurine plus anti-TNF.
Perianal Crohn sequence is non-negotiable: drain the abscess and place setons first, then start biologic; dose-optimized infliximab on an undrained abscess is the wrong move.
Post-operative high-risk patients start prophylactic anti-TNF within four weeks; smoking cessation is the single modifiable factor that meaningfully reduces recurrence.
Rutgeerts scope at six to twelve months is universal regardless of risk, and the middle grade or higher triggers escalation.
In pregnancy the dominant threat is active disease, not medication: continue most drugs, stop methotrexate and JAK inhibitors.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and one disease, many faces
(01:11) - Montreal classification and natural history
(02:37) - Risk stratification and the top-down decision
(04:46) - Medical therapy, steroids, and mesalamine
(07:03) - Immunomodulators: thiopurines and methotrexate
(09:38) - Biologics by mechanism and safety
(15:06) - Perianal Crohn algorithm
(16:52) - Stricturing disease and post-operative recurrence

Chapter 14, Ep 3 of 3: Pouch Dysplasia EIM Pregnancy

Board Pearls — Sun, 12 Jul 2026 15:48:56 -0500

The long-arc complications of IBD after induction and maintenance: the ileal pouch and its inflammations, dysplasia surveillance in long-standing colitis, the extraintestinal manifestations, and pregnancy. The unifying board move is that active disease, not active medication, is the threat, so biologics usually continue through delivery. Localization, timing of surveillance, and whether a manifestation tracks bowel activity are what get tested.

Topics covered

Ileal pouch-anal anastomosis and pouchitis
Cuffitis and the Crohn's-like pouch
Chronic antibiotic-dependent vs refractory pouchitis
Dysplasia surveillance in colitis
Chromoendoscopy and dysplasia management
Extraintestinal manifestations of IBD
Pre-biologic vaccination timing
Pregnancy and biologics in IBD

Key decisions

Pouch patient with new bleeding and a normal-appearing pouch body is cuffitis: treat with topical mesalamine, not systemic escalation.
For antibiotic-refractory chronic pouchitis, vedolizumab carries the strongest randomized evidence and is the favored biologic; clear C. diff, CMV, ischemia, NSAIDs, and celiac before escalating.
Surveillance colonoscopy in extensive UC or Crohn's colitis begins 8 to 10 years after symptom onset (not date of diagnosis), but begins immediately at diagnosis of primary sclerosing cholangitis.
Resectable visible dysplasia with clear margins is removed endoscopically; non-resectable visible dysplasia and invisible high-grade dysplasia both go to proctocolectomy; confirm all dysplasia with a second pathologist.
Live vaccines (MMR, varicella, yellow fever, oral typhoid, intranasal flu) are contraindicated during biologics and for 3 months after, so give at least 4 weeks before starting; infant live/rotavirus vaccines are deferred until in-utero biologic clears, except certolizumab.
Continue most biologics in pregnancy; stop methotrexate and JAK inhibitors; certolizumab crosses the placenta minimally and is preferred late in pregnancy.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: the longer arc of IBD
(00:58) - The pouch and pouchitis
(03:10) - Chronic pouchitis, cuffitis, and the Crohn's-like pouch
(05:22) - Dysplasia surveillance in long-standing colitis
(06:54) - Chromoendoscopy and managing dysplasia
(08:57) - Extraintestinal manifestations
(14:23) - Vaccinations before biologics
(15:34) - Pregnancy in IBD

Chapter 15, Ep 1 of 2: CRC Screening Biology Treatment Polyps

Board Pearls — Sun, 12 Jul 2026 15:49:12 -0500

Episode one of two on the Colorectal Cancer, Polyps, and Diverticular Disease chapter, tracing the neoplastic pathway from average-risk screening through molecular subtyping to stage-based treatment and polyp surveillance. The organizing thread is mechanism: why screening starts at forty-five, why MLH1 loss reflexes to BRAF, and why histology sets the surveillance interval.

Topics covered

Average-risk CRC screening at 45
Screening modalities and intervals
Adenoma-carcinoma vs serrated pathways
Universal mismatch-repair reflex testing
TNM staging and workup
Stage-based and molecular treatment
Rectal cancer and total mesorectal excision
Post-polypectomy surveillance intervals

Key decisions

Average-risk screening starts at 45, runs to 75, shared decision 76 to 85; FDR with CRC or advanced adenoma starts at 40 or 10 years before youngest case with 5-year intervals.
A positive stool DNA with a high-quality negative colonoscopy needs no further GI workup; any positive noninvasive test is an indication for diagnostic colonoscopy.
MLH1 loss reflexes to BRAF or MLH1 methylation testing; MLH1 loss with positive BRAF is sporadic serrated disease with no germline implication, while MSH2, MSH6, or isolated PMS2 loss goes straight to germline testing.
At least 12 lymph nodes must be examined for adequate node staging; there is no lower fallback minimum.
MSI-high stage II tumors do not benefit from single-agent fluorouracil and are usually observed; stage III gets mandatory oxaliplatin-based adjuvant chemotherapy.
Anti-EGFR therapy is used only in RAS-wild-type left-sided primaries; MSI-high metastatic disease gets first-line pembrolizumab; BRAF-mutant disease gets a BRAF inhibitor plus cetuximab.
Advanced adenoma is 10 mm or larger, villous or tubulovillous histology, or high-grade dysplasia, any one sufficient, and gets a 3-year surveillance interval; any proximal hyperplastic polyp 10 mm or larger is managed as a sessile serrated lesion.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction
(01:06) - Screening ages and risk tiers
(02:01) - Screening modalities and intervals
(04:30) - Molecular pathways and subtypes
(05:48) - Reflex MMR and Lynch testing
(08:34) - Staging and treatment by stage
(09:57) - Stage four molecular therapy
(12:57) - Polyps and surveillance intervals

Chapter 15, Ep 2 of 2: Diverticular Disease

Board Pearls — Sun, 12 Jul 2026 15:49:22 -0500

Diverticular disease as its own entity, following a management algorithm that shifted meaningfully in the last decade while the boards catch up. Uncomplicated diverticulitis is now an inflammatory process treated with selective rather than reflex antibiotics, and prophylactic resection by episode count is dead. Complicated disease grades on Hinchey and splits at the four-centimeter abscess threshold.

Topics covered

Diverticulosis anatomy and false diverticula
Acute diverticulitis and CT grading
Hinchey classification of complicated disease
Selective antibiotics in uncomplicated disease
Complicated disease and abscess thresholds
Recurrence and elective surgery indications
Segmental colitis (SCAD) as IBD mimic
Modifiable risk factors and post-episode workup

Key decisions

Well-appearing immunocompetent outpatient with uncomplicated left-sided diverticulitis gets supportive care with selective, not reflex, antibiotics; ciprofloxacin plus metronidazole is the wrong move.
Antibiotics remain standard for the immunocompromised, frail, septic, admitted, or any complicated CT feature, because these hosts cannot mount the response that drives spontaneous resolution.
Pericolic abscess under four centimeters resolves with antibiotics alone; four centimeters or larger gets percutaneous drainage plus IV antibiotics, not urgent sigmoidectomy.
Elective resection is reserved for debilitating recurrences, prior complicated attacks, or immunocompromise, never a fixed episode count in immunocompetent patients.
Colonoscopy six to eight weeks after a first episode is mandatory to exclude a perforating sigmoid cancer masquerading on CT.
Segmental colitis spares the rectum and proximal colon, rests on segmental distribution not histology, and responds to mesalamine, not an IBD diagnosis.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Why the algorithm shifted
(00:54) - Anatomy of diverticulosis
(02:00) - Acute diverticulitis and CT grading
(03:05) - Selective antibiotics in uncomplicated disease
(05:06) - Complicated disease and abscess thresholds
(06:48) - Recurrence and elective surgery
(09:13) - Segmental colitis, the IBD mimic

Chapter 16, Ep 1 of 3: Chronic Constipation Pharmacology and OIC

Board Pearls — Wed, 15 Jul 2026 22:29:15 -0500

Episode one of the Pelvic Floor and Anorectal Disorders chapter works through chronic constipation as a symptom-defined syndrome, the empiric laxative sequence that resolves most patients, and the prescription drugs for refractory disease mapped to four molecular targets. The organizing idea: match the drug to the mechanism, and keep opioid-induced constipation separate because the enteric receptor never develops tolerance. Definitions, alarm features, secondary causes, secretagogues, prucalopride, and the peripherally acting opioid antagonists throughout, all framed around the exam stem that names the mechanism.

Topics covered

Symptom-defined diagnosis of chronic constipation
Three mechanistic subtypes: normal-transit, slow-transit, defecatory
Alarm features and secondary causes
Empiric sequence: diet, fiber, osmotic, stimulant laxatives
Prescription secretagogues and their four targets
Prucalopride as the serotonin-4 prokinetic
Opioid-induced constipation and tolerance asymmetry
Peripherally acting opioid antagonists and the obstruction contraindication

Key decisions

Chronic constipation is diagnosed on symptoms over at least three months, not stool frequency alone; infrequent movements without straining, hard stools, or incomplete evacuation is bowel-frequency variation and gets reassurance, not a secretagogue.
Alarm features (new symptoms over age fifty, weight loss, bleeding or iron-deficiency anemia, family history of colorectal cancer or IBD) send the patient to colonoscopy now instead of empiric polyethylene glycol.
The empiric sequence is education and diet, soluble fiber titrated toward twenty-five to thirty grams a day with psyllium preferred, polyethylene glycol seventeen grams daily first-line, then bisacodyl or senna, run over four to eight weeks.
Lubiprostone is dosed at twenty-four micrograms twice daily for chronic constipation versus eight micrograms twice daily for IBS-C; linaclotide is one hundred forty-five micrograms daily versus two hundred ninety for IBS-C on an empty stomach.
Prucalopride is the two-milligram serotonin-4 prokinetic and the natural next step when secretagogues fail, because the deficit is slow propulsion; unlike the withdrawn earlier agents it was designed for selectivity and spares the cardiac targets.
Opioid-induced constipation needs standard stimulant-plus-osmotic laxatives first; when they fail, a peripherally acting antagonist (naloxegol, methylnaltrexone, naldemedine) is added, contraindicated in known or suspected mechanical GI obstruction.
Alvimopan is for postoperative ileus only under a short-term inpatient program, not chronic opioid constipation, and lubiprostone is an opioid-independent non-antagonist option when an antagonist isn't tolerated.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the organizing idea
(00:30) - Constipation is symptom-defined, not frequency
(01:59) - Three mechanistic subtypes
(03:08) - Alarm features and secondary causes
(05:35) - The empiric laxative sequence
(07:52) - Prescription secretagogues and their targets
(10:05) - Prucalopride the prokinetic
(11:44) - Opioid-induced constipation and tolerance
(13:10) - Peripherally acting antagonists and contraindications

Chapter 16, Ep 2 of 3: Dyssynergia and Slow-Transit Constipation

Board Pearls — Wed, 15 Jul 2026 22:29:19 -0500

Episode two covers the constipation phenotypes that need more than pharmacology: defecatory disorders diagnosed on anorectal manometry and balloon expulsion and treated with biofeedback, and slow-transit constipation documented on a marker or capsule study. The organizing discipline is to decide the mechanism before the next drug, because escalating laxatives in unrecognized outlet dysfunction produces overflow and urgency without relief. The central pitfall runs the whole episode: unrecognized outlet dysfunction falsifies the transit study and sends the wrong patient to colectomy, so check the outlet before you cut the colon. Testing thresholds, the two-of-three diagnostic rule, and precise colectomy criteria throughout.

Topics covered

Deciding phenotype before the next drug
Dyssynergic defecation mechanism and rectal exam clue
Balloon expulsion screening test
Anorectal manometry parameters and the rectoanal inhibitory reflex
Defecography and structural lesions
Two-of-three diagnostic rule and biofeedback
Slow-transit constipation and transit studies
Subtotal colectomy indications and disqualifiers

Key decisions

After empiric therapy fails, the first decision is which phenotype the patient has, not which drug comes next, because more laxative in outlet dysfunction produces urgency and overflow around a still-closed sphincter.
Balloon expulsion is the first-line screen: a rectal balloon is inflated with fifty milliliters of warm water and failure to expel within sixty seconds is abnormal and supports a defecatory disorder.
Anorectal manometry reads resting pressure, squeeze pressure, the push maneuver (dyssynergia is a paradoxical rise in anal pressure), and the rectoanal inhibitory reflex, whose absence is the hallmark of Hirschsprung disease.
The diagnosis of a defecatory disorder requires at least two of three positive studies among manometry, defecography, and balloon expulsion, because a paradoxical contraction on manometry alone is too soft.
Biofeedback is the treatment for a confirmed defecatory disorder and outperforms laxatives in this population, but it does not help slow transit without dyssynergia because that lesion is not mechanical at the outlet.
The radiopaque marker study retains twenty-four markers with a plain film on day five; more than five markers retained indicates slow transit, and rectosigmoid clustering points back to outlet dysfunction.
Subtotal colectomy with ileorectal anastomosis requires severe intractable symptoms, objectively confirmed slow transit, and a defecatory disorder excluded, disqualified by prominent abdominal pain, generalized dysmotility, or pseudo-obstruction.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the phenotype decision
(00:29) - Which phenotype, not which drug
(01:34) - Dyssynergic defecation and the rectal exam
(03:03) - Balloon expulsion, manometry, and defecography
(05:06) - Two-of-three rule and biofeedback
(07:07) - Sequencing and the central pitfall
(07:58) - Slow-transit constipation and transit studies
(09:45) - Colectomy criteria and disqualifiers

Chapter 16, Ep 3 of 3: Fecal Incontinence and Benign Anorectal Disorders

Board Pearls — Wed, 15 Jul 2026 22:29:25 -0500

Episode three covers fecal incontinence managed in a fixed sequence and the benign anorectal disorders anchored to the dentate line. Incontinence rarely fails for a single reason, so the workup canvasses the whole continence stack and the treatment runs from optimizing the modifiable factor through loperamide and biofeedback to sacral neuromodulation, which has displaced sphincteroplasty as first-line surgery for refractory disease. The benign disorders follow the anatomy: above the dentate line means painless bleeding, below it means sharp pain, and that landmark predicts management for hemorrhoids, anal fissure, and pruritus ani. Manometry, endoanal ultrasound, the seventy-two-hour rule, and the atypical-fissure workup throughout.

Topics covered

The continence stack and multifactorial failure
Etiologic grid: sphincter, rectal, neurologic, consistency, overflow
History and targeted testing with manometry and endoanal ultrasound
Fixed treatment sequence from modifiable factors to loperamide and biofeedback
Sacral neuromodulation versus sphincteroplasty
Internal and external hemorrhoids and the dentate line
Anal fissure mechanism and atypical-location workup
Pruritus ani as a symptom, not a diagnosis

Key decisions

Endoanal ultrasound is the test of choice for sphincter integrity, mapping anterior defects from obstetric trauma the exam misses, while anorectal manometry is the most informative single test and changes management in most cases.
Soluble fiber like psyllium is the counterintuitive first move in leakage of liquid stool because firm stool is easier to retain than soft stool even with a damaged sphincter, alongside treating impaction and any diarrheal disease.
Loperamide is the drug that follows, a peripheral opioid agonist that slows transit, raises internal sphincter tone, and inhibits the rectoanal inhibitory reflex, all three helping.
For refractory fecal incontinence, sacral nerve stimulation is the favored answer and has displaced sphincteroplasty; the staged trial requires at least fifty percent symptom improvement before permanent implantation.
Sphincteroplasty is reserved for the younger woman with an isolated external sphincter defect from obstetric injury, buying time because outcomes decline over years as pudendal neuropathy undoes the repair.
Thrombosed external hemorrhoids are excised within seventy-two hours of onset for faster pain relief, but after seventy-two hours conservative management is preferred, and the procedure is excision of the whole hemorrhoid, not incision and drainage.
A posterior or anterior midline anal fissure is idiopathic, but a lateral, multiple, or atypical fissure demands a Crohn's and infection workup before topical therapy; treatment layers topical calcium channel blockers, then botulinum toxin, then lateral internal sphincterotomy.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the continence stack
(01:27) - The etiologic grid of incontinence
(02:48) - History and targeted testing
(04:28) - The fixed treatment sequence
(05:52) - Sacral neuromodulation versus sphincteroplasty
(08:01) - Hemorrhoids and the dentate line
(10:03) - Thrombosed external hemorrhoids and the 72-hour rule
(11:05) - Anal fissure
(13:42) - Pruritus ani

Chapter 17, Ep 1 of 2: The R Ratio and the Two Workup Tracks

Board Pearls — Wed, 15 Jul 2026 22:31:59 -0500

Episode one of the Liver Test Interpretation chapter turns abnormal liver enzymes into a workup by computing the R ratio and committing to a track before ordering another test. The organizing idea: which enzyme dominates and by how many multiples of normal it sits at frames the entire differential, because hepatocellular and cholestatic patterns share almost nothing. The hepatocellular track runs five layers in order (viral, autoimmune, metabolic, ischemic, drug); the cholestatic track branches on a single ultrasound finding, dilated tree or not. Thresholds, magnitude anchors, and reflex panels throughout.

Topics covered

The R ratio and sorting hepatocellular from cholestatic
Hepatocellular injury and magnitude-based differential
AST-to-ALT ratio and the redefined normal range
Hepatocellular workup: viral, autoimmune, metabolic layers
Ischemic (shock liver) and drug-induced injury with Hy's Law
Cholestatic workup and the ultrasound branch point
Intrahepatic cholestasis: PBC, PSC, and IgG4 disease
The mixed pattern and the synthesis

Key decisions

Compute the R ratio first on any liver vignette: R over five is hepatocellular, R under two is cholestatic, and two to five is mixed, and commit to that track before ordering another test.
Acetaminophen and ischemic hepatitis are the two causes that cross an ALT of five thousand; ischemia carries an LDH-to-ALT ratio over one and a half with a hypotensive precedent, while an AST-to-ALT ratio over two with AST under four hundred in a drinker is alcoholic hepatitis until proven otherwise.
Use the current normal ALT of under twenty-five for women and under thirty-three for men, because the old range was inflated by undiagnosed fatty liver and hepatitis C.
Run the hepatocellular workup in order: viral first (hepatitis B surface antigen and hepatitis C antibody with reflex RNA), autoimmune second (ANA, smooth-muscle, anti-LKM-one, quantitative IgG), metabolic third (transferrin saturation over forty-five percent before HFE testing, ceruloplasmin in anyone under fifty-five).
Hy's Law is the drug-injury prognostic anchor: an ALT over three times normal with bilirubin over two without obstruction carries about ten percent mortality even after stopping the drug.
In the cholestatic track, get a right-upper-quadrant ultrasound first; a dilated tree goes to MRCP then endoscopic ultrasound for a mass, with ERCP reserved for therapy, while a non-dilated tree triggers anti-mitochondrial antibody and IgM for primary biliary cholangitis.
A positive anti-mitochondrial antibody with an alkaline phosphatase over one and a half times normal and AST under five times normal allows a no-biopsy diagnosis of primary biliary cholangitis, and MRCP showing beaded multifocal strictures diagnoses sclerosing cholangitis without ERCP.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The organizing idea and the R ratio
(00:41) - Computing R at the front door
(01:18) - Hepatocellular injury and magnitude
(03:19) - Redefining the normal range
(03:58) - The hepatocellular workup, layered in order
(08:39) - Shock liver, drug injury, and Hy's Law
(11:11) - The cholestatic workup and the ultrasound branch
(12:43) - Intrahepatic cholestasis: PBC, PSC, IgG4
(16:42) - The mixed pattern and the synthesis

Chapter 17, Ep 2 of 2: Isolated Abnormalities, Imaging, and Biopsy

Board Pearls — Wed, 15 Jul 2026 22:32:06 -0500

Episode two of the Liver Test Interpretation chapter covers what to do when a single value is up with everything else normal, or when the labs aren't the bottleneck and imaging and fibrosis assessment are. Each case forces the same question in a different form: what's the next reflex test, and does it commit you to an invasive workup or excuse you from it? Isolated bilirubin splits on direct versus indirect, isolated alkaline phosphatase splits on GGT, and the fibrosis workup runs FIB-4 before elastography before biopsy. Thresholds, mimic vignettes, and the percutaneous-versus-transjugular decision throughout.

Topics covered

Isolated hyperbilirubinemia and the direct versus indirect split
Separating hemolysis from Gilbert on the indirect side
Direct hyperbilirubinemia: Dubin-Johnson and Rotor
Isolated alkaline phosphatase and the GGT discriminator
Imaging modalities: structure versus fibrosis
Transient and MR elastography cutoffs by etiology
Serum fibrosis biomarkers and the FIB-4 sequence
Liver biopsy indications and technique
Percutaneous versus transjugular and the pressure gradient

Key decisions

Split isolated hyperbilirubinemia at the first line of the panel into indirect versus direct, because the two branches share almost nothing and both are mostly benign.
On the indirect side, run a five-value hemolysis screen (haptoglobin, reticulocyte count, smear, LDH, direct Coombs); a clean screen in the right stem is Gilbert, and G6PD hemolysis after trimethoprim-sulfamethoxazole shows bite cells and Heinz bodies.
Truly isolated direct hyperbilirubinemia with a normal biliary tree narrows to Dubin-Johnson (black liver, inverted urinary coproporphyrin ratio) or Rotor, both benign, so the answer is reassurance, not biopsy.
For isolated alkaline phosphatase, order GGT: elevated GGT confirms a hepatic source, while a normal GGT points to bone and triggers calcium, phosphorus, vitamin D, and a bone fraction or scan.
In the fibrosis workup, reach for FIB-4 first (under one point three rules out advanced fibrosis, over two point six seven supports it, with the lower cutoff shifting to two point zero over age sixty-five), then elastography, then biopsy, and anchor elastography cutoffs to etiology.
Diagnose hepatocellular carcinoma in a cirrhotic by multiphase MRI or CT showing arterial enhancement, washout, capsule, and threshold growth without biopsy, since biopsy of a definite cancer risks needle-tract seeding.
Choose transjugular biopsy over percutaneous for tense ascites, uncorrectable coagulopathy, morbid obesity, or when the hepatic venous pressure gradient is needed, where a gradient of ten or more marks clinically significant portal hypertension and twelve or more correlates with variceal hemorrhage risk.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The reflex-test framing
(00:54) - Isolated hyperbilirubinemia: the first split
(01:56) - Hemolysis versus Gilbert on the indirect side
(04:27) - Direct hyperbilirubinemia: Dubin-Johnson and Rotor
(05:52) - Isolated alkaline phosphatase and GGT
(09:00) - Imaging: structure versus fibrosis
(10:36) - Elastography and etiology-specific cutoffs
(12:35) - Serum biomarkers and the FIB-4 sequence
(14:27) - Biopsy indications and the transjugular decision

Chapter 18, Ep 1 of 3: Acute Viral Hepatitis and the Fecal-Oral Viruses

Board Pearls — Wed, 15 Jul 2026 22:32:13 -0500

Episode one of the Viral Hepatitis chapter builds the acute-hepatitis framework and covers the two fecal-oral viruses, hepatitis A and hepatitis E. The organizing idea: acute viral hepatitis looks the same no matter which virus caused it, so you read the virus off the serology, not the symptoms. It walks the four clinical phases, the four-test acute panel with its two named traps, and then hepatitis A as a post-exposure-prophylaxis decision that splits by age and host. Hepatitis E closes it with its two high-yield scenarios: twenty to thirty percent mortality in third-trimester pregnancy and chronic infection in the immunocompromised.

Topics covered

The acute-hepatitis mechanism and its four phases
The four-test first-line serologic panel
Serology interpretation rules and two named traps
Differential, alarm features, and treatment by virus
Hepatitis A course, risk factors, and atypical variants
Hepatitis A vaccine and post-exposure prophylaxis
Hepatitis E genotypes and when to test
Hepatitis E in pregnancy and chronic infection with ribavirin

Key decisions

The first move on any acute hepatitis stem is the serologic panel, not the history, because the clinical phases are identical across viruses.
The first-line acute panel is four tests, hepatitis B surface antigen, hepatitis B core IgM, hepatitis C antibody with reflex to RNA, and hepatitis A IgM, adding hepatitis E IgM in the returning traveler or when the panel is negative.
Surface antigen positive with core IgM positive is acute hepatitis B, while surface antigen positive with core IgM negative but total core positive is chronic hepatitis B.
A high-suspicion hepatitis C patient with a negative antibody is not cleared, because the antibody lags viremia by a couple of months, so the RNA closes the question.
Post-exposure prophylaxis splits by host: immunocompetent persons aged twelve months to forty get a single vaccine dose within two weeks, while those over forty, the immunocompromised, chronic liver disease patients, and infants under twelve months get immunoglobulin.
Vaccinate all patients with chronic liver disease of any cause against hepatitis A, because a superimposed acute hepatitis A decompensates them at a much higher rate.
Chronic hepatitis E is defined by persistent RNA beyond three to six months in an immunocompromised host, diagnosed by RNA not IgM, and treated by reducing immunosuppression first, then ribavirin for three months.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the organizing idea
(00:28) - Mechanism and the four phases of acute hepatitis
(02:32) - The serologic panel and its two named traps
(04:54) - Differential, alarm features, and treatment by virus
(06:25) - Hepatitis A: course and atypical variants
(08:09) - Hepatitis A vaccine and post-exposure prophylaxis
(09:26) - Hepatitis E: genotypes and when to test
(11:53) - Hepatitis E treatment by host

Chapter 18, Ep 2 of 3: Hepatitis B and D

Board Pearls — Wed, 15 Jul 2026 22:32:19 -0500

Episode two steps inside hepatitis B, where the serologic panel is not just diagnostic but a phase grid that determines treatment, the pregnancy strategy, the reactivation rule, and the hepatitis D testing decision. It reads two grids: the serologic grid of surface antigen, core antibody, and surface antibody that places the patient, and the phase grid of e-antigen, DNA, and ALT that decides whether to treat. From there it covers the nucleoside analogs, the three-pillar pregnancy bundle, the preemptive reactivation prophylaxis rule under immunosuppression, and hepatitis D with its new entry inhibitor bulevirtide. Every threshold, drug, and cutoff is named as the boards test it.

