Board Pearls

Chapter 1, Ep 1 of 3: Esophageal Symptoms: Evaluating Dysphagia

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

The organizing idea is that the history decides the first test, so locate the dysphagia before ordering anything. Food that sticks in the chest seconds after a normal swallow is esophageal dysphagia. Solids first suggest a narrowing, and solids and liquids together suggest a motility disorder. Esophageal dysphagia goes to endoscopy with biopsies from two levels, with alarm features setting the urgency rather than the test. Food impaction is biopsied once cleared, and the history screens for prior surgery, scleroderma, dry mouth, radiation, and amyloid. Trouble at the start of the swallow is oropharyngeal and goes to modified barium swallow, with neuromuscular causes excluded before a Zenker diverticulum is treated by dividing the cricopharyngeus.

Topics covered

Oropharyngeal versus esophageal dysphagia
Narrowing versus motility pattern
Endoscopy with biopsies first
Eosinophilic esophagitis diagnosis
Barium and manometry as next steps
Alarm features and urgency
Food impaction
History clues: surgery, scleroderma, Sjogren, radiation, amyloid
Neuromuscular causes of oropharyngeal dysphagia
Zenker diverticulum and cricopharyngeal myotomy

Key decisions

Decide where dysphagia arises from the history: coughing, choking, nasal regurgitation, or drooling at the start of the swallow is oropharyngeal, and food stopping in the chest seconds later is esophageal.
In esophageal dysphagia, read solids first as a narrowing (Schatzki ring, web, peptic stricture, eosinophilic esophagitis, cancer) and solids and liquids together from the start as a motility disorder.
Send nearly all esophageal dysphagia to upper endoscopy with biopsies first, taking two to four biopsies from both the proximal and distal esophagus even when the lining looks normal, because eosinophilic esophagitis is diagnosed at fifteen or more eosinophils per high-power field.
Use a timed barium esophagram and then high-resolution manometry when endoscopy is non-diagnostic or a motility disorder is suspected, and use barium first after a fundoplication.
Scope urgently when alarm features such as age over fifty, weight loss, or progressive solid-food dysphagia raise the chance of cancer, and go from biopsy to staging with CT, PET, and endoscopic ultrasound if a mass is found.
Remove an impacted food bolus by urgent endoscopy when the patient cannot swallow saliva, and biopsy the esophagus in the same session.
Evaluate oropharyngeal dysphagia with a modified barium swallow done with a speech pathologist, and avoid endoscopy first, since a blind scope can perforate a Zenker pouch.
Treat a Zenker diverticulum by dividing the cricopharyngeus with an open, transoral stapled, or Z-POEM approach, and avoid a fundoplication in scleroderma esophagus.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and Cases
(01:32) - Locating Dysphagia by History
(02:15) - Narrowing Versus Motility Pattern
(03:34) - Endoscopy With Biopsies First
(05:34) - Alarm Features and Urgency
(06:49) - Food Impaction Management
(07:21) - Surgery, Systemic Disease, and Radiation
(10:45) - Oropharyngeal Dysphagia and Neuromuscular Causes
(15:32) - Zenker Diverticulum and Its Treatment
(19:03) - Board Traps and Summary

Chapter 1, Ep 2 of 3: Esophageal Workup: Odynophagia and Reflux Mimics

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

Painful swallowing and a failed proton pump inhibitor trial share one idea: the symptom tells you what kind of problem you have. Odynophagia means injury to the lining, so the episode asks about pills, immune status, and prior reflux, caustic ingestion, or radiation, then separates Candida, herpes, and cytomegalovirus, decides between empiric treatment and endoscopy, and aims biopsies at the ulcer edge or base. Acute radiation mucositis follows. The second half treats a PPI failure with a normal workup as a result to interpret, working through rumination, globus, and functional chest pain, and ending with the rule to rethink the diagnosis rather than raise the dose.

Topics covered

Odynophagia as mucosal injury
Three history clues
Pill esophagitis
Candida, herpes, and cytomegalovirus esophagitis
Empiric treatment versus endoscopy
Biopsy site for each virus
Acute radiation mucositis
Rumination syndrome
Globus
Functional chest pain and heartburn

Key decisions

Treat odynophagia as mucosal injury until proven otherwise, and ask about a recent pill, immunosuppression, and prior reflux, caustic ingestion, or radiation.
For pill esophagitis, stop the drug, give sucralfate, and teach patients to take pills upright with a full glass of water.
Give empiric fluconazole only to a mildly symptomatic patient with a clear Candida risk factor, and go straight to endoscopy for severe odynophagia, an immunocompromised host, a failed fluconazole trial, or a story suggesting a virus or a pill.
Biopsy the ulcer edge for herpes, treated with acyclovir, and the ulcer base for cytomegalovirus, treated with intravenous ganciclovir then oral valganciclovir; when unclear, biopsy both and brush for Candida.
Manage acute radiation mucositis supportively with topical anesthetics, opioids for severe pain, fluids, and nutritional support, and do not confuse it with a late radiation stricture, which causes dysphagia to solids.
Diagnose rumination from effortless regurgitation of recognizable food within minutes of eating, confirm doubtful cases with high-resolution manometry with impedance showing R waves, and treat with diaphragmatic breathing while stopping the PPI.
For globus, screen for alarm features such as true dysphagia, weight loss, hoarseness, a neck mass, or smoking, and reassure rather than image or prescribe a PPI.
Call chest pain functional only after heart, reflux, eosinophilic esophagitis, and motility disorders are excluded, and treat with a low-dose tricyclic, imipramine or amitriptyline 25 to 50 mg at bedtime, not a higher PPI dose.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and five patients
(01:57) - Three history clues for odynophagia
(02:36) - Pill esophagitis from history alone
(03:49) - Candida, herpes, and cytomegalovirus
(05:19) - Empiric treatment or endoscopy now
(06:41) - Where to biopsy each virus
(07:57) - Acute radiation mucositis
(08:39) - Rumination syndrome and failed PPI
(12:49) - Globus and reflux-type treatment failures
(14:19) - Functional chest pain and neuromodulators

Chapter 1, Ep 3 of 3: Esophageal Workup: Dysphagia After Surgery

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

The organizing idea is that the operation predicts the failure. The episode starts with a man who has dysphagia three weeks after a Nissen fundoplication. It shows how the design of the wrap predicts four complications, why barium comes before endoscopy, and how timing and symptoms separate a tight wrap, a slipped wrap, telescoping, and gas-bloat. It then covers treatment, the need for objective proof of reflux and a working esophagus before surgery, and what to tell patients about reflux over time. A woman with dysphagia and new heartburn after a sleeve gastrectomy then shows where to look after a sleeve and after a bypass, and why bypass suits an obese patient with reflux.

Topics covered

Dysphagia after fundoplication
Nissen, Toupet, and Dor wraps
Four wrap failures
Barium swallow before endoscopy
Tight wrap versus slipped wrap
Gas-bloat syndrome
Treating wrap complications
Selecting patients for fundoplication
Sleeve gastrectomy and the incisura
Gastric bypass strictures and marginal ulcers

Key decisions

After a fundoplication, order a barium swallow first and follow it with endoscopy, which reverses the usual order for esophageal dysphagia.
Dysphagia starting right after surgery with a well-placed wrap and a narrow channel is a tight wrap, treated with pneumatic dilation and surgical revision if dilation fails.
Recurrent reflux together with dysphagia means a slipped wrap or telescoping, and a slipped wrap with reflux gets a PPI restarted, with revision kept for nonresponders.
Inability to belch with bloating after meals is gas-bloat, caused by a wrap that blocks the transient relaxations that vent air.
Document reflux objectively before a fundoplication, and do not wrap a scleroderma esophagus, which treats better with aggressive acid suppression and dilation.
After a sleeve gastrectomy, look for a kink or stricture at the incisura angularis, and avoid a sleeve in an obese patient with reflux, choosing Roux-en-Y gastric bypass instead.
After a bypass, examine the gastrojejunal anastomosis, dilating a stricture with through-the-scope balloon and treating a marginal ulcer with a high-dose PPI.
For a marginal ulcer, stop smoking, stop NSAIDs, and eradicate H. pylori if present, because a PPI alone fails if the patient keeps smoking.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:42) - Dysphagia after a Nissen
(01:16) - How the wrap predicts failure
(02:16) - Why barium comes first
(03:22) - Telling the complications apart
(04:34) - Fixing the tight wrap
(04:58) - Selecting patients for fundoplication
(06:18) - Sleeve gastrectomy and reflux
(07:39) - Gastric bypass weak points
(08:44) - Board traps and summary

Chapter 2, Ep 1 of 4: Esophageal Motility: Achalasia and Its Mimic

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

Achalasia is loss of the inhibitory neurons of the myenteric plexus, leaving a sphincter that won't relax and an esophageal body with no propagated wave. The episode follows a thirty-eight-year-old man from his history, which already points to achalasia, through endoscopy before manometry, then barium and high-resolution manometry that confirms the diagnosis and assigns a type that predicts response. It then turns to opioids and to pseudoachalasia, shown by a sixty-eight-year-old woman with the same tracing. Treatment choice by type follows: dilation, Heller with a partial wrap, POEM, and the limited roles of botulinum toxin and drugs. It closes with lifelong follow-up and the exam traps.

Topics covered

Achalasia history and presentation
Heartburn that is not acid reflux
Loss of inhibitory myenteric neurons
Endoscopy before manometry
Barium esophagram findings
High-resolution manometry and IRP
Achalasia types one, two, and three
Opioid effect and pseudoachalasia
Dilation, Heller myotomy, and POEM
Blown-out myotomy and cancer risk

Key decisions

Do not escalate acid suppression for heartburn in a patient with dysphagia to solids and liquids from the start, because achalasia heartburn comes from retained fermenting food and not from acid.
Perform endoscopy before manometry to exclude a tumor at the junction, and do not treat a normal endoscopy as ruling out achalasia, since up to forty percent of patients have a normal scope.
Diagnose achalasia from an elevated integrated relaxation pressure with no normal peristalsis, then assign the type: type one has a silent body, type two has panesophageal pressurization on at least twenty percent of swallows, and type three has premature spastic contractions.
Ask about chronic opioids before trusting the tracing, and stop them before any procedure, because they can produce an achalasia-like pattern.
In an older patient with a short history and weight loss out of proportion to dysphagia, obtain endoscopic ultrasound and CT of the chest and abdomen to look for pseudoachalasia before any myotomy.
For types one and two, choose among pneumatic dilation, laparoscopic Heller myotomy with a Dor or Toupet partial fundoplication, and POEM based on local expertise, patient preference, and trade-offs, and avoid a full Nissen wrap.
For type three, avoid pneumatic dilation and choose POEM with the myotomy extended over the spastic segment.
Reserve botulinum toxin, eighty to one hundred units in four quadrants, for elderly or frail patients who cannot have definitive treatment, and avoid it in young fit patients who will need a myotomy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 Episode Overview
(00:44) - First Patient and Classic History
(02:32) - Neuronal Loss Behind the Findings
(03:39) - Endoscopy and Barium First
(04:39) - Manometry and Achalasia Types
(08:02) - Excluding Pseudoachalasia
(09:28) - Choosing Definitive Treatment
(12:01) - Type Three and Other Options
(13:15) - Long-Term Complications and Follow-Up
(14:10) - Board Traps and Summary

Chapter 2, Ep 2 of 4: Esophageal Motility: Outflow Obstruction

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

A manometry report reading esophagogastric junction outflow obstruction is not yet a diagnosis, and on its own it is often a false positive. The episode follows a fifty-nine-year-old man on daily opioids with obesity and dysphagia. It first defines the three tracing requirements, then explains why the diagnosis is clinically inconclusive without fitting symptoms and a confirmatory test. Next it works through the imitators: opioids, obesity, hernia, eosinophilic esophagitis, cancer, prior fundoplication, and evolving achalasia. It then confirms obstruction with a timed barium esophagram or FLIP, and ends by choosing treatment according to the cause the workup finds.

Topics covered

Outflow obstruction on high-resolution manometry
Chicago version four criteria
Three-part rule for clinical relevance
Opioid effect and taper
Obesity as a confounder
Structural imitators and endoscopic workup
Rapid drink challenge
Timed barium esophagram
FLIP and Dallas criteria
Mechanism-based treatment

Key decisions

Treat an outflow obstruction tracing as clinically inconclusive on its own, and call it relevant only with fitting symptoms (dysphagia, chest pain, or both) plus a confirmatory test.
Require an elevated median IRP both supine and upright (upright threshold twelve millimeters of mercury), some preserved peristalsis, and increased intrabolus pressure on at least twenty percent of swallows.
Taper opioids and repeat manometry before calling the pattern a disease, and if the opioid cannot stop, treat symptoms only rather than the sphincter.
Take eosinophil biopsies in any unexplained outflow obstruction even when the mucosa looks normal, use CT for hernia, outside compression, and mass, and add endoscopic ultrasound when cancer is strongly suspected.
Confirm obstruction with a timed barium esophagram, where a column over five centimeters at five minutes or a tablet that hangs up at the junction supports it.
Confirm obstruction with FLIP at a sixty-milliliter fill, where a distensibility index under two with a maximum diameter under twelve millimeters is reduced opening and an index of at least two with a diameter of at least sixteen millimeters is normal.
For confirmed obstruction with dysphagia, give achalasia-style treatment (pneumatic dilation, Heller myotomy with partial fundoplication, or POEM), and choose POEM when the body is spastic.
For mild symptoms with normal or weak peristalsis, observe on a PPI with diet changes, and for a mechanical cause fix that cause with hernia repair, eosinophilic esophagitis treatment, or cancer care.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Episode introduction
(00:42) - The patient and his report
(01:10) - What the tracing shows
(02:44) - Why the pattern is inconclusive
(03:46) - Opioids and obesity first
(04:45) - Structural imitators and workup sequence
(07:30) - Timed barium esophagram
(08:00) - FLIP measurement and reading
(10:29) - Treating the mechanism
(12:34) - Board traps

Chapter 2, Ep 3 of 4: Esophageal Motility: Spasm and Jackhammer

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

Chest pain and dysphagia from an esophagus whose sphincter opens normally but whose body squeezes too early or too hard are worked up in a fixed order. Two patients carry the episode. A woman with distal esophageal spasm shows why a negative cardiac workup leads to endoscopy with biopsies first, how a normal IRP separates spasm from type three achalasia, how distal latency defines the disease, and which contributors to exclude. Treatment then climbs from smooth muscle relaxants to neuromodulators to procedures. A man with jackhammer esophagus shows the same path, with a high contractile integral and an obstruction below it to rule out.

Topics covered

Chest pain after a negative cardiac workup
Endoscopy with biopsies before manometry
PPI trial when heartburn is present
Normal IRP versus type three achalasia
Distal latency and Chicago version four spasm
Excluding opioids, reflux, and eosinophilic esophagitis
Smooth muscle relaxants and neuromodulators
Botulinum toxin and POEM for refractory disease
Hypercontractile (jackhammer) esophagus
Board traps in workup and treatment

Key decisions

Complete the cardiac workup first, then send a patient with negative testing and pain provoked by swallowing, hot or cold liquids, or large boluses to a GI evaluation.
Do endoscopy with biopsies before manometry, to exclude a stricture or junction lesion and eosinophilic esophagitis, which can mimic or produce a motility pattern.
Start a PPI trial when the patient has heartburn, since reflux coexists in many of these patients and acid can provoke contractions.
Read the IRP first: a normal IRP with premature contractions is spasm, while an elevated IRP with spastic contractions is type three achalasia, treated with POEM.
Diagnose distal esophageal spasm only with symptoms, a normal IRP, and distal latency under 4.5 seconds on at least 20 percent of swallows, and diagnose hypercontractile esophagus with a DCI over 8,000 on at least 20 percent of swallows.
Stop opioids before treating spasm, and treat reflux and eosinophilic esophagitis, because each can produce a tracing that looks like spasm.
Treat in order: diltiazem 60 to 90 mg four times a day or a nitrate, then a tricyclic such as amitriptyline 25 to 50 mg at bedtime, then botulinum toxin, and POEM only for disabling disease that has not responded, avoiding short-acting nifedipine.
Tell the patient up front that no regimen is proven and response is unpredictable, and do not offer myotomy when symptoms are tolerable.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:50) - Chest pain moves to GI clinic
(02:05) - Why endoscopy comes first
(02:57) - Manometry: IRP and type three achalasia
(03:37) - Distal latency and the spasm definition
(05:48) - Excluding opioids and other contributors
(06:21) - Counseling and stepwise treatment
(06:52) - Relaxants, neuromodulators, and procedures
(08:48) - Second patient: jackhammer esophagus
(11:11) - Board traps and summary

Chapter 2, Ep 4 of 4: Esophageal Motility: The Weak Esophagus

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

The organizing idea is that a weak esophagus cannot push food past a wrap, so manometry comes before every fundoplication. Two patients carry the episode. The first has failed swallows with a normal IRP, which is absent contractility, and a very low sphincter pressure that points to scleroderma. The episode then covers the history and serologies that confirm it, and the reflux-directed plan that replaces surgery: lifelong PPI, head-of-bed elevation, stricture dilation, a search for gastroparesis, and Barrett surveillance. The second patient has ineffective esophageal motility with proven reflux, and multiple rapid swallows decide whether he can have a wrap and which one.

Topics covered

Manometry before fundoplication
Chicago version four reading order
IRP and the weak esophagus
DCI and counting ineffective swallows
Ineffective motility versus absent contractility
Absent contractility versus type one achalasia
Low sphincter pressure and scleroderma
Workup for systemic disease
Reflux-directed treatment without a wrap
Multiple rapid swallows and choice of wrap

Key decisions

Order high-resolution manometry before every fundoplication, because a wrap on weak peristalsis can turn mild dysphagia into severe dysphagia.
Read the IRP first: a normal IRP (under 15 mmHg supine, under 12 upright) rules out achalasia and outflow obstruction, while every swallow failed with an elevated IRP is type one achalasia, which needs the sphincter weakened.
Diagnose ineffective esophageal motility when the IRP is normal and more than 70 percent of swallows are ineffective or at least half are failed, and diagnose absent contractility when every swallow fails (DCI under 100).
Treat failed peristalsis plus a resting sphincter pressure under 10 mmHg as scleroderma until proven otherwise, and ask about Raynaud, skin changes, and other causes while sending ANA, anti-centromere, Scl-70, and RNA polymerase III.
Do not offer fundoplication, magnetic sphincter augmentation, or transoral incisionless fundoplication in scleroderma esophagus; treat with a twice-daily PPI for life and head-of-bed elevation of six to eight inches.
Add vonoprazan if symptoms stay refractory, dilate peptic strictures with Savary bougie or balloon, look for gastroparesis, and keep up Barrett surveillance.
In a surgical candidate with ineffective motility, perform multiple rapid swallows (five 2 mL sips, two to three seconds apart) to look for contraction reserve.
Prefer a partial wrap, usually a Toupet at 270 degrees, over a full Nissen when motility is weak.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:42) - Patient one: dysphagia before wrap
(01:11) - Why manometry precedes fundoplication
(01:48) - Reading the tracing and counting swallows
(04:17) - Low sphincter pressure and scleroderma
(05:31) - Finding the systemic disease
(07:08) - Protecting the esophagus without surgery
(09:12) - Patient two: ineffective motility
(10:14) - Multiple rapid swallows and wrap choice
(11:13) - Board traps and key takeaways

Chapter 3, Ep 1 of 3: GERD and Refractory Reflux: Erosive Esophagitis

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

Reflux is a failure of the barrier between stomach and esophagus before it is a problem of acid, and the episode follows two patients through that idea. A man with grade C erosive esophagitis and a hiatal hernia shows what the Los Angeles grade decides, why transient sphincter relaxations, the hernia, lying flat, and obesity cause reflux, and why H2 blockers fade. It then covers PPI timing and speed, vonoprazan, maintenance, and the safety of long-term PPI use. A woman with non-erosive reflux shows how to step down and confirm the diagnosis. The episode closes with board traps.

Topics covered

Los Angeles grading of esophagitis
What grade C and D decide
Hiatal hernia and the reflux barrier
Transient lower esophageal sphincter relaxations
Acid pocket, nighttime reflux, and obesity
H2 blocker tachyphylaxis
PPI timing, speed, and relative potency
Vonoprazan as a potassium-competitive acid blocker
Maintenance versus step-down therapy
Long-term PPI safety and drug interactions

Key decisions

Read the Los Angeles grade first: grade A is only supportive evidence of reflux, while grade B or worse is objective reflux and needs no reflux monitoring to prove it.
Give twice-daily acid suppression to grade C or D esophagitis, a peptic stricture, or Barrett esophagus, and repeat the endoscopy after healing in grade C or D because inflammation can hide Barrett esophagus.
Do not treat erosive esophagitis with an H2 blocker, because tachyphylaxis sets in within days.
Take a PPI thirty to sixty minutes before breakfast, and before dinner if twice daily; a PPI taken at bedtime or with food is functionally untreated, and it takes three to five days to work, so it is not for on-demand relief.
Choose vonoprazan, 20 mg daily for eight weeks of healing and then 10 or 20 mg for maintenance, as a reasonable first choice in severe disease or when a correctly timed PPI fails, and avoid it while breastfeeding.
Continue maintenance therapy at the healing dose after severe erosive disease, and never stop the PPI in severe erosive esophagitis, a peptic stricture, or Barrett esophagus.
In non-erosive or mild erosive disease, step down to the lowest effective dose, on-demand use, or a drug holiday once symptoms are controlled, and do reflux monitoring off PPI if she does not respond.
Do not avoid a PPI in a patient on clopidogrel; pantoprazole or rabeprazole can be chosen if there is concern about the CYP2C19 interaction.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:49) - First patient and endoscopy findings
(01:47) - Los Angeles grades and what they decide
(03:05) - Why he refluxes: barrier failure
(07:52) - Acid suppression: H2 blockers and PPIs
(11:47) - Vonoprazan and when to prefer it
(13:47) - Second patient: non-erosive reflux
(14:35) - Is long-term PPI use safe?
(16:53) - Board traps in reflux

Chapter 3, Ep 2 of 3: GERD and Refractory Reflux: Workup and Surgery

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

Most heartburn that persists on a PPI is not refractory acid reflux, so this episode treats that label as a diagnosis to be tested. The workup starts with how the drug is taken, then intensifies acid suppression, then adds endoscopy with biopsies and the reflux test that fits the patient, read as one of four diagnoses. It then covers medical options for proven reflux that persists and the need for objective testing in extraesophageal symptoms. The second half turns to antireflux surgery: proof of reflux first, the three-test workup, what a wrap rebuilds, matching the wrap to motility, the magnetic ring and transoral options, and the effect of weight.

Topics covered

PPI timing and optimization
Intensifying acid suppression
Endoscopy with two-level biopsies
Off-PPI versus on-PPI reflux testing
Lyon consensus acid exposure time
Reflux hypersensitivity and functional heartburn
Mimics: rumination and supragastric belching
Baclofen and alginates
Extraesophageal symptoms and testing
Surgical workup and choice of wrap
Magnetic ring and transoral fundoplication
Obesity and gastric bypass

Key decisions

Ask exactly when and how the PPI is taken before escalating, and teach dosing thirty to sixty minutes before breakfast, and before dinner when twice daily.
If correct timing fails, move to twice-daily dosing, a more potent PPI such as rabeprazole or esomeprazole, or vonoprazan, and consider a bedtime H2 blocker for documented night-time breakthrough.
Perform endoscopy with two to four biopsies from each of the proximal and distal esophagus even if a prior endoscopy was normal, to catch eosinophilic esophagitis.
Test off PPI with a wireless pH capsule when reflux has never been proven, and on PPI with impedance-pH when reflux is proven and symptoms persist.
Read acid exposure time as over six percent definitive, under four percent against reflux, and four to six percent borderline; with normal acid exposure, a positive symptom association means reflux hypersensitivity and a negative one means functional heartburn, treated with a neuromodulator and never surgery.
Require objective proof of reflux before any antireflux procedure, and complete endoscopy with hernia size, high-resolution manometry, and an off-PPI pH study when reflux is not already proven.
Match the wrap to motility: Nissen for normal peristalsis, Toupet for weak motility, and no full wrap in scleroderma.
Exclude the magnetic ring for a hernia over three centimeters, a body mass index over thirty-five, Barrett esophagus, grade C or D esophagitis, or absent motility, require a hernia under two centimeters for transoral fundoplication, and choose Roux-en-Y gastric bypass rather than sleeve gastrectomy for obesity.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode overview
(01:10) - Patient one: heartburn despite PPI
(02:42) - Intensifying acid suppression
(03:31) - Endoscopy with biopsies
(04:15) - Choosing the reflux test
(07:20) - Four diagnoses and their treatments
(09:49) - Persistent reflux and cough testing
(12:28) - Surgical candidate and required proof
(16:09) - What a wrap rebuilds, which wrap
(19:20) - Magnetic ring and transoral options

Chapter 3, Ep 3 of 3: GERD and Refractory Reflux: Strictures and Rings

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

The organizing idea is that reflux patients whose food sticks fall into two groups, and the pattern of dysphagia tells them apart before any test. A progressive, worsening narrowing in a patient with decades of untreated reflux is a peptic stricture, even when heartburn improves. The episode covers the endoscopy and biopsies it requires, gradual dilation by the rule of threes, and lifelong twice-daily PPI with timing checks and a repeat endoscopy after severe esophagitis heals. It then turns to the man with intermittent steak impactions and a Schatzki ring, which is fixed rather than tightening, so it is fractured with one large dilator instead of stretched.

Topics covered

Dysphagia pattern in peptic stricture
Why improving heartburn is a warning
Biopsies for cancer and eosinophilic esophagitis
Los Angeles grade C esophagitis and hernia size
Dilation and the rule of threes
Twice-daily PPI and correct timing
Repeat endoscopy for hidden Barrett esophagus
Schatzki ring versus stricture
Fracturing a ring with one large dilator
Board traps in strictures and rings

Key decisions

Treat progressive solid-food dysphagia with decades of untreated reflux as a peptic stricture until proven otherwise, and do not take improving heartburn as reassurance.
Biopsy the stricture to exclude malignancy and biopsy the esophagus for eosinophilic esophagitis before or during dilation, and always report the hernia size.
Dilate a fibrotic stricture with a balloon or wire-guided bougies, going up no more than three dilator sizes in a session once moderate resistance is felt, to avoid perforation.
Start a high-dose PPI twice daily, 30 to 60 minutes before breakfast and dinner, continue it indefinitely, and expect about 30 percent of patients to need a repeat dilation.
When a stricture recurs despite a PPI, ask about timing first, since wrong timing is the first thing to check in any PPI failure.
Repeat the endoscopy after healing when the esophagitis was Los Angeles grade C or D, because severe inflammation can hide Barrett esophagus; if found, measure it, biopsy four quadrants, and start surveillance.
Recognize intermittent sudden impaction with normal swallowing between episodes as a Schatzki ring, and biopsy for eosinophilic esophagitis.
Fracture a Schatzki ring in one pass with a single large bougie or balloon of 45 to 60 French, not small gradual dilations, and give a PPI afterward to reduce recurrence.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 two patients
(00:19) - Dysphagia pattern points to stricture
(02:20) - Improving heartburn is a warning
(03:00) - Endoscopy and biopsies
(04:13) - Dilation and the rule of threes
(05:02) - Keeping it open with a PPI
(06:48) - Repeat endoscopy for hidden Barrett
(07:26) - Schatzki ring versus stricture
(09:05) - Fracturing the ring
(09:43) - Board traps

Chapter 4, Ep 1 of 3: Barrett Esophagus and Cancer: Without Dysplasia

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

This episode follows one fifty-eight-year-old man with long-standing heartburn to show that non-dysplastic Barrett esophagus is a field at risk, not a cancer, and that every decision aims to find dysplasia without over-labeling. It begins with who qualifies for a single screening endoscopy and why those criteria are limited. It then covers the American definition of Barrett, with a view and a biopsy, followed by Prague measurement and Seattle sampling. Next come how Barrett forms and progresses, how his risk sets a one-year then three-year surveillance interval, the role of PPI and aspirin, and when surveillance should stop.

Topics covered

Screening criteria for Barrett esophagus
Limits of screening and non-endoscopic cell collection
American versus British definition of Barrett
The one-centimeter rule and irregular Z line
Prague classification and Seattle protocol
How Barrett forms and progresses to cancer
Progression risk and tissue biomarkers
Surveillance intervals
PPI, aspirin, and antireflux surgery
When to stop surveillance

Key decisions

Offer a single screening endoscopy to a patient with chronic reflux, meaning weekly symptoms for five years or more, plus at least three other risk factors, and do not count a relative by marriage as a first-degree relative.
Diagnose Barrett only when salmon mucosa extends at least one centimeter above the gastroesophageal junction and biopsy shows goblet cells, and do not biopsy an irregular Z line with tongues under one centimeter.
Record the segment with Prague C and M, inspect slowly for more than a minute per centimeter, resect visible lesions by endoscopic mucosal resection, and take four-quadrant biopsies every two centimeters, tightening to every centimeter once dysplasia is found.
Repeat endoscopy one year after the diagnosis of non-dysplastic Barrett, then every three years for a segment of three centimeters or more and every five years for a shorter one.
Keep every Barrett patient on a PPI at least once daily, individualize high-dose esomeprazole forty milligrams twice daily and aspirin three hundred milligrams daily, and do not offer antireflux surgery for cancer prevention.
Stop non-dysplastic surveillance when life expectancy no longer supports it, at about eighty-one in a healthy man and seventy-three with severe illness, and about seventy-five in a healthy woman and sixty-nine with severe illness.
Repeat endoscopy after PPI healing in a patient with Los Angeles grade C or D erosive esophagitis, because severe inflammation can hide Barrett.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and Case Setup
(01:20) - Who Qualifies for Screening
(02:34) - Screening Limits and Non-Endoscopic Options
(03:49) - Defining Barrett: View and Biopsy
(05:42) - Prague Measurement and Seattle Sampling
(08:32) - How Barrett Forms and Progresses
(10:17) - Progression Risk and Tissue Tests
(11:54) - Setting Surveillance Intervals
(12:50) - PPI and Aspirin Chemoprevention
(13:49) - When Surveillance Stops

Chapter 4, Ep 2 of 3: Barrett Esophagus and Cancer: Dysplasia Treatment

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

Barrett esophagus with dysplasia is followed through one patient, a sixty-four-year-old woman whose community biopsy reads high-grade dysplasia. The organizing idea is that every step follows cancer risk and tissue evidence. An expert GI pathologist confirms the reading first, and the grade sets the next step. A slower second endoscopic look comes before treatment because a cancer may be hidden. Anything visible is resected before any ablation, and the depth of the resected lesion decides between endoscopy and surgery. The remaining Barrett is then ablated, usually with radiofrequency ablation, with cryotherapy as salvage. Eradication is not cure, so lifelong twice-daily PPI and intensive early surveillance follow.

Topics covered

Expert GI pathology confirmation
Grades of dysplasia and cancer risk
Indefinite and low-grade dysplasia management
High-grade dysplasia and hidden cancer
Careful second endoscopic look
Resect first, ablate second
Mucosal resection versus submucosal dissection
Depth of invasion and node risk
Radiofrequency ablation and cryotherapy
Complications and surveillance after eradication

Key decisions

Send any community dysplasia reading to an expert GI pathologist before treating, because in one cohort only about a quarter of low-grade dysplasia diagnoses were confirmed.
For indefinite dysplasia, give twice-daily PPI for three to six months and repeat endoscopy with biopsies, moving to surveillance every twelve months if the reading is still indefinite.
For confirmed low-grade dysplasia, choose between endoscopic eradication and surveillance every twelve months by shared decision, favoring eradication when life expectancy is reasonable.
Treat expert-confirmed high-grade dysplasia endoscopically in nearly everyone, beginning with a slow high-definition and chromoendoscopy exam with four-quadrant biopsies every centimeter.
Resect any visible nodule before ablating, using mucosal resection for small lesions and submucosal dissection for lesions over two centimeters or depressed ones, so the specimen can be staged.
Treat intramucosal cancer endoscopically, but send submucosal invasion toward esophagectomy unless the lesion is under five hundred micrometers deep, well or moderately differentiated, and without lymphovascular invasion.
Ablate the remaining Barrett with radiofrequency ablation every two to three months until no intestinal metaplasia remains, use cryotherapy if it fails, and continue twice-daily PPI indefinitely.
After high-grade dysplasia or intramucosal cancer, perform endoscopy at three, six, and twelve months and then yearly, with biopsies of the junction and the distal two to three centimeters of new squamous lining.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and the case
(00:45) - The patient with high-grade dysplasia
(01:40) - Expert pathologist confirmation first
(02:20) - What each grade calls for
(04:52) - The careful second look
(05:18) - Resect first, ablate second
(07:25) - Depth decides endoscopy or surgery
(08:57) - Ablating the remaining Barrett
(11:34) - Expected complications of treatment
(12:29) - Surveillance after eradication

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

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

Histology comes first, because adenocarcinoma and squamous cell carcinoma differ in cause, location, and treatment before surgery. Two patients with T3 N1 M0 disease carry the episode. The first, a man with distal adenocarcinoma, is taken through risk factors, then staging in a fixed order: endoscopy, CT, PET-CT, and endoscopic ultrasound last. Next come the TNM definitions and what each depth decides, then perioperative FLOT versus chemoradiation, esophagectomy at a high-volume center, and postoperative strictures and reflux. The second patient, with squamous cell carcinoma, shows chemoradiation before surgery, adjuvant nivolumab for residual disease, and definitive chemoradiation without surgery. Metastatic disease and common board traps close the episode.

Topics covered

Warning pattern of progressive dysphagia
Adenocarcinoma versus squamous cell risk factors
Fixed order of staging tests
Endoscopic resection as staging for early lesions
TNM definitions
Stage-based treatment from T1a to metastatic
Treatment before surgery by histology
Esophagectomy outcomes and postoperative problems
Adjuvant nivolumab and definitive chemoradiation
Metastatic disease and board traps

Key decisions

Order staging as endoscopy with biopsies, CT of chest and abdomen, PET-CT, then endoscopic ultrasound with fine-needle aspiration, because distant metastasis makes precise local depth irrelevant.
Stage a small visible lesion that may be confined to the mucosa or just below it with endoscopic mucosal resection or submucosal dissection, because forceps biopsies cannot measure depth.
Treat T1a cancer endoscopically with resection followed by radiofrequency ablation of remaining Barrett mucosa, and send T1b to esophagectomy unless invasion is under 500 micrometers, well or moderately differentiated, and without lymphovascular invasion.
Give locally advanced disease (T3, T4a, or node-positive without metastasis) multimodality treatment followed by esophagectomy, and treat metastatic disease palliatively.
Choose perioperative FLOT, four cycles before and four after surgery, for adenocarcinoma in a fit patient, and reserve chemoradiation for an adenocarcinoma patient who cannot tolerate it.
Give squamous cell carcinoma neoadjuvant chemoradiation with carboplatin, paclitaxel, and 41.4 gray in 23 fractions, then add adjuvant nivolumab for up to a year if any tumor remains in the specimen.
Use definitive chemoradiation of 50.4 gray in 28 fractions with concurrent chemotherapy for squamous patients who cannot have surgery or who have cervical or very proximal tumors.
Refer for esophagectomy at a high-volume center, dilate an anastomotic stricture that presents as new dysphagia months later, and continue a proton pump inhibitor for life.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:49) - First patient: dysphagia and adenocarcinoma
(01:50) - Risk factors for the two cancers
(03:53) - Staging tests in fixed order
(05:22) - TNM definitions and stage-based treatment
(08:28) - Treatment before surgery by histology
(09:54) - Esophagectomy and postoperative problems
(11:09) - Second patient: squamous cell carcinoma
(13:29) - Metastatic disease and palliation
(14:14) - Board traps and summary

Chapter 5, Ep 1 of 2: Eosinophilic Esophagitis: Diagnosis and Treatment

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

Eosinophilic esophagitis is a food-driven Th2 allergic disease that scars the esophagus if it is left untreated, so the episode is organized around telling inflammation from fibrosis. It starts with a young man's food impaction and the rule to biopsy every adult impaction. It then covers the mechanism, the diagnosis at fifteen eosinophils per high-power field with no PPI trial, and EREFS scoring with its inflammatory and fibrostenotic split. First-line options are a high-dose PPI, a swallowed steroid, or a step-up diet, with biopsy-confirmed remission and ongoing maintenance. A second patient who is refractory leads to adequacy checks, dupilumab, and dilation.

Topics covered

Biopsy of adult food impaction
Typical patient and presentation
Th2 mechanism and fibrosis
Diagnostic criteria and biopsy sampling
Reflux versus eosinophilic esophagitis on pathology
No PPI trial needed for diagnosis
EREFS scoring
PPI, swallowed steroid, and elimination diet
Maintenance after remission
Refractory disease, dupilumab, and dilation

Key decisions

Take esophageal biopsies at the endoscopy for every adult food impaction, even when the esophagus looks normal.
Diagnose eosinophilic esophagitis with at least fifteen eosinophils per high-power field on at least six biopsies from at least two levels, in a patient with esophageal symptoms, without requiring a PPI trial.
Use the EREFS split to guide treatment: edema, exudates, and furrows are inflammation that drugs treat, while rings and strictures are fibrosis that also needs dilation.
Choose among a PPI at omeprazole twenty to forty milligrams twice daily, a swallowed steroid, or a step-up diet starting with milk and wheat, based on adherence, allergic history, and patient preference.
Judge treatment response by biopsy at eight to twelve weeks, with remission below fifteen eosinophils per high-power field, rather than by symptoms, and continue maintenance at the lowest effective dose because relapse after stopping is the rule.
Before calling disease refractory, confirm each trial was adequate: PPI dose and duration, steroid technique with nothing by mouth for thirty minutes, and diet adherence.
Give dupilumab three hundred milligrams subcutaneously every week for refractory disease, because only weekly dosing improved dysphagia.
Dilate fibrotic narrowing gradually toward fifteen to eighteen millimeters alongside maintenance medical therapy, and treat persistent dysphagia with clean biopsies by dilation rather than a different biologic.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:53) - Food impaction and biopsy rule
(03:13) - Th2 mechanism and fibrosis
(04:48) - Diagnosis without a PPI trial
(06:39) - Scoring the endoscopy with EREFS
(08:08) - Choosing first-line treatment
(13:52) - Remission and maintenance
(14:19) - Confirming refractory disease
(16:49) - Dupilumab mechanism and dosing
(19:35) - Dilation for fibrotic narrowing

Chapter 5, Ep 2 of 2: Infectious Esophagitis: Infection and Injury

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

Each infection or injury in this episode is explained by where the agent acts and how long it stays. Candida takes hold when local defenses fail, so unexplained disease prompts an HIV test, and severe or atypical cases are scoped before treatment. Persistent pain after Candida clears suggests cytomegalovirus, biopsied at the ulcer base, while herpes is biopsied at the ulcer edge. Chemical injury follows the chemical and contact time: alkali penetrates the esophagus, the airway comes first, nothing is given that adds injury, and endoscopy at 24 to 48 hours grades the damage and sets disposition. Survivors need stricture care and long-term cancer surveillance. Pill esophagitis is prevented by upright dosing with a full glass of water.

Topics covered

Candida esophagitis and failed host defenses
HIV testing and empiric versus endoscopic approach
Confirming and treating Candida
Cytomegalovirus ulcers and base biopsy
Herpes simplex esophagitis and edge biopsy
Alkali versus acid caustic injury
Airway and what not to do after ingestion
Zargar grading and disposition
Stricture and cancer surveillance
Pill esophagitis and upright dosing

Key decisions

Test for HIV when Candida esophagitis is unexplained, give an empiric fluconazole trial only to a low-risk patient with classic symptoms and thrush, and send severe pain, immunocompromise, or atypical findings to endoscopy with biopsy first.
Treat confirmed Candida esophagitis with fluconazole 200 to 400 mg daily for 14 to 21 days, intravenously if the patient cannot swallow, and reserve echinocandins for fluconazole failure, critical illness, or azole-resistant species, with antiretroviral therapy rather than lifelong fluconazole to prevent recurrence in HIV.
Treat persistent pain after Candida clears in an immunosuppressed patient as a second infection, and biopsy the base of a cytomegalovirus ulcer but the raised edge of a herpes ulcer, because each virus lives in different cells.
Treat moderate to severe cytomegalovirus esophagitis with intravenous ganciclovir 5 mg/kg every 12 hours for 14 to 21 days, then valganciclovir 900 mg daily, refer for an eye exam, and use foscarnet for resistance or marrow suppression, while herpes gets acyclovir for 7 to 10 days if immunocompetent and 14 to 21 days if immunocompromised.
After caustic ingestion, intubate early for drooling, stridor, or a changed voice, and give no emetics, neutralizing agents, activated charcoal, blind nasogastric tubes, or routine antibiotics.
Scope within 24 to 48 hours unless the patient is unstable, perforated, or has severe respiratory distress or airway swelling, in which case get CT and surgical consultation, and send Zargar grade 2B and higher to the ICU without giving steroids for grade 3.
Expect strictures within weeks, treated with repeated endoscopic dilation, and start surveillance endoscopy about 15 to 20 years after a significant caustic injury because of squamous cell cancer risk.
For pill esophagitis, stop the offending drug, coat the ulcer with sucralfate slurry, and teach taking pills upright with at least 8 ounces of water and staying upright for 30 minutes, looking for a motility disorder or stricture if it recurs.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and four patients
(01:29) - Candida esophagitis and failed defenses
(04:14) - Confirming and treating Candida
(06:29) - Cytomegalovirus esophagitis after Candida
(10:14) - Herpes esophagitis and edge biopsy
(13:00) - Chemical injury and caustic chemistry
(15:44) - Airway first and what to avoid
(16:58) - Endoscopy timing and Zargar grading
(19:38) - Strictures and cancer surveillance
(21:01) - Pill esophagitis and prevention

Chapter 6, Ep 1 of 2: Peptic Ulcer Disease and H. pylori: Test to Cure

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

H. pylori care rests on two ideas: the organism's biology explains every test and its false negatives, and resistance patterns explain which drugs can be reused and which cannot. The episode follows a woman with a duodenal ulcer through who gets tested, how PPIs and antibiotics spoil testing, and why antral infection causes duodenal ulcer. It then covers why clarithromycin triple therapy fell, optimized bismuth quadruple therapy and the vonoprazan alternatives, how penicillin and macrolide history pick the regimen, and test of cure. A man whose infection survives two courses then shows how to confirm failure, which drugs to reuse, when to test for resistance, and when rifabutin triple therapy is the last step.

Topics covered

Who should be tested for H. pylori
Urease biology and active tests
Test timing and false negatives
Serology limits
Antral versus whole-stomach infection
Clarithromycin resistance
Optimized bismuth quadruple therapy
Vonoprazan regimens
Penicillin allergy and macrolide history
Test of cure
Confirming treatment failure
Resistance testing and rifabutin salvage

Key decisions

Test anyone with a past or active ulcer, MALT lymphoma, dyspepsia, long-term NSAID or low-dose aspirin use, or unexplained iron deficiency, and hold PPIs for one to two weeks and antibiotics or bismuth for four weeks before an active test.
When the PPI cannot be held, use histology with a special stain on a body biopsy, and never use serology to diagnose active infection or confirm cure.
Do not give empiric clarithromycin triple therapy, because resistance commonly exceeds fifteen percent, and never give it to a patient who has had any macrolide such as azithromycin.
Give optimized bismuth quadruple therapy as first line: a potent PPI (esomeprazole or rabeprazole), bismuth subsalicylate, tetracycline 500 mg four times daily, and metronidazole 500 mg three or four times daily for 14 days, not 10 days and not with doxycycline.
Test to remove a penicillin allergy label when it decides the regimen, and avoid bismuth subsalicylate in a patient with aspirin allergy.
Retest everyone at least four weeks after antibiotics, with the PPI held for one to two weeks, using a urea breath test or stool antigen.
After a confirmed failure, never reuse clarithromycin or levofloxacin without proven susceptibility, and give optimized bismuth quadruple therapy if the failed regimen lacked bismuth, tetracycline, and metronidazole.
After more than one failed regimen, order molecular resistance testing of stool or biopsy and treat to the result, and use rifabutin triple therapy after bismuth quadruple therapy has failed.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Opening and the first patient
(01:14) - Who gets tested for H. pylori
(02:04) - Urease biology and test pitfalls
(04:42) - Why duodenal rather than gastric ulcer
(06:30) - Clarithromycin failure and bismuth therapy
(09:27) - History that picks the regimen
(10:53) - Confirming cure after treatment
(11:21) - Confirming failure and reusable drugs
(15:23) - Resistance testing after two failures
(16:25) - Rifabutin triple therapy as last resort

Chapter 6, Ep 2 of 2: Peptic Ulcer Disease and H. pylori: Ulcer Itself

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

The organizing idea is that every ulcer has a cause to find and a complication to anticipate. The episode starts with how NSAIDs injure the stomach however they are given, then tallies risk factors into tiers that decide PPI protection, followed by celecoxib after a bleed, H. pylori testing, and what aspirin and clopidogrel change. It then asks why an ulcer fails to heal, with proper H. pylori retesting, hidden NSAIDs, adherence, and repeat biopsy for cancer, before the rarer causes and the gastrinoma pattern. Last come free perforation, with CT, resuscitation, and a Graham patch, then penetration that mimics pancreatitis, and endoscopic closure.

Topics covered

How NSAIDs injure the stomach
Risk factors and risk tiers
PPI, misoprostol, and celecoxib protection
H. pylori testing in NSAID and aspirin users
Aspirin and clopidogrel after a myocardial infarction
Non-healing ulcer and missed causes
Repeat biopsy for gastric cancer and lymphoma
Rarer causes of refractory ulcer
Zollinger-Ellison syndrome testing
Free perforation, Graham patch, penetration, and endoscopic closure

Key decisions

Give a high-risk patient, meaning a prior complicated ulcer or more than two risk factors, a PPI with any non-selective NSAID for as long as the NSAID continues.
After an NSAID ulcer bleed in a patient who still needs an anti-inflammatory, start celecoxib with a daily PPI, and recognize that adding aspirin cancels much of celecoxib's advantage.
Test and treat H. pylori in every long-term NSAID or low-dose aspirin user, testing off PPI for one to two weeks or by histology on biopsies.
In a non-healing ulcer, retest H. pylori properly, ask specifically about over-the-counter NSAIDs, check PPI timing, and rebiopsy a gastric ulcer at both the rim and the base.
Suspect Zollinger-Ellison syndrome with multiple ulcers beyond the bulb, and screen with fasting gastrin and gastric pH off PPI: gastrin over 1000 picograms per milliliter with pH under 2 confirms it, and 100 to 1000 needs a secretin test with a rise above 120.
Confirm a free perforation with CT, since a normal chest film does not exclude it, and resuscitate with crystalloid, broad-spectrum antibiotics such as piperacillin-tazobactam, a nasogastric tube, and an intravenous PPI while going to surgery without delay.
Repair a free perforation with a Graham omental patch and do not add vagotomy or antrectomy at the emergency operation.
Manage a penetrating posterior duodenal ulcer medically, and close an endoscopic perforation with clips or suturing only in a stable patient without diffuse peritonitis, with surgery consulted.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patients
(00:59) - NSAID ulcer and how NSAIDs injure
(02:59) - Risk tiers and protection choices
(07:00) - Aspirin and clopidogrel change the plan
(08:25) - The ulcer that will not heal
(13:55) - Gastrinoma pattern and idiopathic ulcer
(15:53) - Free perforation and surgical repair
(20:07) - Penetration that mimics pancreatitis
(21:32) - Perforations made at endoscopy
(22:35) - Board traps across all patients

Chapter 7, Ep 1 of 2: Gastritis and Gastric Cancers: Acid and Atrophy

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

Every patient here is read through what has happened to acid. Autoimmune gastritis destroys body parietal cells and spares the antrum, so iron deficiency comes before B12 deficiency, gastrin runs high, and type one neuroendocrine tumors can form. Separately labeled antral and body biopsies, antibodies, and H. pylori testing confirm it, and B12 and iron are replaced. Intestinal metaplasia after H. pylori is eradicated, staged with OLGIM, and surveyed by stage and risk modifiers. Zollinger-Ellison syndrome is proven by gastrin with pH, then localized and treated, with MEN1 changing the plan. Menetrier disease ends the episode with giant folds and low acid.

Topics covered

Autoimmune atrophic gastritis and pernicious anemia
Why iron deficiency precedes B12 deficiency
Sydney protocol biopsies and serologic markers
B12 and iron replacement and type one gastric NETs
H. pylori and the path to intestinal-type cancer
Eradication and test of cure
OLGA and OLGIM staging and surveillance
Zollinger-Ellison syndrome and the secretin test
Gastrinoma localization and MEN1
Menetrier disease

Key decisions

Consider autoimmune gastritis in an older patient with unexplained iron deficiency and no H. pylori, and take antral and body biopsies in separately labeled jars, using the Sydney protocol of two antrum, two body, and one incisura.
Replace B12 with intramuscular cyanocobalamin 1000 micrograms weekly for one to two months then monthly for life, or with oral 1000 to 2000 micrograms daily, and give intravenous iron when oral iron fails because there is no acid.
Survey autoimmune gastritis every three to five years, remove type one neuroendocrine tumors over one centimeter endoscopically, watch smaller ones, and never perform gastrectomy for the tumor alone.
Treat H. pylori at every stage with a regimen such as optimized bismuth quadruple therapy for fourteen days, confirm cure with a breath test off the PPI, and test first-degree relatives of gastric cancer patients.
Stage metaplasia with OLGIM using biopsies from both antrum and body, and survey about every three years at stage three or four, or at a lower stage with risk modifiers such as incomplete metaplasia, family history, or immigration from a high-risk country.
Diagnose Zollinger-Ellison syndrome with fasting gastrin and gastric pH off the PPI for seven days when safe: gastrin over 1000 with pH under 2 is diagnostic, and intermediate gastrin with acid present needs a secretin test, positive with a rise over 120 picograms per milliliter.
In MEN1 with gastrinoma, control acid with a high-dose PPI, fix the hyperparathyroidism first, and reserve surgery for duodenal tumors over about two to two and a half centimeters, while sporadic localized gastrinomas are explored for cure.
Treat Menetrier disease, with giant body folds, low acid, and protein loss, using cetuximab, and reserve gastrectomy for refractory protein loss, severe symptoms, or high-grade dysplasia.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patient roadmap
(00:56) - Autoimmune gastritis and pernicious anemia
(04:16) - Biopsies, antibodies, and replacement
(08:48) - H. pylori to intestinal metaplasia
(11:03) - Eradication, staging, and surveillance
(15:20) - Zollinger-Ellison syndrome presentation
(17:04) - Gastrin, pH, and secretin testing
(18:43) - Finding the tumor and MEN1
(22:02) - Menetrier disease and giant folds
(24:13) - Board traps and episode summary

Chapter 7, Ep 2 of 2: Gastric Tumors: Diagnosis and Drug Choice

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

Every gastric tumor in this episode is sorted by one feature that sets its treatment. For adenocarcinoma it is the Lauren type, signs of spread, and the molecular profile that picks the drug. For lymphoma it is MALT versus large cell, and the t(11;18) result that predicts whether H. pylori eradication will work. For neuroendocrine tumors it is the gastrin and gastric pH that define type one, two, or three. For GIST it is endoscopic ultrasound, risk by size, mitoses, site, and rupture, and the mutation that chooses imatinib or another drug. The episode closes with the traps the boards set.

Topics covered

Intestinal versus diffuse gastric adenocarcinoma
Signs of metastatic spread on exam
Staging with endoscopic ultrasound, CT, and laparoscopy
Molecular profiling for HER2, PD-L1, MMR, and claudin
Endoscopic, perioperative, and surgical management
Linitis plastica and CDH1 testing
Gastric MALT lymphoma and H. pylori eradication
Diffuse large B-cell lymphoma and R-CHOP
Gastric neuroendocrine tumor types by gastrin and pH
GIST diagnosis, risk, and mutation-directed therapy

Key decisions

Biopsy a hard left supraclavicular (Virchow's) node before planning surgery, because cancer in the node means metastatic disease and no curative operation.
Perform staging laparoscopy with peritoneal washings before any curative gastrectomy, especially for diffuse-type tumors and tumors through the serosa.
Profile every advanced gastric cancer for HER2, PD-L1, mismatch repair or microsatellite instability, Epstein-Barr virus, and claudin 18.2, and give pembrolizumab alone to a mismatch-repair-deficient tumor even if PD-L1 is low.
Treat locally advanced resectable cancer with perioperative FLOT and gastrectomy with D2 dissection, using total gastrectomy for proximal or diffuse-type tumors, and refer young diffuse-type patients or family clusters for CDH1 testing.
Order FISH for t(11;18) in gastric MALT lymphoma, and treat early, H. pylori-positive, translocation-negative disease with 14 days of bismuth quadruple therapy, confirming eradication at least 4 weeks later with the PPI held.
Send translocation-positive, H. pylori-negative, stage two or higher, or persistent MALT lymphoma to radiation (24 to 30 gray for localized disease) or rituximab, never surgery, and treat large B-cell lymphoma with R-CHOP, not antibiotics alone.
Type a gastric neuroendocrine tumor by fasting gastrin and gastric pH, resect type one tumors over 1 cm endoscopically and watch smaller ones, and treat type three tumors like adenocarcinoma with gastrectomy.
Resect gastric GISTs over 2 cm and all non-gastric GISTs without node dissection, give imatinib 400 mg daily for three years after high-risk resection (higher dose for exon nine), and use avapritinib for PDGFRA D842V.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:07) - Adenocarcinoma and the Lauren types
(03:58) - Signs of spread and staging
(05:52) - Molecular profile picks the drug
(08:57) - Diffuse type and linitis plastica
(09:51) - MALT lymphoma and antibiotics
(14:22) - Aggressive large B-cell lymphoma
(15:35) - Neuroendocrine types one and two
(19:42) - Type three neuroendocrine tumor
(21:48) - GIST diagnosis, risk, and therapy

Chapter 8, Ep 1 of 2: Gastric and Small Bowel Motility: Slow Emptying

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

Gastroparesis is delayed gastric emptying without a mechanical obstruction, and every cause breaks one of three things the stomach needs: an intact vagus, intact interstitial cells of Cajal, and working smooth muscle. The episode follows a man with long-standing type one diabetes, starting with causes, especially the opioids, cannabis, and GLP-1 agonists that can be fixed. Symptoms cannot make the diagnosis, so endoscopy comes first to exclude obstruction, followed by a four-hour solid-meal scintigraphy done with drugs held and glucose under two hundred. Treatment then steps up from fluids, glucose, drugs, and diet through prokinetics and antiemetics to pyloric and surgical procedures.

Topics covered

Reservoir, pump, and pacemaker physiology of the stomach
Diabetic and other causes of gastroparesis
Drugs that slow gastric emptying
Why symptoms cannot make the diagnosis
Endoscopy before emptying study
Four-hour gastric emptying scintigraphy and grading
GLP-1 agonist testing pitfall
Diet, glucose, and medication review
Prokinetics and antiemetics
Refractory disease procedures

Key decisions

Perform endoscopy before any emptying study, because a stricture, bezoar, or pyloric stenosis causes the same symptoms and changes the pathway.
Use a four-hour solid-meal scintigraphy with a low-fat egg-white meal, and call over ten percent retention at four hours delayed, graded mild at ten to fifteen percent, moderate at fifteen to thirty-five, and severe above thirty-five.
Hold prokinetics for forty-eight to seventy-two hours, hold opioids, anticholinergics, cannabis, and tobacco for at least forty-eight hours, and start the study with glucose under two hundred.
Stop semaglutide in a patient with a delayed study on the drug, and repeat the study off the drug only if symptoms persist.
Start treatment by correcting fluids and nutrition, improving glucose control, and stopping slowing drugs, then use small frequent low-fat, low-insoluble-fiber meals, with jejunal feeding for weight loss of ten percent or more over three to six months or repeated hospitalizations.
Give metoclopramide five to ten milligrams before meals and at bedtime, and reassess by twelve weeks because of the tardive dyskinesia boxed warning.
Obtain a baseline ECG before domperidone, with QTc under 450 milliseconds in men and 470 in women, and use intravenous erythromycin at three milligrams per kilogram every eight hours for acute flares because oral effect fades.
Do not inject botulinum toxin into the pylorus, and offer G-POEM only to highly selected refractory patients, especially those with more than twenty percent retention at four hours.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 Episode Overview
(01:32) - Reservoir, Pump, and Pacemaker
(02:37) - Diabetes and Other Causes
(04:24) - Medications That Slow Emptying
(06:14) - Endoscopy Excludes Obstruction First
(06:54) - Scintigraphy Method and Grading
(10:04) - The Semaglutide Testing Pitfall
(10:34) - Fluids, Glucose, Drugs, and Diet
(12:02) - Prokinetics and Antiemetics
(16:13) - Refractory Disease and Procedures

Chapter 8, Ep 2 of 2: Gastric and Small Bowel Motility: Three Syndromes

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

Each syndrome in this episode is defined by a pattern, and the work is ruling out its mimics before treating by mechanism. Stereotyped vomiting attacks with symptom-free intervals are cyclic vomiting or cannabinoid hyperemesis, separated by asking about cannabis and hot showers. Obstruction without a lesion is pseudo-obstruction: exclude a mechanical cause, confirm dysmotility, separate neuropathic from myopathic disease, and search for a cause such as scleroderma or an anti-Hu paraneoplastic syndrome. Then comes supportive treatment. Functional dyspepsia is sorted into postprandial distress and epigastric pain, with alarm features and age deciding whether endoscopy comes first, and the subtype choosing the drug.

Topics covered

Cyclic vomiting syndrome phases and mimics
Prevention and abortive therapy for cyclic vomiting
Cannabinoid hyperemesis and TRPV1
Chronic intestinal pseudo-obstruction workup
Neuropathic versus myopathic disease and antroduodenal manometry
Secondary causes: scleroderma and paraneoplastic disease
Nutrition, overgrowth, and prokinetics in pseudo-obstruction
Functional dyspepsia definition and subtypes
Alarm features and when to scope first
Subtype-directed dyspepsia treatment

Key decisions

Diagnose cyclic vomiting syndrome from at least two stereotyped attacks in six months or three in a year with symptom-free intervals, and always ask about cannabis, hot showers, and eating and weight.
Prevent cyclic vomiting with bedtime amitriptyline or nortriptyline titrated from 25 to 100 mg, and treat attacks with fluids, ondansetron, lorazepam, and subcutaneous sumatriptan.
In a daily cannabis user who finds relief in hot showers, have him stop cannabis with addiction support, since attacks usually stop within one to two weeks, and do not rely on tricyclics or ondansetron.
Call it pseudo-obstruction only after CT or MR enterography, barium study, or endoscopy excludes a mechanical cause, then confirm dysmotility and use antroduodenal manometry to separate neuropathic from myopathic disease.
Look for a secondary cause in every patient: megaduodenum and scleroderma in a woman with systemic sclerosis, and anti-Hu antibodies with a chest CT in an older smoker with rapid weight loss.
Treat pseudo-obstruction with jejunal feeding through a combined venting tube, rotating antibiotics for bacterial overgrowth, and prucalopride 2 mg daily (1 mg over age 65) as the preferred prokinetic, avoiding routine octreotide.
In functional dyspepsia, test and treat H. pylori and then give a standard-dose PPI for 4 to 8 weeks if the patient is under 60 without alarm features, but scope first at 60 or older or with any alarm feature such as weight loss over 5 percent.
Match refractory dyspepsia treatment to the subtype: mirtazapine 7.5 mg at bedtime, up to 15 to 30 mg, for postprandial distress with weight loss, and a low-dose tricyclic at 10 to 50 mg for refractory epigastric pain.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and three problems
(00:57) - Cyclic vomiting syndrome case
(05:23) - Cannabinoid hyperemesis syndrome
(07:23) - Pseudo-obstruction with scleroderma
(08:41) - Workup and manometry
(13:24) - Supportive treatment and surgery
(15:42) - Paraneoplastic pseudo-obstruction in a smoker
(17:12) - Functional dyspepsia and postprandial distress
(24:11) - Epigastric pain subtype path
(26:46) - Start to finish review

Chapter 9, Ep 1 of 2: Upper GI Bleeding: Non-Variceal Bleeding Care

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

Upper GI bleeding is a perfusion problem first, a diagnosis problem second, and an endoscopy problem third, so the first hour follows a fixed order: resuscitate, prepare the stomach, estimate risk, then scope. The episode follows a man with a bleeding duodenal ulcer through restrictive transfusion, pre-endoscopy drugs, risk scoring, Forrest-guided dual therapy, PPI protection, rebleeding, and H. pylori eradication. It then turns to bleeding on blood thinners, where two risks compete, the bleed now and the clot the drug prevented. That covers apixaban, aspirin, warfarin, dabigatran, and a recent stent.

Topics covered

Resuscitation and airway
Restrictive transfusion thresholds
Pre-endoscopy PPI and erythromycin
Glasgow-Blatchford and other risk scores
Timing of endoscopy
Forrest classification and dual therapy
High-dose PPI after hemostasis
Rebleeding: repeat endoscopy, embolization, surgery
H. pylori, NSAIDs, and follow-up endoscopy
Reversal and restart of anticoagulants and antiplatelets

Key decisions

Transfuse when hemoglobin falls below 7 g/dL, aiming for 7 to 9, and do not transfuse a stable patient with cirrhosis to 9 or 10.
Give an intravenous PPI and erythromycin 250 mg before endoscopy, and never give tranexamic acid.
Manage a patient with a Glasgow-Blatchford score of 0 or 1 as an outpatient, and scope non-variceal bleeding within 24 hours without rushing it at the expense of resuscitation.
Treat Forrest 1A, 1B, and 2A lesions with dual therapy, epinephrine plus a thermal method, ethanol, or clips, never epinephrine alone, and give no endoscopic treatment for a flat spot or clean base.
After treating a high-risk lesion, give high-dose intravenous PPI for 72 hours, then oral PPI twice daily for two weeks, then once daily to complete four to eight weeks.
Send a rebleed to repeat endoscopy with an over-the-scope clip, then embolization, and reserve surgery for failure of those.
Eradicate H. pylori, stop the NSAID, and re-scope a gastric ulcer at six to twelve weeks, but not a duodenal ulcer.
Hold but do not reverse a factor Xa inhibitor in a stable patient, use four-factor PCC for major warfarin bleeding and idarucizumab 5 g for life-threatening dabigatran bleeding, and restart anticoagulation within about seven days.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patients
(02:05) - Resuscitation, airway, and transfusion
(03:40) - Drugs before the scope
(04:55) - Risk scores and timing
(06:43) - Forrest classification and dual therapy
(11:07) - Rebleeding and rescue options
(11:59) - Preventing the next bleed
(13:42) - Apixaban and aspirin
(17:31) - Warfarin and dabigatran reversal
(19:32) - Recent stent and antiplatelets

Chapter 9, Ep 2 of 2: Upper GI Bleeding: Varices and Hidden Sources

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

Variceal bleeding is managed as a bundle that mostly starts before the endoscope, while the other sources in this episode escape the standard approach unless someone suspects them. The episode begins with a cirrhotic man vomiting blood: airway protection, restrictive transfusion, no routine correction of clotting tests, octreotide, ceftriaxone, band ligation within twelve hours, and early covered TIPS in high-risk patients. It then covers tamponade and stent bridges, gastric varices, and secondary prophylaxis. Next come a Dieulafoy lesion, an aortoenteric fistula, GAVE and Cameron lesions, small bowel angiodysplasia with aortic stenosis, and hereditary hemorrhagic telangiectasia, ending with the board traps.

Topics covered

Why esophageal varices bleed
Pre-endoscopy variceal bundle
Restrictive transfusion and coagulopathy
Band ligation and early TIPS
Tamponade, stents, and gastric varices
Secondary prophylaxis
Dieulafoy lesion
Aortoenteric fistula
GAVE versus portal hypertensive gastropathy
Cameron lesions
Small bowel angiodysplasia and Heyde syndrome
Hereditary hemorrhagic telangiectasia

Key decisions

Intubate electively before endoscopy a patient with grade three or four encephalopathy and active bleeding.
Transfuse restrictively to a hemoglobin of about seven and do not give routine plasma, platelets, or cryoprecipitate for abnormal clotting tests in cirrhosis.
Start octreotide, a fifty-microgram bolus then fifty micrograms per hour for two to five days, on suspicion before endoscopy, and give ceftriaxone one gram daily for up to seven days to every bleeding patient with cirrhosis rather than a fluoroquinolone.
Perform endoscopy within twelve hours and treat bleeding esophageal varices with band ligation rather than sclerotherapy.
Place a covered TIPS within seventy-two hours in Child-Pugh C patients with ten to thirteen points or Child B patients with active bleeding at endoscopy, even if bleeding has stopped, and use salvage TIPS when endoscopy cannot control bleeding.
Limit balloon tamponade to no more than twenty-four hours in an intubated patient, as a bridge, and treat fundal varices with cyanoacrylate glue or coils while searching for splenic vein thrombosis.
Scope a suspected Dieulafoy lesion during active bleeding after erythromycin, treat with hemoclips plus injection or thermal therapy rather than epinephrine alone, and tattoo the site.
Treat GAVE endoscopically, with band ligation increasingly favored over argon plasma coagulation, and do not use beta-blockers or TIPS for it.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patient list
(02:28) - The variceal bleeding bundle
(06:03) - Early TIPS for high-risk patients
(08:10) - Gastric varices and fundal treatment
(09:49) - Dieulafoy lesion between bleeds
(13:09) - Aortoenteric fistula and herald bleeds
(15:03) - GAVE and Cameron lesions
(18:21) - Small bowel angiodysplasia and Heyde syndrome
(19:52) - Hereditary hemorrhagic telangiectasia
(22:19) - Board traps and summary

Chapter 10, Ep 1 of 2: Celiac Disease and Sprue Spectrum: Test and Treat

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

Adult celiac disease usually hides behind another diagnosis, and the mechanism of gluten injury explains every test used to find it. This episode follows one young woman with iron deficiency, loose stools, and a fracture. It starts with the atypical presentations and the autoimmune associations that raise suspicion. It then covers the immune mechanism, including HLA-DQ2 and DQ8, and the rule that testing happens on gluten. Next come tissue transglutaminase IgA with total IgA, the biopsy protocol and Marsh grading, and the limited role of HLA testing. The silent, potential, and seronegative forms and dermatitis herpetiformis follow. It ends with the gluten-free diet, vaccination, bone protection, and follow-up.

Topics covered

Atypical adult presentations of celiac disease
Autoimmune associations and family risk
Gluten, tissue transglutaminase, and HLA-DQ2 or DQ8
Epidemiology and screening of relatives
Testing while eating gluten and the gluten challenge
Tissue transglutaminase IgA with total IgA
Duodenal biopsy protocol and Marsh classification
Role and limits of HLA testing
Silent, potential, and seronegative celiac disease
Dermatitis herpetiformis and dapsone
Gluten-free diet, vaccination, and bone care
Serology and biopsy follow-up

Key decisions

Check celiac serology before accepting an irritable bowel diagnosis, and suspect celiac disease in iron deficiency that fails oral iron with no blood loss to explain it.
Test while the patient is still eating gluten; if already gluten-free, use a gluten challenge of about ten grams a day, roughly three slices of bread, for one to three months, or use HLA testing to exclude the disease.
Order tissue transglutaminase IgA together with a total IgA level, and if total IgA is low switch to IgG tests, preferring deamidated gliadin peptide IgG.
Take at least four distal duodenal biopsies plus one or two from the bulb, because about ten percent of patients have damage confined to the bulb, and diagnose from serology and biopsy together since raised lymphocytes and villous atrophy have other causes.
Use HLA-DQ2 and DQ8 testing only to exclude celiac disease, resolve discordant results, screen high-risk children, or settle ambiguous cases, since a negative result essentially excludes the disease and a positive one shows only susceptibility.
For dermatitis herpetiformis, biopsy skin next to a lesion for granular IgA, treat with the gluten-free diet, and check G6PD before dapsone and monitor the liver.
Prescribe a strict lifelong gluten-free diet with a dietitian, labeled gluten-free food under twenty parts per million, and certified gluten-free oats introduced carefully.
Vaccinate against pneumococcus, replace calcium and vitamin D, repeat DEXA every three years if abnormal or five if normal, expect tissue transglutaminase IgA to normalize by twelve months, and rebiopsy at about two years to confirm healing.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and roadmap
(00:44) - The patient and her clues
(03:36) - Mechanism, HLA, and epidemiology
(06:21) - Serology on a gluten diet
(08:03) - Biopsy protocol and Marsh grading
(10:55) - Silent, potential, seronegative forms
(11:46) - Dermatitis herpetiformis
(13:30) - Gluten-free diet and protection
(15:20) - Monitoring serology and healing
(16:40) - Board traps and summary

Chapter 10, Ep 2 of 2: Celiac Disease and Sprue Spectrum: When Diet Fails

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

The organizing idea is that most celiac patients who fail the diet are not refractory, so the order of the workup matters. Using one 61-year-old man with watery diarrhea and weight loss, the episode starts with a dietitian review for hidden gluten, then confirms the original diagnosis with serology, HLA typing, and expert biopsy review. It then looks for coexisting causes such as microscopic colitis, pancreatic insufficiency, and bacterial overgrowth, and for drugs like olmesartan that mimic the disease. Only then does it define refractory disease, show how fresh biopsies and flow cytometry separate type one from type two, and compare their treatment and outcomes. It closes with enteropathy-associated lymphoma, ulcerative jejunitis, small bowel adenocarcinoma, and who needs surveillance.