Topics covered

The six hepatitis B markers and what each means
The serologic grid and the isolated core antibody
The phase grid of chronic infection
Treatment principles, thresholds, and the drug menu
Reactivation under immunosuppression and prophylaxis
Pregnancy: the three-pillar vertical-transmission bundle
Hepatitis D: coinfection versus superinfection
Hepatitis D treatment and bulevirtide

Key decisions

Read the serologic grid of surface antigen, core antibody, and surface antibody to place the patient, with isolated core antibody positivity worked up by viral DNA and a repeat panel.
The phase grid of e-antigen status, viral DNA, and ALT decides treatment: immune-tolerant and inactive-carrier phases are not treated, while both immune-active phases are.
Treat with entecavir or a tenofovir prodrug indefinitely, choosing alafenamide for renal or bone protection and tenofovir disoproxil in pregnancy.
Reactivation is prevented preemptively, not rescued: surface-antigen-negative core-antibody-positive patients starting rituximab or transplant get prophylaxis because their risk approaches the surface-antigen-positive group.
The pregnancy bundle is universal surface-antigen screening, infant immunoglobulin plus vaccine within twelve hours regardless of viral load, and maternal tenofovir disoproxil from twenty-eight to thirty-two weeks when DNA exceeds two hundred thousand.
Tell coinfection from superinfection by the core antibody: coinfection shows core IgM with acute B and D, while superinfection shows total core without IgM because the underlying B is chronic.
Test for hepatitis D when a chronic hepatitis B patient has an ALT flare with low DNA, because hepatitis D drives injury using circulating surface antigen without needing active B replication.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the phase-grid idea
(00:47) - The six hepatitis B markers
(02:10) - The serologic grid and isolated core antibody
(03:29) - The phase grid of chronic infection
(06:04) - Treatment principles and the drug menu
(08:25) - Reactivation under immunosuppression
(11:10) - Pregnancy: the three-pillar bundle
(13:52) - Hepatitis D: coinfection versus superinfection
(16:16) - Hepatitis D treatment and bulevirtide

Chapter 18, Ep 3 of 3: Hepatitis C

Board Pearls — Wed, 15 Jul 2026 22:32:25 -0500

Episode three covers hepatitis C, now a curable disease, and tests the entire workflow of cure: identify the virus, confirm replication, stage the liver, pick the regimen, document cure, then ask the one remaining cancer question. It runs the reflex antibody-then-RNA diagnosis, the two pangenotypic direct-acting antiviral regimens plus the salvage regimen, and a special-populations set built on a few absolute rules. Decompensated cirrhosis forbids protease inhibitors; advanced kidney disease no longer forbids sofosbuvir. It closes on the highest-yield post-cure point: cancer surveillance continues forever in F4 cirrhosis but stops in F3 fibrosis short of cirrhosis.

Topics covered

Hepatitis C as a curable disease and the drug classes
The reflex antibody-then-RNA diagnostic algorithm
Universal screening and the pre-treatment workup
The two pangenotypic regimens and the salvage regimen
Sustained virologic response and what cure buys
Decompensated cirrhosis and the protease-inhibitor rule
Kidney disease, transplant, and pregnancy
Post-cure cancer surveillance by fibrosis stage

Key decisions

Diagnose in two tests in fixed order, the hepatitis C antibody then a reflex RNA, because the antibody persists for life and cannot distinguish active from resolved infection.
A high-suspicion patient with a negative antibody is not cleared, because the antibody lags viremia by a couple of months, so the RNA confirms acute hepatitis C.
The two preferred first-line regimens are pangenotypic: sofosbuvir-velpatasvir for twelve weeks and glecaprevir-pibrentasvir for eight weeks, the eight weeks holding even in treatment-naive compensated cirrhosis.
Sustained virologic response means undetectable RNA twelve weeks after the end of treatment, not twelve weeks of treatment, and that is the trap.
Protease inhibitors are unsafe in decompensated Child-Pugh B or C cirrhosis, so the regimen there is sofosbuvir-velpatasvir with ribavirin for twelve weeks or without for twenty-four.
Advanced kidney disease no longer forbids sofosbuvir, but glecaprevir-pibrentasvir is the simplest choice in renal impairment or dialysis when liver function is preserved.
Post-cure cancer surveillance continues every six months indefinitely in patients who had F4 cirrhosis at cure, while patients with F3 fibrosis short of cirrhosis stop surveillance after clearance.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: hepatitis C is curable
(00:27) - The cure framework and drug classes
(01:33) - The reflex antibody-then-RNA diagnosis
(03:41) - Screening and the pre-treatment workup
(04:30) - The two pangenotypic regimens and salvage
(06:36) - Sustained virologic response and what cure buys
(08:03) - Special populations and decompensated cirrhosis
(09:51) - Kidney disease, transplant, and pregnancy
(12:20) - Post-cure cancer surveillance by fibrosis stage

Chapter 19, Ep 1 of 2: Drug-Induced Liver Injury and Acetaminophen

Board Pearls — Wed, 15 Jul 2026 22:32:38 -0500

Episode one of the Drug-Induced Liver Injury and Acute Liver Failure chapter builds drug injury from a single mechanism: cytochrome oxidation makes a reactive intermediate, phase-two conjugation quenches it or fails, and injury appears where phase one outpaces phase two. That frame makes the offender lists predictable, the histology readable, and the severity rules non-arbitrary. Hy's Law converts biochemistry into a triage decision, R value predicts trajectory, and histology patterns map backward to drug classes. Acetaminophen is the prototype that runs the whole sequence at speed, with the Rumack-Matthew nomogram, N-acetylcysteine, and time-to-treatment mortality all board-tested cold.

Topics covered

Drug injury as the diagnosis for any new abnormal liver tests
Intrinsic versus idiosyncratic versus indirect hepatotoxicity
Epidemiology and environmental plus genetic risk factors
Herbal and dietary supplement injury
Metabolic activation and the phase-one, phase-two two-step
Agent-specific patterns from isoniazid to amiodarone
Hy's Law, R value, and causality assessment
Histology patterns mapped to drug classes
Acetaminophen toxicity, the nomogram, and N-acetylcysteine

Key decisions

Hy's Law is met when transaminases exceed three times normal, total bilirubin exceeds two times normal, alkaline phosphatase is under two times normal, and no other cause explains it, at which point mortality is about ten percent and the drug is stopped with transplant-center awareness.
The R value classifies pattern, hepatocellular over five, cholestatic under two, mixed between, with hepatocellular injury more likely to evolve to acute failure and cholestatic or mixed more likely to become chronic.
Acetaminophen toxicity occurs when NAPQI production exceeds glutathione capacity, so a chronic alcohol user with CYP2E1 induction and glutathione depletion can develop fulminant injury on therapeutic-range dosing without ever taking an overdose.
An acute single ingestion of seven and a half grams or more in an adult, or over a hundred fifty milligrams per kilogram in a child, puts the patient in the toxic window.
The Rumack-Matthew treatment line runs from a hundred fifty micrograms per milliliter at four hours down to about five at twenty-four hours, and a level above that line within the four-to-twenty-four-hour window indicates N-acetylcysteine.
Intravenous N-acetylcysteine is dosed as a hundred fifty milligrams per kilogram over sixty minutes, then fifty over four hours, then a hundred over sixteen hours, totaling three hundred over twenty-one hours, and started the moment the diagnosis is suspected because mortality roughly doubles with each block of delay.
Drug-induced autoimmune-like hepatitis from nitrofurantoin, minocycline, hydralazine, or methyldopa usually remits when the drug stops and does not need long-term immunosuppression, unlike idiopathic autoimmune hepatitis which flares on steroid taper.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the mechanistic frame
(01:17) - Intrinsic, idiosyncratic, and indirect injury
(02:18) - Epidemiology and risk factors
(04:46) - Herbal and dietary supplements
(05:56) - Metabolic activation: the hepatic two-step
(08:21) - Agent-specific patterns
(11:21) - Hy's Law, R value, and causality
(14:34) - Histology patterns by drug class
(20:11) - Acetaminophen: nomogram and antidote

Chapter 19, Ep 2 of 2: Acute Liver Failure and the King's College Criteria

Board Pearls — Wed, 15 Jul 2026 22:32:52 -0500

Episode two shifts from the drug to the failing organ, asking whether the liver can still recover on its own, how much time you have to decide, and when a different liver is the only answer. It anchors on the four-criterion definition of acute liver failure, then shows how etiology maps directly to the probability of spontaneous recovery. Two special causes, Wilsonian and herpes acute liver failure, each carry a distinctive fingerprint that demands empiric therapy before the workup completes. The King's College Criteria then triage who gets listed, with separate acetaminophen and non-acetaminophen paths calibrated to that recovery probability.

Topics covered

The four-criterion definition of acute liver failure
Distinction from acute-on-chronic failure and cerebral edema
Encephalopathy grading one through four
Etiology distribution and its link to prognosis
Non-cerebral and cerebral edema management
Wilsonian acute liver failure and its fingerprint
Herpes acute liver failure and empiric acyclovir
N-acetylcysteine in non-acetaminophen failure
King's College Criteria and transplant listing

Key decisions

Acute liver failure requires all four criteria: an INR of at least one and a half, hepatic encephalopathy of any grade, total illness duration under twenty-six weeks, and no pre-existing cirrhosis.
Cerebral edema risk rises sharply at grade three or four encephalopathy, and arterial ammonia above roughly a hundred fifty to two hundred marks the threshold where herniation risk climbs, managed with head-of-bed elevation, hypertonic saline, mannitol, and continuous renal replacement.
The Wilsonian fingerprint is Coombs-negative hemolysis with high indirect bilirubin, an alkaline-phosphatase-to-bilirubin ratio under four, an AST-to-ALT ratio over two, low uric acid, and Kayser-Fleischer rings, treated with urgent transplant and bridged by plasmapheresis while avoiding penicillamine.
Herpes acute liver failure shows very high transaminases with a normal or low bilirubin, the anicteric pattern, so empiric intravenous acyclovir at five to ten milligrams per kilogram every eight hours is started in any pregnant or immunocompromised patient with indeterminate failure.
N-acetylcysteine improves transplant-free survival in non-acetaminophen failure only with grade one or two encephalopathy, not grade three or four, so it is given empirically inside the early-grade window at the same dosing as for acetaminophen.
The acetaminophen King's College path is met by an arterial pH under seven point three after resuscitation, or by grade three or four encephalopathy plus an INR over six and a half plus a creatinine over three point four.
The non-acetaminophen path is met by an INR over six and a half alone, or by any three of five features: age under ten or over forty, indeterminate or drug-induced etiology, jaundice over seven days before encephalopathy, an INR over three and a half, and a bilirubin over seventeen and a half.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: from the drug to the failing organ
(00:46) - The four-criterion definition
(02:22) - Acute-on-chronic distinction and grading
(03:31) - Etiology distribution and prognosis
(04:49) - Non-cerebral and cerebral edema management
(06:49) - Wilsonian acute liver failure
(09:25) - Herpes acute liver failure
(11:05) - N-acetylcysteine in non-acetaminophen failure
(12:09) - King's College Criteria and listing

Chapter 21, Ep 1 of 2: MASLD: Diagnosis Through Pharmacotherapy

Board Pearls — Wed, 15 Jul 2026 22:32:57 -0500

Episode one of the Steatotic Liver Disease chapter reframes fatty liver as MASLD, a positive diagnosis built on hepatic steatosis plus at least one of five cardiometabolic criteria rather than an exclusion. The organizing idea: fibrosis stage, not the transaminase or the degree of steatosis, is the prognostic anchor, so the workup runs a tiered noninvasive sequence and management is graded by how much fibrosis is present. It walks the biology of insulin resistance and lipotoxicity, the PNPLA3 and TM6SF2 variants, lean disease and cryptogenic cirrhosis as the same entity, then the FIB-4 into elastography algorithm. Management climbs from weight-loss targets through bariatric surgery, including compensated cirrhosis, to the newly on-label drugs resmetirom and semaglutide.

Topics covered

Positive cardiometabolic diagnosis and the five criteria
Steatohepatitis versus bland steatosis and fibrosis as the prognostic anchor
Alcohol continuum and the intermediate category
Insulin resistance, lipotoxicity, and the PNPLA3 and TM6SF2 variants
Lean disease and cryptogenic cirrhosis
Noninvasive fibrosis testing: FIB-4, transient elastography, MR elastography
Lifestyle, diet, and weight-loss targets
Bariatric surgery including compensated cirrhosis
Pharmacotherapy: resmetirom, semaglutide, pioglitazone, vitamin E

Key decisions

MASLD requires hepatic steatosis on imaging or biopsy PLUS at least one of five cardiometabolic criteria; one criterion is enough, a deliberate change from metabolic syndrome requiring three.
Read prognosis through fibrosis stage, not the inflammatory grade or the transaminase level, because liver-related mortality climbs steeply with fibrosis while ALT does not track outcome.
FIB-4 under one point three rules out advanced fibrosis and over two point six seven flags high risk, with the cutoff shifting to two point zero over age sixty-five; transient elastography under eight kilopascals rules out advanced fibrosis and over twelve to fourteen suggests cirrhosis.
Stiffness over twenty kilopascals with a platelet count under a hundred fifty thousand indicates clinically significant portal hypertension and triggers variceal screening.
Weight loss is dose-responsive: five percent reduces steatosis, seven to ten percent resolves steatohepatitis, and ten percent or more produces fibrosis regression, with the target shifted to three to five percent in lean disease.
Compensated steatohepatitis cirrhosis can undergo bariatric surgery at experienced centers when synthetic function is preserved and there is no significant portal hypertension; a hepatic venous pressure gradient over fifteen is an absolute contraindication, with sleeve gastrectomy generally preferred.
Resmetirom and semaglutide are on-label for non-cirrhotic moderate-fibrosis steatohepatitis, chosen by dominant comorbidity, while pioglitazone is for the diabetic and vitamin E at eight hundred international units for the non-diabetic biopsy-proven patient, avoided in diabetics and cirrhosis.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the organizing idea
(00:25) - Positive diagnosis on cardiometabolic criteria
(02:10) - Fibrosis as the prognostic anchor
(03:23) - Mechanism and the genetic variants
(05:19) - Lean disease and cryptogenic cirrhosis
(06:50) - Noninvasive fibrosis assessment
(10:08) - Lifestyle, diet, and weight-loss targets
(12:23) - Bariatric surgery and cirrhosis
(14:05) - Pharmacotherapy: the new on-label drugs

Chapter 21, Ep 2 of 2: Alcohol-Associated Liver Disease and Early Transplant

Board Pearls — Wed, 15 Jul 2026 22:33:01 -0500

Episode two moves along the alcohol continuum to alcohol-associated liver disease, one biology read across steatosis, steatohepatitis, and cirrhosis, then zeroes in on the acute superimposed syndrome of severe alcoholic hepatitis. The organizing idea: severe disease is defined by a Maddrey above thirty-two or a MELD over twenty, treated with prednisolone only after infection is excluded, with the day-seven Lille score as the binary decision to continue or stop. It works through the AST-greater-than-ALT lab signature, the ethanol-metabolism mechanism that drives it, and the drug interactions that follow. The close is early transplant for selected steroid nonresponders, which retired the old six-month sobriety rule in favor of a structured psychosocial assessment.

Topics covered

Three-stage spectrum: steatosis, steatohepatitis, cirrhosis
Ethanol metabolism, the NADH shift, and drug interactions
Risk modifiers: sex, genetics, and the acetaldehyde variant
The AST-greater-than-ALT lab pattern
Severe alcoholic hepatitis and the consensus diagnostic criteria
Maddrey and MELD severity thresholds
Prednisolone therapy and mandatory infection screening
The day-seven Lille response decision
Early transplant selection criteria

Key decisions

Diagnose probable alcoholic hepatitis from jaundice within two months, heavy use for at least six months, an AST between fifty and four hundred with a ratio over one and a half, and a bilirubin over three, letting you skip biopsy in the typical patient.
Define severe disease by a Maddrey discriminant function above thirty-two or a MELD over twenty; MELD-Na is not used here.
Expect an AST-to-ALT ratio above one and a half, often above two, with both under four hundred; transaminases over four hundred in a drinker signal something on top of alcohol, classically acetaminophen or ischemic hepatitis.
Give prednisolone forty milligrams daily for up to twenty-eight days, but only after culturing blood, urine, and ascites and imaging the chest, because serious infections were roughly twice as common on steroids; AKI with creatinine above two and a half, uncontrolled infection, and GI bleeding defer or contraindicate them.
Calculate the Lille score at day seven: under about half is a responder who completes the course, while at or above that threshold is a nonresponder who stops steroids because continuing adds infection risk without survival benefit.
Add N-acetylcysteine as an adjunct and give nutrition at thirty to forty kilocalories per kilogram and one and a half grams of protein per kilogram by mouth or nasogastric tube, avoiding parenteral nutrition for infection risk.
Refer steroid nonresponders with first decompensation, strong support, no prior treatment failure, and clear insight for early transplant; the six-month sobriety rule is retired, and post-transplant use acamprosate and baclofen for alcohol use disorder.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the organizing idea
(00:29) - The three-stage spectrum and reversibility
(01:22) - Mechanism and drug interactions
(03:39) - The AST-greater-than-ALT lab pattern
(04:34) - Severe alcoholic hepatitis and its criteria
(06:12) - Steroids, the trial, and infection screening
(07:36) - The day-seven Lille decision
(09:12) - Early transplant and retiring the six-month rule
(10:36) - Selection criteria for early transplant

Chapter 20, Ep 1 of 3: Sorting the Immune Liver Diseases and Autoimmune Hepatitis

Board Pearls — Wed, 15 Jul 2026 22:33:05 -0500

Episode one of the Autoimmune and Cholestatic Liver Diseases chapter builds the sorting framework for the three immune liver diseases and then works autoimmune hepatitis in depth. The organizing idea: pattern plus demographics plus antibodies place a patient into autoimmune hepatitis, primary biliary cholangitis, or primary sclerosing cholangitis within the first two sentences of the vignette. Autoimmune hepatitis is then the ANA and smooth-muscle-antibody interface hepatitis of the middle-aged woman with elevated IgG, confirmed on biopsy. The second half is treatment: steroid induction plus a steroid-sparing agent, the type one versus type two split, the simplified score, and why withdrawal is cautious because relapse is the rule.

Topics covered

Sorting framework: target cell sets the biochemical pattern
Demographics and IBD association across the three diseases
Antibody panel and IgG profile as the discriminator
Autoimmune hepatitis pathogenesis and two clinical faces
Type one versus type two serologic subtypes
Simplified scoring system and its blind spots
Interface hepatitis and ancillary histology
Steroid induction, azathioprine, and budesonide
Remission endpoints and cautious withdrawal

Key decisions

Sort the three immune liver diseases by pattern plus demographics plus antibodies: hepatocellular with ANA or smooth-muscle antibody and high IgG is autoimmune hepatitis, cholestatic with anti-mitochondrial antibody is primary biliary cholangitis, and cholestatic in a man with ulcerative colitis needing MRCP is primary sclerosing cholangitis.
Check a TPMT level before starting azathioprine, because TPMT-deficient patients metabolize it to toxic levels and develop severe myelosuppression; induce a non-cirrhotic adult with prednisone thirty to sixty milligrams daily plus azathioprine fifty to one hundred fifty milligrams daily.
Budesonide at nine milligrams daily is an alternative induction agent for non-cirrhotic patients but must not be used in cirrhosis, because portosystemic shunting bypasses first-pass metabolism, lowering efficacy and raising systemic exposure.
Treat acute severe autoimmune hepatitis with high-dose prednisone or IV methylprednisolone without azathioprine or budesonide, reassess every one to two weeks, and refer for transplant on failure to respond rather than escalating the dose.
Maintain biochemical remission (normal transaminases and normal IgG) for at least two years before considering withdrawal, ideally after a confirmatory biopsy, because most patients relapse within a few years of stopping.
Drug-induced autoimmune-like hepatitis from nitrofurantoin, minocycline, methyldopa, hydralazine, statins, or checkpoint inhibitors is the exception to lifelong therapy: it remits with drug withdrawal and a steroid taper, so the medication history is the discriminator.
In pregnancy continue both prednisone and azathioprine, because the risk of a flare on withdrawal exceeds the fetal risk, and postpartum flare is common.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The sorting framework and its variable
(00:30) - Target cell sets the biochemical pattern
(01:35) - Demographics, IBD, and the antibody panel
(04:08) - Autoimmune hepatitis and its two faces
(05:46) - The simplified scoring system
(06:36) - Interface hepatitis on biopsy
(07:22) - Induction and steroid-sparing maintenance
(09:02) - Remission and cautious withdrawal

Chapter 20, Ep 2 of 3: Primary Biliary Cholangitis

Board Pearls — Wed, 15 Jul 2026 22:33:09 -0500

Episode two works primary biliary cholangitis, the anti-mitochondrial-antibody cholestatic disease of the middle-aged woman, as a biochemical-target-driven problem. The diagnosis is usually made on labs alone, treatment starts with ursodeoxycholic acid for everyone, and escalation is driven by where the alkaline phosphatase and bilirubin sit at twelve months, because those numbers are the surrogate for survival. The second-line landscape changed when obeticholic acid left the US market, leaving elafibranor and seladelpar as the two approved PPAR-targeted agents that tend to improve rather than worsen the itch. The close is the stepped, mechanism-targeted pruritus algorithm from cholestyramine through rifampin, sertraline, naltrexone, and the emerging ileal transporter inhibitors.

Topics covered

Clinical picture and pathogenesis of primary biliary cholangitis
Lab-based diagnosis and when biopsy is needed
Florid duct lesion and staging
Biphasic natural history and prognostic scores
Ursodeoxycholic acid mechanism and twelve-month response
Second-line agents after obeticholic acid withdrawal
Fat-soluble vitamins, bone, and the lipid profile
Stepped mechanism-targeted pruritus algorithm
Ileal bile acid transporter inhibitors

Key decisions

Diagnose primary biliary cholangitis on labs alone when there is a positive anti-mitochondrial antibody, an alkaline phosphatase above one and a half times normal, and transaminases under five times normal with no alternative explanation; biopsy is unnecessary and reserved for antibody-negative disease or suspected overlap.
Start every patient on ursodeoxycholic acid thirteen to fifteen milligrams per kilogram per day for life, and assess response at twelve months: the alkaline phosphatase should fall toward one and a half times normal with a normal bilirubin, and failure or intolerance triggers a second agent.
Use the twelve-month continuous risk scores that combine age, bilirubin, alkaline phosphatase, albumin, and platelets to identify the roughly one third of non-responders who face higher risk of cirrhosis, transplant, and death.
Obeticholic acid was withdrawn from the US market in 2025 for liver-injury signals, leaving elafibranor and seladelpar, both PPAR agonists, as the only approved second-line agents, chosen by tolerability rather than a clear efficacy difference.
Do not reflexively add a statin for high total cholesterol, because the profile is dominated by lipoprotein X and HDL and is generally not atherogenic; statins are safe but reserved for patients with conventional risk factors.
Run pruritus as a stepped sequence: cholestyramine first, dosed at least one hour before or four hours after other drugs, then rifampin with liver tests at four to eight weeks, then sertraline, then low-dose naltrexone.
Stop rifampin at any signal of worsening transaminases or rising bilirubin, since idiosyncratic hepatotoxicity occurs in the first couple of months, rather than reducing the dose and continuing.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The middle-aged woman with cholestatic labs
(00:27) - Clinical picture and pathogenesis
(01:23) - Lab-based diagnosis and when to biopsy
(02:50) - Biphasic natural history and risk scores
(04:08) - Ursodeoxycholic acid and twelve-month response
(05:44) - Second-line agents after obeticholic acid
(07:32) - Vitamins, bone, and the lipid trap
(08:23) - The stepped pruritus algorithm

Chapter 20, Ep 3 of 3: Primary Sclerosing Cholangitis and IgG4 Disease

Board Pearls — Wed, 15 Jul 2026 22:33:13 -0500

Episode three works primary sclerosing cholangitis, the multifocal stricturing disease of the man with ulcerative colitis, as a recognition-and-surveillance problem, then covers its steroid-responsive mimic. MRCP not serology makes the diagnosis, the alkaline phosphatase is normal in nearly half of patients at any moment, and because there is no proven medical therapy the work is surveillance for three cancers. The chapter closes on IgG4-related sclerosing cholangitis, the older man with painless jaundice and a sausage-shaped pancreas who responds dramatically to corticosteroids and must not go to a Whipple, plus the two overlap syndromes. Cancer thresholds, the dominant stricture workup, and the high-dose ursodeoxycholic acid harm signal run throughout.

Topics covered

Sclerosing cholangitis presentation and IBD association
MRCP as the diagnostic test and role of ERCP
Natural history and premalignant surveillance rationale
Cholangiocarcinoma surveillance and CA 19-9
Dominant stricture workup and brush cytology ceiling
Gallbladder and colorectal cancer thresholds
No proven therapy and high-dose UDCA harm
IgG4-related sclerosing cholangitis and HISORt
Autoimmune hepatitis overlap syndromes

Key decisions

Diagnose primary sclerosing cholangitis with MRCP, not serology, because a normal alkaline phosphatase occurs nearly half the time and the beaded pattern of multifocal short-segment strictures with intervening normal or dilated segments closes it; reserve ERCP for dominant stricture, cholangitis, or suspected cancer.
Surveil for cholangiocarcinoma with annual MRCP plus CA 19-9 starting at diagnosis, interpreting the CA 19-9 by trajectory from the patient's baseline rather than the absolute number, since it is uninformative in Lewis-negative patients and rises with cholangitis.
Treat every dominant stricture as cancer until proven otherwise with ERCP brushings, molecular testing for chromosomal polysomy, and cholangioscopy-directed biopsy, because brush cytology has a false-negative rate over fifty percent.
Remove the gallbladder for polyps greater than eight millimeters, a lower threshold than the ten-millimeter general-population cutoff, and follow smaller polyps with ultrasound every six months.
Perform colonoscopy at the time of sclerosing cholangitis diagnosis regardless of IBD duration, then every one to two years, because the combination enriches colorectal cancer risk several-fold and the diagnosis resets the surveillance clock.
Do not use high-dose ursodeoxycholic acid above twenty-eight milligrams per kilogram per day, because a large trial showed increased mortality, transplant, and colorectal neoplasia; there is no proven medical therapy.
Check serum IgG4 and add an IgG4 stain to the biopsy at every new diagnosis, and trial prednisone forty milligrams daily for four weeks then taper in the older man with painless jaundice, a distal common bile duct stricture, and a sausage-shaped pancreas rather than defaulting to a Whipple.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - The man with ulcerative colitis and rising ALP
(00:34) - Presentation and the IBD association
(02:07) - MRCP as the diagnostic test
(04:27) - Natural history and premalignant surveillance
(06:17) - The dominant stricture workup
(08:07) - Gallbladder and colorectal thresholds
(10:22) - No proven therapy and transplant
(11:35) - IgG4-related sclerosing cholangitis
(15:09) - The overlap syndromes

Chapter 22, Ep 1 of 3: Hereditary Hemochromatosis

Board Pearls — Wed, 15 Jul 2026 22:33:16 -0500

Episode one of the Inherited Liver Diseases chapter takes hereditary hemochromatosis and reasons from the molecular lesion outward: lose the HFE signal, lose the hepcidin brake, and iron pours in unchecked for decades. The organizing move is that genotype alone is a substrate, not a disease, so diagnosis rests on biochemistry plus genotype, not a positive C282Y result by itself. Iron regulation, the C282Y and H63D alleles, incomplete sex-skewed penetrance, the two-tier diagnostic framework, phlebotomy to a ferritin target, and the reversibility line all run through the episode. The recurring trap is the healthy homozygote with normal iron studies who is surveyed, not treated.