Topics covered

Non-responsive celiac disease
Hidden gluten and dietitian review
Confirming the original diagnosis
Microscopic colitis and other coexisting causes
Drug-induced villous atrophy
Defining refractory celiac disease
Biopsy handling and flow cytometry
Type one versus type two treatment
Enteropathy-associated T-cell lymphoma and ulcerative jejunitis
Small bowel adenocarcinoma and surveillance

Key decisions

Send every non-responsive celiac patient to a dietitian experienced in celiac disease first, and do not treat a normal antibody as proof that the bowel has healed.
Confirm the original diagnosis from the original serology, HLA typing for DQ2 or DQ8, and an expert review of the original biopsies.
Perform colonoscopy with random biopsies for microscopic colitis, check fecal elastase and start enzyme replacement when it is under 200 micrograms per gram, and test for bacterial overgrowth with a breath test or empiric rifaximin.
Review the medication list for olmesartan and other angiotensin receptor blockers, NSAIDs, and mycophenolate, which can cause villous atrophy that looks like active celiac disease.
Send two or three duodenal biopsies fresh for flow cytometry and two or three in formalin for immunohistochemistry and T-cell receptor rearrangement PCR, because formalin destroys the surface markers flow cytometry reads.
Call refractory disease type two when more than 20 percent of intraepithelial lymphocytes lack surface CD3 and CD8 and the rearrangement is monoclonal, and treat it with cladribine, often followed by autologous stem cell transplant, rather than like type one.
Treat type one with the strict diet plus budesonide 9 milligrams a day as 3 milligrams three times daily, with the capsules opened so the drug reaches the small bowel.
When a stable patient relapses on a strict diet, consider gluten, refractory disease, and lymphoma together, and image the small bowel with CT or MR enterography, capsule endoscopy, and balloon-assisted enteroscopy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode roadmap
(00:40) - The patient and hidden gluten
(02:05) - Confirming the original diagnosis
(02:44) - Coexisting conditions and drug mimics
(04:07) - Defining refractory celiac disease
(04:31) - Biopsy handling and typing
(06:06) - Treatment and outlook by type
(07:29) - Lymphoma and ulcerative jejunitis
(09:26) - Adenocarcinoma and surveillance
(11:21) - Board traps and summary

Chapter 11, Ep 1 of 1: Small Bowel Mucosal Disease: Beyond Celiac Disease

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

Six patients show the small bowel problems that sit beside celiac disease, and each case asks what must be excluded, which finding decides, and how the mechanism chooses treatment. The episode begins by excluding celiac disease before labeling wheat symptoms as gluten sensitivity, wheat allergy, or FODMAP intolerance. It then reads the medication list in seronegative villous atrophy, with olmesartan as the model, and moves to autoimmune enteropathy and its immunosuppressive treatment. Tropical sprue follows, separated by low folate and low B12, and then Whipple disease, from migratory arthritis to biopsy, lumbar puncture, and brain-penetrating antibiotics. It ends with bacterial overgrowth, its causes, breath testing, and recurrence.

Topics covered

Excluding celiac disease with HLA testing
Wheat allergy, gluten sensitivity, and FODMAP intolerance
Low-FODMAP diet in three phases
Drug-induced enteropathy and olmesartan sprue
Autoimmune enteropathy
Tropical sprue
Whipple disease
Small intestinal bacterial overgrowth
Board traps across the chapter

Key decisions

In a patient already gluten-free, exclude celiac disease with HLA-DQ2 and DQ8 typing, since a negative result rules it out, or by a gluten challenge of about ten grams a day for one to three months before testing.
In a patient with irritable bowel-type symptoms who feels better off wheat, start a dietitian-supervised low-FODMAP diet (eliminate for four to six weeks, reintroduce, personalize) before committing to lifelong gluten avoidance.
In villous atrophy with negative celiac serology and no response to a gluten-free diet, review the medications first, and stop olmesartan, which is both the treatment and the diagnosis, without restarting it to prove the point.
In suspected autoimmune enteropathy, check quantitative immunoglobulins for common variable immunodeficiency, then treat with budesonide nine milligrams daily with the capsules opened for proximal release.
In a returning traveler with low folate and low B12 and a macrocytic anemia, diagnose tropical sprue, exclude Giardia, and treat with folic acid and tetracycline plus B12 injections.
In suspected Whipple disease, biopsy the distal duodenum and jejunum, confirm PAS-positive, acid-fast negative macrophages with PCR, perform a lumbar puncture in every patient, and treat with ceftriaxone followed by a year of trimethoprim-sulfamethoxazole.
In suspected bacterial overgrowth, use a glucose or lactulose breath test, where a hydrogen rise of at least twenty parts per million within ninety minutes is positive, and treat with rifaximin 550 milligrams three times a day for fourteen days.
When the cause of overgrowth cannot be corrected, such as a permanent afferent limb or a motility disorder, expect recurrence and use cyclic, rotating antibiotics.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and six cases
(01:02) - Wheat symptoms: excluding celiac first
(08:04) - Seronegative villous atrophy and olmesartan
(11:07) - Other drugs that injure the bowel
(13:35) - Autoimmune enteropathy and budesonide
(16:47) - Tropical sprue after travel
(20:05) - Whipple disease from joints to gut
(26:23) - Bacterial overgrowth after gastrectomy
(31:48) - Traps the boards set
(33:28) - Start to finish review

Chapter 12, Ep 1 of 2: Chronic Diarrhea and Malabsorption: First Workup

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

Chronic diarrhea is loose stools for more than four weeks, and small absorptive failures cause big diarrhea. The episode starts with the history, especially the medication list including over-the-counter products and supplements, then the surgical history, the exam, and a rectal exam. It then moves through first blood tests, stool studies, and targeted imaging and endoscopy. The stool osmotic gap sorts diarrhea into osmotic, secretory, inflammatory, or fatty types. Secretory diarrhea is proven with a supervised fast and worked up from common to rare causes: microscopic colitis, bile acid diarrhea, drugs, infection, neuroendocrine tumors such as VIPoma, carcinoid, and gastrinoma, then laxative abuse and idiopathic disease.

Topics covered

Definition and mechanisms of chronic diarrhea
History and medication culprits
Surgical history and exam clues
First labs and stool studies
Imaging and endoscopy
Stool osmotic gap and osmotic diarrhea
Proving secretory diarrhea with a fast
Common causes of secretory diarrhea
Neuroendocrine tumors and VIPoma
Factitious and idiopathic secretory diarrhea

Key decisions

Define chronic diarrhea as loose stools for more than four weeks, and ask specifically about antacids, supplements, vitamins, laxatives, herbal products, and sugar-free foods, because the medication list is the most productive part of the history.
Send a blood count, metabolic panel, CRP, TSH, and tissue transglutaminase IgA with a total IgA as first labs, because selective IgA deficiency invalidates IgA-based celiac serology.
Use fecal calprotectin to separate inflammatory from non-inflammatory diarrhea: under 50 micrograms per gram essentially excludes IBD, 50 to 250 is indeterminate, and over about 250 (150 in some labs) calls for colonoscopy.
Calculate the osmotic gap as 290 minus twice the sum of stool sodium and potassium: under 50 is secretory, over 100 is osmotic, and it cannot be trusted when measured stool osmolality is far from 290.
Confirm secretory diarrhea with a supervised fast of 24 to 48 hours, since persistent high volume means the drive is not something eaten, while stopping with fasting means an osmotic cause was missed.
Work up secretory diarrhea from common to rare: colonoscopy with right and left colon biopsies for microscopic colitis, a cholestyramine trial of 4 grams once to four times a day for bile acid diarrhea, then drugs and chronic infection, and send a neuroendocrine panel only when the picture fits.
Diagnose a VIPoma with a fasting VIP over 200 picograms per milliliter plus cross-sectional and DOTATATE imaging, correct fluids and potassium first, resect if localized, and use octreotide or lanreotide for metastatic disease.
Consider surreptitious laxative use in a young patient with hypokalemia and a normal workup, and screen urine and stool for bisacodyl, anthraquinones, and phenolphthalein.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode overview
(02:09) - History and why small problems matter
(02:51) - Medication list and culprit drugs
(05:51) - First labs for systemic causes
(06:57) - Stool studies, imaging, and endoscopy
(09:05) - Osmotic gap and osmotic diarrhea
(12:36) - Proving secretory diarrhea
(14:40) - Secretory causes, common to rare
(16:46) - VIPoma diagnosis and treatment
(21:05) - Factitious and idiopathic diarrhea

Chapter 12, Ep 2 of 2: Chronic Diarrhea and Malabsorption: Bile and Fat

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

The organizing idea is that chronic diarrhea needs its mechanism identified before it is labeled irritable bowel. The episode starts with bile acids in the colon, how a sequestrant trial confirms the diagnosis, and why a long ileal resection reverses the treatment. It then covers microscopic colitis: culprit drugs, biopsies from both sides of the colon, and staged therapy with budesonide. Next comes fatty stool, proven by fecal fat and split into pancreatic and mucosal causes by fecal elastase. Bloody diarrhea is named by the colonoscopy pattern. Last is the empty workup, with a repeat history, empiric trials in order of likelihood, targeted tests, referral, and only then the irritable bowel label.

Topics covered

Bile acid physiology and bile acid diarrhea
Diagnosing without the SeHCAT scan
Sequestrant dosing and long ileal resection
Microscopic colitis risk factors and biopsy
Staged treatment with budesonide
Celiac disease and microscopic colitis overlap
Steatorrhea testing and fecal elastase
Pancreatic enzyme dosing
Mucosal causes of fat malabsorption
Colonoscopy patterns in bloody diarrhea
Obscure diarrhea and empiric trials
When irritable bowel applies

Key decisions

Suspect bile acid diarrhea in urgent, watery, often nocturnal diarrhea after cholecystectomy, and confirm it with a one to two week sequestrant trial because SeHCAT is not available in the United States.
Start cholestyramine at four grams once daily, up to sixteen grams a day, and take other drugs one hour before or four hours after it, or switch to colesevelam at three point seven five grams a day if the powder is not tolerated.
Do not give a sequestrant after more than one hundred centimeters of ileal resection; use a low-fat diet, medium-chain triglycerides, and fat-soluble vitamins instead.
For suspected microscopic colitis, take random biopsies from both the right and left colon even when the colon looks normal, then stop NSAIDs, PPIs, SSRIs, and smoking before starting budesonide nine milligrams a day for six to eight weeks.
Use maintenance budesonide three to six milligrams a day for relapse, which occurs in sixty to eighty percent after stopping.
In a celiac patient with persistent watery diarrhea despite a normal tissue transglutaminase, perform colonoscopy with right and left colon biopsies, not a repeat duodenal biopsy.
Prove steatorrhea with fecal fat over fourteen grams a day, then use fecal elastase under two hundred on a formed stool to call pancreatic insufficiency and dose enzymes at twenty-five thousand to fifty thousand lipase units with each meal, taken with the first bite.
In unexplained diarrhea, retake the history first, then run empiric trials in order of likelihood starting with a bile acid sequestrant, and do HLA DQ2 and DQ8 typing before any gluten-free trial.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patient list
(01:14) - Bile acid diarrhea after cholecystectomy
(06:50) - Long ileal resection reverses treatment
(07:51) - Microscopic colitis diagnosis and treatment
(13:30) - Celiac disease and microscopic colitis
(14:23) - Steatorrhea and pancreatic insufficiency
(18:33) - Mucosal causes of fat malabsorption
(20:54) - Bloody diarrhea and colonoscopy patterns
(22:20) - Obscure diarrhea and empiric trials
(27:22) - When irritable bowel finally applies

Chapter 13, Ep 1 of 2: IBS and Functional Bowel: Constipation Subtype

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

Irritable bowel syndrome with constipation is a positive diagnosis made from the symptom pattern, and one 34-year-old woman carries the case from first visit to treatment. The episode starts with the Rome IV criteria and then assigns the subtype from Bristol stool form on abnormal days. Next it checks alarm features and decides that no testing is needed without them, while screening for pelvic floor dyssynergia. It then explains her pain and constipation through visceral hypersensitivity and slow colonic transit. Treatment follows in steps: explanation, stopping constipating drugs, psyllium, polyethylene glycol, secretagogues, prucalopride, and pain-directed therapy.

Topics covered

Rome IV criteria
Irritable bowel versus chronic constipation
Subtyping by Bristol stool form
Alarm features
Testing in constipation-predominant disease
Pelvic floor dyssynergia
Visceral hypersensitivity and slow transit
Fiber and polyethylene glycol
Secretagogues
Prucalopride and pain-directed therapy

Key decisions

Diagnose irritable bowel from the Rome IV pattern: abdominal pain at least one day a week for three months, with onset at least six months ago, related to defecation or to a change in stool frequency or form.
Call it chronic idiopathic constipation, not irritable bowel, when hard infrequent stools and bloating come with little or no pain.
Assign constipation-predominant disease when at least a quarter of abnormal movements are Bristol 1 or 2 and fewer than a quarter are Bristol 6 or 7.
With no alarm features, order no labs, imaging, or colonoscopy beyond age-based colon cancer screening, which starts at 45 in average-risk adults.
Send a patient who strains, feels incomplete evacuation, or splints for anorectal manometry with balloon expulsion testing and biofeedback instead of escalating laxatives.
Add soluble fiber (psyllium) toward about 25 grams a day, increased slowly, rather than wheat bran, and stop constipating drugs such as opioids, anticholinergics, calcium channel blockers, iron, and calcium.
Add a secretagogue when pain and constipation travel together: linaclotide 290 micrograms daily on an empty stomach, plecanatide 3 milligrams daily, lubiprostone 8 micrograms twice daily with food, or tenapanor 50 milligrams twice daily.
Use prucalopride 2 milligrams daily (1 milligram in renal impairment, off label here) when secretagogues fail or the colon is slow, and choose an SSRI rather than a tricyclic for pain in a constipated patient.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 Patient Case
(01:36) - Diagnosis by Rome IV Criteria
(02:46) - Assigning the Subtype
(03:44) - Alarm Features and Testing
(05:00) - Screening for Outlet Dysfunction
(05:38) - Why Pain and Constipation Occur
(07:10) - First Steps: Fiber and Laxatives
(08:41) - Secretagogue Drugs Compared
(11:12) - Prucalopride and Pain Therapy
(12:50) - Board Traps and Summary

Chapter 13, Ep 2 of 2: IBS and Functional Bowel: Diarrhea and Bloating

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

Irritable bowel is a positive diagnosis, and treatment follows the mechanism that drives the symptoms. The episode starts with a young man with diarrhea-predominant disease: Rome IV diagnosis, subtype by Bristol form, alarm features, a narrow screen, and the treatable mimics that slip past it. Treatment then runs through loperamide, rifaximin, bile acid sequestrants, eluxadoline, alosetron, and low-dose tricyclics. The second patient has mixed-subtype IBS with fibromyalgia and migraines, so pain is treated through the gut and the brain, with peppermint oil, neuromodulators, and behavioral therapy. Bloating is worked up from the lumen outward, ending with abdomino-phrenic dyssynergia.

Topics covered

Rome IV diagnosis and subtype
Alarm features and the narrow screen
Mimics of diarrhea-predominant IBS
Post-infectious IBS and C. difficile retesting
Drugs for diarrhea-predominant IBS
Eluxadoline and alosetron limits
Visceral hypersensitivity and central pain
Peppermint oil and neuromodulators
CBT and gut-directed hypnotherapy
Bloating workup and low-FODMAP diet
Abdomino-phrenic dyssynergia

Key decisions

Diagnose diarrhea-predominant IBS from the symptom pattern using Rome IV, and set the subtype from stool form on bad days, with at least a quarter Bristol six or seven and under a quarter Bristol one or two.
With no alarm features, send tissue transglutaminase IgA with a total IgA, CRP and fecal calprotectin, and Giardia testing when there is an exposure; send a positive antibody to duodenal biopsy and a high calprotectin to colonoscopy.
Suspect bile acid diarrhea after cholecystectomy, ileal resection, or ileal Crohn disease, and treat with a sequestrant such as cholestyramine four grams once to four times a day; a response within days to two weeks supports the diagnosis.
Do not retest for C. difficile in typical post-infectious IBS without features of active infection, because thirty to fifty percent of positives in that setting are false positives.
Treat frequency and urgency with loperamide, bloating and overall symptoms with rifaximin 550 mg three times a day for fourteen days (up to two retreatments), and pain with low-dose amitriptyline ten to thirty milligrams at bedtime.
Never give eluxadoline after cholecystectomy or with heavy drinking, prior pancreatitis, or biliary disease, and reserve alosetron for women with severe refractory diarrhea-predominant disease, never men or the mixed subtype.
In mixed-subtype IBS with fibromyalgia and migraine, choose duloxetine as the neuromodulator, allow weeks before judging it, and use enteric-coated peppermint oil rather than anticholinergic antispasmodics.
For bloating, check constipation and incomplete evacuation first, then bacterial overgrowth and a three-phase dietitian-guided low-FODMAP diet, and send a patient with a clear lumen and protruding belly to physical therapy for abdomino-phrenic dyssynergia.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(01:05) - Diagnosing IBS with diarrhea
(01:50) - Alarm features and the narrow screen
(03:53) - Treatable mimics and post-infectious IBS
(06:44) - Choosing drugs for diarrhea
(09:32) - Eluxadoline and alosetron limits
(11:38) - Mixed subtype and visceral pain
(14:43) - Neuromodulators and behavioral therapy
(17:34) - Working up bloating from the lumen
(20:10) - Abdomino-phrenic dyssynergia

Chapter 14, Ep 1 of 3: Inflammatory Bowel Disease: Ulcerative Colitis

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

Ulcerative colitis care comes down to matching treatment to where the disease sits, how far it reaches, and how sick the patient is. The episode begins with bloody diarrhea, a high fecal calprotectin, and ileocolonoscopy with biopsies that separate ulcerative colitis from Crohn disease, then classifies extent by Montreal. It covers risk factors and the immune biology behind modern drugs. Treatment follows: mesalamine formulation matched to extent, oral plus topical dosing, and sulfasalazine when arthritis coexists. The episode ends in the hospital with admission criteria, the first-hours plan, the day three decision, a single salvage attempt, and the triggers for colectomy.

Topics covered

Fecal calprotectin and IBD diagnosis
Ileocolonoscopy and biopsy findings
Montreal classification of extent
Crohn disease by comparison
Smoking and other risk factors
Immune pathways and IBD genes
Mesalamine formulation and dosing
Sulfasalazine for peripheral arthritis
Severity scoring and Truelove and Witts criteria
Acute severe colitis: steroids, salvage, and surgery

Key decisions

Suspect IBD when infection is excluded and fecal calprotectin is above about 150 to 200 micrograms per gram, then use ileocolonoscopy with the terminal ileum intubated and biopsies to decide between ulcerative colitis and Crohn disease.
Classify extent as Montreal E1, E2, or E3 and match the mesalamine formulation to it: suppositories reach only the last 15 to 20 centimeters, while 4 gram enemas reach the splenic flexure.
Induce moderate left-sided disease with oral plus topical five-ASA, using oral mesalamine 4.8 grams a day, and step down to 2.4 grams a day once remission holds, aiming for an endoscopic Mayo subscore of 0 or 1.
Escalate to systemic corticosteroids or an advanced therapy when five-ASA gives no response within four to eight weeks.
Choose sulfasalazine when peripheral arthritis coexists, give daily folic acid, and discuss reversible low sperm counts before starting.
Admit for acute severe colitis when there are more than six bloody stools a day plus a temperature over 37.8, heart rate over 90, hemoglobin under 10.5, or ESR over 30; exclude C. difficile and CMV, image for megacolon, start intravenous steroids and clot prophylaxis, let the patient eat, and avoid loperamide and opioids.
On day three, more than eight stools, or three to eight with a CRP over 45 milligrams per liter, means salvage with infliximab (10 milligrams per kilogram if albumin is very low) or cyclosporine rather than a higher steroid dose.
No response to salvage within five to seven days means subtotal colectomy, and perforation, uncontrolled hemorrhage, or toxic megacolon not improving within 24 to 48 hours means emergency colectomy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(00:49) - Bloody diarrhea and calprotectin
(01:54) - Scope, biopsies, and Montreal extent
(03:29) - Crohn disease by comparison
(05:22) - Risk factors and immune biology
(08:56) - Mesalamine formulation and dosing
(14:02) - Sulfasalazine for arthritis
(15:17) - Severity scoring and admission criteria
(17:38) - First hours of acute severe colitis
(18:41) - Day three salvage and surgery

Chapter 14, Ep 2 of 3: Inflammatory Bowel Disease: Crohn Disease Therapy

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

Crohn disease is managed by where it sits and how it behaves, because untreated inflammatory disease often scars into strictures or tunnels into fistulas. The episode begins with Montreal classification and the features that justify early biologic therapy, then covers safe thiopurine use and steroid choices. It next sorts advanced drug classes by what they block and which comorbidities exclude them, including JAK inhibitors and S1P modulators. It then takes perianal disease, where the abscess is drained before any biologic, followed by strictures, choosing dilation or surgery, and prevention of postoperative recurrence with scheduled colonoscopy and the Rutgeerts score.

Topics covered

Montreal classification of Crohn disease
Features predicting an aggressive course
Budesonide and systemic steroid use
Thiopurine testing and monitoring
Treat-to-target with objective markers
Advanced therapy classes and exclusions
JAK inhibitors and S1P modulators
Perianal fistula and abscess management
Stricture dilation versus surgery
Postoperative recurrence and Rutgeerts score

Key decisions

Start infliximab with azathioprine early, after tuberculosis and hepatitis B screening, in a young patient with deep ulcers, smoking, steroid need at presentation, and extensive small bowel disease, and start budesonide nine milligrams a day for low-risk mild ileal disease.
Test TPMT before any thiopurine, giving no drug when activity is absent and half dose when it is intermediate, and add NUDT15 testing in patients of Asian, Hispanic, or Native American ancestry.
Avoid anti-TNF drugs in class three or four heart failure and multiple sclerosis, avoid JAK inhibitors with a clot history or heart disease, and choose vedolizumab or an IL-23 drug instead.
Give anti-TNF therapy rather than vedolizumab when extraintestinal joint or eye disease is prominent, and give the recombinant zoster vaccine before a JAK inhibitor and an ECG and eye exam before ozanimod.
Drain a perianal abscess and place setons before any biologic, then give metronidazole with dose-optimized infliximab, using methotrexate rather than a thiopurine in a young man, and remove setons at three to six months.
Treat inflammation around a stricture medically first, dilate only short accessible strictures under four to five centimeters, and use stricturoplasty rather than resection outside the colon when no abscess, dysplasia, or cancer is present.
Start an anti-TNF drug within four weeks of resection in high-risk patients, require smoking cessation, perform ileocolonoscopy at six to twelve months in everyone, and escalate at Rutgeerts i-two.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and first patient
(01:04) - Classifying Crohn and assessing risk
(04:50) - Steroid choices by disease location
(06:20) - Starting thiopurines safely
(09:37) - Choosing advanced therapy by comorbidity
(16:24) - JAK inhibitors and S1P modulators
(19:06) - Perianal fistula and abscess
(23:58) - Strictures: dilation or surgery
(27:59) - Postoperative colonoscopy and Rutgeerts score
(29:14) - Board traps and summary

Chapter 14, Ep 3 of 3: Inflammatory Bowel Disease: The Pouch and Beyond

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

The organizing idea is that where a problem sits, and whether it follows the bowel, decides the treatment. The episode starts with the ileal pouch: pouchitis, its antibiotic-dependent and antibiotic-refractory forms, cuffitis, Crohn-like disease, and irritable pouch, with endoscopy and biopsies first. It then turns to the colon, covering when surveillance starts, how often, which technique, and what to do with visible and invisible dysplasia. Next come extraintestinal manifestations of the joints, eyes, liver, skin, and kidney, sorted by whether they track bowel activity. It closes with the whole patient: nutrient deficiencies, bone health, vaccines before immunosuppression, and pregnancy for both parents.

Topics covered

Pouchitis causes, risk factors, and diagnosis
Acute, chronic, and refractory pouchitis treatment
Cuffitis, Crohn-like disease, and irritable pouch
Pouch cancer surveillance
Colitis dysplasia surveillance timing and technique
Management of visible and invisible dysplasia
Extraintestinal manifestations and their link to bowel activity
Eye, skin, liver, and kidney complications
Nutrient deficiencies and bone health
Vaccines and pregnancy on immunosuppression

Key decisions

Diagnose pouchitis only after pouchoscopy with biopsies exclude C. difficile, CMV, cuffitis, and Crohn-like disease, then treat acute pouchitis with ciprofloxacin 1000 mg a day or metronidazole 750 to 1500 mg a day for 7 to 14 days.
In antibiotic-refractory pouchitis, first exclude infection, ischemia, NSAID use, and celiac disease, then escalate to a biologic, with vedolizumab best supported but not approved for pouchitis in the United States.
Treat cuffitis topically with mesalamine or topical steroids, not antibiotics, and treat Crohn-like disease of the pouch like luminal Crohn disease, with an anti-TNF drug first.
Start surveillance colonoscopy 8 to 10 years after symptom onset in extensive colitis, and at the diagnosis of primary sclerosing cholangitis, using high-definition chromoendoscopy in remission, yearly in high-risk patients, every 2 to 3 years in intermediate-risk, and every 5 years if low-risk.
Resect visible resectable dysplasia endoscopically and survey at 3 to 6 months then yearly, send non-resectable visible dysplasia and invisible high-grade dysplasia to proctocolectomy, and confirm every dysplasia read with a second pathologist.
Send anterior uveitis or scleritis for same-day ophthalmology, prefer an anti-TNF drug over vedolizumab when extraintestinal disease is prominent, avoid etanercept and IL-17 inhibitors, and do not debride pyoderma gangrenosum.
Use intravenous iron in active inflammation and parenteral B12, 1000 micrograms intramuscularly weekly for four weeks then monthly, after ileal resection.
Give live vaccines at least four weeks before a biologic, aim for remission at conception, stop methotrexate in either parent three to six months before trying, avoid JAK inhibitors in pregnancy, and defer rotavirus in infants exposed to biologics other than certolizumab.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(01:12) - Pouchitis from acute to refractory
(06:52) - Cuffitis, Crohn-like disease, irritable pouch
(09:13) - Colitis cancer surveillance and lesions
(14:44) - Invisible dysplasia and special findings
(16:14) - Extraintestinal manifestations of IBD
(22:13) - Skin and kidney complications
(24:21) - Nutrient deficiencies and bone health
(27:07) - Vaccines before immunosuppression
(28:44) - Pregnancy and conception planning

Chapter 15, Ep 1 of 2: Colorectal Cancer and Polyps: Screening to Therapy

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

This episode follows colorectal neoplasia from screening to treatment. Screening prevents cancer by removing precursors and lowers deaths by finding early cancer, so the first decisions are when to start, which test to use, and what a positive stool test requires. Next come polyps, where histology, size, and number set surveillance, and where serrated lesions are easy to miss. Then a new cancer is tested for mismatch repair, staged, and matched to adjuvant therapy by stage and risk. Metastatic disease is treated by reading the tumor profile in order, with mismatch repair first. The episode ends with rectal cancer, where the pelvis calls for pelvic MRI, total neoadjuvant therapy, and sometimes watch-and-wait.

Topics covered

Why screening works and when it starts
Screening tests and their limits
Positive stool test with a normal colonoscopy
Family history and earlier screening
Adenomas, serrated lesions, and surveillance
Serrated polyposis syndrome
Mismatch repair testing and Lynch syndrome
TNM staging and adjuvant chemotherapy
Metastatic disease and the tumor profile
Immunotherapy for mismatch repair deficiency
Rectal cancer and watch-and-wait

Key decisions

Start average-risk screening at forty-five and continue through seventy-five, individualize from seventy-six to eighty-five, and generally stop after eighty-five.
Send any positive non-invasive test, whether FIT, stool DNA, blood test, or abnormal CT colonography, to diagnostic colonoscopy, and get that commitment before the kit goes home.
Start at forty, or ten years before the youngest case, with colonoscopy every five years when a first-degree relative has colorectal cancer or an advanced adenoma.
Manage a proximal hyperplastic-looking polyp of ten millimeters or more as a sessile serrated lesion, and give an advanced adenoma or a large serrated lesion a three-year colonoscopy.
Test every new colorectal cancer for mismatch repair deficiency, send MSH2, MSH6, or isolated PMS2 loss to germline testing, and test MLH1 loss for BRAF V600E or MLH1 promoter methylation first.
Give stage three disease oxaliplatin chemotherapy, with three months of CAPOX for low-risk T1 to T3 N1 and six months for T4, N2, or FOLFOX, and give stage two chemotherapy only with high-risk features and never fluorouracil alone for microsatellite-unstable tumors.
Add an anti-EGFR antibody in metastatic disease only when the tumor is RAS wild-type and left-sided, use bevacizumab otherwise, and give pembrolizumab first for mismatch repair deficient tumors.
Treat locally advanced rectal cancer after pelvic MRI with total neoadjuvant therapy, offer watch-and-wait after a complete clinical response, and check mismatch repair before radiation.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:15) - Screening tests and start age
(07:03) - Family history moves the start
(07:54) - Polyp histology and surveillance
(13:32) - Serrated polyposis syndrome
(14:19) - Colon cancer, Lynch testing, staging
(20:14) - Node-positive cancer and chemotherapy
(22:41) - Metastatic disease and tumor profile
(26:50) - Immunotherapy for mismatch repair deficiency
(27:40) - Rectal cancer and organ preservation

Chapter 15, Ep 2 of 2: Diverticular Disease: Diagnosis to Follow-Up

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

Diverticular disease is a common, usually silent finding that sometimes turns into inflammation, and the episode follows three patients through the decisions that follow. A man with a first attack shows how CT confirms and grades diverticulitis, who can be managed without antibiotics, why colonoscopy follows a first episode, and how to counsel on modifiable risks. His later attacks show why surgery is no longer tied to attack count. A woman with a pelvic abscess shows when to drain, when to operate, and what a colovesical fistula looks like. A third patient has rectum-sparing colitis in a diverticular segment, treated with mesalamine.

Topics covered

Diverticula and who gets them
Diagnosing diverticulitis with CT
Hinchey classification
Antibiotics or observation in uncomplicated disease
Colonoscopy after a first attack
Recurrence risk and modifiable factors
Abscess drainage and urgent surgery
Fistulas and strictures
Elective resection criteria
Segmental colitis associated with diverticulosis

Key decisions

Use CT to confirm diverticulitis, grade it, and find abscess, perforation, fistula, or obstruction, and stage complicated disease with the Hinchey classification.
Manage an immunocompetent, non-frail outpatient with uncomplicated left-sided diverticulitis, no systemic inflammatory response, and reliable follow-up with supportive care and no routine antibiotics.
Give antibiotics to patients who are immunocompromised, frail, septic, admitted, or have complicated disease, using oral ciprofloxacin plus metronidazole or amoxicillin-clavulanate, and intravenous regimens if admitted.
Perform colonoscopy six to eight weeks after a first episode to exclude cancer, unless a recent high-quality colonoscopy was normal.
Treat a pericolic abscess under four centimeters with antibiotics alone, drain one of four centimeters or more percutaneously with intravenous antibiotics, and send an undrainable abscess to urgent surgery.
Send Hinchey three or four disease with free perforation to urgent sigmoid resection, either with primary anastomosis or as a Hartmann procedure, depending on stability and contamination.
Repair diverticular fistulas, such as a colovesical fistula with pneumaturia, by elective sigmoid resection, and do not recommend prophylactic surgery after a fixed number of attacks, reserving it for debilitating recurrences, complicated disease, and immunocompromised patients.
Treat segmental colitis associated with diverticulosis, which spares the rectum and proximal colon, with mesalamine, and do not use mesalamine or rifaximin to prevent diverticulitis recurrence.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Episode introduction and overview
(00:38) - First patient and diverticula basics
(02:41) - CT diagnosis and Hinchey grading
(03:43) - Antibiotics or supportive care
(05:26) - Colonoscopy after a first attack
(06:10) - Recurrence risk and modifiable factors
(07:04) - Abscess, perforation, and fistula
(08:46) - Elective surgery and attack count
(09:42) - Segmental colitis with diverticulosis
(10:52) - Board traps and summary

Chapter 16, Ep 1 of 3: Pelvic Floor and Anorectal: Chronic Constipation

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

Chronic constipation is diagnosed by symptoms, and the episode's organizing idea is that the mechanism and the response to each step decide what comes next. It starts with the Rome four criteria and the separation from irritable bowel by dominant pain, then the three mechanisms. Patients without alarm features get empiric treatment: education, psyllium, stopping constipating drugs, polyethylene glycol, then stimulants. Alarm features send a patient to colonoscopy first. When fiber, polyethylene glycol, and stimulants fail, a prescription drug is chosen by its target, starting with the secretagogues and moving to prucalopride, which switches mechanism. After several failures, the next move is testing for an outlet or transit problem.