Topics covered

Iron regulation: hepcidin, ferroportin, and HFE
C282Y and H63D genotypes
Non-HFE hemochromatosis and ferroportin disease
Biopsy iron distribution and quantitative thresholds
Incomplete, sex-skewed penetrance
Carrier and homozygote frequencies
Diagnostic criteria and the two-tier framework
Phlebotomy to a ferritin target
Reversibility, cirrhosis, and HCC surveillance

Key decisions

C282Y homozygosity is the classical disease genotype; an isolated H63D allele or compound heterozygosity rarely causes overload and does not warrant phlebotomy or surveillance.
Diagnose on biochemistry plus genotype: a fasting transferrin saturation of at least forty-five percent in men or forty in women plus a ferritin over three hundred in men or two hundred in women, then HFE genotyping for homozygosity.
A high ferritin with a normal transferrin saturation in alcohol, fatty liver, or inflammation is secondary hyperferritinemia and is not treated with phlebotomy; treat the upstream driver instead.
Induction phlebotomy removes about five hundred milliliters of whole blood (roughly two hundred fifty milligrams of iron) weekly to a target ferritin of fifty to a hundred, holding the session if hemoglobin is under eleven.
Homozygotes with normal iron studies are substrates, not patients, and get iron studies repeated every couple of years to catch late conversion.
Once cirrhosis is established, liver cancer risk is high (about a third of cirrhotic patients), so ultrasound every six months continues for life, and phlebotomy does not reverse established cirrhosis, diabetes, or hypogonadism.
Counsel patients to avoid vitamin C supplements and raw shellfish (fulminant Vibrio risk) and reduce red meat; siblings of a proband carry a one-in-four risk and are screened first.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: the two metal-handling diseases
(00:46) - Iron loop: hepcidin, ferroportin, and HFE
(02:06) - The classical genotype and the non-HFE forms
(03:36) - Biopsy pattern and hyperferritinemia mimics
(04:36) - Incomplete penetrance and carrier frequencies
(05:52) - Diagnostic criteria: biochemistry plus genotype
(06:57) - Phlebotomy to target and dietary counseling
(08:14) - Reversibility, cirrhosis risk, and cancer surveillance
(09:47) - One-line summary

Chapter 22, Ep 2 of 3: Wilson Disease

Board Pearls — Wed, 15 Jul 2026 22:34:27 -0500

Episode two takes the other metal-handling disease, Wilson, where the toxin is copper and the ATP7B pump fails at two coupled jobs: pushing copper into bile and loading it onto ceruloplasmin. The diagnostic logic is harder because no single test stands alone, so the Leipzig score integrates weighted features and the chelator choice turns on the speed and site of copper movement. Low ceruloplasmin, high urinary copper, the fulminant fingerprint, and trientine-plus-zinc therapy run through the episode. The board traps are the young steatohepatitis patient without metabolic syndrome and the misread fulminant case that costs the transplant window.

Topics covered

ATP7B and the failed copper exit
Low ceruloplasmin from accelerated degradation
Kayser-Fleischer rings and sunflower cataracts
Hepatic and neuropsychiatric phenotypes
Leipzig diagnostic score and copper tests
The fulminant Wilson fingerprint
Trientine, penicillamine, and zinc
Monitoring with urinary and free copper
Pregnancy and contraception traps

Key decisions

Diagnose Wilson with at least two of five features (Kayser-Fleischer rings, ceruloplasmin under twenty, typical neurologic symptoms, twenty-four-hour urinary copper over forty, hepatic copper over two hundred fifty) using the Leipzig score, where four or higher establishes it.
A ceruloplasmin over thirty essentially excludes Wilson because synthetic capacity is intact, and a hepatic copper under thirty-five excludes it; the intermediate band triggers molecular testing.
Consider Wilson in any patient from about three to forty-five with unexplained liver disease, and specifically in a young steatohepatitis patient with no metabolic syndrome features.
First-line chelation is trientine over penicillamine for neurologic Wilson because penicillamine causes paradoxical worsening in up to half; zinc induces enterocyte metallothionein and is for maintenance or pre-symptomatic patients only.
Trientine chelates oral iron into a toxic complex and chelates zinc, so separate them in time, and overtreatment causes a reversible sideroblastic anemia from copper depletion.
On long-term monitoring, high free copper with low urinary copper signals non-adherence, while low free copper signals overtreatment.
In pregnancy continue chelation at a quarter-to-half reduced dose by the third trimester, avoid estrogen-containing contraceptives and copper IUDs, and replace prenatal vitamins with copper-free formulations.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: the failed copper exit
(00:25) - ATP7B mechanism and low ceruloplasmin
(01:50) - Hepatic and neuropsychiatric phenotypes
(03:01) - The Leipzig score and diagnostic tests
(04:36) - The fulminant Wilson fingerprint
(05:35) - Chelation: trientine, penicillamine, zinc
(07:37) - Monitoring: urinary and free copper
(08:15) - Pregnancy and contraception traps
(09:11) - One-line summary

Chapter 22, Ep 3 of 3: A1AT, CF Liver Disease, PCLD, and Cholestatic Syndromes

Board Pearls — Wed, 15 Jul 2026 22:34:30 -0500

Episode three closes the chapter with the four inherited liver diseases beyond the metal pair: alpha-one antitrypsin deficiency, cystic-fibrosis-associated liver disease, polycystic liver disease, and the familial cholestatic syndromes. The unifying move is that mechanism predicts therapy in each one, and each carries a distinct board trap. Alpha-one antitrypsin is the two-organ split where augmentation rescues the lung and does nothing for the liver; CF liver disease is one causal chain treated at three points; polycystic liver disease is synthetic-function-preserved mass effect; and the cholestatic syndromes split by the GGT pattern and cancer risk. Ileal bile acid transporter inhibitors, CFTR modulators, and the MELD exception anchor the modern management.

Topics covered

Alpha-one antitrypsin two-organ split
PiZZ, the null genotype, and PAS-diastase-resistant globules
Augmentation and NSAID treatment traps
CF-associated liver disease and CFTR modulators
Polycystic liver disease and the MELD exception
Familial cholestatic syndromes and the GGT split
Cancer risk by mechanism
IBAT inhibitors and pruritus therapy
Alagille syndrome

Key decisions

In PiZZ alpha-one antitrypsin deficiency, IV augmentation restores circulating anti-elastase and slows lung decline but does nothing for the liver, because hepatic injury is from intracellular polymer, not circulating deficiency.
Avoid NSAIDs in PiZZ patients because they increase hepatic alpha-one antitrypsin synthesis and worsen the polymer load; diagnose by phenotyping or genotyping, not the level alone, since it is an acute-phase reactant.
The null genotype causes severe early emphysema with normal liver enzymes because no protein is made to accumulate, while PiZZ biopsy shows PAS-positive, diastase-resistant periportal globules.
In cystic-fibrosis-associated liver disease, treat at three points: ursodeoxycholic acid downstream, fat-soluble vitamins in the middle, and CFTR modulators upstream, with triple therapy standard for any patient carrying at least one F508del allele.
Polycystic liver disease is treated by symptom severity, not cyst count: first-line somatostatin analog, then fenestration or partial hepatectomy, then transplant, with a MELD exception because synthetic function is preserved.
The familial cholestatic syndromes split by GGT, with the bile salt export pump and membrane-organizing defects low GGT and the phosphatidylcholine flippase defect high GGT, and the export-pump type carries the highest pediatric liver cancer risk warranting alpha-fetoprotein surveillance.
Ileal bile acid transporter inhibitors are the era-defining therapy for pruritus in the progressive intracellular-cholestasis syndromes and Alagille, combined with rifampin and naltrexone.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction: four diseases, one logic
(00:33) - Alpha-one antitrypsin: the two-organ split
(04:21) - A1AT treatment: augmentation and NSAID traps
(05:57) - CF-associated liver disease: three intervention points
(08:25) - Polycystic liver disease: mass effect and MELD exception
(11:11) - Familial cholestatic syndromes: the GGT split
(13:23) - Cholestasis treatment: IBAT inhibitors and pruritus
(15:16) - Alagille syndrome
(16:13) - Pulling the four together

Chapter 23, Ep 1 of 3: Portal Hypertension and Varices

Board Pearls — Wed, 15 Jul 2026 22:34:34 -0500

Episode one of the Portal Hypertension and Cirrhosis Complications chapter treats portal hypertension as a pressure problem first, then follows that pressure into varices and bleeding. The organizing idea: the hepatic venous pressure gradient is the hemodynamic gold standard, and liver stiffness plus platelets give the noninvasive translation that now drives beta-blocker and screening decisions. Screening thresholds, primary prophylaxis, and the acute variceal hemorrhage bundle all key off the same physiology, with the restrictive transfusion target, mandatory ceftriaxone, and the early-TIPS decision as the cirrhosis-specific layers. It closes on gastric varices, portal hypertensive gastropathy, and GAVE, where anatomy and drainage pick the therapy, not appearance.

Topics covered

Portal hypertension hemodynamics and HVPG thresholds
Beta-blocker response and presinusoidal versus postsinusoidal causes
Noninvasive CSPH detection and the rule of five
Variceal screening and surveillance intervals
Primary prophylaxis: carvedilol versus band ligation
The acute variceal hemorrhage bundle
Early TIPS during the index admission
Gastric varices, portal hypertensive gastropathy, and GAVE

Key decisions

An HVPG over five defines portal hypertension, ten or higher defines clinically significant portal hypertension and identifies who will develop varices and decompensation, and over twelve marks the variceal bleeding threshold; a beta-blocker responder drops the gradient more than a fifth or below twelve.
By the rule of five, a liver stiffness of twenty-five kilopascals or higher rules in clinically significant portal hypertension while stiffness of fifteen or lower with platelets of a hundred fifty thousand or higher rules it out; defer screening endoscopy when stiffness is under twenty and platelets over a hundred fifty thousand.
In compensated cirrhosis with clinically significant portal hypertension, a beta-blocker reduces first decompensation even without high-risk varices, a different indication from variceal prophylaxis, and cirrhosis without CSPH is not an indication.
For medium or large varices choose a nonselective beta-blocker or band ligation, with carvedilol preferred because its alpha-blockade lowers intrahepatic resistance in addition to inflow; hold nonselective beta-blockers when systolic pressure drops under ninety, sodium falls under a hundred thirty, or acute kidney injury develops.
In acute variceal hemorrhage transfuse to a hemoglobin around seven, not higher, and give octreotide plus mandatory ceftriaxone with endoscopic band ligation within twelve hours.
Early TIPS within seventy-two hours improves one-year survival in high-risk bleeds, Child C in the ten-to-thirteen range or Child B with active bleeding, and the decision is made during the index admission rather than after the second bleed.
Isolated fundal varices without esophageal varices should prompt evaluation for splenic vein thrombosis, and GAVE breaks the portal-pressure logic because TIPS is not effective.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the hemodynamic root
(00:31) - Portal hypertension as a pressure problem
(01:08) - HVPG thresholds and their meaning
(03:13) - The noninvasive framework and rule of five
(05:32) - Variceal screening and surveillance
(06:28) - Primary prophylaxis choices
(08:17) - The acute hemorrhage bundle
(09:46) - Early TIPS in the index admission
(11:57) - Gastric varices, gastropathy, and GAVE

Chapter 23, Ep 2 of 3: The Splanchnic Vasodilation Cluster

Board Pearls — Wed, 15 Jul 2026 22:34:38 -0500

Episode two follows the splanchnic vasodilation cluster, where one upstream physiology produces four complications, each with its own bundle, threshold, and drug sequence. Portal hypertension drives splanchnic vasodilation, the kidney reads effective hypovolemia and retains sodium, and from that single mismatch flow ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic encephalopathy. The episode anchors ascites on the serum-ascites albumin gradient and the fixed spironolactone-to-furosemide ratio, then moves through the TIPS-versus-paracentesis decision, hyponatremia thresholds, the peritonitis antibiotic-plus-albumin bundle, terlipressin for hepatorenal syndrome, and lactulose plus rifaximin for encephalopathy. Every threshold is mechanism-derived rather than arbitrary.

Topics covered

One physiology, four complications
Ascites and the serum-ascites albumin gradient
Diuretic management and the spironolactone-furosemide ratio
Large-volume paracentesis and albumin replacement
Refractory ascites: TIPS versus serial paracentesis
Hyponatremia thresholds
Spontaneous bacterial peritonitis bundle
Hepatorenal syndrome and terlipressin
Hepatic encephalopathy: lactulose plus rifaximin

Key decisions

A serum-ascites albumin gradient over one point one supports portal hypertension while a gradient under one point one points toward carcinomatosis, tuberculous, or pancreatic ascites; low ascitic protein under two and a half fits cirrhotic ascites while high protein with a high gradient suggests heart failure or constrictive pericarditis.
The diuretic backbone is spironolactone plus furosemide in a fixed hundred-to-forty ratio, starting at a hundred plus forty and maxing at four hundred plus one hundred sixty, and large-volume paracentesis above five liters needs albumin at six to eight grams per liter removed.
An ascitic neutrophil count over two hundred fifty diagnoses spontaneous bacterial peritonitis; treat empirically with a third-generation cephalosporin and give albumin one and a half grams per kilogram on day one and one gram per kilogram on day three.
Secondary peritonitis prophylaxis is mandatory after a first episode because one-year recurrence exceeds seventy percent, using daily norfloxacin, ciprofloxacin, or trimethoprim-sulfamethoxazole indefinitely.
Hepatorenal syndrome is diagnosed after no improvement following two days of diuretic withdrawal plus albumin at a gram per kilogram, and first-line therapy is terlipressin plus albumin continued up to fourteen days or to creatinine response.
Hyponatremia thresholds are concrete: reduce diuretics under one hundred thirty, stop them and fluid-restrict under one hundred twenty-five, admit for saline under one hundred twenty, correcting no faster than eight to ten per twenty-four hours.
Hepatic encephalopathy is treated with lactulose titrated to two to three soft stools a day plus rifaximin after a first overt episode, and protein restriction is forbidden because muscle is the largest extra-hepatic ammonia detoxifier.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the splanchnic cluster
(00:32) - One physiology, four complications
(01:31) - Ascites and the albumin gradient
(02:50) - Diuretics and the fixed ratio
(04:41) - Refractory ascites and the TIPS decision
(07:31) - Hyponatremia thresholds
(09:01) - Spontaneous bacterial peritonitis
(13:04) - Hepatorenal syndrome and terlipressin
(16:15) - Hepatic encephalopathy

Chapter 23, Ep 3 of 3: Pulmonary, Coagulopathy, and Vascular Complications

Board Pearls — Wed, 15 Jul 2026 22:34:42 -0500

Episode three covers the decompensated complications that do not flow primarily through splanchnic vasodilation, starting with two pulmonary syndromes that look related but are physiologically opposite. Hepatopulmonary syndrome is capillary dilation with shunt physiology, recognized by platypnea and orthodeoxia, while portopulmonary hypertension is arteriolar constriction diagnosed by right heart catheterization, and that single distinction picks the therapy and changes the transplant calculus. The episode then works the coagulopathy where the INR misleads because cirrhotic hemostasis is rebalanced rather than impaired, so paracentesis and thoracentesis need no correction. It closes on the vascular liver diseases sorted by anatomic level, Budd-Chiari, sinusoidal obstruction syndrome, portal vein thrombosis, porto-sinusoidal vascular disease, and shock liver.

Topics covered

Hepatopulmonary syndrome and shunt physiology
Platypnea, orthodeoxia, and contrast echocardiography
Portopulmonary hypertension and the transplant calculus
Hepatic hydrothorax
Rebalanced hemostasis and the misleading INR
Periprocedural transfusion decisions
Budd-Chiari syndrome
Sinusoidal obstruction syndrome
Portal vein thrombosis and tumor thrombus

Key decisions

Hepatopulmonary syndrome is diagnosed by contrast echocardiography showing microbubbles in the left atrium three to six cardiac cycles after the right atrium opacifies, and an arterial oxygen below sixty earns transplant-priority exception points with transplant the only cure.
Portopulmonary hypertension is confirmed by right heart catheterization with a mean pulmonary arterial pressure of at least twenty-five, a pulmonary vascular resistance over three Wood units, and a wedge of at most fifteen; a mean pressure at or above fifty contraindicates transplant while thirty-five to forty-five is a relative contraindication treatable with vasodilators.
Vasodilators help portopulmonary hypertension because the lesion is constriction but do not help hepatopulmonary syndrome because the capillaries are already dilated.
Hepatic hydrothorax is managed with sodium restriction, diuretics, therapeutic thoracentesis, and TIPS for refractory cases, while chest tube placement and pleurodesis are contraindicated.
The INR does not predict bleeding in cirrhosis because hemostasis is rebalanced, so paracentesis and thoracentesis require no correction and viscoelastic testing captures the real state; high-risk procedures keep platelets above fifty thousand and fibrinogen above a floor.
Budd-Chiari mandates a thrombophilia workup with JAK2 the highest-yield test, and treatment escalates stepwise from anticoagulation to angioplasty to TIPS to transplant.
In portal vein thrombosis exclude hepatocellular carcinoma with tumor thrombus before anticoagulating, using arterial enhancement as the discriminator, while sinusoidal obstruction syndrome is treated with defibrotide.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction and the remaining complications
(00:24) - Hepatopulmonary syndrome
(01:05) - Platypnea and orthodeoxia
(02:39) - Portopulmonary hypertension
(04:31) - Hepatic hydrothorax
(06:22) - Coagulopathy and the misleading INR
(10:16) - Vascular liver disease and Budd-Chiari
(12:24) - Sinusoidal obstruction syndrome
(13:53) - Portal vein thrombosis

Chapter 24, Ep 1 of 4: Benign Liver Lesions by Context

Board Pearls — Thu, 16 Jul 2026 07:59:31 -0500

Episode one of the Liver Tumors and Transplant chapter runs the benign masses on a single decision: imaging appearance plus hormonal or drug context usually settles the diagnosis, and biopsy enters only when the imaging is atypical or the lesion has real malignant potential. Peripheral nodular enhancement filling inward is a hemangioma, hepatobiliary-phase retention is focal nodular hyperplasia, and hepatobiliary-phase darkening is an adenoma. From the adenoma you stratify by sex, size, growth, and beta-catenin status, because that subtype is what turns a benign mass into a resection case. The two edge entities, nodular regenerative hyperplasia and peliosis hepatis, round out the pattern-recognition set.

Topics covered

Imaging-plus-context decision rule
Cavernous hemangioma and its enhancement pattern
Kasabach-Merritt syndrome
Focal nodular hyperplasia and the central scar
Hepatic adenoma and oral contraceptives
Adenoma molecular subtypes and beta-catenin
Adenoma resection versus surveillance
Nodular regenerative hyperplasia and peliosis hepatis

Key decisions

A cavernous hemangioma shows peripheral nodular enhancement in the arterial phase that fills inward over the venous phase, and that classical pattern means no biopsy and no surveillance.
Treat a hemangioma only when it is giant and symptomatic, causes Kasabach-Merritt syndrome with thrombocytopenia and consumptive coagulopathy, or drives high-output heart failure.
Focal nodular hyperplasia retains a hepatobiliary contrast agent like gadoxetate because it has functioning hepatocytes and bile ductules, while an adenoma goes dark in that phase, so no needle is needed and the pill is not stopped when imaging is classical.
Resect any hepatic adenoma in a man regardless of size, plus any lesion five centimeters or larger, any growing lesion, any beta-catenin-positive lesion, any that has bled, and resect before a planned pregnancy.
Small adenomas in young women on the pill can be watched: stop the pill first, then image every six months for two years and annually thereafter.
Hepatic adenomatosis, meaning more than ten lesions, is a rare reason to transplant when the disease is unresectable.
A near-normal biopsy behind non-cirrhotic portal hypertension is nodular regenerative hyperplasia revealed on reticulin stain, and blood-filled cavities in a drug-exposed patient is peliosis hepatis managed by removing the offending agent.

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

Questions or feedback: hello@boardpearls.com.

Chapter 24, Ep 2 of 4: Hepatocellular Carcinoma End to End

Board Pearls — Thu, 16 Jul 2026 07:59:41 -0500

Episode two works hepatocellular carcinoma as one continuous algorithm built on a single override: a new lesion in a cirrhotic or chronic hepatitis B liver is HCC until proven otherwise. Surveillance goes to every Child-Pugh A or B cirrhotic and to high-risk hepatitis B, by ultrasound and AFP every six months timed to the tumor doubling time and the curative-size cutoffs. LI-RADS turns that finding into a diagnosis, with the definite category diagnostic by imaging alone and the two special categories forcing biopsy or excluding transplant. The BCLC system then turns the diagnosis into the treatment the physiology will actually permit, from resection and ablation, through transplant within Milan, to locoregional therapy and first-line atezolizumab plus bevacizumab for advanced disease.

Topics covered

Surveillance eligibility and Child-Pugh cutoffs
Non-cirrhotic hepatitis B risk triggers
Ultrasound plus AFP every six months
The role and limits of AFP
LI-RADS categories and the diagnostic five
Major features and their mechanisms
BCLC staging and curative options
Milan and UCSF criteria and down-staging
Locoregional and systemic therapy

Key decisions

Surveil every patient with Child-Pugh A or B cirrhosis of any cause including cured hepatitis C, and surveil Child-Pugh C only when the patient is a transplant candidate.
The modality is right-upper-quadrant ultrasound with AFP every six months, substituting MRI or CT when severe obesity or steatosis makes the ultrasound useless; AFP is never stand-alone, but a value over two hundred nanograms per milliliter with arterial enhancement strongly supports HCC.
LI-RADS five requires a lesion at least one centimeter with arterial-phase hyperenhancement plus a major feature, namely washout, an enhancing capsule, or threshold growth of fifty percent or more in six months, and in a cirrhotic liver that is a diagnosis without biopsy.
A rim-enhancing, peripheral-washout, targetoid lesion is the malignant-but-not-HCC category that you biopsy, because intrahepatic cholangiocarcinoma over two centimeters is a transplant contraindication; an arterially enhancing tumor thrombus takes the patient out of transplant criteria and is not anticoagulated.
Milan criteria are a single lesion at most five centimeters, or up to three lesions each at most three centimeters, with no extrahepatic spread and no macrovascular invasion; UCSF widens this and patients beyond Milan can be down-staged with locoregional therapy and three to six months of imaging stability before listing.
Cirrhotic resection requires a normal bilirubin and a hepatic venous pressure gradient under ten, and thermal ablation substitutes for tumors under three centimeters, limited by the heat-sink effect near vessels.
First-line advanced therapy is atezolizumab plus bevacizumab, requiring a mandatory upper endoscopy within six months with high-risk varices treated first, and durvalumab plus tremelimumab is the alternative when bevacizumab is contraindicated.

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

Questions or feedback: hello@boardpearls.com.

Chapter 24, Ep 3 of 4: Cholangiocarcinoma by Anatomy

Board Pearls — Thu, 16 Jul 2026 07:59:49 -0500

Episode three organizes cholangiocarcinoma anatomy first, biology second, because where the tumor sits dictates the operation and the transplant path. Intrahepatic disease is resected when possible and is a transplant contraindication over two centimeters, distal disease gets a Whipple, and perihilar disease is resected when resectable with a narrow unresectable subset going through a neoadjuvant-then-transplant protocol. The imaging is delayed enhancement without washout, the mirror image of HCC, because the fibrous stroma traps contrast rather than letting it run through. CA 19-9 is a trend rather than a yes-or-no and is unusable in Lewis-negative patients, so sclerosing cholangitis patients with a new dominant stricture get FISH on the brushings when cytology fails them.

Topics covered

Three anatomic subtypes and their operations
Perihilar subclassification and hepatectomy extent
Delayed enhancement versus HCC washout
Shared inflammatory risk factors
CA 19-9 interpretation and Lewis-negative patients
The indeterminate stricture and FISH
Perihilar transplant protocol
First-line systemic therapy
FGFR2 and IDH1 targeted subtypes

Key decisions

Location dictates the operation: intrahepatic tumors come out with the piece of liver, perihilar tumors need a hemihepatectomy plus extrahepatic bile duct plus Roux-en-Y, and distal tumors need a pancreaticoduodenectomy.
Intrahepatic cholangiocarcinoma takes up contrast progressively in the venous and delayed phases with no washout, the opposite of HCC, because the dense fibrous stroma traps and slowly releases contrast.
CA 19-9 is not specific because it rises in benign biliary obstruction and cholangitis, and it is useless in Lewis-antigen-negative patients who cannot make it, so it is best read as a trend in a high-risk patient.
In a sclerosing cholangitis patient with a new dominant stricture and atypical but non-diagnostic ERCP brushings, the right next step is FISH on those brushings, where polysomy carries high specificity for cholangiocarcinoma.
Intrahepatic cholangiocarcinoma larger than two centimeters is a contraindication to transplant, because occult micrometastatic disease drives poor post-transplant survival, so resection is the best chance.
Perihilar transplant applies only to tumors at most three centimeters in radial diameter with no intrahepatic metastases or nodal involvement, following a fixed neoadjuvant chemoradiation, boost, maintenance, and staging-laparotomy sequence, and transperitoneal biopsy is contraindicated because it seeds the tract and disqualifies the patient.
First-line systemic therapy is gemcitabine plus cisplatin plus durvalumab, and intrahepatic tumors earn a molecular workup because FGFR2 fusions are treated with pemigatinib or futibatinib and IDH1 mutations with ivosidenib.

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Chapter 24, Ep 4 of 4: Liver Transplant Scoring to Recurrence

Board Pearls — Thu, 16 Jul 2026 08:00:05 -0500

Episode four follows a patient across the whole transplant arc, organized by two clocks: the allocation score that triages who is sickest, and time itself, which orders both the drop in immunosuppression intensity and the shift from acute risk to cumulative toxicity. The calculated score does the primary triage with its sex and albumin corrections fixing real undervaluation, the workup confirms the operation can succeed medically, infectiously, and psychosocially, and the exception points cover the diseases the labs cannot see. Donor type then sets the complication profile, immunosuppression intensity organizes the early timeline of rejection and opportunistic infection with CMV dominant, and cumulative toxicity organizes the late timeline. The original disease returns in a pattern specific to its cause, which is why surveillance continues indefinitely.

Topics covered

Allocation score components and corrections
Referral triggers and the score-of-fifteen threshold
The three-question workup
Exception points for undervalued diseases
Donor types and their complication signatures
Immunosuppression stepping down over time
The complication timeline by era
Acute and antibody-mediated rejection
CMV and recurrent disease patterns

Key decisions

The allocation score uses capped creatinine, bilirubin, INR, and sodium, adds points for female sex to correct the lower creatinine of lower muscle mass, and subtracts points across the low albumin range to capture catabolic decompensated disease.
List for transplant on decompensation, meaning variceal bleeding, ascites, encephalopathy, HCC, or hepatorenal dysfunction, or on a score of fifteen or higher, the point where the operation stops being a net loss versus medical management.
Exception points cover diseases the score misses: HCC within criteria gets a regional median score after a six-month wait, hepatopulmonary syndrome qualifies at an arterial oxygen under sixty, and portopulmonary hypertension qualifies with a mean pressure under thirty-five after vasodilators while a mean over fifty is an outright contraindication.
Donation after circulatory death carries higher ischemic cholangiopathy and primary non-function from longer warm ischemic time, mitigated by normothermic machine perfusion, and living donor grafts carry higher biliary complication rates but serve high-symptom, low-score patients.
Immunosuppression steps down from high-dose induction steroid, through the first months of triple therapy with steroid taper, mycophenolate, and a calcineurin inhibitor, to calcineurin-inhibitor monotherapy after about a year.
Acute cellular rejection occurs in about a third of transplants, usually in the first six weeks, needs biopsy showing the triad of portal inflammation, bile duct injury, and endothelial inflammation, and is treated with intravenous methylprednisolone five hundred to a thousand milligrams daily for three days.
Tacrolimus is metabolized by CYP3A4, so azole antifungals, macrolides, diltiazem, verapamil, and amiodarone raise its level and cause toxicity, while rifampin, isoniazid, phenytoin, carbamazepine, and St John's wort lower it and risk rejection.