Topics covered

Rome four criteria
Chronic constipation versus irritable bowel with constipation
Normal transit, slow transit, and defecatory disorders
Alarm features
Fiber, constipating drugs, and laxatives
Secretagogues: lubiprostone, linaclotide, plecanatide
Prucalopride and serotonin four selectivity
Tenapanor
Refractory constipation and when to test
Board traps

Key decisions

Diagnose chronic constipation from the Rome four symptom cluster, not stool frequency, because infrequency is only one of six features and a patient with four or five movements a week can qualify.
Call the problem irritable bowel with constipation instead of chronic constipation when abdominal pain dominates the picture.
Treat empirically when there are no alarm features, but send a patient with new symptoms after fifty, weight loss, bleeding or iron deficiency anemia, or a missed colonoscopy to investigation first.
Start with education and gradually increased psyllium toward 25 to 30 grams a day, stop constipating drugs such as calcium channel blockers and calcium supplements, then use polyethylene glycol 17 grams daily, then bisacodyl or senna as stimulants, and avoid magnesium in renal impairment.
Treat failure of a four to eight week trial of fiber, polyethylene glycol, and stimulants as the signal to stop escalating and test with balloon expulsion, anorectal manometry, and a transit study.
Use lubiprostone 24 micrograms twice daily with food, or linaclotide 145 micrograms daily thirty minutes before the first meal (72 micrograms if not tolerated), or plecanatide 3 milligrams daily, and check timing before calling any drug a failure.
Switch mechanism after a secretagogue fails, for example to prucalopride 2 milligrams daily (1 milligram with creatinine clearance under 30), rather than trying another drug with the same mechanism.
After several drug failures, test for a defecatory disorder or slow transit instead of changing drugs again, and remember tenapanor is approved for irritable bowel with constipation, not chronic idiopathic constipation.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and case plan
(01:50) - Rome four criteria and IBS-C
(02:59) - Three mechanisms of constipation
(04:56) - Empiric treatment and laxatives
(07:19) - Alarm features come first
(09:12) - Secretagogues and their dosing
(11:40) - Switching mechanism to prucalopride
(13:15) - Tenapanor and timing rules
(14:19) - When switching drugs stops working
(14:52) - Board traps and summary

Chapter 16, Ep 2 of 3: Pelvic Floor Disorders: Refractory Constipation

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

Constipation that fails the standard drugs usually has a mechanism the drugs cannot reach, and the episode sorts those mechanisms by where the lesion sits. It starts at the outlet with dyssynergic defecation, working through the rectal exam, balloon expulsion, manometry, defecography, and biofeedback, and notes that an absent rectoanal inhibitory reflex suggests Hirschsprung disease. It then turns to slow transit, which is diagnosed only after the outlet is cleared, using the marker study, then prucalopride and other medical options before a narrowly indicated colectomy. It closes with opioid-induced constipation, where standard laxatives come first, then a PAMORA unless obstruction is possible, and alvimopan stays an inpatient drug after bowel resection.

Topics covered

Dyssynergic defecation mechanism
Digital rectal exam and balloon expulsion
Anorectal manometry and defecography
Biofeedback therapy
Hirschsprung disease and the rectoanal inhibitory reflex
Slow-transit constipation and the marker study
Medical therapy and prucalopride
Colectomy criteria and outcomes
Opioid-induced constipation and PAMORAs
Alvimopan after bowel resection

Key decisions

In a constipated patient who has failed empiric therapy, look for a defecatory disorder with a digital rectal exam and a balloon expulsion test (50 mL of warm water, abnormal if not expelled within 60 seconds) instead of escalating laxatives.
Diagnose dyssynergic defecation only when at least two of three studies are positive: anorectal manometry, defecography, and balloon expulsion, since manometry alone is not sufficient, and treat it with biofeedback, six to twelve sessions.
Suspect late-onset Hirschsprung disease when manometry shows an absent rectoanal inhibitory reflex, especially with lifelong constipation and a dilated colon above a narrowed segment.
Order a transit study only after a defecatory disorder is excluded, using a radiopaque marker study with 24 markers, no laxatives, and a day-five film, where more than five retained markers means slow transit and rectosigmoid clustering sends the workup back to the outlet.
Exhaust medical therapy, including prucalopride, before colectomy, and offer subtotal colectomy with ileorectal anastomosis only for disabling refractory slow transit confirmed on a marker study, with the outlet cleared and without dominant abdominal pain, generalized dysmotility, or pseudo-obstruction.
For opioid-induced constipation, try standard laxatives first, then add a PAMORA after excluding mechanical obstruction, such as naloxegol 25 mg daily on an empty stomach, reduced to 12.5 mg with creatinine clearance under 60 mL a minute or a moderate CYP3A4 inhibitor and avoided with strong inhibitors or inducers.
Use lubiprostone 24 micrograms twice daily as an alternative when a PAMORA is not tolerated or is contraindicated.
Give alvimopan only in the hospital to speed GI recovery after partial bowel resection with primary anastomosis, for no more than 15 doses, and never for chronic opioid-induced constipation.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview of the Episode
(01:09) - Dyssynergic Defecation Case
(02:43) - Testing Order and Manometry
(07:00) - Biofeedback Treatment
(07:58) - Absent Reflex and Hirschsprung
(08:35) - Slow-Transit Constipation Case
(10:05) - Marker Study and Medical Therapy
(13:07) - Colectomy Criteria and Results
(14:43) - Opioid-Induced Constipation and PAMORAs
(20:03) - Alvimopan After Bowel Surgery

Chapter 16, Ep 3 of 3: Pelvic Floor and Anorectal: The Anal Canal

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

Every complaint in this episode comes back to which part of the anal canal is involved and what keeps the problem going. Fecal incontinence is usually multifactorial, so the episode looks for every cause, matches urge or passive leakage to the failing sphincter, and tests with manometry and endoanal ultrasound before stepping from fiber, loperamide, and biofeedback to sacral nerve stimulation. It then uses the dentate line to separate painless internal hemorrhoids, which are graded and banded, from painful thrombosed external ones, which are excised within seventy-two hours. Fissures follow, treated stepwise by relaxing the internal sphincter, with lateral ones prompting a search for Crohn disease. Pruritus ani closes the episode, with secondary causes excluded first.

Topics covered

Fecal incontinence causes
Urge versus passive leakage
Anorectal manometry and endoanal ultrasound
Medical therapy and biofeedback
Sacral nerve stimulation and other operations
Overflow incontinence from impaction
Hemorrhoids and the dentate line
Goligher grades and rubber band ligation
Thrombosed external hemorrhoid
Anal fissure stepwise treatment
Atypical fissures and Crohn disease
Pruritus ani workup

Key decisions

Ask directly about fecal incontinence, since patients present with loose stools, and look for every contributing cause because more than eighty percent have more than one.
Read urge leakage as external sphincter weakness and passive leakage as internal sphincter dysfunction or neuropathy, then use anorectal manometry and endoanal ultrasound to find the defect.
Treat incontinence first with psyllium, loperamide at four to sixteen milligrams a day, and a bile acid sequestrant when bile acids contribute, add biofeedback to the drugs, and in refractory disease use sacral nerve stimulation before sphincteroplasty, with a permanent implant if the test improves symptoms by at least fifty percent.
Disimpact and start a maintenance regimen for overflow incontinence, and do the rectal exam before giving loperamide.
Start conservative care for every hemorrhoid grade, band grades two and three above the dentate line, and keep excisional hemorrhoidectomy for grade four, mixed disease, persistent symptoms, or strangulation.
Excise a thrombosed external hemorrhoid whole within seventy-two hours, and after that use sitz baths, analgesics, stool softeners, and topical agents; never just incise and drain.
Treat a chronic fissure by steps: fiber and sitz baths, then topical diltiazem or nitroglycerin for six to eight weeks, then botulinum toxin at twenty to fifty units, then lateral internal sphincterotomy, weighing obstetric injury and age because of incontinence risk.
Work up a lateral or multiple fissure for Crohn disease and other secondary causes before routine treatment, and do not call pruritus ani idiopathic until infection, skin disease, seepage, and neoplasia are excluded and soap and wipes are stopped.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 case overview
(02:05) - Causes of fecal incontinence
(04:30) - Manometry and endoanal ultrasound
(05:35) - Drugs and biofeedback
(06:55) - Sacral nerve stimulation and surgery
(08:59) - Hemorrhoids and the dentate line
(11:46) - Banding and hemorrhoid surgery
(13:14) - Thrombosed external hemorrhoid timing
(14:14) - Anal fissure and Crohn disease
(18:15) - Pruritus ani workup

Chapter 17, Ep 1 of 2: Liver Test Interpretation: Patterns and Workup

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

An abnormal liver test is a screening signal, and the workup is organized by which enzyme dominates and by how many multiples of normal it sits at. The episode first redefines a normal ALT, then sets the pattern with the R ratio, reads the size of the elevation, and uses the AST-to-ALT ratio. Hepatocellular injury is worked up in one round across the viral, autoimmune, metabolic and inherited, ischemic, and drug layers, with a full supplement history, while shock liver and herpes simplex hepatitis are recognized by pattern. Cholestasis starts with ultrasound, then MRCP for dilated ducts, AMA for a normal tree, MRCP for primary sclerosing cholangitis, and IgG4 for stricture mimics.

Topics covered

True upper limit of normal ALT
R ratio and injury pattern
Size of the aminotransferase elevation
AST-to-ALT ratio
Five-layer hepatocellular workup
Supplements, Hy's law, and drug injury
Ischemic hepatitis and herpes simplex hepatitis
Ultrasound first in cholestasis
Primary sclerosing cholangitis and primary biliary cholangitis
IgG4-related sclerosing cholangitis

Key decisions

Treat an ALT above 25 in women or above 33 in men as abnormal, and work up small elevations rather than accepting the lab's upper limit of 40.
Calculate the R ratio from multiples of the upper limit, not raw values: over 5 is hepatocellular, under 2 is cholestatic, and 2 to 5 is mixed.
Treat an aminotransferase level over 5000 as acetaminophen or ischemic hepatitis rather than starting a broad workup, and read an AST-to-ALT ratio over 2 with an AST under 400 in a drinker as alcohol-associated hepatitis.
Send the viral, autoimmune, metabolic and inherited, ischemic, and drug layers in one round for hepatocellular injury, and ask specifically about supplements before accepting a history of no medications.
Apply Hy's law, an ALT over 3 times normal with a bilirubin over 2 mg/dL in drug injury without obstruction, and monitor the INR closely.
Start empiric acyclovir immediately for suspected herpes simplex hepatitis in a pregnant or immunocompromised patient, without waiting for HSV PCR.
Order a right upper quadrant ultrasound before any serology in cholestasis, use MRCP for a dilated tree, and reserve ERCP for planned therapy.
Diagnose primary biliary cholangitis without biopsy from a positive AMA with an alkaline phosphatase over 1.5 times normal, and diagnose primary sclerosing cholangitis from a beaded MRCP in AMA-negative cholestasis with IBD.
Check IgG4 (over 135 mg/dL is suggestive) in a distal stricture with pancreatic fullness before calling it cancer, and use a steroid response as the discriminator.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(02:01) - Redefining a normal ALT
(02:49) - The R ratio sets the pattern
(04:31) - What the size of elevation means
(05:36) - AST-to-ALT ratio clues
(06:38) - Five-layer hepatocellular workup
(13:39) - Shock liver and herpes hepatitis
(15:15) - Cholestasis and primary sclerosing cholangitis
(19:35) - Primary biliary cholangitis and IgG4
(22:34) - Board traps by pattern

Chapter 17, Ep 2 of 2: Liver Test Interpretation: Workup and Staging

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

The organizing idea is to match the test to the question. An isolated bilirubin is split into indirect and direct, hemolysis is excluded, and the benign inherited syndromes are told apart. An isolated alkaline phosphatase is traced to liver or bone with the GGT, and a hepatic source is checked for infiltrative disease. Fibrosis is then staged without biopsy, starting with FIB-4, then FibroScan, then MR elastography when results are unreliable or disagree, with stiffness cutoffs that differ by disease. Biopsy comes last, only when it changes management, and the approach depends on ascites, clotting, and whether portal pressure is wanted. The hepatic venous pressure gradient then measures what no image can.

Topics covered

Direct versus indirect bilirubin
Hemolysis screen
Gilbert and Crigler-Najjar syndromes
Dubin-Johnson and Rotor syndromes
GGT and the source of alkaline phosphatase
Infiltrative causes of high alkaline phosphatase
FIB-4 and blood fibrosis scores
FibroScan and MR elastography
Indications and routes for liver biopsy
Hepatic venous pressure gradient

Key decisions

Split an isolated raised bilirubin into indirect and direct before any other workup.
Diagnose Gilbert syndrome clinically only after a negative hemolysis screen, with no genetic test, and doubt it when the indirect bilirubin is well above five.
Separate Dubin-Johnson from Rotor syndrome by the black liver and the normal total but inverted urinary coproporphyrin, and treat neither.
Check the GGT before any liver workup for an isolated alkaline phosphatase, since a normal GGT in an adult points to bone and a high GGT confirms a liver source.
Stage MASLD fibrosis with FIB-4 first, where under 1.3 (under 2.0 over age 65) is low risk and above 2.67 is high risk, and send the indeterminate range to FibroScan, MR elastography, or ELF.
Use MR elastography when FibroScan is unreliable, as in severe obesity or ascites, or when results disagree, and remember that iron overload disrupts it.
Choose a transjugular biopsy over a percutaneous one for tense ascites, coagulopathy, morbid obesity, vascular liver disease, or when portal pressure is wanted, and do not transfuse for an INR or platelet count alone.
Read an HVPG of 10 or more as clinically significant portal hypertension and 12 or more as a variceal bleeding risk, and treat a normal HVPG with portal hypertension as a pre-sinusoidal or post-sinusoidal cause.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:42) - Indirect bilirubin and Gilbert syndrome
(03:13) - Excluding hemolysis
(05:10) - Isolated direct bilirubin syndromes
(07:13) - High alkaline phosphatase and GGT
(09:29) - Hepatic causes and infiltrative disease
(11:44) - Imaging and FIB-4 staging
(14:33) - FibroScan and MR elastography
(17:50) - When biopsy is indicated
(21:10) - HVPG and portal hypertension patterns

Chapter 18, Ep 1 of 3: Viral Hepatitis: Acute Hepatitis A and E

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

Acute viral hepatitis looks the same whatever the virus, so the serologic panel, not the history, decides the diagnosis. The episode starts with the first panel and how to read it, then shows why a negative hepatitis C antibody can miss acute infection and why acute hepatitis C is treated promptly. It moves to acute hepatitis B, which is treated only if fulminant or protracted, and to core IgM in a chronic flare. Hepatitis E follows, as a mimic of drug injury, as chronic infection in transplant recipients, and as a danger in pregnancy. Hepatitis A closes the episode, with its unusual courses, vaccination, and postexposure prophylaxis.

Topics covered

Course of acute viral hepatitis
First serologic panel and its readings
Acute hepatitis C and antibody lag
Pretreatment workup and vaccination
Acute hepatitis B management
Core IgM in a chronic hepatitis B flare
Hepatitis E mistaken for drug injury
Chronic hepatitis E in transplant recipients
Hepatitis E in pregnancy
Hepatitis A courses, vaccine, and prophylaxis

Key decisions

Order hepatitis B surface antigen, core IgM, hepatitis C antibody with reflex RNA, and hepatitis A IgM first, and add hepatitis E IgM for travelers to South Asia or Africa, pork or game eaters, and unexplained acute hepatitis with a negative panel.
Check HCV RNA when the antibody is negative in a high-risk patient with acute hepatitis, because the antibody can stay negative for the first one to three months.
Treat acute hepatitis C promptly with a direct-acting antiviral such as sofosbuvir-velpatasvir for twelve weeks, after checking hepatitis B serology, and test for HCV yearly if injection continues.
Treat acute hepatitis B with entecavir or tenofovir only if it is fulminant or protracted, with a rising INR and deep jaundice beyond about four weeks, and never use peginterferon.
Send hepatitis E IgM when an apparent drug-induced liver injury does not quite fit, and manage acute hepatitis E in an immunocompetent patient supportively.
Treat chronic hepatitis E in a transplant recipient by reducing immunosuppression first, then ribavirin six hundred to twelve hundred milligrams daily for three months, and avoid peginterferon after heart, lung, and kidney transplants.
Move a pregnant woman with hepatitis E and confusion immediately to a center that can manage acute liver failure, along with her obstetric team.
Give postexposure prophylaxis for hepatitis A within two weeks: vaccine alone from twelve months to forty years, vaccine plus immune globulin for the immunocompromised and those with chronic liver disease, and immune globulin alone under twelve months.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patients
(01:51) - Phases of illness and first panel
(04:08) - Acute hepatitis C and antibody lag
(06:36) - Acute hepatitis B and flares
(08:12) - Hepatitis E mimicking drug injury
(10:09) - Chronic hepatitis E in transplant
(11:23) - Hepatitis E in pregnancy
(12:41) - Hepatitis A course and vaccination
(14:36) - Hepatitis A postexposure prophylaxis
(15:33) - Board traps and episode review

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

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

Hepatitis B decisions follow from reading the markers correctly and asking what is about to happen to the liver or the patient. The episode starts with surface, core, and e markers and the phases of chronic infection, then the isolated core antibody. It moves to treatment criteria, the three first-line drugs, and why therapy is usually indefinite. Reactivation under immunosuppression comes next, with prophylaxis timing, followed by pregnancy: newborn prophylaxis, maternal tenofovir, and the postpartum flare. It ends with hepatitis D, which needs hepatitis B, with testing, coinfection versus superinfection, and bulevirtide, then the common board traps.

Topics covered

Hepatitis B serologic markers
Phases of chronic infection
Isolated core antibody
Treatment criteria and drug choice
Duration of therapy and cure
Reactivation and prophylaxis
Pregnancy and newborn prophylaxis
Postpartum flare
Hepatitis D testing and diagnosis
Bulevirtide and peginterferon

Key decisions

Treat e antigen-negative immune-active disease (DNA above 2,000 with a raised ALT, using limits of 35 in men and 25 in women), stage 2 or higher fibrosis, and compensated cirrhosis with any detectable DNA, while following inactive carriers with a normal ALT and DNA below 2,000 every three to six months.
Treat decompensated cirrhosis with a positive surface antigen regardless of DNA, e antigen, or ALT, and never use peginterferon in cirrhosis.
Choose tenofovir alafenamide when kidney or bone risk is present, tenofovir disoproxil in pregnancy, and entecavir at 1 mg rather than 0.5 mg after prior lamivudine.
Test every patient for surface antigen and core antibody before immunosuppression, and give entecavir or a tenofovir to surface antigen positive patients and to core antibody positive patients on rituximab, obinutuzumab, or stem cell transplant.
Start prophylaxis about a week before immunosuppression and continue it six months after standard immunosuppression, or 12 to 18 months after B-cell depletion or transplant.
Give every infant of a surface antigen positive mother hepatitis B immune globulin and vaccine within 12 hours of birth, and start tenofovir disoproxil at 28 to 32 weeks when maternal DNA exceeds 200,000 IU/mL.
Monitor ALT and DNA for six months after stopping maternal tenofovir because of the postpartum flare, and continue therapy in mothers with advanced fibrosis.
Suspect hepatitis D with an ALT flare and a low HBV DNA, test antibody first and confirm with HDV RNA, separate coinfection from superinfection by core IgM, and treat active infection with bulevirtide or pegylated interferon alfa.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:34) - Reading markers and phases
(06:24) - Isolated core antibody
(07:03) - Who to treat and which drug
(11:51) - Reactivation under immunosuppression
(17:06) - Pregnancy and newborn prophylaxis
(21:09) - Hepatitis D diagnosis
(24:29) - Treating hepatitis D
(26:59) - Board traps

Chapter 18, Ep 3 of 3: Viral Hepatitis: Hepatitis C Screening to Cure

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

Hepatitis C is now curable with pills, so the episode follows one pathway and then shows where it bends. It starts with universal screening and confirming infection with antibody and reflex RNA. Next come the pretreatment workup, the two preferred regimens, and SVR twelve as the test of cure. Salvage after relapse follows. Then three patients leave the standard pathway: a woman with decompensated cirrhosis awaiting transplant, who also shows who needs surveillance after cure, a man on dialysis, and a pregnant woman. The episode closes with the traps the boards set.

Topics covered

Direct-acting antiviral classes
Universal screening and risk factors
Antibody with reflex RNA
Pretreatment workup
Preferred regimens and interactions
SVR twelve and benefits of cure
Salvage after relapse
Decompensated cirrhosis and transplant timing
Cancer surveillance after cure
Dialysis and pregnancy

Key decisions

Screen every adult eighteen and older at least once with hepatitis C antibody and reflex RNA, and screen yearly in people who inject drugs and other high-risk groups.
Check HCV RNA directly when acute infection is suspected, because the antibody can take one to three months to turn positive.
Before treatment, check hepatitis B surface antigen, surface antibody, and core antibody, and stage fibrosis, while treating genotype testing as optional with pangenotypic regimens.
Treat most patients, including those with compensated cirrhosis, with sofosbuvir-velpatasvir for twelve weeks or glecaprevir-pibrentasvir for eight weeks, and do not defer for past or current drug use.
After relapse on an NS5A inhibitor plus sofosbuvir, give sofosbuvir-velpatasvir-voxilaprevir for twelve weeks.
In decompensated cirrhosis, avoid every protease inhibitor and give sofosbuvir-velpatasvir with ribavirin for twelve weeks, or alone for twenty-four weeks when ribavirin is contraindicated.
Treat a transplant candidate before transplant only when MELD is about fifteen to eighteen or lower, albumin is above two point eight, and age is under sixty-five.
Continue ultrasound surveillance every six months indefinitely after cure when cirrhosis was present, but not for stage three fibrosis alone.
On dialysis without decompensation, prefer glecaprevir-pibrentasvir, and in pregnancy wait to treat until after delivery, testing the infant with RNA at two to six months.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Hepatitis C episode overview
(03:08) - Screening and confirming infection
(04:31) - Pretreatment workup
(05:27) - Preferred regimens and interactions
(06:50) - SVR twelve and benefits of cure
(08:04) - Salvage after relapse
(08:27) - Decompensated cirrhosis and transplant
(11:24) - Surveillance after cure
(12:19) - Hepatitis C on dialysis
(13:10) - Hepatitis C in pregnancy

Chapter 19, Ep 1 of 2: Drug Injury and Liver Failure: Causes and Patterns

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

Drug injury happens when a drug's reactive intermediate outruns the liver's ability to neutralize it, and that one idea ties the episode together. It starts with a woman on nitrofurantoin, where Hy's law, the R ratio, and RUCAM set severity, pattern, and causality, and where autoimmune-like injury is told apart from true autoimmune hepatitis. Supplements and HLA testing before abacavir follow, then the metabolic mechanism seen with isoniazid and acetaminophen, and the separate rules for valproate, methotrexate, statins, and amiodarone. Biopsy patterns come next, from cholestasis after amoxicillin-clavulanate to DRESS, granulomas, steatosis, and sinusoidal obstruction. The episode ends with acetaminophen: toxic thresholds, the limits of the nomogram, and N-acetylcysteine dosing.

Topics covered

Three kinds of drug injury and risk factors
Hy's law and the R ratio
RUCAM causality scoring
Drug-induced autoimmune-like hepatitis
Supplements and HLA-B 5701 testing
Reactive metabolites and isoniazid
Valproate, methotrexate, statins, and amiodarone
Biopsy patterns of drug injury
Acetaminophen toxicity and the nomogram
N-acetylcysteine dosing

Key decisions

When drug injury shows an ALT or AST over three times normal, a bilirubin over two times normal, an alkaline phosphatase under two times normal, and no other cause, it meets Hy's law, so stop the drug, admit the patient, and alert a transplant center.
Calculate the R ratio, ALT over its upper limit divided by alkaline phosphatase over its upper limit, to call the pattern: over five is hepatocellular, under two is cholestatic, and two to five is mixed.
Treat drug-induced autoimmune-like hepatitis by withdrawing the drug, reserve steroids for this pattern and for checkpoint inhibitor hepatitis, and biopsy when tests do not improve after stopping or the patient is jaundiced.
Test for HLA-B 5701 before starting abacavir, since it is the one genetic test that is actionable and mandated.
Stop isoniazid when a patient is jaundiced with an ALT over ten times normal, and counsel the patient to stop drinking and avoid acetaminophen.
Monitor methotrexate with periodic liver tests plus a noninvasive fibrosis assessment such as FibroScan, not with ALT alone.
Use the Rumack-Matthew nomogram, with a treatment line from 150 micrograms per milliliter at four hours to 4.7 at 24 hours, only for a single, timed, acute ingestion; for chronic, late, extended-release, or unknown-time ingestion, treat empirically without waiting for a level.
Give intravenous N-acetylcysteine at 150 milligrams per kilogram over 60 minutes, then 50 over four hours, then 100 over 16 hours, and keep repeating the 16-hour dose while encephalopathy, an INR over about 1.5 to 2, or raised aminotransferases persist.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:07) - Nitrofurantoin injury and Hy's law
(05:33) - R ratio pattern and causality
(07:01) - Autoimmune-like drug injury
(08:27) - Supplements and HLA testing
(10:11) - Metabolism, isoniazid, and acetaminophen mechanism
(13:44) - Valproate, methotrexate, statins, amiodarone
(16:22) - Reading the biopsy patterns
(23:03) - Acetaminophen poisoning and treatment
(29:26) - Board traps and summary

Chapter 19, Ep 2 of 2: Drug Injury and Liver Failure: Acute Liver Failure

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

Acute liver failure is a loss of liver function in a previously healthy liver, and the organizing idea is that the cause and the timing drive every decision. The episode defines it with four criteria, separates it from acute-on-chronic failure, and explains why only acute liver failure swells the brain. It then covers causes and which recover alone, followed by ICU management of glucose, coagulopathy, infection, and cerebral edema. Three treatments that start before confirmation come next: fulminant Wilson disease, herpes simplex hepatitis, and N-acetylcysteine for non-acetaminophen failure. It closes with early transfer, the two King's College versions, Status one-A listing, and contraindications.

Topics covered

Four criteria for acute liver failure
Acute-on-chronic failure and cerebral edema
Encephalopathy grades
Causes and spontaneous recovery
ICU management of complications
Intracranial hypertension management
Fulminant Wilson disease
Herpes simplex hepatitis
N-acetylcysteine without acetaminophen
Transfer, King's College criteria, and Status one-A listing

Key decisions

Diagnose acute liver failure when the INR is at least 1.5 with any encephalopathy, illness under 26 weeks, and no cirrhosis, and count fulminant Wilson disease, autoimmune hepatitis, and hepatitis B reactivation despite underlying disease.
Give a continuous dextrose infusion for hypoglycemia, and do not give fresh frozen plasma for an elevated INR unless the patient bleeds or needs an invasive procedure.
Treat cerebral edema, a risk that rises at grade three or four encephalopathy or an arterial ammonia over 150 to 200 micromoles per liter, with head elevation to 30 degrees, sedation, a PaCO2 of 30 to 35, hypertonic saline to a sodium of 145 to 155, mannitol for breakthrough, and renal replacement therapy to remove ammonia.
Suspect fulminant Wilson disease in a young patient with Coombs-negative hemolysis, an alkaline phosphatase-to-bilirubin ratio under 4, an AST-to-ALT ratio over 2.2, and low uric acid, and list for urgent transplant with plasmapheresis as a bridge rather than giving penicillamine.
Start intravenous acyclovir at 5 to 10 mg/kg every 8 hours before the PCR returns in any pregnant or immunocompromised patient with indeterminate acute liver failure.
Give intravenous N-acetylcysteine to patients with indeterminate or drug-induced liver failure and grade one or two encephalopathy, even without acetaminophen, and do not use corticosteroids except for autoimmune hepatitis or high-grade checkpoint inhibitor hepatitis.
Transfer to a transplant center at the first trigger, such as any encephalopathy, persistent acidosis after fluids, an INR over 2 unresponsive to vitamin K, or a rising creatinine in acetaminophen failure, without waiting for the King's College criteria.
Apply the acetaminophen version (pH under 7.30 after fluids, or grade three or four encephalopathy plus INR over 6.5 plus creatinine over 3.4) or the non-acetaminophen version (INR over 6.5, or any three of five features), then list Status one-A and exclude uncontrolled sepsis and irreversible brain injury.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode overview
(01:31) - Defining acute liver failure
(05:11) - Causes and spontaneous recovery
(07:10) - ICU complications and cerebral edema
(10:38) - Fulminant Wilson disease
(13:47) - Herpes simplex hepatitis
(15:58) - N-acetylcysteine without acetaminophen
(17:49) - Transfer and acetaminophen criteria
(20:28) - Status one-A and contraindications
(22:16) - Non-acetaminophen criteria and other scores

Chapter 20, Ep 1 of 3: Immune Liver Disease: Autoimmune Hepatitis

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

Autoimmune hepatitis is first placed among the three immune liver diseases using the biochemical pattern, demographics, and antibodies, and only then confirmed. The episode explains why a mild-looking case can already be cirrhotic, how type one differs from type two, why the simplified score often needs a biopsy to reach definite, and why the drug history is checked before long-term treatment is committed. Treatment follows: prednisone or budesonide with azathioprine after TPMT testing, with budesonide kept out of cirrhosis. The episode then turns to the most common error, stopping too soon, and ends with azathioprine failure, acute severe disease, and pregnancy.

Topics covered

Three immune liver diseases compared
Pathogenesis and presentation
Type one versus type two
Simplified scoring and biopsy
Drug-induced autoimmune-like injury
Low-titer smooth muscle antibody in fatty liver
Induction with prednisone or budesonide plus azathioprine
Remission and timing of withdrawal
Azathioprine failure, acute severe disease, and pregnancy

Key decisions

Treat a middle-aged woman with a hepatocellular pattern, ANA or smooth muscle antibody, and a high IgG as having autoimmune hepatitis, and proceed to biopsy and treatment.
Obtain a biopsy in most suspected cases, because serology and IgG alone often score only probable (six points) and 23 percent of confirmed cases scored six or less without histology.
Recheck the drug history before committing to long-term therapy, since drug-induced injury looks the same on biopsy and remits with a steroid taper once the drug is withdrawn.
Check TPMT before the first dose of azathioprine, and do not start standard-dose azathioprine in a deficient patient.
Stage the liver before choosing the steroid: use budesonide 9 mg a day only without cirrhosis, and use prednisone with azathioprine when cirrhosis is present.
Do not stop treatment when the ALT normalizes; require at least 24 months of biochemical remission, often with a repeat biopsy first, before considering withdrawal.
Switch to mycophenolate mofetil for azathioprine intolerance or non-response rather than stopping treatment.
In acute severe disease, give high-dose steroids without azathioprine or budesonide, reassess every 7 to 14 days, and move to transplant evaluation rather than a higher steroid dose if there is no response.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview and Episode Plan
(04:58) - Telling the Three Diseases Apart
(05:34) - Cause, Presentation, and Type
(07:51) - Scoring, Biopsy, and Drug History
(10:40) - Fatty Liver and a Weak Antibody
(11:40) - Induction and Azathioprine Safety
(14:10) - Remission and Premature Withdrawal
(15:04) - When Azathioprine Fails
(15:41) - Acute Severe Disease
(17:00) - Pregnancy on Immunosuppression

Chapter 20, Ep 2 of 3: Cholestatic Liver Disease: Diagnosis to the Itch

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

Primary biliary cholangitis is autoimmune destruction of the small bile ducts, aimed at a mitochondrial enzyme that the anti-mitochondrial antibody recognizes. The episode first makes the diagnosis from labs without a biopsy, then looks for associated conditions and sets the alkaline phosphatase as the marker to follow. It covers the antibody-negative and antibody-only edges of diagnosis. It then turns to ursodeoxycholic acid dosing, response judged at twelve months, and second-line choices after obeticholic acid's withdrawal. Transplant timing follows. The last section treats itch on its own terms, stepping from cholestyramine through rifampin, naltrexone or sertraline, and linerixibat.

Topics covered

Autoimmune destruction of small bile ducts
Three lab criteria for diagnosis
Associated autoimmune disease and osteoporosis
Lipoprotein X and statin decisions
Histologic stages
AMA-negative disease and AMA-only patients
Ursodeoxycholic acid dosing and response criteria
Second-line PPAR agonists and fibrates
Transplant indications
Stepped treatment of cholestatic itch

Key decisions

Diagnose primary biliary cholangitis without a biopsy when the AMA titer is 1 to 40 or higher, the alkaline phosphatase is above one and a half times normal, and the AST is under five times normal with no other explanation.
Biopsy when the AST is over five times normal, because that raises the possibility of overlap with autoimmune hepatitis.
Treat every patient with ursodeoxycholic acid at 13 to 15 milligrams per kilogram a day for life, and judge response at twelve months.
Call it an inadequate response if the alkaline phosphatase is above about 1.67 times normal at twelve months or the bilirubin is raised, and then add elafibranor or seladelpar while continuing ursodeoxycholic acid.
Monitor, and do not treat or biopsy, a patient with a positive AMA and normal liver tests, and treat her if the alkaline phosphatase rises above one and a half times normal.
Refer for transplant on the clinical picture rather than waiting for the MELD to rise, including for decompensation, refractory itch, or hepatocellular carcinoma within the Milan criteria.
Give cholestyramine at least one hour before or four hours after other oral drugs, then add rifampin with liver tests at four to eight weeks, stopping it if the bilirubin rises.
Start naltrexone at a low dose with a warning about the withdrawal-like reaction, which is not an allergy, and use sertraline when depression coexists.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and roadmap
(00:55) - First patient and disease biology
(03:28) - Diagnosis without a biopsy
(04:29) - Associated conditions, histology, natural history
(07:18) - AMA-negative and AMA-only patients
(08:34) - UDCA dosing and judging response
(11:29) - Second-line drugs after obeticholic acid
(14:51) - When transplant comes in
(15:36) - Cholestatic itch and stepped treatment
(21:22) - Board traps and summary

Chapter 20, Ep 3 of 3: Cholestatic Liver Disease: Sclerosing Cholangitis

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

Primary sclerosing cholangitis is an imaging diagnosis and a premalignant condition, and the episode builds on that idea. It starts with who gets the disease and why MRCP, not ultrasound, antibodies, or ERCP, makes the diagnosis, then covers when to biopsy, the IgG4 stain, and small-duct disease. It then turns to surveillance for cholangiocarcinoma, colorectal cancer, and gallbladder cancer, the sampling of a dominant stricture, and the complications and treatments, including transplant. Next comes IgG4-related cholangitis, the steroid-responsive mimic of pancreatic cancer, diagnosed with the HISORt criteria. The episode ends with the overlaps of autoimmune hepatitis with primary biliary cholangitis and with sclerosing cholangitis.