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Chapter 25, Ep 1 of 3: Acute Pancreatitis: The First Hours

Board Pearls — Thu, 16 Jul 2026 08:00:27 -0500

Episode one of the Acute Pancreatitis chapter follows a single mechanism from trypsin escaping its compartment to the cytokine cascade, third-spacing, and lost pancreatic perfusion. The organizing idea: every first-hours decision reaches back to that mechanism. The two-of-three rule diagnoses around the failure modes of pain, enzymes, and imaging alone; the cause is worked up on admission because the trigger reshapes management; severity stays provisional while organ failure declares; and fluids are moderate lactated Ringer's titrated to hematocrit and BUN. The trial that asked whether more fluid was better answered no and stopped early.

Topics covered

Mechanism: trypsin activation and the calcium convergence point
Triggers: gallstones, alcohol, triglycerides, calcium
Systemic inflammation, third-spacing, and necrosis
Clinical presentation and lipase versus amylase
Revised Atlanta two-of-three diagnosis
Severity grading by organ failure
Etiology workup during the index admission
Severity scores and first-day hematocrit and BUN trends
Moderate goal-directed lactated Ringer's resuscitation

Key decisions

Diagnose acute pancreatitis on the revised Atlanta two-of-three rule: characteristic upper abdominal pain, lipase or amylase over three times the upper limit of normal, or characteristic cross-sectional imaging.
Order lipase rather than amylase because it rises within four to eight hours, stays up for eight to fourteen days, and is pancreas-specific, and remember the enzyme height does not track severity.
Avoid routine early CT because necrosis takes seventy-two to ninety-six hours to demarcate; reserve imaging for diagnostic uncertainty, failure to improve at forty-eight to seventy-two hours, or suspected complications.
Get a right-upper-quadrant ultrasound in everyone, since a positive study means same-admission cholecystectomy, and treat an ALT over three times normal (roughly above one hundred fifty) as a strong pointer to a gallstone cause.
Define severe disease as persistent organ failure beyond forty-eight hours, a modified Marshall score of two or more in the renal, pulmonary, or cardiovascular system, and treat early severity as provisional.
Escalate on rising hematocrit or BUN despite fluids, because hemoconcentration is a surrogate for the hypoperfusion driving necrosis, even before the Marshall score turns positive.
Resuscitate with moderate goal-directed lactated Ringer's at about one and a half milliliters per kilogram per hour after a ten-milliliter-per-kilogram bolus in hypovolemic patients, titrating to urine output of half to one milliliter per kilogram per hour.

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Chapter 25, Ep 2 of 3: Feeding, ERCP, and the Gallbladder

Board Pearls — Thu, 16 Jul 2026 08:00:30 -0500

Episode two works through three first-days decisions where the intuitive older instinct turns out to be net harmful. Pancreatic rest with TPN increases infection because an empty lumen lets villi atrophy and gut bacteria translocate into necrotic tissue, so early enteral feeding wins. Universal urgent ERCP was wrong because most triggering stones have already passed, leaving an empty duct and only post-ERCP risk. And interval cholecystectomy costs roughly one in six patients a recurrent biliary event, so same-admission surgery is now standard. The unifying logic: each intervention earns its place against its own complication profile.

Topics covered

Pancreatic rest versus early enteral feeding
The gut barrier and bacterial translocation
Feeding rules in mild disease
Feeding in predicted severe disease and tube level
TPN as the failure path
ERCP indications and the passed-stone anatomy
The three-patient ERCP decision
Same-admission versus interval cholecystectomy
Exceptions: severe disease and the non-surgical patient

Key decisions

Feed early in mild disease, within twenty-four to forty-eight hours, with a low-fat solid diet if the patient is hungry, has bowel sounds, and isn't vomiting, rather than holding NPO until the lipase normalizes.
Do not force an early nasojejunal tube on predicted severe patients, since early nasojejunal placement showed no difference in major infection or mortality versus oral intake on demand.
When a tube is needed, place a nasogastric tube and start feeding, because nasogastric, nasoduodenal, and nasojejunal feeding are equivalent and standard formulas work as well as elemental ones.
Reserve TPN for the patient who truly cannot tolerate enteral feeding for a prolonged period from severe ileus, hemodynamic intolerance, or surgical anatomy.
Perform ERCP within twenty-four hours for cholangitis and within twenty-four to seventy-two hours for persistent obstruction, but give no ERCP to mild gallstone pancreatitis without cholangitis or obstruction.
Treat the duct, not the pancreas, as the indication for ERCP: a rising bilirubin and dilated duct warrant ERCP regardless of severity score, while a falling ALT and non-dilated duct do not.
Do same-admission cholecystectomy within three days of pain resolution for mild gallstone pancreatitis, deferring four to eight weeks only in severe or necrotizing disease and substituting ERCP with biliary sphincterotomy in patients too high-risk for surgery.

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Chapter 25, Ep 3 of 3: Necrosis, Vascular Traps, and Recurrence

Board Pearls — Thu, 16 Jul 2026 08:01:06 -0500

Episode three picks up where the pancreas has declared itself necrotic and organizes the collection nomenclature on timing and content. Necrosis is managed by delay, drain, then debride, with endoscopic transmural drainage now favored because it never crosses the peritoneum. The vascular complications split by vessel: venous thrombosis usually self-resolves, while a pseudoaneurysm mandates CT angiography and embolization before any drainage. The post-ERCP triad attacks three independent nodes, and recurrent disease is worked up by escalation from baseline labs to MRCP to endoscopic ultrasound for microlithiasis, with the pancreas divisum trap waiting at the end.

Topics covered

Recognizing necrosis and infected necrosis
Collection nomenclature by timing and content
Step-up management: delay, drain, debride
Endoscopic versus surgical step-up
Splanchnic venous thrombosis and left-sided portal hypertension
Arterial pseudoaneurysm and pre-drainage angiography
Post-ERCP pancreatitis and its prevention triad
Recurrent and idiopathic disease workup
Pancreas divisum and prevention by stopping the cause

Key decisions

Diagnose necrosis by non-enhancing parenchyma on contrast CT and read gas in a peripancreatic collection, absent recent intervention, as essentially diagnostic of infected necrosis.
Name collections by timing and content: acute peripancreatic fluid collection and pseudocyst without necrosis, acute necrotic collection and walled-off necrosis with necrosis, split at four weeks.
Follow the step-up principle of delay past four weeks, drain percutaneously or endoscopically first, and debride only when drainage fails or solid debris obstructs it, favoring endoscopic transmural drainage with a lumen-apposing metal stent.
Withhold anticoagulation for isolated splenic vein thrombosis, reserving it for clot extending into the portal or superior mesenteric vein, and treat bleeding gastric varices from left-sided portal hypertension with splenectomy.
Image the arterial anatomy before any necrosectomy or cyst drainage and embolize a pseudoaneurysm first, because manipulation risks catastrophic hemorrhage.
Prevent post-ERCP pancreatitis in high-risk cases with all three pillars: rectal indomethacin one hundred milligrams, a prophylactic pancreatic duct stent, and peri-procedural lactated Ringer's.
Work up recurrent disease by escalation from baseline labs to MRCP to endoscopic ultrasound for microlithiasis and tumors, add genetic testing under thirty-five, and offer cholecystectomy after a second idiopathic episode.

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Chapter 26, Ep 1 of 5: Chronic Pancreatitis Framework and Pain

Board Pearls — Thu, 16 Jul 2026 08:02:33 -0500

Episode one of the Chronic Pancreatitis, Cysts, and Neoplasms chapter builds the framework from a single fact: fewer than three percent of heavy drinkers ever develop the disease, so exposure alone is never enough and a co-modifier has to do the converting. The organizing idea is that tobacco and a genetic background decide who progresses, and where each gene sits in the trypsin-control pathway sets its inheritance, penetrance, and cancer risk. Diagnosis is calibrated to stage, CT for calcification, secretin-MRCP for the duct, endoscopic ultrasound for minimal-change parenchyma, and function testing for the gland that still looks normal. Pain is worked in steps, from cessation and non-opioid analgesics through neuromodulators to decompression, with the randomized shift that moved early surgery ahead of endoscopy the tested pivot. Cause, mechanism, staging, and steps throughout.

Topics covered

Fibroinflammatory disease and the co-modifier concept
Tobacco and genetic background as converters
TIGAR-O etiologic classification
Genetic forms and trypsin regulation
Cationic trypsinogen cancer risk and surveillance
Staged diagnosis: CT, secretin-MRCP, endoscopic ultrasound
Functional testing for early disease
Stepwise pain management
Early surgery in dilated-duct disease

Key decisions

Fewer than three percent of heavy alcohol users develop chronic pancreatitis, so a toxic exposure needs a co-modifier, usually tobacco plus a genetic background, before fibrosis takes hold.
A patient over fifty with a first idiopathic acute pancreatitis episode needs cross-sectional imaging follow-up once inflammation settles, because obstruction from pancreatic adenocarcinoma is the must-not-miss of the obstructive category.
Cationic trypsinogen gain-of-function disease carries the highest cancer risk of any subset, earning routine surveillance with annual MRI alternating with endoscopic ultrasound starting at age forty.
Genetic testing is indicated when the cause is unclear, when there is a family history, or when onset is under about thirty-five.
Work up diagnosis as CT first for calcification, secretin-enhanced MRCP next for duct and side branches, endoscopic ultrasound for minimal-change parenchyma, and secretin-stimulated function testing when structure still looks normal, with a peak duodenal bicarbonate at or above eighty milliequivalents per liter carrying high negative predictive value.
Manage pain in steps starting with alcohol and tobacco cessation, then non-opioid analgesics, neuromodulators such as gabapentin or pregabalin, and enzyme replacement when exocrine insufficiency coexists, with narcotics minimized.
In painful chronic pancreatitis with a dilated main duct, early surgical drainage beats the endoscopy-first approach, so surgery is now the early move rather than the salvage move.

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Chapter 26, Ep 2 of 5: Enzyme Replacement, Type 3c Diabetes, Complications

Board Pearls — Thu, 16 Jul 2026 08:03:55 -0500

Episode two follows three threads that all trace to the same parenchymal loss the framework episode set up. The acini die and enzyme replacement stands in, but only if dosed with the meal and released at the right duodenal pH, so a proton pump inhibitor enters when the coating fails. The islets die and produce a diabetes defined not by insulin lack but by lost glucagon, which makes hypoglycemia the dominant management feature and steers drug choice away from sulfonylureas. The structural disruption produces complications whose management is read directly off the anatomy, drain the symptomatic pseudocyst, recognize disconnected duct as the exception, and take the spleen out when left-sided portal hypertension bleeds. Mechanism first, management second, throughout.

Topics covered

Exocrine reserve and the ten-percent threshold
Enzyme replacement dosing with meals
Structured workup for inadequate response
Pancreatogenic diabetes and lost glucagon
Drug choices: metformin over sulfonylureas
Pseudocyst and disconnected duct syndrome
Distal bile duct stricture from head fibrosis
Splenic vein thrombosis and left-sided portal hypertension
Pancreatic ascites and pseudoaneurysm

Key decisions

Steatorrhea and fat-soluble vitamin deficiency appear only after exocrine output drops below about ten percent of normal, so clinical insufficiency means roughly ninety percent of acinar capacity is already lost.
Start enzyme replacement at forty to fifty thousand lipase units with each main meal and half that with snacks, taken with the meal, titrating up to about ninety thousand per meal by clinical response.
When response is inadequate, escalate the dose, then add a proton pump inhibitor because acidic duodenal pH prevents the enteric coating from releasing enzyme, then verify adherence and exclude bacterial overgrowth, bile acid malabsorption, celiac, and mucosal disease.
Pancreatogenic diabetes loses glucagon alongside insulin, making hypoglycemia brittle, so insulin titration stays conservative, sulfonylureas are avoided, and metformin remains a reasonable adjunct.
Drain a pseudocyst for symptoms, infection, or rapid enlargement rather than size, using an endoscopic-ultrasound-guided cyst-gastrostomy with a lumen-apposing metal stent, and recognize disconnected duct syndrome as the exception needing permanent drainage or resection.
Splenectomy is curative when isolated fundal gastric varices from splenic vein thrombosis bleed, because removing the high-flow inlet decompresses the left-sided portal hypertension.
Embolize a suspected pseudoaneurysm before any necrosectomy or cyst drainage, because manipulating a collection that hides it risks catastrophic hemorrhage.

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

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Chapter 26, Ep 3 of 5: Autoimmune Pancreatitis Types One and Two

Board Pearls — Thu, 16 Jul 2026 08:04:27 -0500

Episode three steps outside the alcohol-and-tobacco gland to a diagnosis that sits at a costly decision point: steroids given to a patient who actually has adenocarcinoma cost the curative resection window. Autoimmune pancreatitis splits on mechanism, type one a systemic IgG4-related plasma-cell disease of older men with painless jaundice, type two a duct-centered process a decade younger tied to inflammatory bowel disease. Demographics, imaging, serology, other-organ involvement, and histology all line up behind that one distinction, and the criteria are structured precisely because the mass mimics cancer. The steroid trial is pulled in as a diagnostic element, but when the differential with adenocarcinoma stays genuinely unresolved, surgery comes first. Mechanism drives the whole call.

Topics covered

Mechanism split: plasma-cell versus duct-centered
Demographics of type one and type two
Imaging and the absent double-duct sign
IgG4 serology and its threshold
Other-organ involvement
Histology: storiform fibrosis versus granulocytic lesion
Steroid response as a diagnostic element
When surgery precedes the steroid trial
Relapse pattern and rituximab

Key decisions

Type one is a systemic IgG4-related plasma-cell disease of older men presenting with painless obstructive jaundice, while type two is a duct-centered process a decade younger with an even sex distribution and an inflammatory bowel disease association in about a third.
Adenocarcinoma produces the double-duct sign with upstream dilation, whereas type one infiltrates and narrows the duct without dilating it, so a sausage-shaped gland with a capsule rim and a non-dilated duct nearly makes the diagnosis.
A mild IgG4 elevation under twofold also occurs in some pancreatic cancers, so only a value greater than two times the upper limit of normal supports autoimmune pancreatitis, and even then it is one criterion among several.
Both types respond to prednisone forty milligrams daily for four weeks then a five-milligram weekly taper, with clinical and biochemical improvement within two weeks part of the criteria and failure to respond the signal to re-evaluate for cancer.
When the noninvasive workup leaves the differential with adenocarcinoma genuinely unresolved, a focal head mass with a double-duct sign, a high CA 19-9, a mildly elevated IgG4, and non-diagnostic histology goes to resection, not empiric steroids.
Type one relapses in a third to a half of patients, so rituximab one thousand milligrams on days one and fifteen with maintenance every six months for two years is the steroid-sparing agent of choice.
Type two rarely relapses because there is no circulating clone, so no maintenance is indicated and the rare relapse is treated like the first episode.

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Chapter 26, Ep 4 of 5: Pancreatic Cystic Lesions and Surveillance

Board Pearls — Thu, 16 Jul 2026 08:05:28 -0500

Episode four takes the incidental cyst through the same endoscopic-ultrasound-and-fluid pathway used for the autoimmune mass, but the cost runs the other way: resecting a cyst that was never going to become cancer commits a patient to major-operation morbidity for nothing. The organizing question is whether the epithelium is mucinous, because only the mucinous lesions carry progressive dysplasia, and the fluid answers it, CEA and glucose for mucin, amylase for duct communication. Demographics and imaging give a pretest guess, then the biochemistry classifies the lesion cleanly. The intraductal mucinous neoplasm is the one left to surveil, where high-risk stigmata mandate resection, worrisome features trigger endoscopic ultrasound, and a size-stratified MRI schedule runs only while it can still change management. Thresholds are the trap throughout.

Topics covered

Mucinous versus non-mucinous as the organizing principle
Demographics and imaging of the five entities
Mucinous cystic neoplasm versus serous cystadenoma
Fluid biochemistry: CEA, glucose, amylase
The four-quadrant classification by CEA and amylase
Clinical pivots by cyst type
High-risk stigmata versus worrisome features
The five- and ten-millimeter thresholds
Size-stratified surveillance and stopping rules

Key decisions

The decision to watch or resect tracks whether the epithelium is mucinous, since intraductal and mucinous cystic neoplasms harbor progressive dysplasia while serous cystadenoma, pseudocyst, and retention cysts have negligible malignant potential.
A cyst fluid CEA above one hundred ninety-two nanograms per milliliter favors mucinous origin, a glucose below fifty is highly sensitive for a mucinous cyst, and an amylase above two hundred fifty units per liter supports duct communication.
A mucinous cystic neoplasm goes to resection in a fit candidate regardless of size, while a confidently diagnosed serous cystadenoma needs no surveillance at all.
Any one of the four high-risk stigmata, obstructive jaundice with a cystic head lesion, an enhancing mural nodule five millimeters or larger, a main pancreatic duct ten millimeters or larger, or suspicious cytology, mandates surgical referral with no confirmatory aspiration needed.
Worrisome features such as a cyst three centimeters or larger, an enhancing nodule under five millimeters, a main duct between five and ten millimeters, or growth of two and a half millimeters or more per year trigger endoscopic ultrasound rather than the operating room.
A new five-millimeter enhancing nodule crosses from worrisome into high-risk regardless of prior stability, so a four-millimeter nodule keeps a patient in surveillance while a five-millimeter nodule is the threshold for resection.
Surveillance continues only while it can change management, stopping when the patient is no longer a surgical candidate or life expectancy is under ten years, with exceptions for younger, familial, or genetically at-risk patients.

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Chapter 26, Ep 5 of 5: Pancreatic Adenocarcinoma and Neuroendocrine Tumors

Board Pearls — Thu, 16 Jul 2026 08:06:22 -0500

Episode five closes the chapter with two tumors that share the same pancreas and almost nothing else. Adenocarcinoma is desmoplastic, poorly enhancing, presents late with painless jaundice, and is staged by its relationship to four vessels into the resectability categories that drive surgery-versus-systemic-therapy. The neuroendocrine tumors are islet-derived, hypervascular, and often announce themselves with a hormone syndrome while still small, sorted by functional pattern and grade. The same core biopsy and multiphase CT serve both, but everything downstream diverges, so the work is holding the two algorithms apart. Biology sets the staging language, and the staging language sets the treatment, from neoadjuvant FOLFIRINOX to somatostatin analogs and radionuclide therapy.

Topics covered

Adenocarcinoma biology and late presentation
Risk factors: modifiable, hereditary, conditioning
Diagnostic sequence and core biopsy
The autoimmune pancreatitis mimic trap
Four-vessel resectability staging
Neoadjuvant, adjuvant, and metastatic chemotherapy
Neuroendocrine tumor biology and imaging
Functional syndromes: insulinoma and gastrinoma
VIPoma, glucagonoma, somatostatinoma
Treatment stratified by size and receptor status

Key decisions

A patient over sixty with a painless head mass and obstructive jaundice has adenocarcinoma until proven otherwise, so a mildly elevated IgG4 does not justify empiric prednisone that would cost the curative window.
Resectability is defined by the tumor relationship to the celiac axis, common hepatic artery, superior mesenteric artery, and superior mesenteric and portal veins, with borderline disease showing arterial contact under one hundred eighty degrees or reconstructable venous involvement.
Borderline resectable and many resectable patients receive neoadjuvant modified FOLFIRINOX for four to six months before re-staging, and upfront-surgery patients receive adjuvant modified FOLFIRINOX when fit.
Metastatic disease is treated with modified FOLFIRINOX or gemcitabine plus nab-paclitaxel by performance status, with olaparib maintenance for germline BRCA or PALB2 mutations whose tumors respond to platinum.
In suspected insulinoma, a suppressed C-peptide with high insulin during hypoglycemia indicates factitious insulin use rather than tumor, and endoscopic ultrasound is the dominant localization tool because most insulinomas are somatostatin-receptor negative.
Gastrinoma diagnosis requires a fasting serum gastrin measured off proton pump inhibitor for seven days, with a gastrin above one thousand picograms per milliliter and gastric pH under two diagnostic, and intermediate values prompting a secretin stimulation test.
Non-functional neuroendocrine tumors under one centimeter may be observed while those over two centimeters warrant resection, and unresectable disease is managed with somatostatin analogs, everolimus or sunitinib, and lutetium-DOTATATE radionuclide therapy.

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Chapter 27, Ep 1 of 4: Gallstones and Acute Cholecystitis

Board Pearls — Thu, 16 Jul 2026 08:06:40 -0500

Episode one of the Biliary Tract Disease chapter starts with the stone, because the phenotype tells you what biochemical environment produced it, and that environment is really the risk-factor list seen from the mechanism side. Cholesterol stones come from supersaturation, dysmotility, or nucleation; black pigment stones from excess unconjugated bilirubin; brown pigment stones form new in the duct under stasis plus bacterial deconjugation. Asymptomatic stones are observed because the math favors it, unless a cancer or surgical-emergency configuration shifts the calculus, and true biliary colic tips a fit patient toward cholecystectomy. When persistent obstruction converts colic into acute cholecystitis, the Tokyo grade dictates how aggressively to operate, with the friable ischemic wall of the acalculous and emphysematous variants pushing drainage back toward the percutaneous route.

Topics covered

Cholesterol stones and the three lithogenic pathways
Gallstone risk factors mapped to mechanism
Black pigment stones and chronic hemolysis
Brown pigment stones and the two-year rule
Observation versus surgery for asymptomatic stones
Prophylactic cholecystectomy indications
Tokyo diagnosis and grading of cholecystitis
Drainage options for the poor surgical candidate
Acalculous and emphysematous variants

Key decisions

Asymptomatic gallstones are observed because progression to symptomatic disease runs only one to four percent per year, which does not exceed the perioperative mortality of elective cholecystectomy.
Prophylactic cholecystectomy is offered for a discrete list of cancer or emergency configurations: patchy porcelain gallbladder, stones three centimeters or larger, coexisting polyps, Native American women with stones, and pancreaticobiliary maljunction with cysts.
In uncomplicated cholecystitis liver chemistries stay normal or under twice normal, so a marked bilirubin or transaminase elevation signals concurrent duct stones or Mirizzi syndrome and should widen the differential.
Tokyo grade one mild disease gets early laparoscopic cholecystectomy within the admission, usually within seven days, while the planes of Calot's triangle still separate.
Tokyo grade three severe disease with organ dysfunction gets ICU resuscitation plus emergent gallbladder drainage first, with cholecystectomy deferred and sometimes never done.
For the poor surgical candidate, endoscopic-ultrasound-guided drainage with a lumen-apposing metal stent is now preferred over percutaneous drainage, but emphysematous cholecystitis is a contraindication because the ischemic friable wall risks catastrophic perforation.
Acalculous and emphysematous variants prioritize rapid percutaneous cholecystostomy with broad-spectrum antibiotics, and gangrene, perforation, or peritonitis forces operation regardless of stability.

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Chapter 27, Ep 2 of 4: Uncommon Gallbladder Presentations

Board Pearls — Thu, 16 Jul 2026 08:06:56 -0500

Episode two covers the less common gallbladder presentations, and the thread running through all of them is the same: chronic inflammatory remodeling around the gallbladder distorts the anatomy enough to change either the operation, the cancer risk, or the diagnostic frame. Stone-driven inflammation at Calot's triangle either compresses the bile duct from outside in Mirizzi, calcifies the wall in porcelain gallbladder, or erodes into bowel in gallstone ileus and Bouveret. The Csendes stage sets the reconstruction, the calcification pattern sets the cancer indication, and the level of stone impaction sets endoscopy versus surgery. Polyps test on a clean size rule with risk-factor modifiers, and functional gallbladder disorder tests on the discipline not to operate, because the failure mode is over-treating a heterogeneous category.

Topics covered

Mirizzi syndrome and the Csendes classification
MRCP staging and open conversion risk
Porcelain gallbladder and calcification pattern
Cholecystenteric fistula and gallstone ileus
Bouveret syndrome and gastric outlet obstruction
Gallbladder polyps and the size threshold
Gallbladder adenocarcinoma biology
Pancreaticobiliary maljunction
Functional gallbladder disorder and over-treatment

Key decisions

In Mirizzi syndrome the Csendes stage dictates the operation: external compression or a small fistula allows cholecystectomy or primary repair over a T-tube, while destruction of two-thirds or more of the duct wall requires hepaticojejunostomy.
MRCP is the study of choice in suspected Mirizzi because it shows the stone, duct compression, and any fistula without instrumenting, and dense inflammation at Calot's triangle mandates open conversion with intraoperative cholangiography.
Mucosal, incomplete, or focal porcelain gallbladder calcification remains an indication for prophylactic cholecystectomy, while complete circumferential transmural calcification can be observed in selected high-risk surgical patients.
Gallstone ileus is managed with enterotomy and stone extraction, and a staged approach that defers fistula takedown lowers perioperative mortality in elderly comorbid patients; Bouveret syndrome is treated first-line with endoscopic lithotripsy because the duodenal stone is within endoscopic reach.
Gallbladder polyps at or above ten millimeters warrant cholecystectomy regardless of other features, and six-to-nine-millimeter polyps warrant surgery if any risk factor is present, with documented growth of two millimeters or more the highest-yield malignancy signal.
Primary sclerosing cholangitis drops the polyp threshold so that any polyp, or one at eight millimeters, warrants cholecystectomy, with annual ultrasound surveillance.
Functional gallbladder disorder demands strict selection: fully met biliary pain criteria, structural disease excluded, functional GI disease optimized first, and explicit counseling that even low-ejection-fraction patients improve only about sixty percent of the time.

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

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Chapter 27, Ep 3 of 4: Duct Stones and Acute Cholangitis

Board Pearls — Thu, 16 Jul 2026 08:07:04 -0500

Episode three takes the stone into the bile duct, and the whole problem sits on a probability question, because ERCP carries its own complication profile, headlined by post-ERCP pancreatitis. You earn the right to do an ERCP by raising the pretest probability of a retrievable stone high enough to justify the procedural risk, so high-probability patients go straight to ERCP while intermediate patients confirm the stone first with MRCP or endoscopic ultrasound. When the same stone turns septic, cholangitis runs on a hydraulic mechanism: the obstruction raises intraductal pressure and refluxes bacteria into the blood, which is why antibiotics alone cannot fix it and decompression is mandatory. The Tokyo grade scales the timing, and clinical improvement on antibiotics is never mistaken for a relieved obstruction.

Topics covered

Post-ERCP pancreatitis and the probability tiers
High, intermediate, and low probability features
MRCP versus endoscopic ultrasound
Large stones and post-cholecystectomy stones
Cholangitis and the hydraulic mechanism
Charcot triad and Reynolds pentad
Tokyo grading and decompression timing
Empiric antibiotics and rescue drainage

Key decisions

High-probability duct stone requires any one of a stone seen on imaging, ascending cholangitis, or a bilirubin over four with a duct dilated above six millimeters, and any one of those sends the patient straight to ERCP.
Intermediate-probability patients should not go straight to ERCP; confirm or refute the stone first with MRCP, or endoscopic ultrasound when small stones or sludge are suspected.
MRCP misses stones under six millimeters while endoscopic ultrasound catches sludge and microlithiasis, so small-stone disease favors EUS and an anatomic duct survey favors MRCP.
Stones a centimeter or larger exceed what a conventional sphincterotomy can extract, so first-line therapy is sphincterotomy plus large-balloon dilation, with cholangioscopy-directed lithotripsy as the alternative.
In cholangitis, decompression is the central intervention because antibiotics only suppress bacteremia while the closed obstructed duct keeps reseeding.
Tokyo severe cholangitis with any organ dysfunction needs biliary decompression within twenty-four hours, moderate disease needs ERCP within forty-eight hours, and ERCP within forty-eight hours reduces mortality across all three grades.
Empiric antibiotics target enteric gram-negatives and anaerobes with a third-generation cephalosporin plus metronidazole, piperacillin-tazobactam, or a carbapenem in healthcare-associated or immunocompromised patients.

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

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Chapter 27, Ep 4 of 4: Cysts, Leaks, Strictures, and Sphincter Dysfunction

Board Pearls — Thu, 16 Jul 2026 08:07:44 -0500

Episode four turns to the duct that is structurally abnormal from birth or made abnormal by an operation, where the recurring move is to read the anatomy and let it dictate whether an endoscopic fix can work at all. Choledochal cysts drive cholangiocarcinoma through decades of epithelial exposure to refluxed enzymes, and the Todani type dictates the operation, with complete excision the rule and the choledochocele the low-risk exception. Bile leak and stricture are the iatrogenic version, where the Strasberg level decides whether endoscopic stenting can bridge the injury at all, so a cystic-stump leak seals with a stent while a complete transection needs hepaticojejunostomy. Sphincter of Oddi dysfunction divides into a true stenosis that sphincterotomy cures, a functional pain that a procedure only harms, and a heterogeneous middle where empiric sphincterotomy beats a manometry-driven workup.

Topics covered

Choledochal cysts and the Todani classification
Cholangiocarcinoma risk and cyst anatomy
Cyst excision and hepaticojejunostomy
Pancreaticobiliary maljunction
Caroli disease and syndrome
Bile leaks and the Strasberg classification
Type E transection and reconstruction
Post-cholecystectomy strictures
Sphincter of Oddi dysfunction reclassified

Key decisions

Todani type one, two, and four choledochal cysts need complete cyst excision, cholecystectomy, and a Roux-en-Y hepaticojejunostomy, because a Whipple leaves proximal cyst epithelium and its cancer risk in place.
The choledochocele is the exception, where the intraduodenal location and very low malignancy risk make endoscopic sphincterotomy or limited excision sufficient.
Whenever pancreaticobiliary maljunction is found, prophylactic cholecystectomy is part of the operation cyst or no cyst, because in maljunction without cysts gallbladder cancer develops in about a third of patients.
After cyst excision, current guidance recommends lifelong MRCP every three to five years to surveil retained at-risk epithelium that can still progress to cholangiocarcinoma.
Strasberg type A cystic-stump leaks seal in most cases with endoscopic sphincterotomy plus a transpapillary stent within four to six weeks, and type C and D injuries with luminal continuity can also be stented.
Strasberg type E complete transection has no continuity for a stent to reach and requires surgical Roux-en-Y hepaticojejunostomy, with the Bismuth level predicting complexity.
The former SOD type one is true mechanical stenosis treated with empiric biliary sphincterotomy without manometry, the former type three is functional pain that should not undergo ERCP, and suspected sphincter dysfunction demands aggressive prophylaxis with rectal indomethacin, lactated Ringer's, and a pancreatic duct stent.

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

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Chapter 29, Ep 1 of 7: Safe Cannulation and PEP Prophylaxis

Board Pearls — Thu, 16 Jul 2026 08:08:05 -0500

Episode one of the ERCP and EUS Procedures chapter starts from the single fact that reorganizes everything: ERCP is a therapy, not a test, so you earn the right to do it only when a non-invasive study cannot answer the question. From there the whole episode is risk management. Wire-guided cannulation replaces the hydraulic contrast push that floods the pancreatic duct, difficult-cannulation maneuvers each solve one anatomic problem, and the prophylaxis stack is held by mechanism because the mechanisms tell you who needs which. The organizing thread: find the duct by guidance, then stack indomethacin, a pancreatic duct stent, and lactated Ringer on the patient whose risk factors say the pancreas will react.

Topics covered

ERCP as therapy, not a diagnostic test
Post-ERCP pancreatitis risk and mechanism
Wire-guided versus contrast-first cannulation
Difficult-cannulation escalation and EUS rendezvous
Rectal indomethacin prophylaxis
Prophylactic pancreatic duct stent
Aggressive lactated Ringer hydration
High-risk patient profile and protective chronic pancreatitis

Key decisions

Reserve ERCP for therapeutic intent (stone extraction, stricture stenting, cholangitis decompression, leak repair); if you only need to image the ducts, order MRCP or EUS, which carry no pancreatitis risk.
Use wire-guided cannulation rather than contrast-first, because threading a soft hydrophilic guidewire avoids the hydraulic acinarization injury that flooding the pancreatic duct with contrast produces.
Give rectal indomethacin one hundred milligrams before every native-papilla ERCP, timed pre-procedure so the drug is therapeutic at the moment of cannulation.
In high-risk patients keep the prophylactic pancreatic duct stent on top of indomethacin, not instead of it, since indomethacin alone was not non-inferior to indomethacin plus a stent.
Run lactated Ringer at three milliliters per kilogram per hour during the procedure, a twenty milliliter per kilogram bolus immediately after, then three milliliters per kilogram per hour for eight hours, chosen over saline because lactate buffers acidosis.
Concentrate the full stack on high-risk patients (suspected sphincter of Oddi dysfunction, prior PEP, female sex, normal bilirubin, difficult cannulation, acinarization), remembering a normal bilirubin raises risk and burnt-out chronic pancreatitis runs it backwards.
Do not use octreotide, gabexate, or intravenous secretin; they sound plausible but do not reduce post-ERCP pancreatitis.

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

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Chapter 29, Ep 2 of 7: Patient Selection and Complications

Board Pearls — Thu, 16 Jul 2026 08:08:23 -0500

Episode two is about the decision that comes before cannulation and the restraint it takes to decline the procedure when objective evidence for benefit is absent. A landmark sham-controlled trial retired type three sphincter of Oddi dysfunction as a sphincterotomy indication, so pain with normal labs and a normal duct becomes a functional pain disorder, not an ERCP. Pregnancy raises the threshold highest because a second patient absorbs all the risk and none of the benefit. The back half turns on two failure mechanisms, the cut that bleeds and the elevator that harbors biofilm, and each names the patient to protect and the device choice that protects them.

Topics covered

Sphincter of Oddi dysfunction types and the landmark trial
Post-cholecystectomy duct dilation as physiologic compensation
ERCP in pregnancy and radiation minimization
Sedation and positioning in pregnancy
Post-sphincterotomy bleeding risk factors
Balloon dilation versus sphincterotomy in coagulopathy
Perforation and the Stapfer classification
Duodenoscope biofilm and single-use scopes

Key decisions

Do not offer sphincterotomy for type three sphincter of Oddi dysfunction (pain with normal enzymes and a non-dilated duct); a sham did at least as well, so manage it as a functional pain disorder with neuromodulators and behavioral therapy.
Treat type one dysfunction (pain, elevated enzymes, dilated duct) with biliary sphincterotomy without manometry, and treat type two as shared decision-making with mandatory indomethacin, lactated Ringer, and a pancreatic duct stent since manometry is the highest-PEP procedure.
Read a ten to twelve millimeter duct in a post-cholecystectomy patient with normal enzymes as physiologic compensation, not sphincter dysfunction, so it alone does not justify ERCP.
In pregnancy avoid diagnostic ERCP entirely: use non-contrast MRCP or EUS, shield the uterus, run pulsed fluoroscopy at four to eight pulses per second aiming under one minute, prefer the second trimester, and keep fetal dose under the fifty milligray threshold.
Prefer propofol for sedation in pregnancy, accept moderate-dose fentanyl, avoid midazolam especially in the first trimester, and position the patient left-lateral to avoid aortocaval compression.
In cirrhosis or coagulopathy choose endoscopic papillary balloon dilation over full sphincterotomy for stone extraction, trading the cut for a stretch to avoid a bleeding bed the mucosa cannot control.
Prevent duodenoscope-transmitted infection with disposable elevator caps or single-use duodenoscopes rather than double high-level disinfection or ethylene oxide, which add no benefit because they cannot reach the elevator interior.

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

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Chapter 29, Ep 3 of 7: The Obstructed and Indeterminate Biliary Tree

Board Pearls — Thu, 16 Jul 2026 08:08:42 -0500

Episode three centers on the stricture you cannot name: painless jaundice, a tight narrowing, and imaging that says cancer without proving it. Tissue acquisition is the whole game, and every step up the diagnostic cascade works by getting closer to the tumor, from a shallow brush that misses submucosal cholangiocarcinoma to intraductal biopsy and FISH to cholangioscopy to an EUS needle in the mass itself. The transplant candidate inverts that hierarchy, because a needle in the hilar primary can seed the peritoneum and disqualify the cure. Then durable drainage follows anatomy: covered metal distally to block ingrowth, uncovered metal at the hilum to preserve side branches, and always enough viable liver drained to clear the bilirubin.

Topics covered

Brush cytology and why it misses cholangiocarcinoma
Intraductal biopsy, FISH, and cholangioscopy
EUS fine needle biopsy of a pancreatic head mass
Transplant candidate and needle-tract seeding
Endoscopic ampullectomy versus Whipple
Distal covered metal stents
Hilar uncovered metal stents and side branches
Draining fifty percent of viable liver

Key decisions

Do not trust a negative brush cytology in a malignant-looking stricture; stack intraductal forceps biopsy and FISH for polysomy, then cholangioscopy with targeted biopsy, because each step samples deeper than superficial shed cells.
For a pancreatic head mass needing tissue before neoadjuvant chemotherapy, use EUS-guided fine needle biopsy of the mass itself, favoring a biopsy needle over aspiration when you need core architecture and immunohistochemistry.
In a transplant candidate never needle the hilar primary by EUS or percutaneous route; stay inside the duct with brush and intraductal biopsy, and biopsy suspicious regional nodes only as a transplant-eligibility test.
Resect an ampullary adenoma en bloc for lesions up to two to three centimeters after EUS excludes intraductal extension, accepting a ten to fifteen percent pancreatitis rate to spare the patient a Whipple.
Place a prophylactic five French pancreatic duct stent after ampullectomy, skip the submucosal lift, and survey the resection bed at three and six months with a side-viewing duodenoscope in FAP.
Use a fully covered self-expanding metal stent for distal malignant obstruction to block tumor ingrowth and allow removal at the Whipple, reserving plastic stents for a life expectancy under three months.
At the hilum use an uncovered metal stent so side-branch bile flows through the mesh, map viable territories with MRCP, and drain at least fifty percent of viable liver while avoiding atrophic segments.

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

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Chapter 29, Ep 4 of 7: When Standard ERCP Fails

Board Pearls — Thu, 16 Jul 2026 08:09:01 -0500

Episode four picks up the moment standard ERCP fails, and it runs on a single habit: name the anatomic barrier and let it choose the technique. When you cannot cannulate the papilla, a dilated duct becomes an EUS target, and the finishing options rank by how much natural drainage they keep, rendezvous over choledochoduodenostomy over hepaticogastrostomy. When surgery has hidden the papilla, the question is how to restore the duodenoscope's en face view through the particular barrier, so EDGE tunnels into the bypassed stomach, balloon enteroscopy reaches a hepaticojejunostomy, and a reversed cautious approach handles Billroth two. Device design and technique are consequences of the anatomy, not lists to memorize.

Topics covered

EUS-guided biliary drainage and the dilated-duct target
EUS-guided rendezvous
Choledochoduodenostomy with a LAMS
Hepaticogastrostomy and anti-migration stents
Roux-en-Y gastric bypass and the EDGE procedure
Balloon enteroscopy for hepaticojejunostomy
Billroth two and the reversed sphincterotomy
En face access as the organizing principle

Key decisions

Reserve EUS-guided biliary drainage for obstruction with upstream dilation, because a dilated duct is the only target you can puncture; a normal-caliber duct offers nothing to aim at.
Choose EUS-guided rendezvous first whenever the papilla is reachable, since advancing a wire across the papilla for a duodenoscope preserves natural drainage and leaves no permanent fistula.
Use choledochoduodenostomy with a lumen-apposing metal stent when the papilla is unreachable but the extrahepatic duct sits within a centimeter of the duodenal bulb with no intervening vessels on Doppler.
Fall back to hepaticogastrostomy with a partially covered stent (covered tract segment, uncovered intraductal segment) only when neither the papilla nor the extrahepatic duct is available and a dilated left intrahepatic duct remains.
Prefer the EDGE procedure over balloon enteroscopy in Roux-en-Y gastric bypass, then remove the LAMS and close the fistula at the end of biliary therapy to prevent weight regain.
Reach a Roux-en-Y hepaticojejunostomy anastomosis with balloon-assisted enteroscopy, using percutaneous transhepatic cholangiography or EUS-guided hepaticogastrostomy as fallbacks.
In Billroth two anatomy prefer a forward-viewing endoscope up the afferent limb given the five to eight percent perforation risk, and cut the sphincterotomy in the reversed direction, ideally a needle-knife over a placed stent.

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

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Chapter 29, Ep 5 of 7: Recurrent Pancreatitis and Duct Decompression

Board Pearls — Thu, 16 Jul 2026 08:09:15 -0500

Episode five holds EUS and ERCP to one standard in the pancreatitis spectrum: they earn their place only when there is structural disease or stone burden to act on, because every procedure carries a real pancreatitis risk weighed against a modest expected benefit. In the recurrent-attack workup, EUS for microlithiasis is the highest-yield study after MRCP, while sphincterotomy for divisum and idiopathic disease is the reflex sham-controlled data have humbled. In the chronic gland you decompress discrete obstructive lesions and read the true predictors of success, disease duration, cessation, and stone burden rather than head calcification. Standing over all of it, a randomized trial favors early surgical drainage for the painful dilated duct.

Topics covered

EUS and ERCP earn their place only with structural disease
Idiopathic recurrent acute pancreatitis workup
EUS for microlithiasis
Sphincter of Oddi manometry caution
Pancreas divisum and the sham-controlled trial
Chronic dilated duct and predictors of success
ESWL and pancreatic duct stone fragmentation
Dominant stricture stenting and surgery versus endoscopy

Key decisions

Work up idiopathic recurrent acute pancreatitis with history, calcium and triglycerides, MRCP, and IgG4 serologies, then EUS as the highest-yield test because it resolves microlithiasis that surface ultrasound misses.
Do not reflexively perform ERCP with manometry after a negative workup; biliary sphincterotomy helps only about half the time even with elevated pressures, so reserve it for documented multiple recurrences with full prophylaxis.
Do not offer routine minor papilla sphincterotomy for recurrent pancreatitis in pancreas divisum, since a sham-controlled trial showed no benefit and the tiny minor papilla carries higher post-procedure pancreatitis risk.
Predict chronic-pancreatitis endotherapy success from short disease duration, smoking and alcohol cessation, limited stone burden, and achievable complete clearance, not from the presence or absence of head calcification.
Fragment pancreatic duct stones larger than five millimeters with extracorporeal shock-wave lithotripsy first (about seventy percent clearance), escalating to pancreatoscopy with electrohydraulic or laser lithotripsy and avoiding mechanical baskets that can impact.
Manage a dominant pancreatic duct stricture with a single largest-feasible plastic stent (typically ten French) for about twelve uninterrupted months, reserving multiple side-by-side stents for refractory strictures.
Favor early surgical drainage with a longitudinal pancreaticojejunostomy over an endoscopy-first strategy in dilated-duct chronic pancreatitis with intractable pain, per the randomized trial.

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

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Chapter 29, Ep 6 of 7: Fluid Collections and Necrosectomy

Board Pearls — Thu, 16 Jul 2026 08:09:32 -0500

Episode six takes the pancreatitis spectrum to its end: the collections the gland leaves behind. Timing runs on wall-maturation logic, waiting about four weeks for a rind strong enough to hold a transmural anastomosis, and the contents decide everything downstream, since a pseudocyst and walled-off necrosis need different stents and different follow-through. Before any puncture you image for a pseudoaneurysm and embolize it first, because needling a shared wall can cause uncontrolled hemorrhage. Drainage is a step-up, transmural first and necrosectomy only when the cavity will not empty, and two failure modes both turn on sequence. Necrosectomy itself carries one non-negotiable safety rule: carbon dioxide insufflation, because air can embolize.

Topics covered

Four-week wall maturation and drainage timing
Pseudocyst versus walled-off necrosis
Pseudoaneurysm check before puncture
Step-up drainage and stent caliber
LAMS dwell time and complications
LAMS occlusion and tract bleeding failure modes
Cyst fluid analysis parallel
Direct endoscopic necrosectomy and the carbon dioxide rule

Key decisions

Wait about four weeks before draining a symptomatic collection so the inflammatory rind matures into a wall strong enough to hold a transmural anastomosis without leaking.
Review the CT angiogram for a pseudoaneurysm before puncturing; when present, have interventional radiology embolize it first, because needling into or near it can cause uncontrolled hemorrhage.
Match stent caliber to contents: a ten millimeter LAMS or double-pigtail plastic stents for thin pseudocyst fluid, and a fifteen or twenty millimeter LAMS for walled-off necrosis so the endoscope can pass for necrosectomy.
Drain transmurally first and escalate to necrosectomy only when the response is inadequate (persistent fever, leukocytosis, or solid debris), because the endoscopic route avoids the peritoneal wound complications of surgery.
For a bleeding LAMS tract, embolize the pseudoaneurysm before removing the stent, since the LAMS may be tamponading the source; for an occluded LAMS, clear it and place double-pigtail plastic stents through it.
Analyze an indeterminate tail cyst by EUS-guided aspiration: CEA above one hundred ninety-two or glucose below fifty favors mucinous, while high amylase indicates ductal communication.
Use mandatory carbon dioxide insufflation and avoid forceful flushing during necrosectomy, because air can enter venous or peritoneal communications and cause air embolism, and debride a portion at a time across two to four sessions.

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

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Chapter 29, Ep 7 of 7: EUS Beyond the Ducts

Board Pearls — Thu, 16 Jul 2026 08:10:01 -0500

The final episode turns EUS from a guide for therapy into a diagnostician and a palliator, and it runs on one habit: reason from substrate to answer. The five alternating wall layers plus echotexture place a subepithelial lesion and narrow the differential before a needle moves, so a hypoechoic layer-four mass is a GIST until tissue proves otherwise. The needle choice then turns on a single distinction, cells versus architecture, because lymphoma, GIST, and autoimmune pancreatitis all live in structure a core preserves and cytology destroys. Finally the same probe that finds the tumor treats its pain: alcohol neurolysis for cancer, a reversible steroid block for benign disease, with complications that read straight off the interrupted sympathetic outflow.

Topics covered

The five EUS gut-wall layers
Layer-four GIST versus leiomyoma
Size threshold for sampling muscularis lesions
Other layers by echotexture
Fine needle aspiration versus biopsy
Rapid on-site evaluation and cyst fluid
Celiac plexus neurolysis for cancer pain
Neurolysis versus reversible block in benign disease
Complications from interrupted sympathetic outflow

Key decisions

Place a subepithelial lesion by its wall layer and echotexture: a hypoechoic homogeneous mass arising from layer four, the muscularis propria, is a GIST until proven otherwise.
Do not call a layer-four hypoechoic mass a leiomyoma on imaging, because GIST (CD117 and DOG1 positive) and leiomyoma (desmin and smooth muscle actin positive) are indistinguishable sonographically and separate only on immunohistochemistry.
Obtain tissue for any muscularis-propria lesion two centimeters or larger, since within layer four increasing size correlates with malignant behavior.
Choose the needle by whether the diagnosis lives in cells or architecture: cytology suffices for pancreatic adenocarcinoma, but lymphoma, GIST, and autoimmune pancreatitis need a fine needle biopsy core, which also largely obviates rapid on-site evaluation.
Read pancreatic cyst fluid against the epithelium: CEA above one hundred ninety-two or glucose below fifty favors a mucinous cyst, while high amylase points to ductal communication.
Perform celiac plexus neurolysis with absolute alcohol plus bupivacaine for unresectable pancreatic cancer pain, targeting visible ganglia directly when you can see them for better analgesia.
For benign chronic pancreatitis pain use a reversible celiac plexus block with bupivacaine and a corticosteroid, not alcohol neurolysis, because the nerve regenerates and irreversible destruction risks lasting deafferentation.

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Chapter 28, Ep 1 of 4: Fasting and Periprocedural Antithrombotics

Board Pearls — Thu, 16 Jul 2026 08:10:13 -0500

Episode one of the Endoscopy Practice and Sedation chapter frames the morning of the procedure around two preventable disasters: aspiration and thromboembolism. The organizing idea is that fasting intervals are gastric-emptying kinetics on a clock, and every anticoagulant decision sits at the intersection of procedure bleeding risk and patient thromboembolic risk. That grid tells you who holds, who continues, and who bridges. A single asymmetry runs the antiplatelet decisions: an unrecognized stent thrombosis dwarfs endoscopically manageable bleeding, which is why aspirin usually stays on. Reversal closes the loop, each agent matched to its target.

Topics covered

Fasting intervals and delayed-emptying exceptions
GLP-1 receptor agonists and aspiration risk
Procedure bleeding risk versus patient thromboembolic risk
Warfarin holds and morning-of INR
DOAC holds scaled to half-life and kidney function
The narrowing of bridging
Antiplatelet management after coronary stenting
Reversal agents in active bleeding

Key decisions

Follow the two-two-six-eight fasting rule for all sedation depths: clear liquids to two hours, breast milk to four, formula or a light meal to six, a fatty or heavy meal to eight.
For elevated-risk GLP-1 patients (active GI symptoms, dose escalation, weekly dosing), give a clear liquid diet for at least twenty-four hours before the procedure while continuing the drug, rather than a reflex hold.
Hold warfarin five days before a high-bleeding-risk procedure and confirm an INR below one and a half the morning of, because prothrombin's roughly sixty-hour half-life is the rate-limiting factor.
Hold apixaban and rivaroxaban one to two days for low-risk and two to three days for high-risk procedures; extend dabigatran holds as creatinine clearance falls since it is renally cleared.
Reserve bridging for high-thromboembolic-risk patients only (mechanical mitral valve, recent stroke or TIA, prior clot on warfarin, recent VTE, severe thrombophilia), because trials showed no benefit and excess bleeding in lower strata.
Defer elective procedures for thirty days after a bare-metal stent and six months after a drug-eluting stent, continuing aspirin throughout and using cangrelor as a true bridge when a procedure must proceed early.
Reverse life-threatening warfarin bleeding with four-factor PCC plus vitamin K, dabigatran with idarucizumab or dialysis, and factor Xa inhibitors now with four-factor PCC since the decoy agent left the US market.

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

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Chapter 28, Ep 2 of 4: Sedation Depth and Agents

Board Pearls — Thu, 16 Jul 2026 08:10:25 -0500

Episode two frames procedural sedation around one trade: the depth you want versus the depth your team can rescue from. The ASA continuum sets the rescue rule, the practitioner must be able to manage a patient one level deeper than intended, and ASA physical status predicts who tolerates endoscopist-supervised moderate sedation versus who needs anesthesia. Midazolam and fentanyl carry the easy case at the cost of multiplicative respiratory depression; propofol buys fast onset and offset for the complex case at the cost of no antagonist. The alternative agents each solve one problem the standard pair cannot.

Topics covered

The intended-versus-rescuable depth trade
ASA sedation continuum and the rescue rule
ASA physical status classification
Midazolam plus fentanyl pharmacology and dosing
Multiplicative benzodiazepine-opioid respiratory depression
Propofol kinetics and staffing implications
Etomidate, ketamine, and dexmedetomidine

Key decisions

Qualify to rescue one level deeper than the intended target, because a moderate-sedation plan reliably drifts into deep sedation in a subset of patients.
Carry ASA class one and two patients with endoscopist-supervised midazolam and fentanyl for routine EGD and colonoscopy, and involve anesthesia for class three and above.
Titrate midazolam in one milligram increments (0.5 to 2 mg initial) every two to five minutes and fentanyl in twenty-five to fifty microgram increments, waiting for peak effect at three to five minutes before redosing.
Choose propofol for long, complex, ASA three-plus, or high-aspiration-risk cases, with airway-trained personnel immediately available because it has no antagonist and produces predictable apnea.
Pick etomidate (0.1 to 0.2 mg/kg) for the hemodynamically unstable patient such as active hemorrhage with severe aortic stenosis, accepting six to twenty-four hours of adrenal suppression and avoiding it in sepsis.
Reach for ketamine when propofol-induced apnea is unacceptable or IV access is absent, and for dexmedetomidine when airway maintenance is critical in severe OSA or achalasia.

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

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Chapter 28, Ep 3 of 4: Sedation Monitoring and Special Populations

Board Pearls — Thu, 16 Jul 2026 08:10:42 -0500

Episode three covers the monitoring, prediction, and rescue that catch the patient when the drug carries them past the intended depth. Capnography detects apnea within one to two breaths while pulse oximetry lags on supplemental oxygen, so a flat waveform with a reassuring saturation is apnea. Mallampati and the airway predictors decide whether the standard plan is safe before the first dose, and flumazenil and naloxone reverse the agents but wear off faster than what they reverse. The special populations are not exceptions, they are the same framework run through a shifted pharmacokinetic and aspiration-risk profile.

Topics covered

Capnography versus pulse oximetry lag
Mallampati and difficult-airway predictors
Aspiration risk and rapid sequence induction
Flumazenil and naloxone reversal
Cirrhosis and altered sedative handling
Elderly dose reduction
Obstructive sleep apnea and STOP-BANG
Pregnancy agent selection
Updated GLP-1 periprocedural guidance

Key decisions

Use capnography as the standard at moderate and deep sedation, because a flat waveform with a saturation of ninety-eight on nasal cannula is an apneic patient, not a stable one.
Obtain anesthesia consultation before deep sedation for Mallampati three or four, thyromental distance under six centimeters, limited cervical mobility, or BMI above thirty-five.
Dose flumazenil at 0.2 mg IV every minute to a cumulative 1 mg (avoiding it in chronic benzodiazepine use, seizure disorder, or TCA co-ingestion) and titrate naloxone to respiratory rate, monitoring hours past reversal since both outlast their doses.
Halve the midazolam dose and lengthen titration in cirrhosis, shifting toward propofol delivered by anesthesia, and avoid benzodiazepines entirely in the Child B patient with prior overt encephalopathy.
Reduce all sedation agents by twenty-five to fifty percent in patients over sixty-five with longer intervals between boluses, and screen with STOP-BANG to flag undiagnosed OSA that changes the plan.
Manage pregnancy beyond the first trimester with full-stomach precautions and left-lateral positioning, choosing propofol (category B) while avoiding midazolam (category D) and ketamine for uterine hypertonus.
For elevated-risk GLP-1 patients give twenty-four hours of clear liquids on the drug, and never delay time-sensitive endoscopy for GLP-1 management, planning the airway aggressively instead.