Topics covered

Who gets primary sclerosing cholangitis
Why labs and ultrasound cannot settle it
MRCP versus ERCP
Biopsy indications and the IgG4 stain
Small-duct disease
Cholangiocarcinoma and dominant strictures
Colorectal and gallbladder cancer surveillance
Complications, treatments, and transplant
IgG4-related sclerosing cholangitis
Autoimmune hepatitis overlap syndromes

Key decisions

In a patient with colitis and cholestatic liver tests, order MRCP rather than ultrasound or ERCP to diagnose sclerosing cholangitis, and keep ERCP for a dominant stricture, ascending cholangitis, or suspected cholangiocarcinoma.
Biopsy only for small-duct disease with a normal cholangiogram or a suspected autoimmune overlap, signaled by an ALT over five times normal or a high IgG, and stain every biopsy for IgG4.
Do a yearly MRCP plus CA 19-9 in adults with large-duct disease, and remember that CA 19-9 misleads during cholangitis and in Lewis-negative patients.
Treat a dominant stricture as cancer until proven otherwise: send ERCP brushings for cytology and FISH, add cholangioscopy with directed biopsy if still unclear, and dilate only a stricture proven benign.
Refer for transplant a hilar cholangiocarcinoma that meets the Mayo criteria: a mass under three centimeters, no extrahepatic spread, and no transperitoneal biopsy.
Perform colonoscopy with biopsies at diagnosis and every one to two years, remove the gallbladder for polyps over eight millimeters, screen for liver cancer only with cirrhosis, and never use high-dose UDCA above 28 milligrams per kilogram a day.
In an older man with painless jaundice, a distal bile duct stricture, and a sausage-shaped pancreas, get tissue with IgG4 staining and give prednisone 40 milligrams daily for four weeks, then taper by 5 milligrams weekly, before any Whipple.
Treat an autoimmune hepatitis overlap that meets the Paris criteria with UDCA at 13 to 15 milligrams per kilogram a day plus prednisone with or without azathioprine, because neither drug alone controls both components.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode roadmap
(01:11) - First patient: colitis and cholestasis
(05:06) - Biopsy and the IgG4 stain
(06:07) - Small-duct disease and prognosis
(07:50) - Cholangiocarcinoma and dominant strictures
(11:55) - Colorectal and gallbladder surveillance
(13:46) - Complications, treatments, and transplant
(14:59) - IgG4-related sclerosing cholangitis
(19:25) - Autoimmune hepatitis overlap syndromes
(22:03) - Board traps and summary

Chapter 21, Ep 1 of 2: Steatotic Liver Disease: MASLD to Drug Therapy

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

The organizing idea is that fibrosis stage, not ALT or the amount of fat, predicts the outcome, so every decision in MASLD follows from it. The episode first diagnoses MASLD positively from steatosis plus one cardiometabolic criterion and classifies it by alcohol in grams a week. It then explains why fat becomes injury and why genetics such as PNPLA3 drive progression, and it flags lean MASLD and burned-out cryptogenic cirrhosis. Staging comes next, with FIB-4, then FibroScan read with its pitfalls, then MR elastography. Treatment follows: weight loss as a dose, diet and exercise, bariatric surgery, and then semaglutide, resmetirom, pioglitazone, and vitamin E, with the statin always continued.

Topics covered

New SLD, MASLD, MASH, and MetALD nomenclature
Diagnostic criteria for MASLD
Alcohol in grams a week and the MetALD category
Pathogenesis from insulin resistance to lipotoxicity
PNPLA3, TM6SF2, and HSD17B13 genetics
Fibrosis stage as the prognostic driver
Lean MASLD and cryptogenic cirrhosis
FIB-4, FibroScan, and MR elastography staging
Weight loss, diet, exercise, and bariatric surgery
Semaglutide, resmetirom, pioglitazone, and vitamin E

Key decisions

Diagnose MASLD when hepatic steatosis is present with at least one of five cardiometabolic criteria, not the three that metabolic syndrome requires.
Convert drinks to grams a week at 14 grams per drink: MASLD is under 140 grams in women or 210 in men, MetALD lies between, and alcohol-associated liver disease starts at 350 in women or 420 in men.
Start staging with FIB-4, where under 1.3 (2.0 over age 65) is low risk and repeated in one to three years, over 2.67 is high risk, and the range between needs a second test.
Use VCTE next, where under 8 kilopascals rules out advanced fibrosis and 12 to 14 or more suggests cirrhosis, but discount readings taken within three hours of food or in severe obesity, and send unreliable or discordant results to MR elastography.
Set a weight loss dose: 5 percent is the floor, 7 to 10 percent resolves MASH, 10 percent or more can regress fibrosis, and 3 to 5 percent is the target in lean MASLD.
Offer bariatric surgery at a BMI of 35 or more, or 30 to 34.9 with metabolic disease, and in compensated cirrhosis only at an experienced center with a hepatic venous pressure gradient under 10, since a gradient over 15 is an absolute contraindication.
For MASH without cirrhosis and with stage two to three fibrosis, choose semaglutide 2.4 milligrams weekly when obesity or diabetes is present, or resmetirom 80 milligrams daily under 100 kilograms and 100 milligrams at or above, with statin doses capped.
Reserve pioglitazone for biopsy-proven MASH with diabetes and vitamin E 800 international units daily for biopsy-proven MASH without diabetes or cirrhosis, and never withhold a statin because of MASLD.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patient roadmap
(01:42) - New names and diagnostic criteria
(04:05) - Alcohol in grams decides category
(05:06) - Why fat becomes liver injury
(06:44) - Genetics and fibrosis stage prognosis
(08:48) - Lean MASLD and cryptogenic cirrhosis
(10:35) - Noninvasive fibrosis staging
(16:18) - Weight loss, diet, and exercise
(19:09) - Bariatric surgery and cirrhosis
(22:03) - Drug therapy for MASH

Chapter 21, Ep 2 of 2: Steatotic Liver Disease: Alcohol and Transplant

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

The organizing idea is that abstinence is the treatment at every stage of alcohol-associated liver disease, and that severe alcoholic hepatitis is an acute syndrome with its own decision sequence. The episode begins with what reverses at each stage, how alcohol injures the liver, and what the AST-to-ALT pattern means. It then covers why women, PNPLA3 carriers and ALDH2 star two carriers are harmed at lower doses. It moves to diagnosing alcoholic hepatitis by NIAAA criteria without a biopsy, scoring severity, excluding infection, giving prednisolone, and stopping or continuing it at day seven by Lille score. It closes with nutrition, early transplant selection, and alcohol use disorder treatment afterward.

Topics covered

Stages and reversibility of alcohol-associated liver disease
Alcohol metabolism and liver injury
AST to ALT pattern and the AST over 400 rule
Susceptibility: sex, genes, viral hepatitis, bariatric surgery
ALDH2 star two and cancer risk
NIAAA criteria for alcoholic hepatitis
MELD and Maddrey severity scores
Prednisolone, contraindications, and the Lille score
Nutrition and supportive care
Early transplant selection and alcohol use disorder drugs

Key decisions

Counsel a heavy drinker with advanced fibrosis to stop drinking, because steatosis reverses in four to six weeks, steatohepatitis resolves in about half who stop, and cirrhosis does not reverse.
Treat an AST over 400 in a drinker as a superimposed insult and check an acetaminophen level and medication history rather than blaming alcohol alone.
Do not skip screening endoscopy when platelets are under 150,000, whatever the liver stiffness.
Diagnose probable alcoholic hepatitis by NIAAA criteria without a biopsy, and biopsy only when abstinence has exceeded 60 days, labs are atypical, or another cause is suspected.
Call disease severe at a MELD over 20 or a Maddrey function over 32, screen for infection first, and give prednisolone 40 mg daily for 28 days unless there is a contraindication such as a creatinine over 2.5.
Stop steroids at a day-seven Lille score of 0.45 or higher, and continue the full 28 days when it is under 0.45.
Refer a steroid non-responder or steroid-ineligible patient for early transplant evaluation when criteria are met, including a first decompensation, at least two close supports, no more than one failed treatment, and a commitment to lifelong sobriety, without waiting six months.
Treat alcohol use disorder in significant liver disease with acamprosate or baclofen 10 mg three times a day, and use disulfiram and naltrexone cautiously.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(01:06) - Disease course and reversibility
(03:30) - How alcohol injures the liver
(06:35) - Lower-dose susceptibility and ALDH2
(07:26) - Care after transplant
(07:26) - Day-seven Lille decision
(07:26) - Severity scores and steroids
(07:26) - Nutrition and supportive care
(07:26) - Diagnosing alcoholic hepatitis
(07:26) - Selecting patients for early transplant

Chapter 22, Ep 1 of 3: Inherited Liver Diseases: Hereditary Iron Overload

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

Hemochromatosis is a low hepcidin letting ferroportin release iron unchecked, and every decision in the episode follows from that. The episode starts with the two results that make the diagnosis, a raised fasting transferrin saturation and ferritin, then HFE genotyping. It covers which genotypes load iron, what incomplete penetrance means for relatives, and how to recognize secondary hyperferritinemia and the non-HFE forms. It then turns to staging the liver, phlebotomy induction and maintenance, habits to change, what reverses and what does not, lifelong cancer surveillance in cirrhosis, transplant, and testing of siblings and the spouse.

Topics covered

Hepcidin, ferroportin, and iron absorption
C282Y and H63D genotypes
Ancestry and carrier frequency
Diagnostic thresholds and HFE testing
Incomplete penetrance and monitoring
Secondary hyperferritinemia
Non-HFE hemochromatosis types
Biopsy iron patterns
Staging, phlebotomy, and diet
Reversibility, cancer surveillance, and family screening

Key decisions

Diagnose hemochromatosis with a fasting transferrin saturation of at least 45 percent in men or 40 percent in women plus a ferritin over 300 in men or 200 in women, then send HFE genotyping for C282Y homozygosity.
Do not send HFE testing or phlebotomize for a high ferritin with a normal saturation, as in a woman with MASLD and a saturation of 28 percent, and treat the cause instead.
Do not treat H63D alone, or C282Y with H63D without a cofactor such as alcohol, MASLD, or hepatitis C, and do not phlebotomize a C282Y homozygote with normal iron studies, who is rechecked every two to three years.
When overload is clear and HFE is negative, test for HJV, HAMP, TfR2, and SLC40A1 and quantify liver iron by MRI, reserving biopsy for HFE-negative overload or an unexplained ferritin.
Stage the liver by biopsy or elastography before treatment when ALT is over twice normal, age is over 40 with a ferritin over 1,000, platelets are low, or the genotype is not C282Y homozygosity with diagnostic doubt.
Phlebotomize 500 mL weekly until ferritin is 50 to 100, hold the session if hemoglobin is under 11, then maintain with one to two units every two to four months and a ferritin every six to twelve months.
Stop alcohol, vitamin C supplements, and raw shellfish, and eat less red meat, using iron chelators only when phlebotomy is not tolerated.
Continue liver cancer surveillance every six months for life in cirrhosis, evaluate the heart for iron before transplant, and test siblings and the spouse.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and chapter setup
(00:52) - First patient: knuckle pain and ferritin
(02:36) - HFE genotypes and ancestry
(03:57) - Two results that make the diagnosis
(05:25) - Penetrance and his brother
(06:39) - Non-HFE forms of hemochromatosis
(08:32) - Biopsy iron patterns
(09:51) - Staging, phlebotomy, and habits
(13:52) - What reverses, cancer risk, transplant
(15:31) - Family screening and board traps

Chapter 22, Ep 2 of 3: Inherited Liver Diseases: Wilson Disease

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

Wilson disease is a failed copper pump, and nearly every decision in this episode follows from that. ATP7B failure blocks biliary copper excretion and leaves ceruloplasmin low, so the episode starts with whom to suspect, from about age three to forty-five, including lean patients labeled with MASLD. It then builds the diagnosis with the Leipzig score, shows why ceruloplasmin cannot decide alone, and moves to ATP7B testing and sibling screening. Treatment follows: trientine first, the pitfalls of iron, zinc, and penicillamine, zinc for maintenance, and urine copper targets read with free copper. It closes with pregnancy and contraception, and with transplant for fulminant or decompensated disease.

Topics covered

ATP7B copper pump and who to suspect
Liver and neuropsychiatric presentations
Leipzig score diagnosis
Ceruloplasmin limits and hepatic copper
ATP7B testing and sibling screening
Trientine versus penicillamine
Zinc for maintenance
Urine copper and free copper monitoring
Pregnancy and contraception
Liver transplant indications

Key decisions

Suspect Wilson disease in anyone about three to forty-five with unexplained liver disease, especially a lean patient with steatohepatitis and no insulin resistance or a patient with new neuropsychiatric symptoms.
Diagnose with the Leipzig score, where four or more is diagnostic, three is possible and calls for further testing, and two or less is unlikely.
Treat a ceruloplasmin over thirty or a hepatic copper under thirty-five micrograms per gram as excluding the disease, and send ATP7B genetic testing when hepatic copper is intermediate, fifty to two hundred fifty.
Screen every sibling with ceruloplasmin, a slit-lamp exam, and ATP7B testing, and treat a presymptomatic sibling with zinc before the liver or brain is injured.
Start symptomatic disease with trientine, seven hundred fifty to fifteen hundred milligrams a day in divided doses on an empty stomach, never with iron and separated from zinc by at least an hour, and give pyridoxine twenty-five to fifty milligrams a day if penicillamine is used.
Aim for a twenty-four-hour urine copper of two hundred to five hundred micrograms on a chelator, and when it is under two hundred, a free copper over fifteen means non-adherence and under five means overtreatment, which is treated by lowering the dose and not with iron.
Keep the urine copper at seventy-five or less on zinc, and use zinc for maintenance or presymptomatic disease but not alone for symptomatic disease.
Never stop therapy in pregnancy, reduce the chelator dose instead, avoid estrogen contraceptives, copper IUDs, and copper-containing vitamins, and refer for transplant in fulminant disease or decompensated cirrhosis that has failed medical treatment, but not for isolated neurologic disease.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(00:59) - Teenager with raised ALT and tremor
(03:21) - Liver and neuropsychiatric presentations
(05:28) - Five features and the Leipzig score
(06:31) - Borderline results and liver copper
(08:49) - Screening siblings
(09:16) - Chelators, zinc, and drug interactions
(12:26) - Reading urine and free copper
(13:30) - Pregnancy and contraception
(15:09) - When transplant is the answer

Chapter 22, Ep 3 of 3: Inherited Liver Diseases: Four More Diseases

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

This final episode of the chapter treats each inherited liver disease as a question of mechanism, and the mechanism drives the test and the treatment. Alpha-one antitrypsin deficiency injures the lung through lost protein and the liver through trapped protein, so the serum level misleads and augmentation helps only the lung. Cystic fibrosis causes patchy biliary cirrhosis, so biopsy misleads, portal hypertension can precede liver failure, and the modulator must match the mutation. Polycystic liver disease is treated by symptoms, starting with a somatostatin analog before surgery. Childhood cholestatic syndromes are sorted by GGT and by extrahepatic findings.

Topics covered

Alpha-one antitrypsin deficiency mechanisms
Pi phenotypes and liver risk
Diagnosis and treatment of PiZZ disease
Cystic fibrosis liver disease
Cystic fibrosis modulators by mutation
Genetic forms of polycystic liver disease
Symptom-based treatment of polycystic liver
ARPKD and congenital hepatic fibrosis
PFIC, BRIC, and GGT
Alagille syndrome

Key decisions

Diagnose alpha-one antitrypsin deficiency by Pi typing or SERPINA1 genotyping, not by serum level, because the level rises with inflammation and falls in advanced cirrhosis.
In PiZZ patients, stop smoking, alcohol, and NSAIDs, check liver tests, blood count, and ultrasound or elastography yearly, and start liver cancer surveillance every six months once cirrhosis develops.
Give weekly intravenous augmentation to protect the lung, and refer for liver transplant when the liver fails, since augmentation does not protect the liver and transplant cures it.
Diagnose cystic fibrosis liver disease with labs, ultrasound, and elastography rather than biopsy, and screen for varices even when bilirubin, albumin, and INR are normal.
Treat cystic fibrosis liver disease with ursodeoxycholic acid at 15 to 20 mg/kg a day, replace vitamins A, D, E, and K, and use elexacaftor-tezacaftor-ivacaftor for anyone with at least one F508del allele.
Treat polycystic liver disease only for symptoms, starting with lanreotide or octreotide and judging the response at 6 to 12 months, then fenestration or resection only if enough liver tissue remains.
Request a MELD exception for symptomatic polycystic liver disease with transplant evaluation, because preserved synthetic function gives a low calculated MELD, and consider combined liver-kidney transplant in advanced ADPKD.
Treat a cholestatic infant with severe itch and a normal GGT as PFIC one or two, confirm by genetic testing, relieve itch with odevixibat or maralixibat, and follow AFP in PFIC two.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and four diseases
(01:14) - Alpha-one antitrypsin opposite mechanisms
(03:12) - Pi phenotypes and liver risk
(05:36) - Alpha-one antitrypsin treatment and transplant
(06:58) - Cystic fibrosis liver disease
(09:56) - Modulators matched to mutation
(11:16) - Polycystic liver disease genetics
(13:49) - Drugs, surgery, and transplant for cysts
(15:49) - PFIC, BRIC, and the GGT
(20:24) - Alagille syndrome

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

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

Portal hypertension begins as resistance inside the liver, then splanchnic vasodilation drives the hyperdynamic circulation behind most cirrhosis complications. The episode first measures and estimates portal pressure and starts carvedilol for compensated cirrhosis with clinically significant portal hypertension, then separates presinusoidal and postsinusoidal causes and recognizes acute-on-chronic liver failure. It next decides who can skip screening endoscopy and how to treat each size of varix, including when to hold the beta-blocker. Acute bleeding follows, with the transfusion target, ceftriaxone, octreotide, banding, preemptive TIPS, and secondary prophylaxis. It closes with gastric varices, splenic vein thrombosis, portal hypertensive gastropathy, and GAVE.

Topics covered

How portal hypertension develops
Hepatic venous pressure gradient thresholds
Baveno seven estimation of CSPH
Carvedilol to prevent decompensation
Presinusoidal and postsinusoidal causes
Acute-on-chronic liver failure
Screening endoscopy and primary prophylaxis
Holding the beta-blocker
Acute variceal bleed bundle
Preemptive TIPS and secondary prophylaxis
Gastric varices and BRTO
Splenic vein thrombosis, gastropathy, and GAVE

Key decisions

Start carvedilol, 6.25 mg daily increasing to twice daily as tolerated, in compensated cirrhosis with CSPH, which a stiffness of 25 kilopascals or more establishes without a catheter, to prevent decompensation rather than to prevent varices.
Defer screening endoscopy only when stiffness is under 20 kilopascals and platelets are over 150,000, with yearly elastography and platelet counts; meeting one criterion alone still means a scope.
Give carvedilol or band every two to four weeks until obliteration for medium or large varices, and for small varices with red wale signs or Child-Pugh C cirrhosis; a patient on a beta-blocker needs no surveillance endoscopy.
Hold the beta-blocker for a systolic pressure under 90, a sodium under 130, or acute kidney injury, and switch to banding until it can be resumed.
In an acute variceal bleed, transfuse to a hemoglobin of about 7 without correcting the INR with plasma, give ceftriaxone 1 g daily for up to seven days and octreotide 50 microgram bolus then 50 micrograms an hour, protect the airway, and band within 12 hours.
Place a preemptive covered TIPS within 72 hours for Child-Pugh C with scores of 10 to 13, or Child-Pugh B with active bleeding at endoscopy, unless there is severe right heart failure, pulmonary hypertension, prior overt encephalopathy, sepsis, or biliary obstruction.
For secondary prophylaxis in patients outside those groups, combine a nonselective beta-blocker with banding every seven to fourteen days, with a PPI for two weeks after each session.
Do not band fundal varices; use BRTO when there is a gastrorenal shunt and nothing else to fix, TIPS when ascites or esophageal varices coexist, splenectomy or splenic artery embolization for isolated splenic vein thrombosis, and ablation rather than TIPS or beta-blockers for GAVE.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and scope
(02:59) - Measuring and estimating portal pressure
(05:32) - Presinusoidal and postsinusoidal causes
(06:47) - Acute-on-chronic liver failure
(07:42) - Screening and varix prophylaxis
(10:42) - When to hold the beta-blocker
(11:36) - Acute variceal bleeding bundle
(14:02) - Preemptive TIPS decision
(15:25) - Secondary prophylaxis after a bleed
(16:27) - Gastric varices and other lesions

Chapter 23, Ep 2 of 3: Portal Hypertension: Ascites and Complications

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

Ascites in cirrhosis grows out of splanchnic vasodilation and hormonal sodium retention, so treatment targets sodium rather than water. The episode starts with the diagnostic tap, the SAAG, and diuretic dosing, then covers albumin after large taps and refractory ascites with TIPS. It moves to hyponatremia and its correction limits, then spontaneous bacterial peritonitis with antibiotics, albumin, and prophylaxis, and the secondary peritonitis that needs surgery. Hepatorenal syndrome follows, diagnosed only after an albumin challenge and treated with terlipressin or norepinephrine. The episode ends with hepatic encephalopathy: find the precipitant, titrate lactulose, add rifaximin, and keep protein in the diet.

Topics covered

Pathophysiology of ascites
Diagnostic paracentesis and SAAG
Sodium restriction and diuretics
Drugs to avoid in ascites
Albumin after large-volume paracentesis
Refractory ascites and TIPS
Hyponatremia management
Spontaneous bacterial peritonitis
Secondary bacterial peritonitis
Hepatorenal syndrome diagnosis and treatment
Hepatic encephalopathy and protein intake

Key decisions

Tap every patient with new or worsening ascites, and read a SAAG of 1.1 g/dL or more as portal hypertension, with ascitic protein under 2.5 pointing to cirrhosis.
Restrict sodium to under 2 grams a day, restrict fluid only when serum sodium is under 125, and combine spironolactone and furosemide at 100 to 40 up to 400 to 160, stopping NSAIDs and aminoglycosides.
Give 6 to 8 grams of albumin per liter removed for any paracentesis over 5 liters.
Place TIPS in refractory ascites only after an echocardiogram and without a MELD over about 18 to 22, bilirubin over 3 to 5, INR over 2.5, recurrent encephalopathy, heart failure, or pulmonary hypertension, and give rifaximin for protection.
Correct chronic hyponatremia by 4 to 6 mEq/L in 24 hours and never more than 8, and treat dilutional hyponatremia with diuretic withdrawal, fluid restriction, and albumin rather than saline.
Diagnose spontaneous bacterial peritonitis at an ascitic neutrophil count over 250 per cubic millimeter, treat with ceftriaxone 2 grams daily for 5 to 7 days plus albumin 1.5 g/kg on day one and 1 g/kg on day three, and continue prophylaxis afterward.
Diagnose HRS-AKI only after 2 days of diuretic withdrawal and albumin 1 g/kg a day without improvement, then give terlipressin with albumin unless saturation is under 90 percent, using norepinephrine in that case.
In overt encephalopathy, reverse the precipitant, titrate lactulose to 2 to 3 soft stools a day, add rifaximin 550 mg twice daily after the first episode, and give protein at 1.2 to 1.5 g/kg a day with a bedtime snack.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patient roadmap
(01:29) - How ascites forms and is treated
(04:23) - Albumin after large-volume paracentesis
(05:41) - Refractory ascites and TIPS
(08:11) - Hyponatremia on diuretics
(10:01) - Spontaneous bacterial peritonitis
(13:46) - Secondary peritonitis and empyema
(14:42) - Diagnosing hepatorenal syndrome
(17:31) - Treating HRS-AKI
(19:53) - Hepatic encephalopathy

Chapter 23, Ep 3 of 3: Cirrhosis Complications: Lungs and Vessels

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

This episode is organized around one idea: in cirrhosis, the vessels of the lungs, the clotting system, and the liver's own blood supply each fail in a way that changes management. It starts with the two opposite pulmonary vascular syndromes, hepatopulmonary syndrome and portopulmonary hypertension, and their effects on transplant, then hepatic hydrothorax and why a chest tube is never placed. It then explains why the INR misleads, which procedures need no correction, and when to anticoagulate. It closes with vascular liver disease by level of obstruction: Budd-Chiari syndrome, sinusoidal obstruction syndrome, portal vein thrombosis, and porto-sinusoidal vascular disease.

Topics covered

Hepatopulmonary syndrome
Portopulmonary hypertension and transplant candidacy
Hepatic hydrothorax
Rebalanced hemostasis and the INR
Procedure prophylaxis and viscoelastic testing
Anticoagulation and cirrhotic cardiomyopathy
Budd-Chiari syndrome
Sinusoidal obstruction syndrome
Portal vein thrombosis
Porto-sinusoidal vascular disease

Key decisions

Diagnose hepatopulmonary syndrome with a delayed bubble study (three to six cycles) plus a PaO2 under 80 or a macroaggregated albumin scan, and request MELD exception points when PaO2 is under 60, since only transplant cures it.
Diagnose portopulmonary hypertension by right heart catheterization (mean pressure of 25 or more, resistance over 3 Wood units, wedge of 15 or less), treat with PDE-5 inhibitors, endothelin receptor antagonists, or prostacyclins, and rule out transplant when the mean pressure is 50 or more or fails to respond.
For a suspected hepatic hydrothorax, do a diagnostic thoracentesis, treat a pleural neutrophil count over 250 as spontaneous bacterial empyema, use TIPS for refractory effusion, and never place a chest tube or do pleurodesis.
Do not give plasma or platelets before paracentesis, thoracentesis, or endoscopy without intervention, because the INR does not predict bleeding in cirrhosis, and continue heparin prophylaxis in hospitalized patients.
Use viscoelastic testing to guide correction before high-risk procedures, replacing fibrinogen to over 120 mg/dL and platelets to over 50,000 only with documented bleeding or the highest-risk procedures.
Reserve rivaroxaban and apixaban for Child-Pugh A and some Child-Pugh B patients, and avoid them in Child-Pugh C, severe coagulopathy, or after a recent variceal hemorrhage.
Treat Budd-Chiari syndrome in order, with anticoagulation, then angioplasty and stent, then TIPS, then transplant, after a thrombophilia workup that always includes JAK2.
Exclude arterially enhancing tumor thrombus before anticoagulating portal vein thrombosis, and do not anticoagulate cavernous transformation.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:05) - Hepatopulmonary syndrome
(03:38) - Portopulmonary hypertension
(05:37) - Hepatic hydrothorax
(07:14) - Rebalanced hemostasis and the INR
(10:50) - Anticoagulation and cirrhotic cardiomyopathy
(12:13) - Budd-Chiari syndrome
(14:27) - Sinusoidal obstruction syndrome
(15:41) - Portal vein and porto-sinusoidal disease
(18:21) - Board traps and recap

Chapter 24, Ep 1 of 4: Liver Tumors and Transplantation: Benign Lesions

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

Imaging, not biopsy, sorts a benign liver lesion found by chance in a liver without cirrhosis, and the episode follows three patients through that idea. A young woman's six-centimeter mass is separated on contrast MRI into hemangioma, with peripheral nodular enhancement and centripetal fill-in, focal nodular hyperplasia, which stays bright in the hepatobiliary phase on gadoxetate, and adenoma, which is dark. Adenoma then brings the surgery decisions: subtype, size, sex, bleeding, growth, and planned pregnancy, plus stopping estrogen and surveillance for smaller lesions. A man using anabolic steroids shows why sex changes the rule and what else steroids do to the liver. A woman on azathioprine shows nodular regenerative hyperplasia, which needs a reticulin stain.

Topics covered

Imaging-first approach to benign liver lesions
Hemangioma and Kasabach-Merritt syndrome
Focal nodular hyperplasia and gadoxetate MRI
Hepatic adenoma associations and subtypes
Resection criteria for adenoma
Adenoma surveillance and adenomatosis
Adenoma in men and anabolic steroid liver injury
Peliosis hepatis
Nodular regenerative hyperplasia
Board traps for benign liver lesions

Key decisions

In a liver without cirrhosis, let contrast-enhanced MRI identify a benign lesion and biopsy only atypical ones, while a new lesion in cirrhosis is treated as cancer until proven otherwise.
Reassure a patient whose lesion shows peripheral nodular enhancement with centripetal fill-in, because a classic hemangioma needs no biopsy and no follow-up imaging, and treat only symptomatic giant lesions, high-output heart failure, or Kasabach-Merritt syndrome.
Call a lesion that is bright in the hepatobiliary phase on gadoxetate focal nodular hyperplasia and a lesion that is dark an adenoma, because FNH has working bile ductules and an adenoma has no bile ducts; classic FNH needs no surveillance and no stopping of contraceptives.
Resect any adenoma in a man, any adenoma of five centimeters or more, a growing or bleeding adenoma, a beta-catenin-activated adenoma, and any adenoma before a planned pregnancy.
Stop estrogen-containing contraceptives in any woman with an adenoma and switch to a non-estrogen method, since some adenomas regress when estrogen is withdrawn.
Observe a small adenoma outside the resection criteria with MRI or CT every six months for two years, then yearly, and resect if it grows or bleeds.
Consider liver transplant only as a rare option for hepatic adenomatosis, more than ten adenomas, that cannot be resected.
Suspect nodular regenerative hyperplasia when imaging looks cirrhotic with splenomegaly and varices but routine histology is nearly normal, order a reticulin stain, and consider drugs such as azathioprine as the cause.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and three patients
(00:45) - The patient with a six-centimeter mass
(01:47) - Hemangioma signature and treatment
(03:01) - Focal nodular hyperplasia and gadoxetate
(04:07) - Her MRI points to adenoma
(05:44) - Adenoma resection criteria and pregnancy
(06:45) - Observing a smaller adenoma
(07:19) - Adenoma in a man on steroids
(08:41) - Nodular regenerative hyperplasia on azathioprine
(09:54) - Board traps and key points

Chapter 24, Ep 2 of 4: Liver Tumors and Transplantation: Liver Cancer

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

Hepatocellular carcinoma care runs on a few fixed rules: surveillance follows the cirrhosis, imaging makes the diagnosis, and the BCLC stage picks the treatment. The episode starts with who is surveyed, using ultrasound and AFP every six months, and when MRI or CT replaces ultrasound. It covers hepatitis B without cirrhosis and the groups who are not surveyed. It then reads a new nodule with LI-RADS, including LR-5, LR-M, and tumor in vein. Staging follows, with resection, ablation, and transplant for early disease, chemoembolization or radioembolization for intermediate disease, and systemic drugs for advanced disease. The episode ends with the variceal check before bevacizumab.

Topics covered

Surveillance in cirrhosis, including cured hepatitis C
Ultrasound with AFP every six months
Switching to MRI or CT when ultrasound fails
Hepatitis B surveillance without cirrhosis
Groups who are not surveyed
LI-RADS categories and LR-5 diagnosis
LR-M lesions and tumor in vein
BCLC staging
Resection, ablation, and transplant criteria
TACE, TARE, and mRECIST
Systemic therapy and the variceal check

Key decisions

Survey every six months with ultrasound plus AFP in all Child-Pugh A and B cirrhosis, including hepatitis C cured by sustained virologic response, and survey Child-Pugh C only when the patient is listed or being evaluated for transplant.
Use multiphase MRI or CT every six months instead of ultrasound when severe obesity or marked steatosis makes the ultrasound inadequate.
Survey non-cirrhotic hepatitis B by risk, such as an Asian man over forty, an Asian woman over fifty, a viral load over 200,000 IU/mL, or a PAGE-B score of ten or higher, and survey hepatitis D in any phase, but do not survey stage three fibrosis or MASLD without cirrhosis.
Diagnose hepatocellular carcinoma without a biopsy when a lesion in cirrhosis is LR-5, meaning one centimeter or more with arterial hyperenhancement plus washout, a capsule, or growth of 50 percent in six months, follow LR-3 at three to six months, manage LR-4 with short-interval imaging or biopsy, and biopsy LR-M.
Treat an arterially enhancing portal vein thrombus as tumor in vein, which is not anticoagulated and counts as metastatic disease that excludes transplant.
Match early disease to treatment: ablate tumors under three centimeters, resect only with a normal bilirubin and a hepatic venous pressure gradient under ten, and transplant within Milan criteria or after downstaging with three to six months of stable imaging.
Treat intermediate BCLC B disease with TACE or TARE and judge response by mRECIST, which measures viable enhancing tumor rather than size.
Before atezolizumab plus bevacizumab, obtain an upper endoscopy within six months and treat high-risk varices, and use durvalumab plus tremelimumab when bevacizumab is unsafe.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:09) - Surveillance after hepatitis C cure
(02:13) - Six-month interval and the right test
(03:25) - Hepatitis B without cirrhosis
(04:25) - Patients who are not surveyed
(06:28) - Reading the nodule with LI-RADS
(08:45) - LR-M lesions and tumor in vein
(10:06) - BCLC stage and early treatment
(13:19) - Intermediate disease: TACE and TARE
(14:24) - Advanced disease and systemic therapy

Chapter 24, Ep 3 of 4: Liver Tumors and Transplantation: Biliary Cancer

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

The organizing idea is that the location of a cholangiocarcinoma decides everything. The episode starts with a man with cirrhosis and an intrahepatic mass, then covers how progressive enhancement without washout separates this tumor from hepatocellular carcinoma. It reviews the risk factors and why CA 19-9 misleads, then explains why a transplant cannot cure him and how first-line drugs and FGFR2 and IDH1 testing guide treatment. A second patient with sclerosing cholangitis and a hilar stricture shows the Mayo transplant protocol and why tissue must be taken from inside the duct. A third patient, with a distal tumor, shows that resection is the cure and that IgG4-related disease can imitate cancer.