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

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Chapter 28, Ep 4 of 4: Antibiotics, Devices, Capsule, and Adverse Events

Board Pearls — Thu, 16 Jul 2026 08:11:42 -0500

Episode four closes the chapter on four topics that each test one recognition: when the reflexive answer is wrong because the underlying principle has shifted. Antibiotic prophylaxis turns on closed-space infection, not the prosthetic device, so the 2007 AHA guideline took GI endoscopy off the endocarditis list. Cardiac device management turns on electromagnetic interference, so modern pacemakers tolerate routine polypectomy without reprogramming while ICDs need arrhythmia detection suspended. Capsule endoscopy lives or dies on retention risk addressed by the patency capsule, and the ASGE Cotton lexicon grades adverse events by intensity of intervention.

Topics covered

Endocarditis prophylaxis off the GI list
The closed-space infection principle
Incomplete ERCP drainage and cyst FNA prophylaxis
Pacemakers and monopolar electrosurgery
ICDs and arrhythmia detection
Capsule endoscopy retention
The patency capsule workup
The ASGE Cotton adverse event lexicon

Key decisions

Give no endocarditis prophylaxis for GI endoscopy, including prosthetic valves, pacemakers, ICDs, prosthetic joints, and vascular grafts, because the transient bacteremia risk is too low to justify antibiotics.
Reserve prophylaxis for closed-space scenarios: incomplete biliary drainage at ERCP, EUS-FNA of cystic lesions, PEG or PEJ placement with a single dose of cefazolin, cirrhotic UGI bleeding with ceftriaxone, and PD-patient lower endoscopy.
Withhold prophylaxis for solid-lesion EUS-FNA, diagnostic EGD and colonoscopy, and non-bleeding variceal band ligation, because none creates a closed space the immune system cannot clear.
Do not reprogram pacemakers for routine polypectomy; place the grounding pad away from the heart on the thigh or lower back, and add backup pacing only for the pacemaker-dependent patient in the cardiac field.
Suspend ICD arrhythmia detection with a magnet or formal reprogramming during electrosurgery, leaving the pacing function untouched and placing external defibrillator pads as backup.
Define capsule retention as failure to pass within two weeks (about one to two percent baseline, five to thirteen percent with strictures) and screen with the patency capsule when Crohn or prior surgery raises stricture risk.
Grade adverse events by intervention intensity on the ASGE Cotton lexicon: mild (under three nights, no transfusion), moderate (four to ten nights or transfusion or repeat endoscopy), severe (over ten nights, surgery, or disability), and fatal (death within thirty days).

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Chapter 30, Ep 1 of 5: Screening, Prep, and Detection Metrics

Board Pearls — Thu, 16 Jul 2026 08:13:14 -0500

Episode one of the Colonoscopy Practice and Quality chapter treats screening colonoscopy as a chain of dependencies where the weakest link governs the outcome. The organizing idea: colorectal cancer has a long precursor and a survivable early stage, so everything from the starting age to the withdrawal time exists to make prevention real rather than nominal. It walks the modality menu with the rule that any positive non-invasive test commits the patient to colonoscopy, then the split-dose preparation physiology that delivers a clean right colon. It closes on the detection metrics, adenoma detection rate as the single most validated quality measure and sessile serrated lesion detection rate as its complement on the serrated pathway.

Topics covered

Colorectal cancer screening rationale
USPSTF age forty-five and the upper bound
High-risk starting ages and intervals
The screening modality menu
Split-dose bowel preparation physiology
Boston Bowel Preparation Scale adequacy
Cecal intubation rate and withdrawal time
Adenoma detection rate
Sessile serrated lesion detection and technology

Key decisions

Average-risk screening starts at age forty-five, runs routinely through seventy-five, is individualized from seventy-six to eighty-five, and is generally not offered after eighty-five because lead time exceeds residual life expectancy.
Any positive non-invasive test, whether FIT, multi-target stool DNA, CT colonography, or Shield, is an indication for diagnostic colonoscopy, and repeating or switching the stool test is not a path back to safety.
Split-dose preparation with the second dose finished four to eight hours before the procedure is superior to single-dose evening prep, and PEG-electrolyte is the non-fermentable standard when polypectomy is anticipated because fermentable mannitol risks hydrogen-gas explosion under electrocautery.
Adequate preparation requires a Boston Bowel Preparation Scale total at or above six with no individual segment below two, and inadequate prep brings the patient back within one year rather than continuing standard surveillance.
Cecal intubation rate should be at or above ninety-five percent for screening with photo documentation of the appendiceal orifice and ileocecal valve, and withdrawal time should be at least six minutes diagnostic and eight to nine minutes for a negative screening exam.
Adenoma detection rate is benchmarked around thirty to thirty-five percent in mixed screening populations, with each one percent absolute increase associated with roughly a three percent decrease in interval cancer risk.
Minimum acceptable sessile serrated lesion detection rate is approximately six to seven percent, and any proximal hyperplastic polyp ten millimeters or larger is treated as a sessile serrated lesion for surveillance.

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Chapter 30, Ep 2 of 5: Polyp Recognition and Resection Technique

Board Pearls — Thu, 16 Jul 2026 08:14:05 -0500

Episode two frames polyp management as a reading task that begins before the snare opens: has the lesion grown horizontally along the mucosa or vertically into the submucosa, because vertical growth is what carries cancer risk. Paris morphology, the NICE and JNET optical patterns, Kudo pit pattern, and the lateral spreading granularity types are all ways of reading that same growth signal, and depressed or pseudodepressed surfaces are what deep submucosal invasion looks like from above. The optical read then dictates the resection plan. Cold snare wins on safety for diminutive and small lesions, hot snare is reserved for the vascularized pedunculated stalk, EMR is standard for larger sessile and lateral spreading lesions, and en bloc resection by ESD or band-ligation is reserved for when specimen integrity is needed for staging.

Topics covered

Horizontal versus vertical polyp growth
Paris morphology classification
NICE and JNET optical prediction
Kudo pit pattern
Lateral spreading lesion granularity types
Cold snare and hot snare selection
Endoscopic mucosal resection and the non-lifting sign
Underwater EMR and margin ablation
ESD and Japanese curative criteria

Key decisions

Depressed Paris zero-two-c and mixed zero-two-a-plus-c lesions carry disproportionately high submucosal invasion rates and go to en bloc resection or surgical referral, not piecemeal EMR.
A NICE one or JNET one lesion can be confidently treated with cold-snare polypectomy, while a NICE three or JNET three lesion is a staging problem rather than an endoscopic one.
Cold snare polypectomy is preferred for diminutive polyps and standard for four to ten millimeter polyps because pure mechanical transection avoids thermal injury, dropping delayed bleeding and electrocoagulation syndrome.
Hot snare is reserved for pedunculated polyps over ten millimeters with a defined feeding artery, and thick stalks warrant a prophylactic clip or detachable loop before transection.
For sessile and lateral spreading lesions ten millimeters or larger without high-risk features, submucosal-injection EMR is standard, and a non-lifting sign means biopsy and referral for surgery or ESD.
Snare-tip soft coagulation of the EMR margin gives roughly a four-fold reduction in adenoma recurrence at first surveillance by killing microscopic adenomatous nests at the resection edge.
Japanese ESD curative criteria require en bloc removal with negative vertical and lateral margins, well or moderate differentiation, no lymphovascular invasion, and intramucosal or submucosal invasion under one thousand microns, which drops nodal risk below one percent.

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Chapter 30, Ep 3 of 5: The Malignant Polyp and Surveillance

Board Pearls — Thu, 16 Jul 2026 08:14:12 -0500

Episode three resolves the malignant polyp on one anatomic fact: lymphatics in the colon begin at the muscularis mucosae, so disease confined above it cannot metastasize while submucosal invasion opens the door to nodal spread. Intramucosal adenocarcinoma behaves as high-grade dysplasia and is cured by complete resection, which is why the word on the path report pulls toward unnecessary surgery. The Kikuchi and Haggitt systems describe depth, but the modern algorithm aggregates depth with tumor budding, differentiation, lymphovascular invasion, and margin status rather than acting on depth alone. Surveillance then calibrates the next exam to the worst lesion found, with the shortest interval winning when findings conflict and a separate six-month site check for piecemeal EMR of lesions twenty millimeters or larger.

Topics covered

Muscularis mucosae and metastatic potential
Intramucosal adenocarcinoma versus true cancer
Kikuchi and Haggitt depth systems
Aggregating high-risk histologic features
Tumor budding by ITBCC criteria
USMSTF twenty twenty surveillance intervals
Serrated surveillance intervals
Piecemeal EMR site surveillance

Key decisions

Intramucosal adenocarcinoma is confined above the muscularis mucosae and behaves as high-grade dysplasia, so complete endoscopic resection is curative and surgery is unnecessary morbidity.
Deep submucosal invasion alone, meaning Kikuchi sm three, Haggitt level four, or over one thousand microns, without other adverse features carries only about two and a half percent nodal risk, which can spare surgery in poor operative candidates.
Four high-risk features drive surgical referral regardless of invasion depth: poor differentiation, lymphovascular invasion, high-grade tumor budding, and a positive margin under one millimeter.
High-grade tumor budding by ITBCC is ten or more buds in a zero point seven eight five square millimeter hotspot, defined as single cells or clusters of up to four cells at the invasive front, and pushes the decision toward surgery.
The three-year interval is the default short interval, triggered by any single high-risk feature such as five to ten adenomas, an adenoma ten millimeters or larger, villous histology, high-grade dysplasia, or a large or dysplastic sessile serrated lesion.
More than ten adenomas at the index exam triggers one-year follow-up and evaluation for a hereditary syndrome, and when findings conflict the shortest interval always applies.
Piecemeal EMR of any lesion twenty millimeters or larger gets a site check at six months, then one year, then resumption of standard intervals, because local recurrence runs fifteen to twenty percent without margin ablation.

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Chapter 30, Ep 4 of 5: Post-Polypectomy Adverse Events

Board Pearls — Thu, 16 Jul 2026 08:14:17 -0500

Episode four teaches the post-polypectomy adverse event set through mechanism, because each event has a distinct anatomic or thermal correlate that determines the next move. Immediate bleeding is treated at the visible vessel while delayed bleeding returns for endoscopic hemostasis on the still-recognizable scar, and the prophylactic-clip decision turns on proximal location and antithrombotic risk rather than reflex. Perforation forces a closure decision driven by defect age and size, while post-polypectomy electrocoagulation syndrome mimics perforation but lacks free air and resolves on bowel rest. The unifying frame is that the recognition cue tells you the mechanism and the mechanism tells you the response, so hematochezia, free air, focal peritonitis without free air, and left shoulder pain are not interchangeable.

Topics covered

Immediate versus delayed post-polypectomy bleeding
Endoscopic hemostasis modalities
The prophylactic-clip decision
Perforation rates and recognition
Endoscopic closure versus surgery
Post-polypectomy electrocoagulation syndrome
Splenic injury and the Kehr sign

Key decisions

Immediate bleeding at the polypectomy site is managed at the visible vessel with hemoclips, snare-tip or forceps coagulation, or epinephrine paired with a definitive modality, while delayed bleeding at one to fourteen days returns for repeat colonoscopy with hemostasis on the recognizable scar.
Prophylactic clip closure of large proximal EMR defects reduces delayed bleeding with a number needed to treat around ten in patients on antithrombotics or with proximal lesions over twenty millimeters, but routine closure of small left-sided defects off antithrombotics is not standard.
A fresh perforation under two centimeters recognized during the procedure can be closed endoscopically with through-the-scope clips, over-the-scope clips, or suturing with success above ninety percent.
Larger defects, older perforations, established peritoneal contamination, or poor closure positions go to the operating room.
Post-polypectomy electrocoagulation syndrome presents twenty-four to seventy-two hours after hot snare with fever and focal peritonitis but no free air on imaging, and management is bowel rest, intravenous antibiotics, and observation rather than surgery.
Post-colonoscopy peritoneal signs, fever, leukocytosis, and free air on imaging are perforation until proven otherwise, worked up with cross-sectional imaging and surgical consultation.
Splenic injury from splenocolic-ligament traction presents with left upper quadrant pain radiating to the shoulder as the Kehr sign, and is managed from observation through embolization to splenectomy by hemodynamic stability.

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Chapter 30, Ep 5 of 5: Serrated Pathway, Lynch, and Special Populations

Board Pearls — Thu, 16 Jul 2026 08:14:28 -0500

Episode five closes the chapter on the other half of why colonoscopy quality matters, the serrated pathway where missed right-sided lesions become interval cancer. Sessile serrated lesions run through BRAF V600E, CIMP-high hypermethylation, MLH1 silencing, and microsatellite instability, which is why sessile serrated lesion detection rate is its own quality metric. That molecular route drives the Lynch reflex tree: mismatch repair immunohistochemistry, then BRAF and MLH1 methylation to triage sporadic disease, with the other loss patterns going straight to germline testing because sporadic biology cannot explain them. The special populations then bend the standard algorithm one mechanism at a time, as the kidneys forbid phosphate, the liver forbids morphine, the fetus forbids first-trimester benzodiazepines, and the IBD colon demands chromoendoscopy.

Topics covered

Serrated pathway molecular biology
Lynch universal tumor screening
BRAF V600E as sporadic discriminator
MMR loss patterns and germline testing
Serrated polyposis syndrome criteria
Physiology-driven special populations
Pregnancy, cirrhosis, and ESRD colonoscopy
IBD chromoendoscopy surveillance
Periprocedural antithrombotic management

Key decisions

Combined MLH1 and PMS2 loss on immunohistochemistry reflexes to BRAF V600E testing, and a positive result triages the patient away from germline testing because the cancer is sporadic CIMP-pathway disease.
A negative BRAF result reflexes to MLH1 promoter methylation testing, and only when both BRAF and methylation are negative does germline sequencing for Lynch syndrome become indicated.
Isolated loss of MSH2, MSH6, or PMS2 goes straight to germline testing without BRAF or methylation, because sporadic methylation acts on MLH1 specifically and cannot explain those losses.
The WHO twenty nineteen serrated polyposis definition requires either five or more serrated polyps proximal to the rectum all at least five millimeters with two over ten, or more than twenty serrated polyps with at least five proximal to the rectum.
Elective colonoscopy in pregnancy is deferred when possible, done in the second trimester when necessary, with propofol preferred, first-trimester benzodiazepines avoided, and left lateral decubitus positioning to protect venous return.
Sodium phosphate preparations are contraindicated in chronic kidney disease, on diuretics or ACE inhibitors, in hypertension, and in the elderly, with iso-osmotic PEG-electrolyte the standard alternative and hemodialysis timed to the morning after dialysis.
Elective polypectomy on full dual antiplatelet therapy after a recent stent is deferred until DAPT can be safely de-escalated, and IBD dysplasia surveillance uses chromoendoscopy with targeted biopsies rather than random four-quadrant sampling.

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Chapter 31, Ep 1 of 4: Massive Upper GI Bleeding Resuscitation

Board Pearls — Thu, 16 Jul 2026 08:14:31 -0500

Episode one of the GI Emergencies chapter treats massive upper GI bleeding as a resuscitation problem before it is an endoscopic one. The organizing idea is a clock that starts when the patient arrives, where permissive hypotension protects the clot and the wrong decision made confidently is worse than none. It moves through the timeline the patient is actually on: restrictive transfusion, the balanced massive transfusion ratio and the calcium citrate chelates, anticoagulation reversal run in parallel rather than as a delay, and field-clearing erythromycin before endoscopy. It closes on the two recognition stems the boards reward, the herald bleed of an aortoenteric fistula and the two arteries where failed hemostasis sends you to interventional radiology.

Topics covered

Upper GI bleeding as a resuscitation problem
Restrictive transfusion target and its exceptions
Massive transfusion protocol and calcium repletion
Anticoagulation reversal in the first hour
Pre-endoscopic erythromycin and why TXA fails
Airway protection and endoscopy timing
Aortoenteric fistula recognition
Salvage angiography for failed hemostasis

Key decisions

Transfuse to a restrictive hemoglobin trigger of seven with a target of seven to nine, raising the trigger to eight only in active acute coronary syndrome, and transfuse empirically in uncontrolled hemorrhage because the lab hemoglobin lags real-time loss by thirty to sixty minutes.
Activate the massive transfusion protocol at anticipated need over ten units of red cells in twenty-four hours or four in one hour, delivering a balanced one-to-one-to-one ratio and repleting ionized calcium that citrate chelates.
Reverse warfarin with four-factor prothrombin complex concentrate rather than fresh frozen plasma, reverse dabigatran with idarucizumab five grams and apixaban or rivaroxaban with andexanet alfa, and run reversal in parallel with endoscopy rather than letting the INR delay it.
Give erythromycin two hundred fifty milligrams intravenously thirty to ninety minutes before endoscopy to clear the gastric field, but do not give tranexamic acid because it adds venous thromboembolism risk without benefit in arterial spurting.
Scope non-variceal upper GI bleeding within twenty-four hours and variceal hemorrhage within twelve, reserving sub-six-hour endoscopy for uncontrollable hemorrhage or suspected aortoenteric fistula.
Suspect aortoenteric fistula in a prior aortic graft patient with a herald bleed and image with CT angiography for periaortic gas before EGD, and send failed dual-therapy hemostasis to embolization of the gastroduodenal or left gastric artery.

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Chapter 31, Ep 2 of 4: Lower GI Bleeding and Mesenteric Ischemia

Board Pearls — Thu, 16 Jul 2026 08:14:34 -0500

Episode two moves below the ligament of Treitz and then to the mesenteric vessels, carrying the same rule forward: pick the imaging that feeds the next intervention and recognize the pattern that flips the algorithm. Acute lower GI bleeding branches on hemodynamic stability, CT angiography for the unstable patient because it hands interventional radiology the anatomy and colonoscopy at twelve to twenty-four hours for the stable one, with the etiologies read by pattern. Colon ischemia separates from diverticular bleeding on pain before bleeding, and isolated right colon ischemia flips the workup toward mesenteric imaging. Acute mesenteric ischemia turns on recognizing pain out of proportion to exam and reaching for CT angiography before lactate rises, then matching intervention to each of four etiologies.

Topics covered

Acute lower GI bleeding and the BUN-to-creatinine clue
Hemodynamic split: CT angiography versus colonoscopy
Diverticular, angiodysplastic, and post-polypectomy bleeding
Endoscopic hemostasis and the no-serosa rule
Colon ischemia and pain before bleeding
Isolated right colon ischemia flipping the algorithm
Four etiologies of acute mesenteric ischemia
Etiology-specific intervention
The lactate trap and initial bundle

Key decisions

Send the hemodynamically unstable lower GI bleeder to CT angiography first because it images extravasation at about zero point three milliliters per minute and gives IR the anatomy for superselective embolization, and send the stable patient to colonoscopy at twelve to twenty-four hours after rapid polyethylene glycol prep.
Suspect a brisk upper source in about fifteen percent of presumed lower GI bleeds and when the BUN-to-creatinine ratio exceeds thirty, and exclude anorectal sources by anoscopy before colonoscopy referral.
Treat diverticular and post-polypectomy bleeding with clips or bands rather than deep thermal therapy because the diverticular wall and thinned resection base lack serosa and coagulate to perforation.
Distinguish colon ischemia by cramping pain preceding hematochezia within twenty-four hours, treat mild disease supportively, and add antibiotics when the white count exceeds fifteen thousand, BUN exceeds twenty, or ulceration is severe.
Image the mesenteric vessels in isolated right colon ischemia because that SMA watershed-equivalent territory can herald silent SMA occlusion, and anchor suspected acute mesenteric ischemia on pain out of proportion with CT angiography now, not lactate first.
Match the mesenteric intervention to etiology: embolectomy for SMA embolus, revascularization with bypass or stenting for SMA thrombosis, intra-arterial papaverine with low-flow correction for NOMI, and systemic anticoagulation for mesenteric venous thrombosis, with peritoneal signs sending everyone to laparotomy.

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Chapter 31, Ep 3 of 4: Foreign Body and Caustic Ingestion

Board Pearls — Thu, 16 Jul 2026 08:14:37 -0500

Episode three works two mechanical emergencies that each hand you a recognition cue and a defined intervention with a clock embedded in it. For foreign bodies the urgency of removal follows the mechanism of injury, not the politeness of the object, sorting into three timing tiers from two-hour disc batteries to blunt objects that never come out. The food bolus doubles as the eosinophilic esophagitis biopsy opportunity that closes if you do not take it at the same procedure. For caustic ingestion, substance category drives the injury pattern, the airway is the first priority, and the Zargar grade at endoscopy drives short-term feeding and monitoring while late stricture and squamous cell carcinoma risk drive long-term surveillance.

Topics covered

Urgency follows mechanism, not the object
Three timing tiers for removal
Disc batteries, sharps, and magnets
Drug packers versus stuffers
Food bolus and the eosinophilic esophagitis gateway
Alkali versus acid injury patterns
Airway priority and contraindicated interventions
Zargar grading and feeding safety
Late strictures and cancer surveillance

Key decisions

Remove an esophageal disc battery within two hours because hydroxide drives alkaline liquefactive necrosis within two hours and can perforate, and remove esophageal obstruction with unmanageable secretions or a sharp esophageal object within six hours.
Remove food bolus without complete obstruction, non-sharp esophageal objects, gastric or duodenal sharps, objects longer than six centimeters, and reachable high-power magnets within twenty-four hours, while managing blunt asymptomatic post-duodenal objects expectantly.
Do not endoscope body packers or stuffers because rupture during retrieval risks a fatal toxic dose, reserving laparotomy for symptoms of leak.
Take at least four biopsies from proximal and distal esophagus at the same procedure when no eosinophilic esophagitis diagnosis exists, since roughly half of adult food bolus impactions trace to it and the histologic threshold is fifteen eosinophils per high-power field.
Prioritize the airway in caustic ingestion because alkali can cause supraglottic edema, and avoid induced emesis, activated charcoal, chemical neutralization, and acute nasogastric intubation.
Endoscope caustic ingestion within twelve to twenty-four hours and let the Zargar grade decide: grades zero through two-A feed and observe, two-B and three delay feeding with ICU monitoring and surgical consult, and grade four operate, with dilation in one-to-two-millimeter increments toward fourteen to fifteen millimeters for late strictures.

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Chapter 31, Ep 4 of 4: Esophageal Perforation and Ogilvie Syndrome

Board Pearls — Thu, 16 Jul 2026 08:15:48 -0500

Episode four closes the chapter with two emergencies that run on the same cue-plus-threshold-plus-intervention shape, where the threshold is a mechanism in disguise. For esophageal perforation the clock starts when the wall tears, and the twenty-four hour window separates clean primary closure from sealed stent and drainage because the mediastinal tissue planes change from friend to enemy. For acute colonic pseudo-obstruction the clock starts when the colon stops moving, and a four-step algorithm anchored by a cecal-diameter threshold and a neostigmine-with-cardiac-monitoring decision moves the patient from the conservative bundle to pharmacology to decompression to surgery. Laplace's law explains why the cecum fails first and the neostigmine contraindication list explains why every dose comes with atropine at the bedside.

Topics covered

Causes of esophageal perforation and Boerhaave
The Mackler triad and recognition stem
Perforation site and left-sided effusion
Water-soluble contrast imaging and antibiotics
The twenty-four hour repair-versus-stent window
Ogilvie syndrome and autonomic imbalance
Ruling out mechanical obstruction
Neostigmine and cardiac monitoring
Colonoscopic decompression and surgery

Key decisions

Image suspected esophageal perforation with CT chest and oral water-soluble contrast looking for pneumomediastinum, avoiding barium initially because barium granulomatous mediastinitis is a feared complication, since a normal chest radiograph does not exclude the diagnosis.
Cover both mediastinal compartments with piperacillin-tazobactam or a meropenem-based regimen plus antifungal coverage in severe disease, and place nasogastric decompression under fluoroscopic guidance to avoid the leak.
Repair Boerhaave and large iatrogenic perforations primarily within twenty-four hours while tissue planes hold, shift beyond twenty-four hours to covered self-expanding metal stents with drainage, and clip small iatrogenic perforations caught at the index endoscopy.
Rule out mechanical obstruction and volvulus first in suspected Ogilvie syndrome with CT showing a dilated colon without a transition point, because a mechanical cause will not respond to neostigmine and may perforate during conservative management.
Manage the first forty-eight to seventy-two hours conservatively with decompression, electrolyte correction, and stopping opioids and anticholinergics, then escalate at cecal diameter over twelve centimeters, persistent distension, or impending perforation because Laplace's law makes the cecum fail first.
Give neostigmine two milligrams intravenously over three to five minutes with mandatory cardiac monitoring and atropine at the bedside, honor the contraindication list, and move to colonoscopic decompression then surgery when it fails or is contraindicated.

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Chapter 32, Ep 1 of 4: Refeeding, Malnutrition, and Enteral Access

Board Pearls — Thu, 16 Jul 2026 08:16:24 -0500

Episode one of the GI Nutrition chapter builds the inpatient nutrition framework and the enteral access decisions. The organizing idea is that the labs lie and the instinct to feed faster is usually wrong. Refeeding syndrome is what happens when a starvation-adapted patient meets a carbohydrate load, so the active intervention is restraint with thiamine before glucose. Hospital malnutrition is not what a low albumin says it is, so GLIM separates the phenotypic deficit from the etiologic cause. And the route of nutrition follows the gut's functional state, with a functional gut winning every time.

Topics covered

Refeeding syndrome and the electrolyte shift
Thiamine before glucose and Wernicke
NICE high-risk criteria
Restrained calorie reintroduction
Albumin as an inflammatory marker
GLIM phenotypic plus etiologic criteria
Functional gut and enteral access selection
PEG techniques and complications
Tube-feed diarrhea and the medication list

Key decisions

Refeeding calories start at ten to twenty kilocalories per kilogram per day and advance over four to seven days, with thiamine two hundred to three hundred milligrams given before any glucose load and continued daily for five to seven days.
Any single NICE criterion, a BMI below sixteen, weight loss above fifteen percent, more than ten days of negligible intake, or pre-feeding hypokalemia, hypophosphatemia, or hypomagnesemia, makes a patient high risk for refeeding.
Albumin and prealbumin are negative acute-phase reactants suppressed by IL-six and TNF-alpha, so they are excluded from GLIM criteria and should never be treated as nutrition markers in an inflamed patient.
GLIM malnutrition requires one phenotypic criterion, weight loss, low BMI, or reduced muscle mass, plus one etiologic criterion, reduced intake or assimilation or inflammation.
A functional gut wins, so short-term feeds under four to six weeks use nasogastric or nasojejunal tubes and longer-term feeds use percutaneous endoscopic gastrostomy.
PEG does not prevent aspiration or extend survival in advanced dementia and is not standard of care, so families should be counseled against it.
Tube-feed diarrhea is worked up by reviewing the medication list for sorbitol vehicles, checking recent antibiotics, and sending a stool C. diff test before any formula change.

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Chapter 32, Ep 2 of 4: Parenteral Nutrition and Short Bowel Syndrome

Board Pearls — Thu, 16 Jul 2026 08:17:09 -0500

Episode two takes the patient whose gut cannot do the work. Parenteral nutrition is a tool for a non-functional gut, with composition rules that follow from chemistry rather than biology and indication discipline that follows from trial data. Its long-term complications are driven by the loss of enteral stimulation, from gallbladder stasis and IFALD to manganese parkinsonism and catheter biofilm infection. Short bowel syndrome then turns on residual anatomy, where the colon's presence or absence determines both the rehabilitation trajectory and the complication pattern, and teduglutide's trophic effect explains both its efficacy and its surveillance burden.

Topics covered

When parenteral nutrition is the answer
Composition rules from chemistry
Lipid emulsions and IFALD
Indication discipline versus cachexia
Cholelithiasis and manganese parkinsonism
Catheter-related bloodstream infection
Short bowel anatomic phenotypes
Teduglutide and surveillance
Enteric hyperoxaluria and D-lactic acidosis

Key decisions

Dextrose in parenteral nutrition provides three and four-tenths kilocalories per gram, not four, because pharmaceutical dextrose is a monohydrate whose water contributes no calories, so calculating at four per gram overshoots.
Calcium and phosphate cannot be co-administered freely because they precipitate, so compounding uses solubility tables or split bags, and acetate is the buffer of choice because it is metabolized to bicarbonate.
Parenteral nutrition is reserved for a non-functional gut and is contraindicated or harmful in metastatic cancer cachexia and inferior to enteral feeding in mild-to-moderate acute pancreatitis.
Even enteral feeding at twenty to thirty percent of caloric needs restores CCK-driven gallbladder contraction and reduces parenteral-nutrition-associated cholelithiasis.
Manganese is removed from parenteral nutrition formulations once cholestasis develops or once globus pallidus T1 hyperintensity appears, since impaired biliary excretion drives basal ganglia accumulation and parkinsonism.
Oral rehydration in short bowel uses sodium ninety milliequivalents per liter with glucose ninety to one hundred ten millimoles per liter to match SGLT-one stoichiometry, because plain water and most sports drinks produce net water loss.
Teduglutide requires a baseline colonoscopy with polyp removal within six months before initiation, a follow-up at the end of year one, and surveillance every five years thereafter, and is contraindicated in active GI malignancy.

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Chapter 32, Ep 3 of 4: Fat-Soluble and Water-Soluble Vitamins

Board Pearls — Thu, 16 Jul 2026 08:17:35 -0500

Episode three reads the vitamins the way the boards test them, where every micronutrient produces a stereotyped phenotype that is the recognition cue on a stem. Behind each cue is a biochemical mechanism, and the same mechanism predicts the at-risk population and the replacement strategy. Memorizing the symptom list is the wrong frame; learning the mechanism lets the phenotype, the population, and the treatment fall out of it. The fat-soluble vitamins share a bile-salt absorption requirement, and the water-soluble vitamins carry the acute decisions, thiamine before glucose and B12 before folate.

Topics covered

Bile-salt requirement for fat-soluble vitamins
Vitamin A night blindness and toxicity
Vitamin D metabolic bone disease
Vitamin E neuropathy, hemolysis, and NASH
Vitamin K, warfarin, and the NPO patient
Essential fatty acid deficiency
Thiamine and Wernicke encephalopathy
B12 absorption steps and pernicious anemia
B12-versus-folate masking trap

Key decisions

Anything that disrupts the enterohepatic bile-acid cycle, cholestyramine, cholestasis, ileal disease, cystic fibrosis, or unsupplemented parenteral nutrition, deletes all four fat-soluble vitamins plus essential fatty acids.
Chronic vitamin A intake above roughly fifty thousand international units per day activates hepatic stellate cells into myofibroblasts and produces perisinusoidal fibrosis and portal hypertension, while a single large dose instead causes pseudotumor cerebri.
Vitamin E at eight hundred international units daily improves histology only in non-diabetic biopsy-proven NASH, and extension beyond that phenotype is unsupported given increased prostate cancer and hemorrhagic stroke risk at high doses.
An NPO patient on warfarin started on broad-spectrum antibiotics spikes the INR within days because both dietary and colonic bacterial vitamin K sources are eliminated at once.
Medium-chain triglyceride oil cannot prevent essential fatty acid deficiency because its eight-to-twelve-carbon chains lack the eighteen-carbon backbone, so intravenous lipid emulsion one to two times weekly is required.
Thiamine must precede any glucose load in an at-risk patient, given empirically as five hundred milligrams intravenously three times daily, because glucose without thiamine precipitates Wernicke encephalopathy.
Always check B12 before starting folate, because high-dose folate corrects the megaloblastic anemia while subacute combined degeneration of the cord progresses unchecked.

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

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Chapter 32, Ep 4 of 4: Minerals and Trace Elements

Board Pearls — Thu, 16 Jul 2026 08:17:55 -0500

Episode four closes the chapter with the minerals and trace elements, which run on the same logic as the vitamins: each element has a specific biochemical role and a specific exposure or pathology context that produces its phenotype. The boards favor the pairs that turn on a single mechanism, zinc inducing metallothionein to trap copper, cholestasis blocking biliary manganese excretion, and Brazil nuts concentrating selenium. Each element pairs a recognition cue with a population and a replacement strategy, the same teaching unit used for the vitamins.

Topics covered

Iron deficiency and malabsorptive anatomy
PPI-induced hypomagnesemia and TRPM6
Zinc acrodermatitis and dysgeusia
Copper myeloneuropathy from zinc excess
Copper deficiency mimicking B12
Manganese toxicity in parenteral nutrition
Selenium cardiomyopathy and selenosis
Chromium and glucose intolerance
D-lactic acidosis in short bowel

Key decisions

PPI-induced hypomagnesemia works through impaired TRPM6 channel function, and the testable feature is kinetic asymmetry: magnesium normalizes within about a week of discontinuation but recurs within about two weeks of rechallenge.
Vonoprazan or another potassium-competitive acid blocker is the alternative for the patient with recurrent PPI-induced hypomagnesemia because it does not lower magnesium.
Zinc deficiency is repleted with oral zinc sulfate two hundred twenty milligrams, fifty milligrams elemental, daily, and refractory hepatic encephalopathy in cirrhosis can reflect zinc deficiency through its urea-cycle cofactor role.
Chronic zinc excess from denture cream or supplements induces enterocyte metallothionein that traps copper, producing copper deficiency, so the treatment is copper two milligrams daily plus removing the zinc source.
Copper deficiency mimics B12 subacute combined degeneration with myeloneuropathy, anemia, and neutropenia, and the discriminators are a normal B12 level and a zinc-excess history.
Manganese is removed from parenteral nutrition once cholestasis develops or globus pallidus T1 hyperintensity appears, because impaired biliary excretion drives basal ganglia accumulation and levodopa-unresponsive parkinsonism.
Selenium deficiency on long-term unsupplemented parenteral nutrition produces Keshan cardiomyopathy, while chronic Brazil nut overconsumption, more than three per day, produces selenosis with alopecia, brittle nails, and garlic breath.

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

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Chapter 33, Ep 1 of 5: C. diff Diagnosis and First-Episode Treatment

Board Pearls — Thu, 16 Jul 2026 08:18:04 -0500

Episode one of the GI Infections chapter builds C. diff around two competing problems: the defaults moved off metronidazole and vancomycin, and asymptomatic colonization is common enough that the wrong test drives unnecessary treatment. The organizing idea is that diagnosis exists to separate active disease from colonization, while treatment exists to get the right drug to the colonic lumen at the right concentration for the right duration. Severity thresholds decide treatment intensity, and fulminant features bring surgery into the conversation at presentation rather than after medical failure. Everything reduces to those two problems.

Topics covered

Antibiotic exposure and C. diff risk factors
Presentation and pseudomembranous colitis
Two-step NAAT plus toxin EIA algorithm
Who to test and why test of cure fails
Severity stratification thresholds
Fidaxomicin first-line and vancomycin alternative
Metronidazole in third place and pregnancy
Fulminant disease regimen and surgery

Key decisions

Test only patients with high pre-test probability, three or more unexplained watery stools per day off laxatives, and screen with a sensitive NAAT or GDH before confirming with a specific toxin EIA.
Treat a discordant NAAT-positive, toxin-EIA-negative result as likely colonization and correlate clinically rather than reflexively treating, and never send a test of cure.
Stratify by white count of fifteen thousand and creatinine of one point five: below both is nonsevere, either threshold is severe, and hypotension, ileus, or megacolon makes it fulminant.
Treat a first non-fulminant episode with fidaxomicin two hundred milligrams twice daily for ten days, using oral vancomycin one hundred twenty-five milligrams four times daily when fidaxomicin is unavailable.
Never give intravenous vancomycin for C. diff because it does not reach the colonic lumen, and reserve oral metronidazole for the lowest-risk patients only when neither preferred drug is available.
Choose oral vancomycin first-line in pregnancy on decades of safety data, and stop the inciting antibiotic as part of treatment.
Treat fulminant disease with high-dose oral vancomycin five hundred milligrams every six hours plus intravenous metronidazole, add rectal vancomycin when ileus blocks oral delivery, and engage surgery at presentation.

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

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Chapter 33, Ep 2 of 5: C. diff Recurrence Toolkit

Board Pearls — Thu, 16 Jul 2026 08:18:07 -0500

Recurrence is the dominant management problem in C. diff, and this episode organizes the entire toolkit around a single mechanism: the spore. Surviving spores germinate once the antibiotic stops, so every tool either keeps colonic drug above the killing threshold across successive germination waves or restores the commensal community that denies spores a niche. The drug you reach for depends on what was used first, the structural taper-and-pulse pattern matters more than the molecule, and after two or more recurrences the strategy shifts from antibiotics to microbiome restoration. Bezlotoxumab and prophylaxis close the loop in the right patients.

Topics covered

The spore-germination cycle behind recurrence
Fidaxomicin for a first recurrence
Extended-pulse fidaxomicin dosing
Vancomycin tapered-pulsed dosing
Bezlotoxumab host-immunity layer
Microbiome restoration after multiple recurrences
Live biotherapeutics Rebyota and Vowst
Oral vancomycin prophylaxis

Key decisions

After a first recurrence in a patient treated with vancomycin or metronidazole, switch to fidaxomicin, using extended-pulse dosing in older patients with a prior episode and coverage.
After a first recurrence in a patient treated initially with fidaxomicin, use vancomycin tapered-pulsed dosing rather than repeating a flat ten-day course, because the temporal exposure pattern is what prevents recurrence.
Add bezlotoxumab ten milligrams per kilogram as a single infusion during the antibiotic course in patients with recurrence risk factors, and never substitute it for the antibiotic or use it as monotherapy.
After two or more recurrences, shift from repeat antibiotics, which sustain only about thirty percent cure, to microbiome restoration, which reaches eighty to ninety percent sustained cure.
Give the standardized live biotherapeutic products after a completed antibiotic course: rectal single-dose Rebyota or oral spore Vowst, endorsed by ACG for the second or subsequent recurrence.
Offer oral vancomycin prophylaxis during future antibiotic exposure only to patients with prior CDI, because the benefit does not extend to patients without a prior episode.

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

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Chapter 33, Ep 3 of 5: Travelers' Diarrhea and Bacterial Toxins

Board Pearls — Thu, 16 Jul 2026 08:18:14 -0500

The community-acquired diarrheas separate cleanly once you group by acquisition pattern rather than symptoms, because the exposure history predicts the pathogen and the pathogen predicts the treatment. Travelers' diarrhea selects the empiric antibiotic by region and resistance, while rifaximin stays in the noninvasive niche because it is non-absorbed. Shiga-toxin-producing E. coli flips the rule entirely, since antibiotics release more toxin and loperamide prolongs exposure. Nontyphoidal Salmonella, Shigella, Yersinia, Vibrio, and Listeria each run on their own biology, and the foodborne toxin syndromes are recognized by time to onset that tells you cultures and antibiotics are unnecessary.

Topics covered

Acquisition pattern as the organizing principle
Travelers' diarrhea and region-based empiric therapy
Rifaximin in the noninvasive niche
The no-antibiotics-for-EHEC rule and HUS
Campylobacter and Salmonella treatment rules
Shigella, Yersinia, and Vibrio biology
Listeria in special hosts
Foodborne toxin syndromes by time to onset

Key decisions

Choose empiric travelers' diarrhea therapy by region: azithromycin one gram once or five hundred milligrams daily for three days where Campylobacter and fluoroquinolone resistance dominate, with ciprofloxacin only in low-resistance areas.
Reserve rifaximin for afebrile, non-bloody travelers' diarrhea because it is non-absorbed and cannot reach invasive Salmonella, Shigella, or Campylobacter in the lamina propria.
Withhold antibiotics and loperamide in suspected Shiga-toxin-producing E. coli and give intravenous hydration with renal monitoring, because both interventions raise hemolytic-uremic syndrome risk.
Treat nontyphoidal Salmonella gastroenteritis with antibiotics only when extraintestinal seeding risk exists, such as age extremes, immunocompromise, sickle cell disease, prosthetic grafts, or bacteremia.
Treat most Shigella cases with a fluoroquinolone or azithromycin because the low infectious dose makes reducing fecal shedding a public health priority.
Treat Vibrio vulnificus sepsis with doxycycline plus a third-generation cephalosporin, and treat invasive Listeria with intravenous ampicillin, adding gentamicin for severe disease or meningitis.
Recognize the foodborne toxin syndromes by time to onset and skip stool cultures and antibiotics: one to six hours for Staph aureus and emetic Bacillus cereus, eight to sixteen hours for the diarrheal toxins.

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

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Chapter 33, Ep 4 of 5: Parasitic and Viral Diarrheas

Board Pearls — Thu, 16 Jul 2026 08:18:21 -0500

The parasitic diarrheas sort by exposure history, so the workup follows the suspected pathogen rather than a generic ova-and-parasite exam. Giardia comes from untreated water with a single-dose tinidazole answer, Entamoeba histolytica from endemic travel with two-stage tissue-then-luminal therapy, and Strongyloides is the pre-steroid serology question that prevents seventy-percent-mortality hyperinfection. Anisakis is the raw-fish larva cured by endoscopic removal. On the viral side, norovirus dominates on infectious dose and environmental persistence, which is why soap-and-water and bleach are the outbreak answers, while rotavirus fades under vaccination.

Topics covered

Suspecting parasites by exposure history
Giardia and single-dose tinidazole
Cryptosporidium and immune status
Entamoeba histolytica two-stage therapy
Strongyloides pre-steroid screening and hyperinfection
Anisakis and endoscopic removal
Norovirus and the outbreak pattern
Rotavirus and the viral differential

Key decisions

Diagnose Giardia by stool antigen EIA or PCR over insensitive microscopy, and treat with single-dose tinidazole two grams, choosing paromomycin in pregnancy because it is poorly absorbed.
Treat Entamoeba histolytica sequentially: metronidazole or tinidazole for tissue-invasive trophozoites, followed by a luminal agent like paromomycin to kill the cysts that would otherwise relapse.
Manage most amebic liver abscesses with metronidazole alone, reserving drainage for large or peripheral abscesses at risk of rupture or for treatment failure.
Screen with Strongyloides serology before any glucocorticoid, anti-TNF agent, transplant immunosuppression, or chemotherapy in patients with prior endemic exposure, since stool studies are insensitive.
Treat Strongyloides with ivermectin over albendazole because ivermectin targets the autoinfective filariform larvae, and give empiric ivermectin when immunosuppression is urgent and serology is positive.
Treat norovirus supportively and control outbreaks with soap-and-water hygiene, bleach-based surface disinfection, and excluding symptomatic staff for at least forty-eight hours, because alcohol sanitizers underperform.

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

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Chapter 33, Ep 5 of 5: Immunocompromised-Host Enteric Infections

Board Pearls — Thu, 16 Jul 2026 08:18:35 -0500

The immunocompromised gut expands the pathogen list, and the organizing move is that each organism lives behind a specific cue that names the therapy: name the host, the stain, and the histology, and you name the drug. CMV gives the owl-eye inclusion at the ulcer base treated with ganciclovir, with foscarnet as salvage when UL97 mutations break the prodrug pathway. MAC gives the PAS-positive, acid-fast-positive macrophage treated with a macrolide plus ethambutol, microsporidia turn on beta-tubulin pharmacology, and the coccidians answer to trimethoprim-sulfamethoxazole. The unifying thread is that antimicrobials hold the line while immune reconstitution provides durable clearance.

Topics covered

CMV colitis hosts and presentation
Biopsy from the ulcer base
CMV resistance and foscarnet salvage
MAC enterocolitis and combination therapy
MAC versus Whipple on acid-fast staining
Microsporidia and beta-tubulin pharmacology
Cyclospora and coccidian folate biology
Cystoisospora and its stem-level fingerprint

Key decisions

In acute severe ulcerative colitis refractory to intravenous corticosteroids, look for CMV first, since it is found in roughly a third of these cases and shifts management from biologic escalation to antiviral therapy.
Biopsy the ulcer base rather than the edge or normal mucosa for CMV, add immunohistochemistry because hematoxylin and eosin has sensitivity below fifty percent, and treat with intravenous ganciclovir.
Switch to foscarnet when ganciclovir fails from UL97 mutations, because foscarnet inhibits UL54 polymerase directly and does not require viral phosphorylation.
Treat disseminated MAC with a macrolide plus ethambutol, adding rifabutin in advanced disease, because macrolide monotherapy rapidly selects resistance.
Separate MAC from Whipple on the acid-fast stain: MAC-laden macrophages are PAS-positive and acid-fast positive, while Whipple macrophages are PAS-positive and acid-fast negative.
Treat Encephalitozoon intestinalis microsporidia with albendazole but use fumagillin for Enterocytozoon bieneusi, whose tubulin variant resists albendazole binding.
Treat Cyclospora and Cystoisospora with trimethoprim-sulfamethoxazole, because coccidian folate biology has no salvage pathway, and continue prophylaxis while CD4 stays below two hundred.

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

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Chapter 34, Ep 1 of 4: Solid Organ Transplant GI Disease

Board Pearls — Thu, 16 Jul 2026 08:19:05 -0500

Episode one of the GI in the Immunocompromised Host chapter starts with a single recognition move: a transplant recipient on calcineurin inhibitor plus mycophenolate plus prednisone with diarrhea could be any of five entities at once, and time since transplant is the variable that reorders the differential. The first month belongs to the surgeon, the one-to-twelve-month window belongs to opportunistic infection, and beyond a year belongs to cumulative toxicity and malignancy. From there the reasoning runs on enzymes: donor-recipient serostatus and UL97 versus UL54 for CMV resistance, CYP3A4 for the calcineurin inhibitor trap, and dose-dependent crypt exposure for mycophenolate enteropathy. Sitting over all of it, Epstein-Barr virus drives the post-transplant lymphoproliferative disorder that responds first to reducing the immunosuppression that allowed it.

Topics covered

The five-entity transplant diarrhea differential
Time since transplant as the organizing variable
CMV serostatus stratification and valganciclovir prophylaxis
CMV colitis diagnosis and base-of-ulcer biopsy
Ganciclovir resistance and the UL97 versus UL54 pathway
Mycophenolate enteropathy and its histologic mimics
Calcineurin inhibitor toxicity and CYP3A4 drug interactions
Post-transplant lymphoproliferative disorder and EBV

Key decisions

Before any test or scope, place the patient on the transplant timeline: first month surgical, one to twelve months opportunistic, beyond a year cumulative toxicity and malignancy.
Use valganciclovir nine hundred milligrams daily for solid organ transplant CMV prophylaxis, not letermovir, and give the D-plus R-minus mismatch the longest course at every organ.
Diagnose CMV colitis with a biopsy from the ulcer base plus immunohistochemistry, because inclusions concentrate in granulation tissue and H and E misses up to half of cases.
Treat ganciclovir-resistant CMV from a UL97 mutation with foscarnet or maribavir, and recognize that UL54 mutations produce resistance to both ganciclovir and foscarnet.
Manage mycophenolate enteropathy by mechanism: reduce the dose twenty-five to fifty percent or convert to enteric-coated mycophenolic acid, reserving azathioprine for refractory cases.
Screen every new prescription in a transplant patient against the CYP3A4 list, because azoles, erythromycin and clarithromycin, and verapamil or diltiazem push calcineurin inhibitor levels toxic.
Treat CD20-positive PTLD by reducing immunosuppression first, then adding rituximab, escalating to R-CHOP only in patients without complete response after induction.

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

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Chapter 34, Ep 2 of 4: Hematopoietic Cell Transplant Gut GVHD

Board Pearls — Thu, 16 Jul 2026 08:19:19 -0500

Episode two takes the other host state hiding behind the word transplant: the hematopoietic cell transplant recipient whose donor immune system attacks the host. The post-transplant timeline organizes everything, with the first twenty-one days belonging to conditioning toxicity rather than graft-versus-host disease, so the timeline decides which diagnosis is even allowed. Gut disease is staged by daily stool volume on the Glucksberg-Seattle thresholds, the histology anchors on crypt apoptosis, and the biopsy-bench differential always includes CMV because apoptosis is not pathognomonic. Treatment is methylprednisolone first and ruxolitinib second on the strength of a randomized trial, and the shared move across both host states is to pair every immunosuppression escalation with an infectious workup.

Topics covered

The post-transplant timeline and conditioning toxicity
Sinusoidal obstruction syndrome and defibrotide
Acute GVHD target organs and prognosis
Glucksberg-Seattle gut staging by stool volume
Crypt apoptosis histology and the Lerner system
The biopsy-bench differential and CMV overlap
Steroids first and steroid-refractory definition
Ruxolitinib and mechanism-matched later agents

Key decisions

Read gut symptoms against the timeline: the first twenty-one days belong to conditioning toxicity, which mimics graft-versus-host disease but does not need graft-versus-host therapy.
Stage gut GVHD by daily stool volume, with stage four defined by output greater than two thousand milliliters per day, severe pain, ileus, or hematochezia.
Include CMV polymerase chain reaction and tissue immunohistochemistry in every suspected gut GVHD workup, because crypt apoptosis is not pathognomonic and CMV coexists often.
Start intravenous methylprednisolone two milligrams per kilogram per day with the calcineurin inhibitor continued, reserving budesonide for upper-gut-only mild disease.
Classify non-response at day five to seven as steroid-refractory and move to ruxolitinib rather than pushing methylprednisolone to four milligrams per kilogram or to colectomy.
Give ruxolitinib five to ten milligrams twice daily as the first-line second therapy, matching later agents like vedolizumab or infliximab to the dominant tissue and cytokine.
When CMV reactivates during a steroid course, treat with intravenous ganciclovir and hold immunosuppression escalation until viremia clears rather than reading it as GVHD progression.

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

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Chapter 34, Ep 3 of 4: HIV GI Disease and Typhlitis

Board Pearls — Thu, 16 Jul 2026 08:19:47 -0500

Episode three covers the non-transplant immunocompromised GI host, where two settings that look unrelated share one logic: identify the host state, and the host state opens a tiered differential. In HIV that state is the CD4 count, which converts a long pathogen list into strata that drive workup and surfaces the pre-antiretroviral-era entities still seen in late presenters, AIDS cholangiopathy, gut Kaposi sarcoma, and post-treatment IRIS. In chemotherapy-related neutropenia that state is the absolute neutrophil count, which defines typhlitis as a cecum-predominant enterocolitis managed conservatively with bowel rest and broad-spectrum antibiotics. The recurring move is that the number tells you what to look for and the entity tells you what to do, from antiretroviral therapy as the dominant intervention to the narrow list of surgical indications.

Topics covered

CD4 count as the HIV recognition anchor
CD4-stratified opportunistic infection tiers
AIDS cholangiopathy and papillary stenosis
GI Kaposi sarcoma and HHV-8
Immune reconstitution inflammatory syndrome
Antiretroviral timing and the cryptococcal exception
Typhlitis pathogenesis and the recognition triad
Conservative management and surgical indications

Key decisions

Let the CD4 stratum set pretest probability: below one hundred directs stool studies for Cryptosporidium and microsporidia plus blood cultures for Mycobacterium avium complex.
Add ERCP sphincterotomy for the papillary stenosis pattern of AIDS cholangiopathy, because fixed scar does not reverse with antiretroviral therapy alone.
Diagnose GI Kaposi sarcoma by clinical appearance at endoscopy rather than pinch biopsy, confirming with LANA-1 immunohistochemistry and treating primarily with antiretroviral therapy.
At IRIS, continue antiretroviral therapy without interruption and treat the underlying infection, delaying initiation four to six weeks only for cryptococcal meningitis.
Diagnose typhlitis on CT showing cecal wall thickening greater than four millimeters and avoid colonoscopy, which risks perforation in a friable neutropenic bowel.
Manage typhlitis conservatively with bowel rest and antibiotics covering gram-negatives, anaerobes, and Pseudomonas, adding empiric antifungals after seventy-two hours of persistent fever.
Reserve surgery for perforation, refractory hemorrhage, full-thickness necrosis, persistent sepsis, or abscess failing drainage, accepting operative risk when the alternative is death.

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

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Chapter 34, Ep 4 of 4: Immune Checkpoint Inhibitor Toxicity

Board Pearls — Thu, 16 Jul 2026 08:20:29 -0500

Episode four closes the module on checkpoint inhibitor toxicity, one entity with many organ targets, where releasing the brakes on T cells means the same cells recognize self. Drug class predicts the toxicity rate, with anti-CTLA-4 broad and severe, anti-PD-1 focal and milder, and combination highest, while grade drives therapy through a universal seventy-two-hour escalation window. The colitis algorithm runs grade-based steroids then infliximab or vedolizumab, with the choice turning on hepatic comorbidity and CMV risk. The single most tested distinction is that steroid-refractory hepatitis goes to mycophenolate mofetil, not infliximab, because infliximab is contraindicated by its own hepatotoxicity, and the whole framework extends to pneumonitis, endocrinopathies, and the other immune-related adverse events.