Topics covered

Three anatomic types of cholangiocarcinoma
Bismuth-Corlette classification
Imaging versus hepatocellular carcinoma
Risk factors
Limits of CA 19-9
Transplant contraindication in intrahepatic tumors
First-line therapy and molecular testing
Mayo protocol for hilar tumors
Safe tissue sampling
IgG4 mimic of distal tumors

Key decisions

Classify a tumor as intrahepatic, perihilar or distal by its location, because each type is managed differently.
Suspect cholangiocarcinoma rather than hepatocellular carcinoma when a mass enhances progressively through the venous and delayed phases without washout.
Treat CA 19-9 as one piece of evidence only, since it rises with benign obstruction and cholangitis and stays normal in the 5 to 10 percent of people who are Lewis-negative.
Do not transplant an intrahepatic cholangiocarcinoma larger than 2 centimeters, and reserve resection, the only cure for intrahepatic and distal tumors, for disease without spread.
Give gemcitabine plus cisplatin plus durvalumab for advanced disease, and test every intrahepatic tumor for FGFR2 fusions (pemigatinib or futibatinib) and IDH1 mutations (ivosidenib).
Assume a dominant stricture in sclerosing cholangitis is cholangiocarcinoma, and evaluate it with ERCP brushings for cytology and FISH plus cholangioscopy with directed biopsy.
Offer the Mayo protocol of neoadjuvant chemoradiation and transplant to selected unresectable perihilar tumors of 3 centimeters or less with no intrahepatic metastases or nodal involvement.
Avoid percutaneous or EUS-guided biopsy of a hilar primary in a possible transplant candidate because of tract seeding, but do biopsy a suspicious regional node.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 three patients
(01:18) - Three anatomic types and Bismuth-Corlette
(02:17) - Imaging versus hepatocellular carcinoma
(03:06) - Risk factors to recognize
(03:56) - Why CA 19-9 misleads
(04:25) - Why transplant cannot cure him
(05:00) - Systemic therapy and molecular testing
(05:56) - Hilar tumor and Mayo protocol
(07:43) - How tissue sampling protects eligibility
(08:21) - Distal tumor and IgG4 mimic

Chapter 24, Ep 4 of 4: Liver Tumors and Transplantation: Transplant Care

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

Liver transplant care runs on a calendar and on rules for what MELD cannot measure. The episode begins with referral at a first decompensation or a MELD of 15, then covers MELD 3.0, the evaluation, vaccines before transplant, and sarcopenia. It moves to exception points for cancer within Milan and for lung syndromes, the review board, and what each donor type means. After transplant, complications are read by time since surgery, with rejection diagnosed by biopsy, CMV prevented, and drug toxicities matched to each agent. It closes with late kidney injury and cancers, recurrence of sclerosing cholangitis, hepatitis B and C, autoimmune hepatitis, and MASH, and the tacrolimus interactions to check whenever a drug is added.

Topics covered

Referral triggers and MELD 3.0
Pretransplant evaluation and vaccines
Alcohol assessment and sarcopenia
Exception points for liver cancer
Hepatopulmonary and portopulmonary syndromes
National Liver Review Board conditions
Donor types and graft complications
Complications by time since transplant
Rejection and CMV prevention
Immunosuppressant toxicities
Late cancers and recurrent disease
Tacrolimus drug interactions

Key decisions

Refer for transplant at a first decompensation or a MELD of 15 or higher, without waiting for a higher score, while a compensated patient with a MELD under 15 is not referred yet.
Judge alcohol-related liver disease by structured assessment such as SIPAT or the High Risk Alcoholism Relapse score, not by a rigid six-month rule.
Give live vaccines, varicella and MMR, before transplant, because they are contraindicated afterward.
Give cancer within Milan the regional median MELD after a six-month wait, and accept downstaging into Milan when the cancer is stable on imaging for three to six months.
Grant a hepatopulmonary exception only with a room-air PaO2 under 60, a right-to-left shunt on bubble echocardiography, and no significant primary lung disease, and rule out transplant when the mean pulmonary artery pressure is over 50.
Diagnose suspected rejection by biopsy, treat it with methylprednisolone 500 to 1000 mg daily for three days then a taper, and use thymoglobulin if it resists steroids.
Prevent CMV in D-plus R-minus recipients with valganciclovir 900 mg daily for three to six months or preemptive weekly PCR, and do not use letermovir to treat active disease.
Convert to an mTOR inhibitor when kidney function declines on tacrolimus, and check the tacrolimus level whenever a drug is added.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode overview
(01:33) - Referral timing and MELD 3.0
(03:09) - Evaluation, vaccines, and sarcopenia
(07:03) - Exception points for liver cancer
(09:21) - Review board conditions and donors
(11:56) - Complications by time since transplant
(13:28) - Rejection and CMV prevention
(18:18) - Late kidney injury and cancers
(19:47) - Recurrence of original disease
(20:44) - Tacrolimus interactions

Chapter 25, Ep 1 of 3: Acute Pancreatitis: From Acinar Cell to Severity

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

Acute pancreatitis starts with premature trypsin activation inside the acinar cell, driven by sustained intracellular calcium whatever the trigger, and it becomes dangerous through capillary leak, third spacing, and necrosis that takes days to show. The episode begins with diagnosis by two of three criteria, so a CT on day one is unnecessary, and with why lipase is the better enzyme and why very high triglycerides can hide it. It then works through the cause: gallstones, alcohol, triglycerides, drugs, calcium, tumor after forty, structural, autoimmune, and genetic causes. It ends with severity, defined by organ failure, the early scores and bedside markers, and the timing of CT.

Topics covered

Trypsin activation and the calcium pathway
Systemic inflammation and necrosis timing
Revised Atlanta diagnostic criteria
When to skip the CT
Lipase versus amylase
Lipemic serum and falsely normal enzymes
Gallstone, alcohol, and triglyceride causes
Drugs, calcium, tumors, and genetics
Organ failure and the Marshall score
Early scores, bedside markers, and CT severity index

Key decisions

Diagnose acute pancreatitis when two of three criteria are met: typical pain, lipase or amylase over three times normal, or characteristic imaging, and skip the CT on day one when two are already present.
Order a right upper quadrant ultrasound in every patient, and plan cholecystectomy before discharge when gallstones are found.
Treat an ALT over 150 as pointing to a biliary cause, and use MRCP or EUS when suspected persistent obstruction or cholangitis persists despite a non-diagnostic ultrasound.
Treat triglycerides over 1,000 mg/dL as causal with fasting for at least 24 hours plus an insulin drip, and recheck fasting triglycerides at four to six weeks.
Check calcium and PTH in every unexplained attack, review the drug list, and image a first unexplained attack after age forty for a tumor.
Offer genetic testing for recurrent attacks under age thirty-five, especially with a family history.
Define organ failure as a modified Marshall score of two or more in any system, and call pancreatitis severe when failure persists beyond 48 hours.
Escalate care and consider the ICU when the hematocrit stays over 44 or the BUN rises within 24 hours, and obtain the CT severity index only after 72 hours.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and roadmap
(01:32) - Trypsin activation and calcium pathway
(02:57) - Why patients worsen after admission
(04:33) - Diagnostic criteria and skipping CT
(05:42) - Why lipase is the better enzyme
(06:20) - Milky serum and normal enzymes
(07:00) - Gallstones, alcohol, and triglycerides
(09:35) - Drugs, calcium, tumors, and genetics
(13:58) - Organ failure and severity grading
(16:21) - Early scores, markers, and CT timing

Chapter 25, Ep 2 of 3: Acute Pancreatitis: First Days of Treatment

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

The organizing idea is that early treatment in acute pancreatitis works by restoring perfusion, feeding the gut, and acting on the bile duct only when there is a reason. The episode starts with fluid: which fluid, how much, how to judge response at six to twelve hours, and when a non-responder moves to the ICU. It then covers feeding, from early oral diet in mild disease to tube choice and the limited role of parenteral nutrition. Last come the biliary decisions: who needs ERCP and when, timing of cholecystectomy in mild versus necrotizing disease, and sphincterotomy for patients who cannot have surgery.

Topics covered

Why fluid resuscitation is urgent
Lactated Ringer's versus normal saline
Moderate goal-directed fluid dosing
Reassessing response and escalating to the ICU
Fluid caution in heart and kidney disease
Early oral and enteral feeding
Tube choice and parenteral nutrition
ERCP indications and timing
Cholecystectomy timing
Sphincterotomy when surgery is not possible

Key decisions

Give lactated Ringer's as the first fluid rather than normal saline, and do not give hydroxyethyl starch.
In a hypovolemic patient give a ten milliliter per kilogram bolus then one and a half milliliters per kilogram per hour, with no bolus when heart rate, blood pressure, urine output, and hematocrit are normal, and give more cautious dosing in heart or kidney disease.
Reassess at six to twelve hours using hematocrit, BUN, and a urine goal of half to one milliliter per kilogram per hour, and move a non-responder to the ICU instead of raising the rate.
In mild pancreatitis start a low-fat solid diet within twenty-four to forty-eight hours as tolerated, without clear liquids first and without waiting for lipase to normalize.
When tube feeding is needed use a nasogastric tube with a standard polymeric formula, and reserve parenteral nutrition for patients who cannot tolerate enteral feeding for a prolonged period.
Perform ERCP within twenty-four hours for cholangitis and within twenty-four to seventy-two hours for persistent obstruction, but not for gallstone pancreatitis alone, even when predicted severe, and use MRCP or EUS first when obstruction is uncertain.
Remove the gallbladder during the same admission in mild gallstone pancreatitis once pain settles, and defer it four to eight weeks in severe or necrotizing disease.
Offer ERCP with biliary sphincterotomy before discharge to a patient with gallstone pancreatitis who is unfit for cholecystectomy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and first patient setup
(00:51) - Fluid urgency in the first patient
(01:41) - Choosing lactated Ringer's
(02:14) - Moderate goal-directed fluid dosing
(03:38) - Reassessing response and escalation
(04:51) - Early feeding and tube choice
(06:47) - Mild gallstone pancreatitis and ERCP
(09:43) - Same-admission cholecystectomy
(10:39) - Severe disease and delayed surgery
(11:23) - Sphincterotomy when surgery is impossible

Chapter 25, Ep 3 of 3: Acute Pancreatitis: Necrosis and Recurrence

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

Necrosis changes the tempo of acute pancreatitis, and the organizing idea is that timing and cause decide every step. The episode begins with a man in week three whose gas-containing collection proves infected necrosis, treated with antibiotics that penetrate tissue, while sterile necrosis gets none. It then names collections by content and time, applies the delay, drain, debride sequence, and requires excluding a pseudoaneurysm before drainage and deciding whether venous thrombosis needs anticoagulation. The second half turns to a young woman with recurrent attacks: second-pass MRCP and EUS, genetic testing, divisum, post-ERCP pancreatitis prevention, cholecystectomy, removing the cause, and screening for diabetes and exocrine insufficiency.

Topics covered

Infected pancreatic necrosis
Antibiotics for infected versus sterile necrosis
Atlanta collection terms
Delay, drain, debride step-up
Pseudoaneurysm and splanchnic vein thrombosis
Recurrent and idiopathic pancreatitis workup
Genetic testing
Pancreas divisum
Post-ERCP pancreatitis prevention
Cholecystectomy and follow-up after discharge

Key decisions

Diagnose infected necrosis in weeks two to four from gas in a collection without a recent procedure, along with fever, a rising white count, or deterioration, and reserve EUS-guided aspiration for equivocal imaging.
Treat infected necrosis with a carbapenem, a fluoroquinolone, or piperacillin-tazobactam plus metronidazole, and give no prophylactic antibiotics for sterile necrosis.
Call an encapsulated collection with solid debris after four weeks walled-off necrosis, not a pseudocyst.
Delay intervention about four weeks, drain percutaneously or endoscopically first, and debride only if drainage fails to control sepsis or solid debris blocks it, using percutaneous catheter drainage earlier only for instability with gas, persistent organ failure, or a fistula.
Embolize a pseudoaneurysm before any drainage when hemoglobin falls or a collection enlarges, and anticoagulate splanchnic venous thrombosis only when it extends into the portal or superior mesenteric vein.
Do a second-pass MRCP and EUS before calling recurrent pancreatitis idiopathic, and test PRSS1, SPINK1, CFTR, CTRC, and CASR in patients under thirty-five, especially with a family history.
Do not perform minor papilla sphincterotomy for divisum seen on imaging alone, and in a high-risk ERCP use rectal indomethacin 100 milligrams, a prophylactic pancreatic stent, and lactated Ringer's solution.
Consider cholecystectomy after a second idiopathic attack, lower triglycerides below 500 milligrams per deciliter, and check hemoglobin A1c at three to six months and ask about steatorrhea after discharge.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and roadmap
(01:31) - Infected necrosis and antibiotics
(03:41) - Naming Atlanta collections
(04:28) - Delay, drain, then debride
(06:32) - Pseudoaneurysm and venous thrombosis
(08:05) - Second patient: recurrent pancreatitis workup
(09:40) - Genetic testing for young patients
(10:16) - Pancreas divisum and sphincterotomy
(11:22) - Preventing post-ERCP pancreatitis
(12:26) - Cholecystectomy, prevention, and follow-up

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

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

Chronic pancreatitis is scar replacing the tissue that secretes and drains, and each decision in this episode follows from that idea. The episode starts with the finding that proves the disease, pancreatic calcification on CT, then classifies the cause with TIGAR-O, weighs alcohol against tobacco, and keeps obstructing cancer in mind. It then covers who needs genetic testing and what PRSS1, SPINK1, and the other genes mean. Next it shows how to make the diagnosis when CT is normal, using secretin MRCP, EUS, and function tests. It closes with pain: medical therapy first, then drainage of an obstructed duct, then total pancreatectomy with islet autotransplantation for a narrow group.

Topics covered

Definition and pathognomonic calcification
TIGAR-O classification of causes
Alcohol, tobacco, and CLDN2
Excluding obstructing adenocarcinoma
Selective genetic testing and PRSS1 surveillance
CT, secretin MRCP, and EUS Rosemont criteria
Why ERCP is not used for diagnosis
Fecal elastase and secretin function testing
Sources of pain and medical management
Endoscopic versus surgical drainage and pancreatectomy with islet autotransplantation

Key decisions

Diagnose chronic pancreatitis from parenchymal calcification on CT alone, with no function test or biopsy needed.
Stop both alcohol and tobacco, because smoking is an independent dose-dependent risk, with a hazard ratio of about three above a pack a day, and quitting only beer lets the gland keep worsening.
Exclude a tumor before any other label in an older patient with a first unexplained attack or a single main duct stricture with upstream dilation.
Order genetic testing when the cause is unclear, there is a family history, or onset is before age thirty-five, and offer surveillance only for PRSS1, with annual MRI alternating with EUS from age forty.
When CT is normal but suspicion stays high, use secretin MRCP or EUS graded by the Rosemont criteria, and do not use ERCP for diagnosis because post-ERCP pancreatitis occurs in three to ten percent overall.
Trust a fecal elastase below one hundred micrograms per gram, distrust values from one hundred to two hundred in watery stool, and use a secretin peak bicarbonate of eighty milliequivalents per liter or more to argue against early disease.
Treat pain with acetaminophen, NSAIDs, and a neuromodulator such as pregabalin, minimize opioids, and do not use enzymes as primary pain therapy.
Refer a fit patient with a dilated obstructed duct for early lateral pancreaticojejunostomy, use lithotripsy for stones over five millimeters when surgery is not chosen, and reserve total pancreatectomy with islet autotransplantation for intractable hereditary or small-duct disease, done early in PRSS1.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and three patients
(01:48) - What chronic pancreatitis is
(02:49) - TIGAR-O classification of causes
(04:01) - Alcohol, tobacco, and the cause not to miss
(05:36) - Who needs genetic testing
(09:10) - Imaging when the CT is normal
(11:09) - Function tests and their pitfalls
(12:27) - Sources of pain and medical therapy
(14:53) - Endoscopic versus surgical drainage
(16:09) - Total pancreatectomy with islet autotransplantation

Chapter 26, Ep 2 of 5: Chronic Pancreatitis and Cysts: Late Complications

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

This episode follows the pancreas after scarring, through what it stops making and the structural trouble it causes. A man with a calcified gland shows that steatorrhea appears only when exocrine function falls below about ten percent, so bone density, vitamins, and B12 are checked, enzymes are given with meals, timing and adherence are fixed before the dose rises, and type three c diabetes is managed cautiously because glucagon is lost. A woman then shows the complications by anatomy: a symptomatic pseudocyst drained endoscopically, a recurrence from a disconnected duct, a fibrotic bile duct stricture, splenic vein thrombosis with gastric varices, high-amylase ascites, and long-term cancer risk.

Topics covered

Late onset of steatorrhea
Baseline bone density, vitamins, and B12
Pancreatic enzyme replacement dosing
Poor response to enzymes
Type three c diabetes
Pseudocyst drainage with LAMS
Disconnected duct syndrome
Distal bile duct stricture
Splenic vein thrombosis and gastric varices
Pancreatic ascites and cancer risk

Key decisions

Diagnose clinical malabsorption as exocrine function below about ten percent of normal, and check bone density, fat-soluble vitamins, and B12 before treatment.
Start PERT with meals at forty thousand to fifty thousand USP lipase units per main meal and half that with snacks, titrating up to ninety thousand USP per meal, and do not confuse international units with USP units.
For a poor enzyme response, check timing and adherence first, then raise the dose, add a PPI, and look for SIBO, bile acid malabsorption, or celiac disease.
Judge enzyme response by weight, stool consistency, vitamin levels, and fecal fat rather than a repeat fecal elastase.
Treat type three c diabetes with metformin and cautiously titrated insulin, avoiding sulfonylureas and GLP-1 agonists after pancreatitis, because glucagon is lost.
Observe asymptomatic pseudocysts whatever their size, and drain symptomatic, infected, or enlarging ones with an EUS-guided LAMS after considering a pseudoaneurysm.
Treat a pseudocyst that recurs after stent removal as disconnected duct syndrome, needing long-term transmural plastic stents or resection after MRCP.
Treat a fibrotic distal bile duct stricture with a fully covered metal stent for six to twelve months or surgery, and treat splenic vein thrombosis with bleeding gastric varices by splenectomy without anticoagulation unless clot reaches the portal or superior mesenteric vein.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(02:48) - Enzyme replacement dosing and timing
(03:42) - Poor response to enzymes
(05:13) - Type three c diabetes
(06:50) - Pseudocyst in chronic pancreatitis
(08:09) - Endoscopic pseudocyst drainage
(09:08) - Recurrence and disconnected duct
(10:18) - Fibrotic bile duct stricture
(11:03) - Splenic vein thrombosis and varices
(11:53) - Duct leak ascites and cancer risk

Chapter 26, Ep 3 of 5: Chronic Pancreatitis and Cysts: Autoimmune Types

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

Autoimmune pancreatitis imitates pancreatic cancer and melts away with steroids, so the organizing idea is excluding cancer before treating. The episode follows an older man with painless jaundice who has type one disease, then a younger woman with ulcerative colitis who has type two. It covers the clues outside the pancreas, why an IgG4 level cannot settle the diagnosis, how the HISORt and international consensus criteria are applied, histologic differences between the types, prednisone dosing, what no response means, and who relapses and what maintains remission.

Topics covered

Autoimmune pancreatitis in TIGAR-O
Type one features and imaging
Other organ involvement in IgG4-related disease
Limits of serum IgG4
HISORt and consensus criteria
Histology of type one and type two
Prednisone induction and taper
Relapse and rituximab maintenance
Type two and ulcerative colitis
Board traps

Key decisions

Suspect type one autoimmune pancreatitis in an older man with painless jaundice, a sausage-shaped gland with a rim, a non-dilated irregular duct, and other organ involvement, and remember that severe pain argues against it.
Do not diagnose on IgG4 alone, because a mild elevation under twice normal occurs in up to about ten percent of pancreatic adenocarcinoma.
Apply the HISORt or international consensus criteria and obtain tissue before steroids in a patient with a focal head mass, since steroids given to an undiagnosed cancer delay resection and worsen outcome.
Give prednisone forty milligrams a day for four weeks, then taper by five milligrams a week, without routine maintenance.
Expect a clinical and biochemical response within two weeks, and if there is none, re-evaluate for adenocarcinoma rather than continuing steroids.
Use rituximab for relapsing or steroid-intolerant type one disease, or add azathioprine, six-mercaptopurine, or mycophenolate overlapping with prednisone for at least eight weeks.
Recognize type two in a younger patient with recurrent pancreatitis or a mass, a normal IgG4, and often ulcerative colitis, confirmed by the granulocytic epithelial lesion on biopsy.
Treat type two with the same prednisone induction but no maintenance therapy, and retreat a relapse with steroids.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:54) - Older man with painless jaundice
(01:58) - Features of type one disease
(02:55) - Organs outside the pancreas
(03:29) - Why IgG4 cannot settle it
(04:13) - HISORt and consensus criteria
(04:57) - Histology separating the types
(05:36) - Prednisone dosing and nonresponse
(06:14) - Relapse and maintenance therapy
(07:13) - Type two in ulcerative colitis

Chapter 26, Ep 4 of 5: Chronic Pancreatitis and Cysts: Naming the Cyst

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

The organizing idea is that every pancreatic cyst is first sorted as mucinous or not, because mucin carries the cancer risk. The episode starts with a woman's incidental tail cyst and the five cyst types, then reads fluid CEA, glucose, and amylase, combines CEA and amylase into a two-by-two, and adds cytology, KRAS, GNAS, and the string sign. A young woman's part-solid mass shows the cyst cured by resection. A man with a branch-duct IPMN then shows MRI surveillance intervals, worrisome features that lead to EUS, high-risk stigmata that lead to surgery, the growth threshold, and when surveillance stops.

Topics covered

Why mucinous cysts matter
Five pancreatic cyst types
Fluid CEA, glucose, and amylase
The CEA and amylase two-by-two
Cytology, KRAS, GNAS, and string sign
Solid pseudopapillary neoplasm
MRI surveillance of branch-duct IPMN
Worrisome features and EUS
High-risk stigmata and surgery
When surveillance stops

Key decisions

Decide first whether a cyst is mucinous, then resect or survey mucinous cysts and usually do nothing for non-mucinous ones.
Call a cyst mucinous when fluid CEA is above 192 nanograms per milliliter or glucose is below 50 milligrams per deciliter, and call it duct-communicating when amylase is above 250 units per liter.
Name the cyst by combining CEA and amylase: high CEA with high amylase is IPMN, high CEA with low amylase is MCN, low CEA with high amylase is pseudocyst, and low CEA with low amylase is serous cystadenoma.
Resect a confirmed MCN in a fit patient, resect a solid pseudopapillary neoplasm, and neither resect nor survey an asymptomatic serous cystadenoma.
Survey branch-duct IPMN with MRI and MRCP at intervals set by size, such as yearly for two years for a 1 to 2 centimeter cyst, and shorten the interval as the cyst grows.
Send a patient with a worrisome feature, such as growth of 2.5 millimeters or more a year, to EUS with aspiration, but send a patient with a high-risk stigma straight to surgery if fit.
Stop surveillance when the patient would no longer have surgery or life expectancy is under ten years, and continue in younger patients and those with familial risk.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode roadmap
(01:30) - Why mucin matters first
(02:16) - The five cyst types
(04:07) - Fluid CEA, glucose, and amylase
(05:11) - The CEA and amylase two-by-two
(05:58) - Cytology, KRAS, GNAS, string sign
(07:01) - Solid pseudopapillary neoplasm in young women
(07:48) - Branch-duct IPMN imaging intervals
(09:13) - Worrisome features and EUS
(11:01) - High-risk stigmata and stopping

Chapter 26, Ep 5 of 5: Pancreatic Cysts and Neoplasms: Two Solid Tumors

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

This episode covers the two solid tumor families of the pancreas through two patients. A woman with painless jaundice and new diabetes shows adenocarcinoma: ultrasound confirms obstruction, pancreas-protocol CT or MRI stages the tumor, CA 19-9 is read with caution, and EUS core biopsy gives tissue. Vessel contact sets resectable, borderline, or locally advanced disease, and borderline disease gets neoadjuvant modified FOLFIRINOX. Germline testing follows. A woman with fasting hypoglycemia shows insulinoma: prove it with a seventy-two-hour fast, exclude injected insulin with C-peptide, find it with EUS, and check for MEN1. Short cases then cover rarer functioning tumors, incidental tumors, and metastatic treatment.

Topics covered

Pancreatic adenocarcinoma presentation and risk factors
Ultrasound, then pancreas-protocol CT or MRI
Limits of CA 19-9
EUS biopsy and biliary drainage
Resectable, borderline, and locally advanced disease
Neoadjuvant and adjuvant chemotherapy
Germline testing and screening
Insulinoma and the seventy-two-hour fast
Gastrinoma, VIPoma, glucagonoma, and somatostatinoma
Non-functioning tumors and metastatic treatment

Key decisions

In a jaundiced patient, start with transabdominal ultrasound to confirm extrahepatic obstruction, then stage with a pancreas-protocol contrast CT or MRI.
Do not trust CA 19-9 for diagnosis or screening, since it is falsely low in Lewis antigen-negative patients and falsely raised in cholestasis, and use it mainly to track treatment response.
Obtain tissue by EUS-guided fine-needle biopsy rather than aspiration, and place a biliary stent at ERCP when the patient is jaundiced and neoadjuvant therapy is planned.
Classify a tumor with arterial contact under 180 degrees or a reconstructable vein as borderline resectable and give neoadjuvant modified FOLFIRINOX for four to six months before restaging and surgery.
After upfront resection in fit patients, give adjuvant modified FOLFIRINOX, and in a germline BRCA2 carrier with metastatic disease, give olaparib maintenance only after a response to first-line platinum.
Diagnose insulinoma with the Whipple triad and a supervised seventy-two-hour fast, and use C-peptide to exclude injected insulin, since it is high with endogenous insulin and suppressed with exogenous insulin.
Find an insulinoma with EUS rather than a somatostatin receptor scan, because the tumor is usually under two centimeters and over seventy percent are negative on scintigraphy, and check calcium for MEN1.
Observe sporadic non-functioning neuroendocrine tumors under one centimeter, resect those over two centimeters, and individualize the decision for tumors of one to two centimeters.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview of the two tumor families
(00:58) - Painless jaundice and new diabetes
(02:21) - Imaging and the limits of CA 19-9
(03:36) - Getting tissue and draining the bile duct
(04:23) - Resectability and neoadjuvant chemotherapy
(06:42) - Germline testing and palliative care
(08:34) - Fasting hypoglycemia and neuroendocrine tumors
(09:50) - Proving and finding an insulinoma
(12:11) - Rarer hormone-secreting tumors
(14:47) - Incidental tumors and metastatic treatment

Chapter 27, Ep 1 of 4: Biliary Tract Disease: Stones and Cholecystitis

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

Gallstones cause one clear symptom, biliary colic, and almost every decision in this episode follows from whether stones are causing trouble or are likely to. A woman with colic shows how to separate her dyspepsia from what stones cause, why her gallbladder should come out, and how her stones trace to cholesterol, black pigment, or brown pigment mechanisms. Asymptomatic stones are then observed unless cancer risk or the surgical setting justifies removal. Acute cholecystitis follows: diagnosis by the Tokyo criteria, ultrasound first and HIDA second, liver tests that point to a duct stone, grading, and timing of surgery. The episode ends with drainage for a patient too sick to operate.

Topics covered

Biliary colic recognition
Dyspepsia and gallstones
Indications for cholecystectomy
Cholesterol and pigment stone formation
Asymptomatic gallstones
Prophylactic cholecystectomy indications
Diagnosis of acute cholecystitis
Tokyo grading and timing of surgery
Gallbladder drainage in poor surgical candidates

Key decisions

Tell a patient with colic and dyspepsia that cholecystectomy should stop the attacks but may not relieve bloating and belching, because only colic is clearly caused by stones.
Refer a fit patient for laparoscopic cholecystectomy after a first episode of colic, since only thirty percent stay symptom-free and severe complications occur at about one percent a year.
Observe asymptomatic stones in an average-risk patient, but operate when the gallbladder is incompletely calcified, stones are three centimeters or more, a polyp of one centimeter or more is present, or the patient is at high-risk ethnicity.
Order right upper quadrant ultrasound first for suspected cholecystitis and reserve HIDA for an equivocal ultrasound or suspected acalculous disease.
Look for a common bile duct stone or Mirizzi syndrome before surgery when transaminases or bilirubin are markedly raised, rather than blaming cholecystitis alone.
Treat Tokyo grade one with fluids, antibiotics, and early laparoscopic cholecystectomy within seven days, before dense fibrosis hides Calot's triangle.
In grade two, give antibiotics with early surgery at a high-volume center or use percutaneous cholecystostomy with cholecystectomy delayed about six weeks.
In grade three, resuscitate in the intensive care unit and drain the gallbladder, preferring a lumen-apposing metal stent under endoscopic ultrasound, but choose percutaneous drainage when ascites, perforation, emphysematous cholecystitis, or coagulopathy is present.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(00:47) - Biliary colic in a young woman
(02:06) - Dyspepsia and the case for surgery
(02:57) - Why stones form: three types
(06:24) - Asymptomatic stones and observation
(07:05) - Prophylactic cholecystectomy indications
(08:47) - Diagnosing acute cholecystitis
(11:43) - Tokyo grading and surgical timing
(13:50) - Draining the gallbladder without surgery
(15:18) - Board traps and summary

Chapter 27, Ep 2 of 4: Biliary Tract Disease: Gallbladder Complications

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

Gallbladder disease goes well beyond simple cholecystitis, and each complication has a recognizable setting and its own treatment rule. The episode begins with the two dangerous acute variants, acalculous cholecystitis in the fasting, sedated ICU patient and emphysematous cholecystitis in the diabetic patient, both needing rapid decompression and broad antibiotics. It then turns to what a stone left for years can do: Mirizzi syndrome, porcelain gallbladder, gallstone ileus, and Bouveret syndrome. Next it covers the four types of gallbladder polyp and the size and risk factor thresholds that separate surgery from rescanning. It ends with gallbladder cancer, which presents late and is usually unresectable.

Topics covered

Acalculous cholecystitis in the ICU
Morphine-augmented HIDA scan
Percutaneous cholecystostomy
Emphysematous cholecystitis
Mirizzi syndrome and Csendes classification
Porcelain gallbladder
Gallstone ileus and Bouveret syndrome
Gallbladder polyp types and size thresholds
Polyps in primary sclerosing cholangitis
Gallbladder cancer risk factors

Key decisions

Consider acalculous cholecystitis in any fasting, sedated ICU patient on TPN or vasopressors with unexplained sepsis and right upper quadrant tenderness, and do not delay treatment for a perfect test.
Use a morphine-augmented HIDA scan as a tiebreaker, remembering that prolonged fasting and TPN cause false positives, and choose percutaneous cholecystostomy with piperacillin-tazobactam or a carbapenem for the unstable patient.
Treat emphysematous cholecystitis with antibiotics covering enteric gram-negatives, anaerobes, and Clostridium, then cholecystectomy if stable or percutaneous cholecystostomy if not, and never use an EUS-guided lumen-apposing metal stent.
Confirm suspected Mirizzi syndrome with MRCP, decompress with ERCP and stenting, and warn the surgeon beforehand because the distorted Calot's triangle raises bile duct injury risk, with a deeper Csendes fistula needing hepaticojejunostomy.
Recommend prophylactic cholecystectomy for incompletely calcified porcelain gallbladder, while complete calcification can be observed in selected high-risk surgical patients with counseling.
Treat gallstone ileus, diagnosed by the Rigler triad, with enterotomy and stone extraction alone in elderly or frail patients, and treat Bouveret syndrome with endoscopic removal or lithotripsy before duodenotomy.
Offer cholecystectomy for a polyp of 10 mm or more, or a 6 to 9 mm polyp with a risk factor such as age over 60, PSC, sessile shape, Asian ethnicity, or growth of 2 mm; otherwise rescan 5 to 9 mm polyps at 3 to 6 months and polyps under 5 mm at 12 months.
In primary sclerosing cholangitis, advise cholecystectomy for polyps over 8 mm, with ultrasound every 6 months for smaller polyps and annual ultrasound for everyone with the disease.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(01:00) - Acalculous cholecystitis in the ICU
(03:27) - Imaging and drainage in the ICU
(04:28) - Emphysematous cholecystitis
(06:05) - Mirizzi syndrome and staging
(08:49) - Porcelain gallbladder
(09:36) - Gallstone ileus and Bouveret syndrome
(11:37) - Gallbladder polyps and size thresholds
(14:17) - Gallbladder cancer and its risks
(16:12) - Board traps and final summary

Chapter 27, Ep 3 of 4: Biliary Tract Disease: Stones and Cholangitis

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

Duct stones and the infection they cause are managed by probability and by the clock. The episode begins with the ASGE 2019 system, which sorts suspected choledocholithiasis into high, intermediate, and low probability and so decides who goes straight to ERCP, who needs EUS or MRCP first, and who goes to cholecystectomy. It then covers stones of one centimeter or more and the frail patient whose gallbladder stays in. It turns to acute cholangitis, an obstructed, infected duct that antibiotics cannot sterilize, graded by Tokyo 2018 to set drainage within 24 or 48 hours, followed by antibiotic choice and rescue drainage when ERCP cannot reach the papilla.