Topics covered

Checkpoint biology and the CTLA-4 versus PD-1 distinction
Colitis rates by drug class and onset windows
Colitis recognition, mimics, and endoscopic predictors
Grade-based colitis management and the seventy-two-hour window
Infliximab versus vedolizumab and CMV risk
Checkpoint hepatitis workup and the autoimmune contrast
Mycophenolate replacing infliximab in hepatitis
The irAE framework across organ systems

Key decisions

Exclude Clostridioides difficile before any steroid escalation in every checkpoint colitis patient, and add CMV testing in anyone already steroid- or biologic-pretreated.
Grade colitis by stools above baseline: grade one gets loperamide with the drug continued, grade two holds the drug and starts budesonide or prednisone, grade three to four discontinues anti-CTLA-4 and starts intravenous methylprednisolone.
Use the seventy-two-hour response window as the universal escalation trigger, adding a biologic when the diffuse T-cell infiltrate escapes steroid effect.
Choose vedolizumab over infliximab when there is hepatic dysfunction or active immune-mediated hepatitis, because it is gut-selective and spares systemic anti-CMV immunity.
Give steroid-refractory checkpoint hepatitis mycophenolate mofetil one gram twice daily, because infliximab is contraindicated by immune-mediated hepatotoxicity.
Treat CMV reactivation during a prednisone taper with intravenous ganciclovir and defer infliximab while CMV is active, since anti-TNF therapy precipitates fulminant viremic disease.
Manage endocrine immune-related adverse events with hormone replacement rather than steroid taper, because the gland is already irreversibly damaged by the time it is recognized.

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

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Chapter 35, Ep 1 of 6: Pregnancy Physiology and Hyperemesis

Board Pearls — Thu, 16 Jul 2026 08:20:46 -0500

Episode one of the GI in Pregnancy chapter sets the physiologic baseline that every later stem depends on. The organizing idea is that pregnancy shifts a predictable set of labs, so any deviation pregnancy does not itself cause is by definition pathologic. From there it walks the volume, CBC, and liver-test changes, the fetal-protective imaging menu, and the antiemetic sequence for nausea and hyperemesis. The through-line is that you interpret a pregnant patient against a moved reference range, and you treat vomiting on a mechanistic ladder that ends with an absolute safety rule.

Topics covered

The shifted-baseline principle
Volume expansion and hepatic blood flow
CBC and creatinine dilutional shifts
Liver tests and the ALP versus GGT rule
Fetal-protective imaging menu
Nausea and hyperemesis gravidarum defined
The antiemetic treatment sequence
Thiamine before glucose and Wernicke prevention

Key decisions

AST, ALT, and bilirubin do not rise in normal pregnancy, so any elevation is pathologic and starts a workup, while an isolated alkaline phosphatase rise with a normal GGT is placental and needs only reassurance.
A pregnancy creatinine is usually below zero point eight, so a value of one point zero is high for this patient and warrants a workup rather than a shrug.
Ultrasound without doppler is first-line in all trimesters, MRI without gadolinium is preferred over CT, and CT is reserved for when diagnostic benefit clearly exceeds a fetal dose kept generally below fifty milligray.
First-line therapy for nausea and hyperemesis is pyridoxine ten to twenty-five milligrams three to four times daily combined with doxylamine, escalating to ondansetron or metoclopramide as second-line.
Any pregnant patient with prolonged vomiting who needs IV fluids gets thiamine one hundred milligrams before or with any glucose-containing fluid, because glucose loading in a thiamine-depleted patient precipitates Wernicke encephalopathy.
Refractory hyperemesis escalates to methylprednisolone sixteen milligrams every eight hours, held until after ten weeks of gestation for the cleft palate signal, with total parenteral nutrition as the last resort.
Hyperemesis liver abnormalities resolve with hydration, which distinguishes them from intrahepatic cholestasis and viral hepatitis, and elevated bile acids with palmoplantar pruritus point to cholestasis rather than hyperemesis.

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

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Chapter 35, Ep 2 of 6: GERD and Peptic Ulcer Disease

Board Pearls — Thu, 16 Jul 2026 08:21:02 -0500

Episode two takes the upper-GI symptom that rides on the same pregnancy physiology as hyperemesis. GERD dominates because progesterone loosens the lower esophageal sphincter while estrogen strengthens the gastric mucosal barrier, so ulcers stay uncommon. The management is a stepwise sequence built on local-then-systemic safety logic, and the reasoning is that the rules fall out of mechanism rather than memorization. The one hard contraindication anchors the section: misoprostol is off the table because the same prostaglandin effect that heals ulcers induces labor.

Topics covered

Why heartburn dominates in pregnancy
Lifestyle and mechanical first measures
Local-acting antacids and alginates
Sucralfate as a non-absorbed add-on
Famotidine as the preferred H2 blocker
Proton pump inhibitors and the omeprazole detail
Misoprostol contraindication
Endoscopy for alarm features

Key decisions

Calcium carbonate is the preferred antacid because it neutralizes acid without aluminum or sodium bicarbonate, and aluminum-only antacids and sodium bicarbonate are avoided for fetal aluminum and maternal alkalosis concerns.
Famotidine is the preferred H2 blocker on class-specific safety, while ranitidine is withdrawn for NDMA and cimetidine is avoided for antiandrogenic and P450 effects.
The PPI panel was largely category B, and omeprazole is the one historical category-C detail even though it carries the longest pregnancy track record.
Misoprostol is prohibited in pregnancy for reflux or peptic disease because it is a prostaglandin E1 analog that produces uterine contractions.
New dyspepsia in pregnancy is usually GERD, but dyspepsia with iron deficiency anemia or melena warrants endoscopic evaluation regardless of trimester.
H. pylori testing and treatment are deferred to postpartum unless complicated peptic ulcer disease forces the issue, because standard quadruple regimens contain agents problematic in pregnancy.
Endoscopy is reserved for alarm features and timed to the second trimester, with benzodiazepine sedation minimized in the first trimester for cleft lip and palate concerns.

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

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Chapter 35, Ep 3 of 6: Pregnancy-Specific Liver Diseases

Board Pearls — Thu, 16 Jul 2026 08:22:18 -0500

Episode three covers the liver diseases that exist only because pregnancy is occurring, the syndromes for which delivery is the definitive treatment. It opens on intrahepatic cholestasis, where a stillbirth-risk curve inflecting at bile acids of one hundred drives delivery timing and a normal GGT separates it from obstruction. It then works through the preeclampsia, HELLP, and AFLP spectrum, teaching the distinction as a mechanism problem: vascular fibrin-and-shear versus fetal LCHAD-driven mitochondrial overwhelm. It closes on hepatic capsular rupture, the catastrophic complication that hemodynamic status triages.

Topics covered

The two halves of liver disease in pregnancy
Intrahepatic cholestasis and its genetics
Diagnosis and the normal-GGT discriminator
Ursodeoxycholic acid treatment
Bile-acid-stratified delivery timing
Preeclampsia and HELLP
AFLP and the LCHAD mechanism
Hepatic rupture as the catastrophe

Key decisions

Intrahepatic cholestasis is diagnosed at total bile acids above ten micromol per liter, and a normal GGT with elevated bile acids and transaminases discriminates it from obstructive cholestasis, which lifts GGT and prompts ultrasound and MRCP.
Ursodeoxycholic acid ten to fifteen milligrams per kilogram per day is the treatment, with cholestyramine as second-line, and vitamin K is given around delivery because cholestasis impairs fat-soluble vitamin absorption.
Delivery timing follows the bile-acid tier: below forty deliver at thirty-nine weeks, forty to ninety-nine between thirty-six and thirty-nine, and at or above one hundred at thirty-six to thirty-seven weeks because stillbirth risk inflects sharply.
HELLP is defined by the Tennessee criteria of LDH at or above six hundred, AST at or above seventy, and platelets at or below one hundred thousand, and twenty percent of cases occur without hypertension.
Preeclampsia and HELLP are treated by delivery because the placental endothelial dysfunction does not resolve until the placenta is gone, with magnesium for seizure prophylaxis and platelet transfusion to above forty thousand for delivery.
AFLP is separated from HELLP by looking for mitochondrial failure, hypoglycemia, encephalopathy, coagulopathy, and lactic acidosis with an AST-to-ALT ratio above one, versus HELLP's schistocytes, high LDH, and deep thrombocytopenia.
Hepatic capsular rupture is triaged by hemodynamics: an unstable patient gets resuscitation with surgery or hepatic artery embolization, while a stable contained hematoma is managed conservatively with coagulopathy correction and serial imaging.

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

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Chapter 35, Ep 4 of 6: Incidental and Pre-Existing Liver Disease

Board Pearls — Thu, 16 Jul 2026 08:23:34 -0500

Episode four takes the hepatic disease that is not caused by pregnancy but is reshaped by it. Viral hepatitis turns on virus-specific decisions: the tenofovir-plus-HBIG-and-vaccine stack that decisively cuts HBV vertical transmission, universal HCV screening with treatment deferred, genotype-driven HEV severity, and the empiric acyclovir that any pregnant patient with high transaminases and low bilirubin earns before HSV PCR returns. The pre-existing diseases follow an immune and pharmacokinetic principle: continue what is working and swap out the teratogens, with the specifics being mycophenolate out, azathioprine acceptable, trientine over penicillamine, and propranolol not nadolol.

Topics covered

Hepatitis A and vaccination safety
Hepatitis B and the tenofovir decision
Hepatitis C and universal screening
Hepatitis E and genotype severity
Disseminated HSV and empiric acyclovir
Autoimmune hepatitis and PBC continuation
Wilson disease and chelation
Cirrhosis and portal hypertension

Key decisions

Maternal antiviral therapy for hepatitis B is added when HBV DNA exceeds two hundred thousand international units per milliliter by week twenty-eight, using tenofovir disoproxil fumarate three hundred milligrams daily started at twenty-eight to thirty-two weeks.
All infants of HBsAg-positive mothers receive HBIG plus the first vaccine dose within twelve hours of birth, taking transmission from over ninety percent down to under five percent, and cesarean delivery is not indicated for HBV alone.
Ribavirin is essentially absolutely contraindicated as a teratogen requiring two forms of contraception for six months, and HCV is screened universally but treated before conception or after pregnancy, while hepatitis E genotypes one and two carry twenty to thirty-three percent third-trimester maternal mortality by geography.
Disseminated HSV produces anicteric liver failure with transaminases twenty-five to forty times normal and bilirubin below three, and empiric IV acyclovir is started before PCR returns because it cuts mortality from thirty to fifty percent down to eight to twenty-five percent.
Azathioprine is continued because the fetal liver cannot activate it, while mycophenolate is strictly contraindicated with a six-month pre-conception washout, and methotrexate-class exposure is avoided.
In Wilson disease chelation must continue with trientine preferred over penicillamine, the dose reduced twenty-five to fifty percent in the third trimester, copper IUDs contraindicated, and levonorgestrel IUDs preferred.
For variceal prophylaxis in cirrhotic pregnancy propranolol is preferred over nadolol, and vasopressin is avoided because it activates myometrial V1 receptors and induces contractions.

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

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Chapter 35, Ep 5 of 6: Inflammatory Bowel Disease in Pregnancy

Board Pearls — Thu, 16 Jul 2026 08:23:39 -0500

Episode five flips a deeply intuitive instinct: pregnancy is not the time to back off immunosuppression, because the measured danger to the fetus is active maternal disease, not active maternal medicine. Once that principle is in place the medication rules become predictable, anything that maintained remission is continued and a small set of mechanism-toxic drugs is held. The molecular centerpiece is FcRn-mediated placental transfer, which loads IgG anti-TNF into cord blood by term but spares the Fab-fragment certolizumab, and that fact drives dose timing near term and infant vaccine decisions.

Topics covered

Active disease as the fetal danger
The central teaching against backing off
The safe-to-continue drugs
FcRn placental transfer and certolizumab
Dose timing near term
Infant live virus vaccination
The contraindicated drugs
Assessing disease activity in pregnancy

Key decisions

Biologic therapy is continued through delivery rather than held in the third trimester, because active disease at conception, not the medication, is what predicts adverse pregnancy outcomes.
Sulfasalazine requires folic acid supplementation bumped to two to three milligrams daily because the sulfa moiety antagonizes folate, and thiopurines are safe because the fetal liver cannot activate the prodrug.
Infliximab, adalimumab, and golimumab are IgG antibodies that cross via FcRn so cord levels can exceed maternal by term, while certolizumab is a Fab fragment with no Fc region and minimal transfer in any trimester.
For IgG anti-TNF agents the final dose is often spaced to roughly week thirty-two through thirty-eight so birth occurs at trough, and the biologic is resumed twenty-four hours after vaginal or forty-eight hours after cesarean delivery.
Live virus vaccination such as rotavirus was conservatively delayed six to twelve months in IgG-biologic-exposed infants, though the 2025 consensus now permits rotavirus for anti-TNF, IL-23 inhibitor, and vedolizumab exposure.
Methotrexate is absolutely contraindicated and stopped three to six months before conception, and tofacitinib, JAK inhibitors, ozanimod, thalidomide, and rifaximin are avoided.
CRP is unreliable in pregnancy because it rises physiologically, so fecal calprotectin is used for activity assessment and a C. difficile stool test is sent whenever a flare presentation comes through the door.

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

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Chapter 35, Ep 6 of 6: Post-Bariatric Pregnancy and Biliary Disease

Board Pearls — Thu, 16 Jul 2026 08:23:44 -0500

Episode six closes the chapter on two luminal problems governed by anatomy and timing. Post-bariatric pregnancy reads every rule off what the surgery changed: bypassed duodenum drops iron and calcium, reduced parietal cell exposure drops B12, the bypassed pylorus invalidates the OGTT, and mesenteric defects plus a gravid uterus produce internal hernia, so right upper quadrant pain after gastric bypass is internal hernia until proven otherwise. Cholelithiasis is governed by the trimester window: conservative when mild, second-trimester laparoscopic cholecystectomy when complicated, and ERCP built around keeping fetal dose under one milligray.

Topics covered

Anatomy and timing as the organizing logic
Post-bypass malabsorption pattern
Gestational diabetes screening after bypass
Internal hernia emergency
Marginal ulcers after RYGB
Cholelithiasis and the trimester window
ERCP and radiation minimization
Antibiotic selection

Key decisions

Conception is delayed twelve to twenty-four months after bariatric surgery because the rapid weight-loss phase and unrepleted micronutrient stores create a compromised environment for fetal growth.
Micronutrient supplementation is mandatory through pregnancy after bypass and sleeve, with B12, iron, folate, calcium, vitamin D, and thiamine all followed and adjusted.
The oral glucose tolerance test is avoided after Roux-en-Y because the bypassed pylorus produces dumping that makes the curve uninterpretable, and fasting glucose with home monitoring replaces it.
Severe right upper quadrant pain in a post-Roux-en-Y patient in late pregnancy is internal hernia until ruled out, and CT with abdominal shielding is appropriate because missing it allows incarcerated bowel necrosis within hours.
Mild biliary colic is managed conservatively, while recurrent colic, complicated cholelithiasis, or gallstone pancreatitis goes to laparoscopic cholecystectomy in the second trimester where all three windows align.
ERCP is reserved for cholangitis, persistent obstruction, or a large stone with refractory symptoms, and keeps fetal dose under one milligray using limited pulsed fluoroscopy, lead shielding, and non-fluoroscopic cannulation when feasible.
Fluoroquinolones and tetracyclines are avoided for their fetal tissue targets, and beta-lactam plus beta-lactamase inhibitor or cephalosporin plus metronidazole are the appropriate antibiotic choices.

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

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Chapter 36, Ep 1 of 5: Tumor Screening and Reflex Testing

Board Pearls — Thu, 16 Jul 2026 08:23:55 -0500

Episode one of the Hereditary GI Cancer Syndromes chapter builds the diagnostic framework the rest of the series depends on. The organizing idea: universal tumor testing catches the carriers that pedigree gatekeeping misses, because family history alone overlooks thirty to fifty percent of them. The four-protein immunohistochemistry pattern then decides the next move, with combined MLH1 and PMS2 loss running a sporadic-cancer rule-out before germline sequencing and everything else reflexing straight to the blood test. The through-line is that protein-loss pattern drives testing, and once a proband is confirmed, cascade testing of relatives becomes the highest-yield step.

Topics covered

Why tumor testing replaces pedigree gatekeeping
Universal four-protein MMR immunohistochemistry
Universal endometrial IHC and the sentinel cancer
The reflex pathway and IHC patterns
MLH1 and PMS2 loss with the BRAF and methylation gate
EPCAM and the MSH2 and MSH6 pattern
Multi-gene panels and phenotype overlap
Cascade testing and multidisciplinary referral

Key decisions

Run universal four-protein mismatch-repair immunohistochemistry, MLH1, MSH2, MSH6, and PMS2, on every newly diagnosed colorectal and endometrial cancer, because pedigree-based screening misses thirty to fifty percent of carriers.
On combined MLH1 and PMS2 loss, test the tumor for BRAF V600E first and then MLH1 promoter methylation; only when both are absent does the patient reflex to germline sequencing, because roughly seventy percent of that pattern is sporadic.
Isolated loss of MSH2, MSH6, or PMS2 has no sporadic counterpart and reflexes directly to germline sequencing without the BRAF and methylation gate.
On the combined MSH2 and MSH6 pattern, the germline test must include EPCAM, because three-prime EPCAM deletions silence the MSH2 promoter and mimic a primary MSH2 mutation.
Choose the multi-gene panel by dominant clinical phenotype, and require pre-test counseling before drawing blood because positive, negative, and uncertain results all carry consequences.
Once a pathogenic variant is confirmed in the proband, prioritize cascade testing of first-degree relatives, each of whom is fifty-fifty at risk and carries the same surveillance program.

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

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Chapter 36, Ep 2 of 5: Lynch Syndrome and Gene-Specific Risk

Board Pearls — Thu, 16 Jul 2026 08:24:12 -0500

Episode two takes Lynch syndrome, the syndrome the diagnostic framework most often surfaces, and anchors everything to one idea: lifetime cancer risk varies sharply by gene, and that gene-specific risk sets each surveillance interval to the dwell time of preinvasive disease in that organ. MLH1 and MSH2 carriers drive high colorectal and endometrial risk, while MSH6 flips uterine cancer above colorectal and MSH2 concentrates the upper urothelial risk. The reasoning extends to why the colonoscopy interval is short, why the cancer operation is extended, why endometrial surveillance is a bridge to hysterectomy, and why aspirin and pembrolizumab both trace back to the mutational burden the syndrome generates.

Topics covered

Mismatch-repair genetics and the MSI phenotype
Classic Lynch tumor histology and late-presenting carriers
Amsterdam and Bethesda criteria
Gene-specific lifetime cancer risk
Colorectal surveillance and extended colectomy
Endometrial surveillance as a bridge to hysterectomy
Urothelial, gastric, and pancreatic programs
Aspirin chemoprevention and checkpoint inhibition
Lynch variants and Syndrome X

Key decisions

Run colonoscopy every one to two years starting age twenty to twenty-five, or five years before the youngest affected relative, because Lynch adenomas progress faster than sporadic ones and a three-year interval is too long.
When a Lynch carrier develops colorectal cancer, particularly an MLH1 or MSH2 carrier, perform extended colectomy with ileorectal anastomosis rather than segmental resection, because metachronous risk in the residual colon is high, then surveil the rectum annually.
Treat MSH6 as the exception where uterine cancer outranks colorectal, discuss risk-reducing hysterectomy earlier, and offer total hysterectomy with bilateral salpingo-oophorectomy after childbearing as a bridge target rather than relying on surveillance permanently.
Gate pancreatic surveillance on family history, enrolling only carriers with a first-degree or second-degree relative with pancreatic cancer in annual EUS or MRI at age fifty, because absolute Lynch pancreatic risk near six percent sits below the surveillance threshold.
Offer daily aspirin for chemoprevention across a tolerable dose range, counseling that the colorectal benefit emerges only beyond five years and the per-protocol effect exceeds the intention-to-treat estimate.
Give pembrolizumab first-line for advanced MSI-high or mismatch-repair-deficient Lynch cancers before chemotherapy, because the high mutational burden generates the neoantigens checkpoint inhibition needs.

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

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Chapter 36, Ep 3 of 5: Adenomatous Polyposis: FAP and MUTYH

Board Pearls — Thu, 16 Jul 2026 08:24:20 -0500

Episode three works the adenomatous polyposis syndromes by their governing logic: if you know the gene, you know the polyp count, the polyp type, and the surgery. APC drives classic FAP toward near-certain colorectal cancer by forty, the same gene at its ends produces the softer attenuated phenotype, and biallelic MUTYH mimics attenuated FAP through an autosomal recessive pattern of affected siblings and unaffected parents. The surgical pivot is not whether to take the colon but whether to take the rectum, which decides itself on polyp burden. After the colon is gone the duodenum becomes the surveillance organ, with Spigelman staging turning ampullary adenomas into an EGD interval and a pancreaticoduodenectomy conversation.

Topics covered

Reasoning from gene to polyp count to surgery
Classic FAP and APC on Wnt signaling
Attenuated FAP and the Ashkenazi variant
MUTYH-associated polyposis and recessive inheritance
FAP extracolonic stigmata and desmoids
Prophylactic colectomy and the rectal decision
Spigelman-staged duodenal surveillance
Chemoprevention as adjunct not substitute

Key decisions

Start annual colonoscopy at puberty, age ten to twelve, in classic FAP, and delay attenuated FAP and MUTYH-associated polyposis to age twenty to twenty-five because the polyps and cancer arise later.
Move to prophylactic colectomy for polyps larger than ten millimeters, high-grade dysplasia, rising polyp number, burden too high to clear endoscopically, or symptoms.
Let the rectum decide the operation: total proctocolectomy with ileal pouch-anal anastomosis when the rectum carries burden, total colectomy with ileorectal anastomosis with annual rectal surveillance when it can be cleared.
Test for biallelic MUTYH in a patient with multiple adenomas who is APC-negative, especially when a sibling is affected and the parents are not, because the pattern is autosomal recessive.
Stage the duodenum by Spigelman and set the interval to the stage: EGD every four years at stage zero down to every year at stage three, with side-viewing ampulla inspection each time, because stage four carries a fourteen to thirty-six percent cancer risk and triggers surgical evaluation.
Treat sulindac and celecoxib as adjuncts only, since they reduce polyp number but do not prevent colorectal cancer or remove the need for surgery.

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

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Chapter 36, Ep 4 of 5: Hamartomatous Polyposis and Diffuse Gastric Cancer

Board Pearls — Thu, 16 Jul 2026 08:24:33 -0500

Episode four moves from adenoma to hamartoma, where the dominant risk shifts away from colorectal cancer. STK11 drives Peutz-Jeghers, and the resection threshold is calibrated to intussusception rather than cancer, so any small bowel polyp over one centimeter comes out. PTEN drives Cowden, where the cancer burden tracks baseline PI3K signaling into breast and thyroid and the GI role is recognition through mixed-histology polyposis. CDH1 flips the algorithm hardest: multifocal submucosal signet-ring disease beneath intact mucosa makes endoscopy unreliable, so prophylactic total gastrectomy between twenty and thirty is the standard of care. The thread is constant, the gene dictates the histology, the histology dictates the natural history, and the natural history dictates whether the answer is surveillance, polyp-by-polyp resection, or removal of the organ.

Topics covered

Peutz-Jeghers, STK11, and buccal pigmentation
Arborizing hamartomas and intussusception risk
Small bowel resection thresholds
Peutz-Jeghers multi-organ cancer surveillance
PTEN hamartoma spectrum and Cowden
Hereditary diffuse gastric cancer and CDH1
Prophylactic total gastrectomy
The Cambridge surveillance protocol
GAPPS as the HDGC differential

Key decisions

Resect any Peutz-Jeghers small bowel polyp greater than one centimeter, any symptomatic polyp regardless of size, and any polyp showing rapid growth, because growth velocity predicts intussusception better than absolute size.
Start Peutz-Jeghers surveillance young with baseline EGD and colonoscopy at age eight to ten plus small bowel capsule or MR enterography, avoiding CT enterography because of cumulative radiation across decades.
Enroll STK11 carriers in pancreatic surveillance on the gene alone, unlike BRCA, ATM, PALB2, and Lynch, because STK11 lifetime pancreatic risk clears the absolute-risk threshold without a family-history modifier.
Read Cowden as a breast and thyroid syndrome, with annual thyroid ultrasound from diagnosis, breast MRI and mammography from the early thirties, and no prophylactic thyroidectomy because the cancers are follicular and papillary rather than medullary.
Recommend prophylactic total gastrectomy with Roux-en-Y reconstruction between ages twenty and thirty for confirmed CDH1 carriers, because random biopsy misses multifocal submucosal signet-ring foci that sit beneath grossly intact mucosa.
Offer the Cambridge protocol of annual EGD with thirty to fifty random biopsies only as a fallback for CDH1 carriers awaiting or declining surgery, counseling explicitly that surveillance failure is documented despite rigorous adherence.
Add annual breast MRI plus mammography from age thirty for female CDH1 carriers, because lobular breast cancer risk reaches forty to fifty-five percent and mammography detects it less reliably.

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

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Chapter 36, Ep 5 of 5: Hereditary Pancreatic Cancer and Coordination

Board Pearls — Thu, 16 Jul 2026 08:24:49 -0500

Episode five closes the chapter with hereditary pancreatic cancer and the family-systems coordination that binds every syndrome together. The gating principle is absolute lifetime risk, not relative risk: surveillance begins above roughly five percent, so STK11, CDKN2A, PRSS1, and familial kindreds qualify on genotype alone while BRCA1, BRCA2, ATM, PALB2, and Lynch enter only with a family-history driver. The treatment side ties platinum and PARP inhibitors back to synthetic lethality in homologous-recombination-deficient tumors. The coordination side names the real failure mode, the carrier whose colonoscopy stays on schedule while gynecologic or urologic surveillance lapses, and the board traps around cascade testing, the GINA insurance gap, and the non-actionable variant of uncertain significance.

Topics covered

Germline genes behind pancreatic cancer
The absolute-risk surveillance threshold
Which carriers qualify on gene alone
Surveillance starting ages and modality
PRSS1 hereditary pancreatitis
Synthetic lethality, platinum, and PARP inhibitors
Multi-organ coordination and cascade testing
Risk-reducing surgery and reproductive counseling
GINA limits and variants of uncertain significance

Key decisions

Gate pancreatic surveillance on absolute lifetime risk above approximately five percent, above which cancer detection outweighs the false positives, procedural complications, and cyst-driven anxiety below it.
Enroll STK11, CDKN2A, PRSS1, and familial pancreatic cancer kindreds on genotype or pedigree alone, but enroll BRCA1, BRCA2, ATM, PALB2, and Lynch carriers only with a first-degree or second-degree relative with pancreatic cancer.
Start surveillance at thirty to thirty-five for STK11, forty for CDKN2A and PRSS1, and fifty for BRCA, ATM, PALB2, and Lynch, or ten years before the earliest family pancreatic cancer, whichever is younger.
Alternate annual EUS and pancreatic-protocol MRI with MRCP because they are complementary, EUS for solid lesions and same-session sampling, MRI for cysts and ductal anatomy without procedural risk.
Offer maintenance olaparib after at least sixteen weeks of platinum-based chemotherapy without progression in germline BRCA metastatic pancreatic cancer, because it roughly doubled progression-free survival and germline panel testing is now standard at diagnosis.
Do not act on a variant of uncertain significance: it does not justify cascade testing or gene-specific surveillance, and the program stays anchored to personal and family history.
Counsel carriers that GINA covers health insurance and employment but not life, disability, or long-term care insurance, and advise obtaining those policies before testing.

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

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