Topics covered

Presentation of duct stones
ASGE 2019 probability levels
EUS versus MRCP for small stones
When ERCP is the wrong move
Stones of one centimeter or more
Gallbladder after duct clearance in frail patients
Acute cholangitis and the Charcot triad and Reynolds pentad
Tokyo 2018 severity grades and drainage timing
Empiric antibiotic choice
Rescue drainage after altered anatomy

Key decisions

Send a patient with high probability of a duct stone (stone seen on imaging, clinical cholangitis, or bilirubin over 4 with a duct wider than 6 millimeters) straight to ERCP, and send intermediate probability patients (abnormal liver tests, dilated duct, or age over 55) to EUS or MRCP first.
Prefer EUS, with sensitivity of 94 percent, over MRCP when small stones or sludge are suspected, since MRCP is only about 70 percent sensitive for stones under 6 millimeters.
Treat stones of one centimeter or more with sphincterotomy plus large-balloon dilation or cholangioscopy-directed lithotripsy, because sphincterotomy alone fails in about 10 to 15 percent.
Avoid ERCP in gallstone pancreatitis without ongoing obstruction or cholangitis, and do cholecystectomy during the same admission.
Leave the gallbladder in a frail, high-risk patient after duct clearance, accepting symptoms in about 10 percent a year, but remove it in a fit patient.
Drain grade 3 cholangitis by ERCP within 24 hours and grade 2 within 48 hours, and do not cancel ERCP because the patient improves on antibiotics.
Start a third-generation cephalosporin plus metronidazole or piperacillin-tazobactam for cholangitis, use a carbapenem after recent biliary instrumentation, in healthcare-associated infection, or with immunocompromise, and narrow after cultures.
Use EUS-guided biliary drainage or percutaneous transhepatic cholangiography within the same window when ERCP fails or anatomy such as Roux-en-Y bypass blocks the papilla.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and chapter setup
(02:05) - ASGE probability levels and ERCP
(03:48) - EUS or MRCP for intermediate risk
(04:50) - Large stones and when to avoid ERCP
(06:12) - Gallbladder in a frail patient
(06:46) - Acute cholangitis and its signs
(08:27) - Tokyo grades and drainage timing
(10:19) - Improvement does not cancel ERCP
(11:01) - Choosing empiric antibiotics
(11:36) - Rescue drainage when ERCP fails

Chapter 27, Ep 4 of 4: Biliary Tract Disease: Functional Pain and Ducts

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

This episode separates biliary problems that look structural from those that are functional, and then covers the bile duct defects a patient is born with or given at surgery. It starts with Rome four functional gallbladder pain, the weak meaning of a low ejection fraction, and why sphincter of Oddi dysfunction now justifies ERCP only when enzymes or duct size are abnormal, with full pancreatitis prophylaxis. It then turns to choledochal cysts, where the Todani type sets the operation, and to Caroli disease. It ends with bile leaks and strictures after cholecystectomy, classified by Strasberg type, treated with a stent, hepaticojejunostomy, or serial dilation.

Topics covered

Rome four functional gallbladder pain
Low HIDA ejection fraction
Pain after cholecystectomy
Sphincter of Oddi dysfunction
Post-ERCP pancreatitis prophylaxis
Choledochal cysts and Todani types
Cyst excision and surveillance
Caroli disease
Bile leak and Strasberg classification
Stenting, ERCP pitfalls, and strictures

Key decisions

Do not recommend cholecystectomy for biliary-type pain on a low ejection fraction alone, including a value below thirty-five percent, and treat functional dyspepsia and irritable bowel syndrome first.
After cholecystectomy with persistent pain, reimage with EUS or MRCP before blaming the sphincter, and accept a duct up to about ten millimeters as possibly normal.
Treat sphincter of Oddi stenosis, meaning pain with enzymes over one point one times normal and a duct over eight to ten millimeters, with empiric sphincterotomy without manometry, and give no ERCP for pain alone with normal labs and imaging.
Give full prophylaxis for any sphincter procedure: rectal indomethacin one hundred milligrams, lactated Ringer's solution, and a pancreatic duct stent in high-risk anatomy.
Treat Todani type one and four cysts with complete excision, cholecystectomy, and Roux-en-Y hepaticojejunostomy rather than a Whipple, then repeat MRCP every three to five years.
Treat a Strasberg type A leak with a plastic stent across the papilla, which seals ninety percent or more, adding sphincterotomy only for a retained stone.
Send complete transection, type E, to hepaticojejunostomy, and get MRCP when bile keeps draining after a normal-looking ERCP.
Treat benign postoperative strictures first with serial balloon dilation and multiple plastic stents over twelve months, reserving hepaticojejunostomy for refractory strictures.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and three patients
(01:43) - Rome four functional gallbladder pain
(02:17) - Why a low ejection fraction misleads
(04:39) - Sphincter of Oddi dysfunction and ERCP
(08:16) - Choledochal cyst and Todani types
(09:50) - Cyst excision and surveillance
(10:44) - Caroli disease
(11:57) - Bile leak and Strasberg types
(13:41) - Stenting the leak and ERCP pitfalls
(14:57) - Postoperative strictures

Chapter 28, Ep 1 of 7: ERCP and EUS Procedures: Preventing Pancreatitis

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

Post-ERCP pancreatitis is the complication that shapes every step of the procedure, and this episode follows a young woman with a bile duct stone through each decision. ERCP is reserved for therapy, because MRCP and EUS answer diagnostic questions without pancreatitis risk. Cannulation starts with a wire rather than contrast, and difficult cannulation escalates from the double-wire technique to septotomy, precut over a pancreatic stent, and EUS rendezvous. The episode then covers who is high risk and the three proven preventive measures: rectal indomethacin, a prophylactic pancreatic duct stent, and aggressive lactated Ringer's. A man with chronic pancreatitis shows why a scarred gland is protected.

Topics covered

ERCP as therapy, not diagnosis
Accepted ERCP indications
Wire-guided cannulation
Escalation for difficult cannulation
Risk factors for post-ERCP pancreatitis
Rectal indomethacin
Prophylactic pancreatic duct stent
Lactated Ringer's protocol
Chronic pancreatitis as protective
Board traps

Key decisions

Use ERCP for therapy rather than diagnosis when MRCP or EUS can answer the question, since those studies carry no risk of post-ERCP pancreatitis.
Cannulate with a hydrophilic guidewire before any contrast is injected, which lowers post-ERCP pancreatitis compared with contrast-first cannulation.
In difficult cannulation, escalate from least to most added risk: double-wire technique, transpancreatic septotomy, precut needle-knife papillotomy over a pancreatic stent, then EUS-guided rendezvous.
Recognize high-risk patients: suspected sphincter of Oddi dysfunction, prior post-ERCP pancreatitis, female sex, a normal bilirubin, difficult cannulation, and acinarization.
Give rectal indomethacin 100 mg immediately before every ERCP with a native papilla.
Add a prophylactic pancreatic duct stent to indomethacin in high-risk patients, because indomethacin alone was not shown to be non-inferior.
Give lactated Ringer's at 3 mL/kg/hour during the procedure, a 20 mL/kg bolus immediately after, and 3 mL/kg/hour for 8 hours, in preference to saline.
Do not use octreotide, gabexate, or secretin for prevention, and expect protection in chronic pancreatitis while still giving indomethacin if the papilla is native.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(00:46) - The first patient
(01:16) - ERCP is therapy, not a test
(02:24) - Wire-guided cannulation first
(03:03) - Escalating difficult cannulation
(04:24) - Who is high risk
(05:20) - Rectal indomethacin dosing
(06:24) - Pancreatic duct stent
(07:05) - Lactated Ringer's protocol
(08:16) - Chronic pancreatitis is protective

Chapter 28, Ep 2 of 7: ERCP and EUS Procedures: Bile Duct and Ampulla

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

This episode is about proving whether a narrowed bile duct is cancer and removing an ampullary adenoma without a Whipple. It starts with a hilar stricture in primary sclerosing cholangitis, where negative brushings do not reassure and sampling escalates to forceps biopsy, FISH, and cholangioscopy, with a ban on needling the primary in a transplant candidate. It then covers EUS for a pancreatic head mass and why pain alone after cholecystectomy is not a reason for ERCP. Next come ampullectomy candidacy, staging, technique, stenting, complications, and surveillance, ending with why familial adenomatous polyposis duodenal disease is different.

Topics covered

Brush cytology sensitivity in strictures
Forceps biopsy, FISH, and cholangioscopy
Transplant candidates and needle seeding
Sampling suspicious lymph nodes
EUS for pancreatic head masses
Sphincter of Oddi dysfunction and ERCP
Ampullary adenoma and ampullectomy
Ampullectomy stents and complications
Surveillance for recurrence
Duodenal polyposis in familial adenomatous polyposis

Key decisions

Treat negative ERCP brushings as non-reassuring, since brush cytology detects only thirty to forty percent of cancers, and escalate to forceps biopsy with FISH (about sixty percent) and then cholangioscopy-directed biopsy (more than seventy percent).
Never use EUS-guided aspiration or percutaneous biopsy on a hilar cholangiocarcinoma in a transplant candidate, because tumor seeding creates extrahepatic disease; sample the primary with brushings and intraductal biopsy at ERCP.
Sample a suspicious regional lymph node, by EUS if needed, because positive nodes contraindicate transplant however they are found.
Use EUS-guided needle biopsy for a distal duct stricture or pancreatic head mass, where sensitivity exceeds ninety percent.
For suspected sphincter of Oddi dysfunction, give sphincterotomy without manometry for stenosis, individualize the decision for the former type two with rectal indomethacin, lactated Ringer's, and a pancreatic stent, and decline ERCP for pain alone with normal tests.
Offer endoscopic ampullectomy for adenomas confirmed by EUS or intraductal ultrasound to lack intraductal extension or invasion, and send those with intraductal extension to surgery.
Resect in one piece without submucosal injection for lesions up to two to three centimeters, place a pancreatic stent and a biliary stent, and remove both at four to eight weeks.
Survey at three and six months after ampullectomy, and refer familial adenomatous polyposis patients with Spigelman stage four disease for duodenectomy or pancreaticoduodenectomy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(01:10) - Hilar stricture with negative brushings
(02:23) - Escalating stricture sampling step by step
(03:23) - Transplant candidates and needle seeding
(04:43) - EUS for a pancreatic head mass
(05:31) - Sphincter of Oddi dysfunction and ERCP
(07:05) - Ampullary adenoma and staging first
(08:57) - One-piece resection and two stents
(10:01) - Complications and recurrence surveillance
(11:29) - Duodenal polyposis in FAP

Chapter 28, Ep 3 of 7: ERCP and EUS Procedures: Malignant Duct Drainage

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

Draining a bile duct blocked by cancer comes down to where the obstruction is, whether the tumor is resectable, and how long the patient will live. The episode starts with distal obstruction before neoadjuvant chemotherapy, which calls for a fully covered metal stent, and asks whether resectable tumors need drainage at all. It then turns to the hilum, where the stent choice reverses to uncovered metal, drainage is planned by viable liver volume, and plastic is reserved for short survival. Last, it covers failed ERCP and the EUS-guided rescues, chosen in order: rendezvous, choledochoduodenostomy, then hepaticogastrostomy, as the anatomy allows. It closes with the classic board traps.

Topics covered

Stent choice in malignant biliary obstruction
Fully covered metal stent for distal obstruction
Same-session EUS biopsy and ERCP
When to drain resectable pancreatic cancer
Uncovered metal stents at the hilum
Draining half of viable liver
Plastic stents for short survival
EUS-guided rendezvous
EUS-guided choledochoduodenostomy with LAMS
EUS-guided hepaticogastrostomy and its complications

Key decisions

For distal obstruction from pancreatic head cancer, distal cholangiocarcinoma, or ampullary cancer before neoadjuvant therapy, combine EUS-guided biopsy with same-session ERCP and a fully covered metal stent, which lasts four to six months and is removable at the Whipple.
Do not drain resectable pancreatic head cancer routinely before prompt surgery; drain for cholangitis, severe jaundice that interferes with chemotherapy, or planned neoadjuvant therapy.
For unresectable hilar tumors of Bismuth type three or four with life expectancy over three months, use uncovered metal stents, because a covered membrane would block side-branch orifices at the confluence.
At the hilum, define viable territories by MRCP, drain at least fifty percent of viable liver, and do not stent atrophic segments; stent bilaterally when both lobes hold similar viable volume and unilaterally when one lobe is atrophic.
Reserve plastic stents for life expectancy under three months, and drain a blocked stent with cholangitis within twenty-four hours for severe disease and forty-eight hours for moderate disease.
After failed ERCP with a dilated duct, use EUS-guided rendezvous when the papilla can be reached, and choledochoduodenostomy with a LAMS when only the extrahepatic duct is accessible from the duodenal bulb.
Use hepaticogastrostomy with a partially covered or dedicated stent, not a fully covered one, when neither the papilla nor the extrahepatic duct is accessible but a dilated left intrahepatic duct is visible from the stomach.
Offer percutaneous transhepatic drainage when EUS drainage is not possible, since every EUS option requires a dilated duct.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview of three cases
(01:52) - Covered stent for distal obstruction
(02:49) - Should resectable tumors be drained
(03:29) - Hilar tumors need uncovered stents
(04:36) - Planning drainage by liver volume
(06:29) - EUS rescue after failed ERCP
(07:41) - Rendezvous when papilla is reachable
(08:21) - Choledochoduodenostomy with LAMS
(09:13) - Hepaticogastrostomy and stent design
(11:13) - Choosing among EUS drainage options

Chapter 28, Ep 4 of 7: ERCP and EUS Procedures: Altered Anatomy Access

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

Altered anatomy changes the question from how to perform ERCP to how to restore a face-on view of the papilla, or how to reach the anastomosis when the papilla is bypassed. The episode starts with Roux-en-Y gastric bypass, comparing laparoscopy-assisted ERCP, balloon enteroscopy, and EDGE, and the need to remove the stent and close the fistula afterward. It then turns to the hepaticojejunostomy after a Whipple, reached by enteroscopy with backups planned in advance. It ends with the Billroth two afferent limb, where perforation risk is highest and the sphincterotomy direction reverses.

Topics covered

Why a standard duodenoscope fails after gastric bypass
Laparoscopy-assisted ERCP
Balloon enteroscopy and its success rate
EUS-directed transgastric ERCP (EDGE)
LAMS removal and fistula closure
Interval cholecystectomy after duct clearance
Hepaticojejunostomy stricture after Whipple
Backup drainage when enteroscopy fails
Billroth two afferent limb and perforation risk
Inverted papilla and sphincterotomy direction

Key decisions

After Roux-en-Y gastric bypass, recognize that the papilla lies a hundred to a hundred and fifty centimeters or more away and is beyond a standard duodenoscope.
Prefer EDGE over laparoscopy-assisted ERCP or balloon enteroscopy in gastric bypass anatomy when local expertise is available, because enteroscopy succeeds in only sixty to seventy percent.
Use laparoscopy-assisted ERCP when EDGE expertise is lacking, and treat enteroscopy as possible but less successful.
Remove the LAMS and close the fistula once biliary therapy is complete, because a persistent gastrogastric communication risks weight regain.
Discuss interval cholecystectomy when the gallbladder remains, since residual gallbladder stones cause symptoms in about ten percent of patients a year after duct clearance.
After a Whipple, target the hepaticojejunostomy rather than a papilla using single-balloon or double-balloon enteroscopy, and plan percutaneous transhepatic cholangiography or EUS-guided hepaticogastrostomy as backup for a febrile patient.
In a Billroth two, avoid forcing a duodenoscope up the afferent limb, consider a cap-assisted forward-viewing scope, and cut the sphincterotomy in the opposite direction, with a needle-knife over a biliary stent sometimes safer.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and three patients
(00:46) - Gastric bypass patient with duct stone
(01:19) - Why the papilla is out of reach
(02:08) - Three routes to the papilla
(03:13) - Why EDGE is preferred
(03:58) - EDGE aftercare and fistula closure
(04:34) - Whipple stricture and hepaticojejunostomy
(05:23) - Backup plans for failed enteroscopy
(05:48) - Billroth two and perforation risk
(07:08) - Board traps and summary

Chapter 28, Ep 5 of 7: ERCP and EUS Procedures: Pancreatic Duct Therapy

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

The organizing idea is that endoscopy can fix a discrete pancreatic duct obstruction, but the threshold for ERCP in pancreatitis stays high because the benefit is modest and post-ERCP pancreatitis is a real risk. The episode starts with a woman with painful chronic pancreatitis, a duct stone, and a stricture who declines surgery. It covers who does well with endotherapy, shock-wave lithotripsy for stones over five millimeters, and single plastic stenting of a dominant stricture. It then turns to a new isolated head obstruction that may be cancer, idiopathic recurrent pancreatitis with its workup, manometry, and divisum, and the autoimmune pancreatogram.

Topics covered

Endotherapy versus surgery in chronic pancreatitis
Predictors of endotherapy success
Components of pancreatic endotherapy
Pancreatic duct stone fragmentation
Dominant stricture stenting
Isolated head obstruction and cancer risk
Workup of idiopathic recurrent pancreatitis
Manometry and sphincterotomy evidence
Pancreas divisum and minor papilla sphincterotomy
Autoimmune pancreatitis pancreatogram

Key decisions

In a fit patient with dilated-duct chronic pancreatitis and intractable pain, prefer early surgical drainage, and reserve endotherapy for patients who are not surgical candidates or who have discrete lesions that can be decompressed in one session.
Expect endotherapy to work best with short disease duration, abstinence from smoking and alcohol, limited stone burden, and complete duct clearance, and steer diffusely calcified disease toward surgical drainage.
Fragment pancreatic duct stones larger than five millimeters with extracorporeal shock-wave lithotripsy first, which clears the duct in roughly seventy percent, and use pancreatoscopic electrohydraulic or laser lithotripsy if it fails or the stone is impacted.
Avoid basket mechanical lithotripsy in the pancreatic duct because the basket can become impacted in the narrow duct.
Treat a dominant stricture with dilation and a single plastic stent of the largest feasible caliber, typically ten French, left in place for about twelve months, reserving multiple side-by-side stents for refractory strictures.
Sample the duct and obtain cross-sectional imaging and EUS-guided fine-needle biopsy when a new isolated pancreatic head obstruction appears in a calcified gland, because it may be cancer.
Complete the idiopathic recurrent pancreatitis workup, including EUS for microlithiasis after MRCP, before considering ERCP, and do not offer manometry-guided sphincterotomy or minor papilla sphincterotomy for divisum alone.
Suspect autoimmune pancreatitis rather than cancer when the pancreatogram shows long skip strictures without upstream dilation, whereas an abrupt cutoff with upstream dilation points to cancer.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(01:26) - Endotherapy or surgery for obstruction
(02:25) - Predictors of endotherapy success
(03:05) - Four parts of endotherapy
(03:25) - Breaking pancreatic duct stones
(04:19) - Stenting the dominant stricture
(04:57) - Isolated head obstruction and cancer
(06:01) - Workup before ERCP in recurrence
(06:53) - Manometry, divisum, and ERCP risk
(08:27) - Autoimmune pancreatitis pancreatogram

Chapter 28, Ep 6 of 7: ERCP and EUS Procedures: Walled-Off Necrosis

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

This episode is about draining walled-off necrosis through the stomach and cleaning it out from the inside. A woman six weeks after necrotizing pancreatitis shows the sequence. A collection is drained only after about four weeks, once the wall has matured, and imaging is checked for pseudoaneurysm first. Solid debris calls for a fifteen or twenty millimeter lumen-apposing metal stent, while a man with a simple pseudocyst shows what suits thin fluid. Necrosectomy follows only if response is inadequate, always with carbon dioxide. The episode then covers recurrent fever, bleeding through the stent, timed stent removal, and a tail cyst that must be aspirated before it is drained.

Topics covered

Walled-off necrosis versus pseudocyst
Timing of transmural drainage
Step-up approach
Pseudoaneurysm check before drainage
Stent choice for necrosis and pseudocyst
Direct endoscopic necrosectomy
Carbon dioxide insufflation
LAMS occlusion and bleeding
LAMS removal and pigtail stents
Aspirating a suspicious tail cyst

Key decisions

Drain a symptomatic collection by EUS-guided transmural drainage at four weeks or later, once the wall has matured enough to support an opening into the gut.
Review CT angiography or contrast-enhanced imaging for a pseudoaneurysm before any puncture, and have interventional radiology embolize one first if it is found.
Use a fifteen or twenty millimeter LAMS for walled-off necrosis with solid debris, and a single ten millimeter LAMS or two double-pigtail plastic stents for a simple pseudocyst.
Add direct endoscopic necrosectomy only after an inadequate response, meaning persistent fever, leukocytosis, or solid debris, and expect a median of two to four sessions.
Use carbon dioxide, never air, and avoid forceful pressurized flushing during necrosectomy, because of the risk of air embolism through vascular communications.
Treat recurrent fever after improvement as LAMS occlusion, with urgent esophagogastroduodenoscopy to clear it and double-pigtail stents placed through the LAMS.
Treat bleeding through the stent with interventional radiology embolization before the LAMS is removed, because the stent may be tamponading the vessel.
Remove the LAMS at about four weeks once the cavity has resolved clinically and on imaging, place double-pigtail stents across the tract, and aspirate a persistent tail cyst before draining it.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(00:42) - Walled-off necrosis and drainage timing
(02:21) - Checking for pseudoaneurysm first
(02:56) - Choosing the stent for necrosis
(03:25) - Pseudocyst stent contrast
(04:25) - Direct endoscopic necrosectomy
(05:23) - Why carbon dioxide, never air
(06:30) - Recurrent fever and stent bleeding
(07:27) - Planned LAMS removal
(08:08) - The tail cyst that mimics

Chapter 28, Ep 7 of 7: ERCP and EUS Procedures: EUS Tissue and Safe ERCP

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

This episode asks how to get the most from the needle and how to take the most care with ERCP. It starts with a subepithelial lesion identified by its EUS layer, then covers which lesions need tissue and which stains separate GIST from leiomyoma. Biopsy needles come next, followed by celiac plexus neurolysis for cancer pain versus a steroid block for benign pain. The ERCP half covers pregnancy, where only urgent indications qualify and radiation is kept minimal. It then turns to sphincterotomy bleeding in coagulopathy, perforation classification, post-ERCP cholangitis, and why duodenoscopes spread resistant bacteria.

Topics covered

Five EUS layers and subepithelial lesions
GIST versus leiomyoma staining
Layer-based differential for other lesions
Biopsy needles and rapid on-site evaluation
Celiac plexus neurolysis and its adverse effects
Celiac plexus block for chronic pancreatitis
ERCP indications and radiation limits in pregnancy
Sedation and positioning in pregnancy
Post-sphincterotomy bleeding and balloon dilation
Perforation and post-ERCP cholangitis
Duodenoscope infection and reprocessing

Key decisions

Sample a layer four subepithelial lesion of two centimeters or more with fine-needle biopsy, and call it a GIST only when it is CD117 and DOG1 positive, since leiomyoma is desmin and smooth muscle actin positive and CD117 negative.
Use Franseen-tip or fork-tip biopsy needles when architecture matters, as in lymphoma, GIST, or autoimmune pancreatitis, because rapid on-site evaluation is then largely unnecessary.
Offer EUS-guided celiac plexus neurolysis with alcohol for unresectable pancreatic cancer pain when opioids cause unacceptable side effects, and use a bupivacaine plus triamcinolone block for chronic pancreatitis because the plexus regenerates.
Warn before neurolysis about diarrhea, orthostatic hypotension, and a transient pain flare, and about rare paraplegia from injection into a spinal radicular artery.
In pregnancy, reserve ERCP for indications that can't wait, such as cholangitis, and use non-contrast MRCP or EUS instead of diagnostic ERCP.
Keep pregnancy fluoroscopy under one minute, pulsed at four to eight pulses per second, collimated, and shielded, with propofol, no midazolam in the first trimester, and left lateral tilt.
In cirrhosis or coagulopathy, choose endoscopic papillary balloon dilation over a full sphincterotomy for duct stones when it will do.
Prevent post-ERCP cholangitis with complete biliary drainage at the first procedure, give antibiotics when it can't be assured, and prevent duodenoscope transmission with disposable elevator components and traceability rather than double disinfection or ethylene oxide.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(01:24) - Five EUS layers and GIST
(02:20) - Staining GIST versus leiomyoma
(03:35) - Why biopsy needles replaced on-site cytology
(04:55) - Celiac plexus neurolysis and block
(07:38) - ERCP in pregnancy
(10:45) - Bleeding after sphincterotomy
(12:18) - Perforation and post-ERCP cholangitis
(13:12) - Duodenoscope infection and reprocessing

Chapter 29, Ep 1 of 4: Endoscopy Practice and Sedation: Before the Scope

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

Everything that has to be right before the scope goes in comes down to matching the preparation to the patient. The episode starts with fasting windows by what was eaten and who counts as a full stomach, then pregnancy testing. It next covers risk-stratified GLP-1 agonist management, with urgent endoscopy never delayed, and the three to four day SGLT-2 inhibitor hold that prevents euglycemic ketoacidosis. It then turns to antithrombotics, weighing procedural bleeding risk against the patient's clotting risk. That means warfarin holds and the near end of bridging, direct oral anticoagulant holds, stent timing and antiplatelet drugs, and finally reversal by drug.

Topics covered

Fasting windows and full stomach
Pregnancy testing before endoscopy
GLP-1 agonist risk stratification
SGLT-2 inhibitors and euglycemic ketoacidosis
Procedure bleeding risk categories
Thromboembolic risk groups
Warfarin hold, INR check, and restart
Why bridging has narrowed
Direct oral anticoagulant holds
Coronary stents and antiplatelet drugs
Reversal of anticoagulants

Key decisions

Allow clear liquids up to two hours before sedation, breast milk up to four, formula or a light meal up to six, and a fatty meal up to eight, and manage gastroparesis, achalasia, gastric outlet obstruction, retained content on a GLP-1 agonist, and pregnancy after the first trimester as a full stomach.
Check a urine pregnancy test in women of reproductive age before elective endoscopy, with a serum quantitative test for ambiguous results, remembering that pregnancy is not an absolute contraindication to a necessary procedure.
Give elevated-risk GLP-1 agonist patients, meaning those with symptoms, in dose escalation, or on weekly dosing, twenty-four hours of clear liquids while continuing the drug, and do not delay endoscopy for bleeding or obstruction, using rapid sequence intubation.
Hold SGLT-2 inhibitors three to four days before elective endoscopy, and if one was taken the night before, reschedule or check a basic metabolic panel, since an anion gap with a normal glucose means euglycemic diabetic ketoacidosis.
Continue warfarin for low-bleeding-risk procedures, but for high-risk ones such as endoscopic mucosal resection hold it five days, confirm a morning INR below 1.5, and restart within twenty-four to forty-eight hours once hemostasis is secure.
Bridge with heparin only high thromboembolic risk patients, such as those with a mechanical mitral valve, a stroke or venous clot within three months, or a CHADS2 of five or six, and never bridge a direct oral anticoagulant.
Hold apixaban or rivaroxaban forty-eight to seventy-two hours before high-risk procedures, and lengthen dabigatran holds as creatinine clearance falls below fifty and thirty milliliters per minute.
Defer elective procedures thirty days after a bare metal stent and six months after a drug-eluting stent, continue secondary-prevention aspirin, hold clopidogrel or prasugrel five to seven days and ticagrelor three to five, and reverse bleeding with 4F-PCC for warfarin and factor ten A inhibitors (plus vitamin K for warfarin) and idarucizumab for dabigatran.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview of the two patients
(01:29) - Fasting windows and full stomach
(02:59) - Pregnancy testing before endoscopy
(03:52) - GLP-1 agonist risk and preparation
(05:47) - SGLT-2 inhibitors and ketoacidosis
(07:51) - Warfarin and the two risks
(11:20) - Why bridging has narrowed
(12:50) - Direct oral anticoagulant holds
(14:29) - Coronary stents and antiplatelets
(16:57) - Reversal agents by drug

Chapter 29, Ep 2 of 4: Endoscopy Practice and Sedation: The Sedation Plan

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

Sedation planning starts with the patient's risk, not the drug. A man with COPD, poorly controlled diabetes, and a BMI of 42 is booked for EUS with fine-needle aspiration, and his case drives the episode. First the ASA class frames his risk. Then the defined depths of sedation show what he means by wanting to be completely out, and why the team must rescue one level deeper. Next comes midazolam with fentanyl, its dosing, and why it suits healthier patients. Propofol follows, with its advantages, its lack of an antagonist, and who should give it. Short cases then place etomidate, ketamine, and dexmedetomidine, before the common board traps.

Topics covered

ASA physical status classes
Minimal, moderate, deep sedation, and general anesthesia
Rescue one level deeper
Midazolam and fentanyl dosing
Respiratory synergy and capnography
Propofol indications and dosing
Propofol hazards and who gives it
Etomidate in unstable patients
Ketamine and dexmedetomidine
Board traps in sedation

Key decisions

Classify COPD, poorly controlled diabetes, or a BMI over 40 as ASA three, and favor propofol with anesthesia support for ASA three and four patients.
Make sure whoever gives sedation can rescue the patient from one level deeper than intended, because depth is a continuum.
Use moderate sedation with midazolam (0.5 to 2 mg start, then 1 mg boluses every 2 to 5 minutes) plus fentanyl (25 to 100 micrograms start) for ASA one and two patients having routine endoscopy.
Give benzodiazepine and opioid doses in small increments, wait for the previous dose to peak at 3 to 5 minutes, and use capnography, because the respiratory depression is multiplicative.
Choose deep propofol sedation (0.5 to 1 mg/kg induction) for ASA three and four patients, long or complex procedures such as EUS and ERCP, and high aspiration risk, with airway-trained staff present because it has no antagonist.
Titrate propofol cautiously in hypovolemic, cirrhotic, or cardiac patients because it lowers vascular resistance and causes hypotension.
Use etomidate (0.1 to 0.2 mg/kg) for hemodynamically unstable patients such as those bleeding, but avoid it in sepsis because it suppresses cortisol for 6 to 24 hours.
Use ketamine (0.5 to 1 mg/kg) when breathing must be preserved or for opioid-tolerant patients while watching blood pressure, and dexmedetomidine for opioid-sparing sedation when the airway is critical.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and sedation plan
(00:48) - The patient and his ASA class
(02:26) - Depths of sedation and rescue
(03:47) - Midazolam plus fentanyl
(05:17) - Why propofol suits this patient
(06:17) - Propofol dangers and who gives it
(07:24) - Etomidate for unstable patients
(08:04) - Ketamine and dexmedetomidine
(09:07) - Board traps in sedation

Chapter 29, Ep 3 of 4: Endoscopy Practice and Sedation: Safe Sedation

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

Safe sedation depends on catching apnea early and on knowing which patients change the standard plan. The episode starts with a colonoscopy patient whose capnography goes flat while her saturation looks normal. It then covers airway prediction with Mallampati class and other markers, full-stomach precautions, titrated naloxone, and flumazenil, including who must never receive it and how long to keep monitoring after reversal. Four more patients follow: a man with cirrhosis, an older woman living alone, a man with sleep apnea, and a pregnant woman needing urgent ERCP. The episode closes with the board traps and a start-to-finish summary.

Topics covered

Capnography versus pulse oximetry
Rescuing a patient from deeper sedation
Predicting the difficult airway
Full-stomach and aspiration risk
Naloxone dosing and monitoring
Flumazenil dosing and contraindications
Sedation in cirrhosis
Sedation in patients over sixty-five
Sedation in sleep apnea
Sedation in pregnancy

Key decisions

Use capnography for all moderate and deep sedation, because the waveform detects apnea within one to two breaths while pulse oximetry on supplemental oxygen lags by thirty to ninety seconds.
Get anesthesia consultation before deep sedation when Mallampati class three or four, thyromental distance under six centimeters, or BMI over thirty-five predicts a difficult airway, and give full-stomach patients airway control with rapid sequence induction and a cuffed endotracheal tube, or delay the procedure.
Reverse opioid oversedation with naloxone at forty micrograms to four-tenths of a milligram intravenously every two to three minutes, titrated to breathing, and monitor for at least four hours because re-sedation can occur.
Give flumazenil at two-tenths of a milligram over fifteen seconds, repeated each minute to a total of one milligram, monitor for at least two hours, and never use it with chronic benzodiazepine therapy, seizure disorders, or mixed tricyclic overdose.
In cirrhosis, halve midazolam or avoid it, and prefer carefully titrated propofol with close attention to blood pressure, because sedation can precipitate encephalopathy.
In patients over sixty-five, cut all sedative doses by twenty-five to fifty percent, use smaller boluses with longer intervals because peak effect is delayed, and plan fall precautions and a discharge that accounts for living alone.
In sleep apnea, use capnography and airway-trained staff, screen undiagnosed patients with STOP-BANG, and use CPAP in recovery.
In pregnancy after the first trimester, use full-stomach precautions and a left lateral tilt, prefer propofol, accept low-dose fentanyl, avoid ketamine, monitor the fetus after twenty-two to twenty-four weeks, and defer elective procedures to the second trimester or after delivery.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(01:21) - Flat capnography with normal saturation
(02:29) - Airway prediction and full stomach
(04:30) - Naloxone dosing and monitoring
(05:26) - Flumazenil and its contraindications
(06:51) - Sedation in cirrhosis
(08:36) - Dose reduction in older patients
(09:37) - Sleep apnea and airway plan
(10:31) - Sedation in pregnancy
(12:12) - Board traps in sedation safety

Chapter 29, Ep 4 of 4: Endoscopy Practice and Sedation: Hardware and Harm

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

The episode is built on one idea: decisions follow the procedure or the event, not the label on the patient. A prosthetic valve, joint, pacemaker, or defibrillator does not by itself call for antibiotics, which are reserved for procedures that introduce bacteria into a closed space that cannot drain. The first case then covers electrosurgery, with the grounding pad kept away from a pacemaker and detection suspended and restored for an ICD. The second case turns to capsule endoscopy: modern cardiac devices are not a barrier, retention is the real risk, and a patency capsule or enterography comes first in high-risk patients. It ends with ASGE grading of adverse events by what they required.

Topics covered

Antibiotic myths with valves and joints
Closed-space principle for prophylaxis
ERCP and EUS cyst prophylaxis
PEG, cirrhosis bleeding, and dialysis prophylaxis
ICD management during electrosurgery
Pacemakers and grounding pad placement
Capsule endoscopy contraindications
Capsule retention and patency capsule
Retrieving a retained capsule
ASGE adverse event grading

Key decisions

Give no antibiotic prophylaxis for prosthetic joints, prosthetic valves alone, pacemakers, defibrillators, vascular grafts, prior endocarditis, diagnostic endoscopy, aspiration of solid lesions, or elective variceal banding.
Give antibiotics for ERCP when drainage is expected to be incomplete, covering enteric gram-negatives and enterococci, and continue them afterward while drainage stays incomplete.
Give a dose before EUS aspiration of a cyst and three to five days of oral antibiotics after; give one gram of intravenous cefazolin thirty minutes before PEG placement.
Give ceftriaxone one gram intravenously daily for the duration of bleeding in cirrhosis with acute upper gastrointestinal bleeding, and ampicillin plus an aminoglycoside before lower endoscopy in peritoneal dialysis patients.
For an ICD, suspend arrhythmia detection by magnet or reprogramming, place external defibrillator pads, leave pacing on, and restore detection right after the procedure.
For a pacemaker, do not reprogram routinely and place the grounding pad away from the heart and device, such as on the lower back or thigh.
In a high-risk patient such as one with Crohn disease, prior bowel surgery, or NSAID enteropathy, do a patency capsule or CT or MR enterography before the diagnostic capsule, and treat a patency capsule still present at thirty hours as a stricture.
Grade adverse events by the intervention required: mild up to three nights, moderate for four to ten nights, one ICU night, transfusion, or repeat endoscopic or radiology treatment, severe beyond that or with surgery or disability, and fatal within thirty days.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and the two patients
(00:51) - Patient with valve, knee, and ICD
(02:14) - The closed-space antibiotic principle
(03:44) - Other antibiotic indications
(04:48) - ICD and pacemaker electrosurgery plans
(06:43) - Capsule endoscopy and cardiac devices
(08:09) - Capsule retention risk
(08:52) - Patency capsule and retrieval
(10:05) - ASGE adverse event grading
(12:20) - Board traps and summary

Chapter 30, Ep 1 of 5: Colonoscopy Practice and Quality: Prep and Quality

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

Colonoscopy protects patients only as far as its quality allows. The episode follows a man with a positive stool test, which shows that every positive non-invasive test leads to colonoscopy, with the commitment secured before the test is chosen. Preparation comes next: split dosing finished four to eight hours before the procedure, avoiding sodium phosphate and mannitol, and scoring with the Boston scale, where any segment under two makes the preparation inadequate. Completeness follows, shown by cecal photographs and a withdrawal time of at least eight minutes. A woman with an interval cancer then shows the endoscopist's own numbers: the adenoma detection rate, the serrated detection rate, and the techniques and tools that raise detection.

Topics covered

Positive non-invasive test leads to colonoscopy
Securing the colonoscopy commitment first
Split-dose preparation timing
Choosing and avoiding preparation agents
Boston Bowel Preparation Scale
Cecal intubation and withdrawal time
Interval cancer and adenoma detection rate
Serrated lesion detection rate
Techniques and devices that raise detection

Key decisions

Send any positive non-invasive test, whether FIT, stool DNA, abnormal CT colonography, or blood-based cell-free DNA, to diagnostic colonoscopy instead of repeating the stool test, and secure the commitment to colonoscopy before a non-invasive test is chosen.
Prescribe split-dose preparation with the second dose finished four to eight hours before the procedure, and write the actual finishing window on the patient's instructions.
Use split-dose polyethylene glycol for a patient with kidney disease, hypertension, and angiotensin-converting enzyme inhibitor or thiazide use, avoiding sodium phosphate, and avoid mannitol whenever electrocautery is planned.
Call preparation adequate only when every segment scores at least two on the Boston scale, a total of six or more, and repeat within a year, often three to twelve months, when it is inadequate.
Prove a complete examination with photographs of the appendiceal orifice and ileocecal valve, aim for cecal intubation in at least ninety-five percent, and average at least eight minutes of withdrawal in normal examinations.
Track the adenoma detection rate against the 2024 targets of thirty-five percent overall, forty in men, and thirty in women, and track a serrated detection rate of at least six percent as well.
Raise detection with withdrawal technique first, including washing and full distension with carbon dioxide, then add computer-aided detection, which adds about ten percent, or a mucosal exposure device, which adds about seven percent.
Give a hyperplastic polyp of ten millimeters or more a three-to-five-year interval.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(01:16) - Positive stool test means colonoscopy
(02:23) - Split-dose timing and preparation choice
(04:22) - Scoring preparation with Boston scale
(05:42) - Proving a complete examination
(07:23) - Interval cancer and adenoma detection
(08:19) - Serrated lesion detection rate
(09:40) - Raising detection: technique and tools
(12:14) - Start to finish review

Chapter 30, Ep 2 of 5: Colonoscopy Practice and Quality: Shape and Snare

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

The organizing idea is that a lesion is described before it is touched, because its shape and surface decide how it comes out. The episode starts with the Paris classification, then reads vessels and surface with NICE, JNET, and Kudo. It sets cancer risk by lateral spreading subtype and reviews serrated polyp recognition. It then matches the tool to the lesion: cold snare for small polyps, hot snare with a clip or loop for thick stalks, and EMR with a lift test for larger lesions. It closes with margin treatment, underwater EMR for scar, and when a lesion must come out in one piece by dissection.

Topics covered

Paris classification and invasion risk
NICE, JNET, and Kudo optical diagnosis
Lateral spreading lesion subtypes and cancer risk
Choosing a technique by lesion type
Serrated polyp recognition
Cold snare versus forceps
Hot snare for pedunculated polyps
EMR and the non-lifting sign
Margin treatment and underwater EMR
Endoscopic submucosal dissection and curative criteria

Key decisions

Describe every lesion by Paris class and optical pattern before any resection, because snaring first risks a piecemeal resection that cannot be staged.
Treat depression (Paris 0-IIc or mixed 0-IIa plus IIc), NICE or JNET type three, and Kudo type five as signs of invasion, and do not remove them with a piecemeal snare.
Resect granular homogeneous lateral spreading lesions, with under one percent cancer risk, piecemeal by EMR, and remove non-granular pseudodepressed lesions, with risk approaching thirty percent, in one piece.
In a granular mixed nodular lesion, target the dominant nodule and remove it in one piece or biopsy it.
Remove polyps of four to ten millimeters, and diminutive polyps, with a cold snare rather than forceps, which tend to leave residual tissue.
Use a hot snare for pedunculated polyps over ten millimeters, with a clip or detachable loop at the base of a thick stalk before cutting.
Biopsy and refer a lesion that does not lift, because failure to lift means deep invasion or fibrosis, and do not snare across it.
Treat the EMR defect margin with snare-tip soft coagulation, which cut adenoma recurrence about fourfold, and use underwater EMR for scarred lesions without deep invasion.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(02:04) - Paris classification and invasion
(03:00) - Optical diagnosis: NICE, JNET, Kudo
(04:58) - Lateral spreading lesions and technique
(06:42) - Recognizing serrated polyps
(07:58) - Cold snare for small polyps
(08:50) - Hot snare for thick stalks
(09:48) - EMR and the non-lifting sign
(11:10) - Margin treatment and underwater EMR
(12:28) - En bloc resection and ESD criteria

Chapter 30, Ep 3 of 5: Colonoscopy Practice and Quality: Polyp Pathology

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

Pathology decides two things after polypectomy: whether the patient needs surgery, and when to look again. The episode starts with why intramucosal adenocarcinoma in the colon is cured by complete resection, then describes invasion depth by Kikuchi or Haggitt level. It then covers the four high-risk features, any one of which sends a patient to surgery, and why deep invasion alone does not in a poor surgical candidate. Next come the 2020 surveillance intervals, set by the highest-risk lesion, and the separate schedule for a piecemeal resection site. It closes with MLH1 loss, where BRAF or methylation separates sporadic cancer from Lynch syndrome, and with serrated polyposis.

Topics covered

Intramucosal adenocarcinoma in the colon
Kikuchi and Haggitt invasion depth
Four high-risk histologic features
Deep invasion in poor surgical candidates
One-piece resection of suspicious lesions
2020 surveillance intervals
Serrated lesion intervals
Piecemeal EMR site surveillance
MLH1 loss and Lynch syndrome
Serrated polyposis syndrome

Key decisions

Treat intramucosal adenocarcinoma (T1a, sm0) like high-grade dysplasia, because the colon's lymphatics begin at the muscularis mucosae; complete endoscopic resection cures it and surveillance replaces colectomy.
Describe T1 depth with the Kikuchi system for sessile lesions and the Haggitt system for pedunculated ones, remembering that Haggitt level four carries risk like deep submucosal invasion.
Send the patient to surgery for any single high-risk feature: poor differentiation (grade three or higher), lymphovascular invasion, tumor budding of ten or more, or a margin under one millimeter.
Do not treat deep invasion alone (sm3, beyond one thousand microns) as an automatic colectomy in a poor surgical candidate, since its nodal risk is about two and a half percent without other adverse features.
Resect any lesion that looks malignant in one piece, because piecemeal removal makes depth, margin, budding, and lymphovascular invasion impossible to assess.
Set the colon-wide interval by the highest-risk lesion: ten years for a normal exam or small distal hyperplastic polyps, three years for an adenoma of ten millimeters or more, villous histology, or high-grade dysplasia, and one year plus hereditary evaluation for more than ten adenomas.
After piecemeal EMR of a lesion twenty millimeters or larger, check the site at six months, a year later, and three years after that, alongside the colon-wide schedule.
With MLH1 and PMS2 loss, BRAF V600E or MLH1 promoter methylation means sporadic cancer, while loss of MSH2, MSH6, or isolated PMS2 goes straight to germline testing; serrated polyposis needs colonoscopy every one to two years.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patients
(00:58) - Malignant polyp and colonic invasion
(02:27) - Describing depth: Kikuchi and Haggitt
(03:29) - Four features that mandate surgery
(04:32) - Deep invasion in a frail patient
(05:35) - Why suspicious lesions come out whole
(06:11) - 2020 surveillance intervals
(08:23) - Piecemeal resection site schedule
(10:28) - MLH1 loss: sporadic or Lynch
(11:55) - Serrated polyposis syndrome

Chapter 30, Ep 4 of 5: Colonoscopy Practice and Quality: Adverse Events

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

Each complication after polypectomy has its own anatomic or thermal mechanism, and that mechanism, along with the timing and location of symptoms, decides management. The episode starts with a woman on aspirin after a large cecal resection. It covers immediate versus delayed bleeding, which proximal defects benefit from clip closure, and how a perforation is handled depending on when it is found. It then turns to a man with fever after a hot snare whose CT shows no free air, which points to post-polypectomy syndrome. It closes with splenic injury after a difficult examination, then a symptom pattern review and the board traps.

Topics covered

Post-polypectomy bleeding risk and aspirin
Immediate versus delayed bleeding
Clip closure of large proximal defects
Perforation recognized during the procedure
Delayed perforation and surgery
Post-polypectomy electrocoagulation syndrome
Splenic injury and the Kehr sign
Symptom patterns after colonoscopy
Board traps

Key decisions

Continue aspirin taken for secondary prevention after a coronary stent, because stent thrombosis is deadlier than procedural bleeding that can usually be treated at the scope.
Manage immediate bleeding at the time with hemoclips, thermal coagulation, or epinephrine injection, and manage delayed bleeding, which appears one to fourteen days later, with repeat colonoscopy and endoscopic hemostasis.
Clip closed large EMR defects of twenty millimeters or more in the proximal colon to prevent delayed bleeding, and do not expect benefit from closing distal defects.
Close a perforation recognized during the procedure and smaller than two centimeters endoscopically, with through-the-scope clips, over-the-scope clips, or suturing, and send larger, older, contaminated, or unclosable perforations to surgery.
Send a delayed perforation with diffuse peritonitis, fever, and free air to surgery rather than attempting endoscopic closure.
Diagnose post-polypectomy syndrome when fever, focal lower quadrant tenderness, and leukocytosis appear twenty-four to seventy-two hours after a hot snare and CT shows no free air, and treat with bowel rest, intravenous antibiotics, and observation.
Suspect splenic injury when left upper quadrant pain, a Kehr sign, and falling blood pressure follow a difficult examination, observing a stable contained injury and using splenic artery embolization or splenectomy when the patient is unstable.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(00:44) - Cecal resection patient on aspirin
(01:46) - Immediate versus delayed bleeding
(02:27) - Clip closure of proximal defects
(03:45) - Perforation: timing decides treatment
(05:24) - Fever after a hot snare
(07:08) - Splenic injury away from the polyp
(07:50) - Symptom patterns point to cause
(08:17) - Board traps in these patients
(09:04) - Start to finish recap

Chapter 30, Ep 5 of 5: Colonoscopy Practice and Quality: Special Patients

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

Special populations change the four phases of colonoscopy, preparation, sedation, intervention, and recovery, and the underlying physiology decides which standard step must change. The episode begins with a dialysis patient on apixaban: safe preparation, timing around dialysis, and an anticoagulant hold planned from the expected procedure. It then turns to cirrhosis, covering rectal varices, why INR should not drive transfusion, and sedation choices. Next comes pregnancy, with when colonoscopy proceeds and how it is done. It closes with a recent drug-eluting stent and when an elective polypectomy should wait, then reviews the board traps.

Topics covered

Special populations and physiology
Bowel preparation in dialysis patients
Scheduling around dialysis
Apixaban and direct oral anticoagulant holds
Rectal varices in cirrhosis
Coagulation and transfusion in cirrhosis
Sedation in cirrhosis
Colonoscopy in pregnancy
Recent coronary stents and timing
Board traps and review

Key decisions

Use polyethylene glycol electrolyte solution for a dialysis patient, avoid sodium phosphate because of acute phosphate nephropathy, and use magnesium-based preparations only with caution in advanced kidney disease.
Schedule a dialysis patient's colonoscopy for the morning after a session, so a Monday, Wednesday, Friday patient is booked on a Tuesday or Thursday.
When polypectomy is anticipated, hold apixaban for forty-eight to seventy-two hours as for a high-risk procedure, rather than twenty-four to forty-eight hours for a low-risk one, and restart one to three days after the procedure once hemostasis is secure.
Do not transfuse plasma to normalize the INR in cirrhosis, because coagulation is rebalanced and the extra volume raises portal pressure; for a high-risk procedure use viscoelastic testing and correct fibrinogen or platelets only when truly low.
Inspect the rectum carefully in a patient with portal hypertension, and do not snare a polyp next to rectal varices the way you would in another patient.
In cirrhosis, prefer fentanyl over morphine and propofol with anesthesia over benzodiazepines, which can precipitate hepatic encephalopathy.
In pregnancy, defer elective colonoscopy, but proceed for hemodynamically significant lower GI bleeding, suspected obstruction, or a severe inflammatory bowel disease flare needing tissue, preferably in the second trimester, with left lateral positioning and no midazolam in the first trimester.
Defer an elective polypectomy for six months after a drug-eluting stent and thirty days after a bare metal stent, rather than operating on full dual antiplatelet therapy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Overview of special populations
(00:50) - Dialysis patient and preparation choice
(02:30) - Timing around dialysis
(03:02) - Planning the apixaban hold
(05:11) - Cirrhosis and rectal varices
(05:54) - INR and transfusion in cirrhosis
(06:53) - Sedation in cirrhosis
(07:26) - Colonoscopy in pregnancy
(08:43) - Recent coronary stent timing
(09:45) - Board traps and summary

Chapter 31, Ep 1 of 4: GI Emergencies: Massive Upper GI Bleed

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

A massive upper GI bleed is a resuscitation problem before it is an endoscopy problem, because the decisions that drive outcome happen in the first hour. The episode follows a man on warfarin and ibuprofen who arrives in shock. It starts with restrictive transfusion and the point where a massive transfusion protocol takes over. It then covers drug-specific anticoagulant reversal and whether it must finish before the scope, erythromycin before endoscopy and tranexamic acid never, and intubation for airway protection. Next come the timing of endoscopy, dual therapy for high-risk stigmata, and embolization or surgery when endoscopy fails. A second patient with an old aortic graft and a herald bleed shows the cause that cannot be missed.

Topics covered

Resuscitation before endoscopy
Restrictive transfusion thresholds
Massive transfusion protocol and calcium
Anticoagulant reversal
Reversal and the timing of endoscopy
Erythromycin and tranexamic acid
Airway protection before EGD
Timing of endoscopy
Dual therapy, embolization, and surgery
Aortoenteric fistula and the herald bleed

Key decisions

Transfuse red cells below a hemoglobin of 7 g/dL with a target of 7 to 9, raise the threshold to 8 with active acute coronary syndrome, and transfuse on clinical grounds when the patient is visibly exsanguinating.
Activate a massive transfusion protocol when bleeding continues despite initial resuscitation, with red cells, plasma, and platelets in a 1:1:1 ratio, and check and replace calcium.
Reverse warfarin in life-threatening bleeding with 4F-PCC rather than plasma, add vitamin K for sustained reversal, give idarucizumab 5 g IV for dabigatran, and use 4F-PCC for apixaban, rivaroxaban, and edoxaban because andexanet alfa was withdrawn.
Do not delay endoscopy for an INR of 1.5 to 2.5, but reverse an INR above 2.5 before endoscopy in most situations.
Give IV erythromycin 250 mg over 20 to 30 minutes, 30 to 90 minutes before endoscopy, to clear the stomach, and do not give tranexamic acid in acute upper bleeding.
Intubate before the scope for grade 3 to 4 hepatic encephalopathy, massive hematemesis with aspiration risk, hemodynamic collapse, or inability to protect the airway.
Scope non-variceal bleeding within 24 hours and variceal bleeding within 12 hours, and reserve endoscopy under 6 hours for unstabilizable massive hemorrhage or a suspected aortoenteric fistula.
Treat high-risk stigmata with epinephrine plus a second modality, send failures to angiographic embolization (gastroduodenal artery for posterior bulb ulcers, left gastric artery for lesser curve ulcers), and operate when embolization fails.
In a patient with a prior aortic graft and a herald bleed, get CT angiography before EGD or surgery, and send a confirmed fistula to surgery.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 first patient
(01:56) - Restrictive transfusion targets
(03:18) - Massive transfusion protocol and calcium
(04:13) - Reversing warfarin and DOACs
(05:33) - Erythromycin yes, tranexamic acid no
(06:24) - Securing the airway first
(07:01) - How soon to scope
(07:59) - Endoscopic therapy for high-risk ulcers
(08:33) - Embolization and surgery after failure
(09:27) - Aortoenteric fistula and the herald bleed

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

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

This episode is organized around one idea: in both lower bleeding and bowel ischemia, the next step depends on stability and on the cause, not on the label. For lower bleeding, the order is to exclude an upper source with the BUN to creatinine ratio, stabilize, do anoscopy, then choose colonoscopy for the stable patient or CT angiography for the unstable one, and clip or band a bleeding diverticulum. Pain before blood points to colon ischemia and, if right-sided, to the mesenteric arteries. Acute mesenteric ischemia follows: recognize pain out of proportion to the examination, get CT angiography despite a normal lactate, resuscitate, then treat by cause or operate for peritoneal signs.

Topics covered

Excluding an upper source in lower bleeding
Anoscopy and stabilization
Oakland score and disposition
CT angiography versus colonoscopy
Diverticular bleeding and clips
Post-polypectomy bleeding and angiodysplasia
Colon ischemia severity and antibiotics
Acute mesenteric ischemia recognition and CT angiography
Resuscitation without vasopressors
Embolus, thrombosis, nonocclusive and venous causes

Key decisions

Suspect an upper source when the BUN to creatinine ratio is above thirty, and do upper endoscopy first when it is about forty with a fast pulse.
Perform bedside anoscopy before referring for colonoscopy, and manage patients with an Oakland score of eight or below as outpatients.
Send a stable patient to colonoscopy twelve to twenty-four hours after rapid preparation with four liters of polyethylene glycol, and send an unstable patient first to CT angiography with embolization if positive.
Treat diverticular stigmata and post-polypectomy bleeding with clips or band ligation rather than deep thermal therapy, because of perforation risk.
Treat mild colon ischemia with fluids and bowel rest, and add antibiotics when the white count is above fifteen thousand, the BUN is above twenty, or ulceration is severe; image the mesenteric vessels in isolated right colon ischemia.
Order CT angiography with arterial and portal venous phases for pain out of proportion to the examination, and do not wait for or be reassured by a lactate.
Resuscitate with crystalloid and broad-spectrum antibiotics while avoiding vasopressors, and proceed to laparotomy with a second look at twenty-four to forty-eight hours for peritoneal signs.
Match treatment to cause: remove an embolus, revascularize a thrombosed SMA origin, give intra-arterial papaverine at thirty to sixty milligrams an hour for nonocclusive ischemia, and anticoagulate mesenteric venous thrombosis.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(01:02) - Painless maroon stools case
(02:44) - Anoscopy and stabilization
(03:02) - CT angiography versus colonoscopy
(05:42) - Diverticular bleeding and clips
(07:36) - Pain first: colon ischemia
(09:14) - Acute mesenteric ischemia presentation
(11:53) - Treatment depends on the cause
(13:25) - Thrombosis, nonocclusive, and venous causes
(16:32) - Board traps and summary

Chapter 31, Ep 3 of 4: GI Emergencies: Esophageal Emergencies

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

The organizing idea is that urgency follows how fast an injury escalates. The episode starts with a food impaction, where complete obstruction means endoscopy within six hours, glucagon rarely helps, nothing is pushed blindly, and biopsies look for eosinophilic esophagitis. It then moves to the two-hour button battery and the removal windows for sharp, long, wide, magnetic, blunt, and drug-packet objects. Next comes Boerhaave syndrome: the Mackler triad, CT with water-soluble contrast, antibiotics with antifungals in severe disease, and the twenty-four-hour line between primary repair and a covered stent. It ends with caustic ingestion: airway first, what never to do, and the Zargar grade deciding disposition.

Topics covered

Food bolus impaction and the six-hour rule
Glucagon and blind pushing
Eosinophilic esophagitis biopsies
Button battery and the two-hour clock
Removal windows by object type
Drug packets
Boerhaave syndrome and the Mackler triad
CT, antibiotics, and antifungals
Repair versus stent at twenty-four hours
Caustic ingestion and Zargar grades

Key decisions

Perform endoscopy within six hours, and sooner if possible, for esophageal obstruction with inability to manage secretions, a sharp esophageal object, or a disc battery, and remove an esophageal disc battery within two hours.
Do not let glucagon, which is given as 1 mg intravenously and works in under twenty percent, delay endoscopy, and never push a bolus blindly with a nasogastric tube or bougie.
Take at least four biopsies each from the proximal and distal esophagus at the first impaction without a known diagnosis, looking for fifteen eosinophils per high-power field.
Remove sharp gastric or duodenal objects, objects longer than six centimeters, and high-power magnets within twenty-four hours, remove objects wider than two and a half centimeters from the stomach, and follow blunt objects past the duodenum with serial radiographs.
Never retrieve drug packets endoscopically, and observe the patient under monitoring with laparotomy for symptoms of a leak.
Suspect Boerhaave even with an incomplete Mackler triad or a normal chest film, and confirm with CT using water-soluble oral contrast, not barium.
Give piperacillin-tazobactam or meropenem, add fluconazole or micafungin from the start in severe disease, and place a nasogastric tube only under fluoroscopy.
Repair primarily with drainage within twenty-four hours of a perforation, and after that use a covered self-expanding metal stent with drainage.
After caustic ingestion, intubate early for stridor, drooling, voice change, or extensive burns, avoid emesis, charcoal, neutralizers, and blind tubes, and scope within about twelve to twenty-four hours but not after forty-eight.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:11) - Steak impaction and the six-hour rule
(03:54) - Eosinophilic esophagitis underneath the bolus
(04:49) - Button battery and the two-hour clock
(05:38) - Removal windows for other objects
(07:39) - Boerhaave syndrome and the Mackler triad
(09:43) - CT, contrast, and antimicrobial coverage
(11:36) - Repair or stent by time
(13:19) - Caustic ingestion: airway and what to avoid
(14:44) - Zargar grades and disposition

Chapter 31, Ep 4 of 4: GI Emergencies: Ogilvie Syndrome

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

Acute colonic pseudo-obstruction is massive colonic dilation without a mechanical blockage, driven by autonomic imbalance that opioids, surgery, and electrolyte disturbances unmask. The episode follows a 76-year-old man after hip surgery through four ordered steps. First, CT excludes mechanical obstruction, volvulus, and toxic megacolon, and sets a baseline cecal diameter. Second, supportive care corrects electrolytes, stops opioids, and decompresses with tubes, resolving about 80 percent of cases. Third, a cecum over 12 centimeters or persistent distension triggers neostigmine, given on a monitor after contraindications are checked. Fourth, colonoscopic decompression follows if neostigmine fails or is contraindicated, and surgery is reserved for perforation, peritonitis, or failure of everything else.

Topics covered

Pathophysiology of colonic pseudo-obstruction
Precipitants and who gets it
CT to exclude mechanical obstruction
Supportive care bundle
Methylnaltrexone for opioid cases
Cecal diameter and perforation risk
Neostigmine dosing and monitoring
Contraindications to neostigmine
Colonoscopic decompression technique
Indications for surgery

Key decisions

Obtain CT of the abdomen and pelvis with contrast before treating, to exclude mechanical obstruction, volvulus, and toxic megacolon, and record the baseline cecal diameter.
In a stable patient with a cecum below 12 centimeters, start 48 to 72 hours of supportive care: nothing by mouth, nasogastric and rectal tubes, mobilization, position changes, electrolyte correction, and stopping opioids and anticholinergics.
Correct potassium, magnesium, calcium, and phosphate, since electrolyte disturbances unmask the autonomic imbalance.
Escalate when the cecum exceeds 12 centimeters, distension persists beyond 48 to 72 hours despite supportive care, or perforation is impending.
Give neostigmine 2 milligrams intravenously over 3 to 5 minutes with cardiac monitoring and atropine 1 milligram at the bedside, optionally with glycopyrrolate to blunt bradycardia.
Withhold neostigmine for mechanical obstruction, recent myocardial infarction, severe bradyarrhythmia, active reactive airway disease, seizure history, peritoneal signs, suspected ischemia, perforation, or hypersensitivity.
Use colonoscopic decompression when neostigmine fails, is contraindicated, or cannot be repeated, with no prep, minimal carbon dioxide insufflation, no narcotic sedation, a check for ischemia, and a decompression tube placed in the right colon.
Send the patient to surgery for perforation, peritonitis, clinical deterioration, or a cecum that stays above 12 centimeters after medical and endoscopic options are exhausted.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(00:35) - The post-hip-surgery patient
(01:00) - Diagnosis and autonomic mechanism
(02:55) - CT to exclude mechanical causes
(03:46) - The supportive care bundle
(05:07) - Cecal diameter and escalation triggers
(05:59) - Neostigmine dosing and monitoring
(06:56) - Checking neostigmine contraindications
(08:32) - Colonoscopic decompression technique
(09:31) - Surgery as the last step

Chapter 32, Ep 1 of 4: GI Nutrition: Deciding to Feed and How

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

The organizing idea is that feeding is a decision with risks on both sides: starved patients can be harmed by food, and inflamed patients can be mislabeled as starved. The episode begins with a starved man with alcohol use disorder, covering refeeding risk, thiamine before glucose, and a slow start. It then turns to a septic woman whose low albumin is not malnutrition, the GLIM criteria, and when support is indicated. Last, it follows a man with oropharyngeal cancer through choosing the gut, picking a nasal tube or PEG, introducer placement, a buried bumper, other PEG problems, and tube-feed diarrhea. A woman with advanced dementia shows who should not get a tube.

Topics covered

Refeeding syndrome physiology
Thiamine before glucose and Wernicke encephalopathy
NICE criteria for refeeding risk
Slow calorie start and electrolyte monitoring
Albumin and prealbumin as inflammatory markers
GLIM criteria and nutrition screening
Indications for nutrition support
Enteral versus parenteral nutrition
Nasal tube versus PEG and placement technique
PEG complications and tube-feed diarrhea

Key decisions

Give thiamine before any glucose in an at-risk patient, 200 to 300 mg daily for refeeding prevention, or 500 mg intravenously three times daily for 2 to 3 days if Wernicke encephalopathy is suspected.
Call a patient high risk for refeeding with a BMI under 16, weight loss over 15 percent in 3 to 6 months, more than 10 days of negligible intake, or low potassium, phosphate, or magnesium, or any two of the lesser criteria.
Start high-risk patients at 10 to 20 kilocalories per kilogram per day, advance over 4 to 7 days, check electrolytes twice daily for 72 hours, and hold calories while phosphate is falling.
Do not diagnose malnutrition or start parenteral nutrition from a low albumin or prealbumin, and use GLIM, which needs one phenotypic and one etiologic criterion.
Start nutrition support when intake will be inadequate for more than 7 days or malabsorption causes weight loss, through the gut if it works.
Use a nasal tube for less than 4 to 6 weeks and a PEG beyond that, with the introducer technique in oropharyngeal cancer and one dose of cefazolin 1 g intravenously 30 minutes before.
Do not place a PEG in advanced dementia, and treat pain with a tube that will not flush or rotate as buried bumper, removed endoscopically or surgically.
In tube-feed diarrhea, review sorbitol-containing medications, antibiotics, and C. difficile before changing the formula.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and patients
(00:58) - Starved patient and refeeding risk
(02:58) - Thiamine before glucose
(05:30) - Starting slowly and monitoring electrolytes
(06:29) - Low albumin is not malnutrition
(07:52) - GLIM criteria and screening tools
(11:08) - Choosing the gut and the tube
(12:19) - Introducer PEG in oropharyngeal cancer
(14:17) - Buried bumper and PEG problems
(15:38) - Tube-feed diarrhea and formula choice

Chapter 32, Ep 2 of 4: GI Nutrition: Parenteral Nutrition and Short Gut

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

The organizing idea is that parenteral nutrition is for a gut that cannot be used, and that a short gut is judged by the anatomy left, not the length lost. The episode starts with who qualifies for parenteral nutrition, then counts calories, avoids precipitation in the bag, chooses lipid and cycling, and handles line infection, gallstones, and liver disease. It then shows who is harmed by it. It turns to short bowel syndrome: anatomy and prognosis, ileal loss, oral rehydration, drugs, cholestyramine, teduglutide with colonoscopy, and the colon's two problems, oxalate stones and D-lactic acidosis.

Topics covered

Indications for parenteral nutrition
Calorie counting and dextrose
Calcium, phosphate, and acetate in the bag
Mixed lipid emulsions and cycling
Line infection and locks
Gallstones and liver disease from parenteral nutrition
When parenteral nutrition harms
Short bowel anatomy and prognosis
Oral rehydration, drugs, and cholestyramine
Teduglutide, oxalate stones, and D-lactic acidosis

Key decisions

Start parenteral nutrition only when the gut cannot be used, as in intestinal failure, ileus beyond seven days, severe pancreatitis that won't tolerate enteral feeding, transplant mucositis, or refractory high-output stomas, and not for low albumin, cancer cachexia, or mild pancreatitis.
Prescribe 25 to 30 kilocalories per kilogram and 1 to 1.2 grams per kilogram of amino acids, count dextrose at 3.4 kilocalories per gram, and give lipid twice weekly to prevent essential fatty acid deficiency.
Keep calcium and phosphate within validated solubility limits and use acetate, not bicarbonate, as the buffer.
Give long-term patients a mixed lipid emulsion rather than pure soybean and cycle feeding over 12 to 18 hours to protect the liver.
Salvage an infected catheter with systemic antibiotics plus a lock when the organism allows, and add ethanol or taurolidine locks after recurrent infections.
Give any enteral intake the patient can absorb, even 20 to 30 percent of needs, to reduce gallbladder stasis and liver injury, and refer for intestinal transplantation when liver failure is established, infections recur, or venous access is lost.
Use a sodium-glucose oral rehydration solution with plain water limited, loperamide before meals, high-dose PPI, and hyperphagia, and give cholestyramine only for 30 to 100 centimeters of ileal resection.
Check colonoscopy within six months before starting teduglutide, at one year, and every five years, avoid it in active gastrointestinal malignancy, and in patients with a colon use a low-oxalate diet with calcium at meals and request D-lactate when confusion follows carbohydrate.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(01:23) - Who needs parenteral nutrition
(02:34) - Calories and dextrose counting
(03:36) - Calcium, phosphate, and acetate
(04:02) - Lipid choice and cycling
(05:12) - Line infection, gallbladder, and liver
(08:06) - When parenteral nutrition harms
(09:22) - Short bowel anatomy and prognosis
(11:16) - Fluids, drugs, and cholestyramine
(13:21) - Teduglutide and colon complications

Chapter 32, Ep 3 of 4: GI Nutrition: Vitamins and Essential Fats

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

Each vitamin and essential fatty acid is traced from its job in the body to the picture its deficiency or excess makes. The episode starts with cholestasis and cholestyramine, which cause all four fat-soluble deficiencies, then covers vitamin D repletion, vitamin E, and vitamin K with warfarin and antibiotics. It turns to vitamin A excess mimicking cryptogenic cirrhosis, then essential fatty acid deficiency and why MCT oil cannot prevent it. The water-soluble section follows B12 absorption, confirmation of a borderline level, folate, and bacterial overgrowth, then pellagra, pyridoxine, thiamine, vitamin C, and biotin.

Topics covered

Fat-soluble vitamin deficiency in cholestasis
Vitamin A deficiency and night blindness
Vitamin D repletion with calcium
Vitamin E deficiency
Vitamin K, warfarin, and antibiotics
Vitamin A hepatotoxicity
Essential fatty acid deficiency and MCT oil
B12 absorption steps and deficiency
Folate deficiency and bacterial overgrowth
Pellagra, pyridoxine, thiamine, vitamin C, and biotin

Key decisions

When one fat-soluble vitamin deficiency is found in a patient with cholestasis or on cholestyramine, look for the other three, because all four depend on bile salts.
Replete vitamin D when 25-hydroxyvitamin D is below 30 ng/mL, or below 20 by a stricter cutoff, using ergocalciferol 50,000 units weekly for 8 to 12 weeks or cholecalciferol 1,000 to 5,000 units daily, always with calcium and a repeat level.
Watch the INR closely in a patient on warfarin who is fasting and receiving broad-spectrum antibiotics, and replace vitamin K under the skin or by mouth, giving intravenous vitamin K slowly because of anaphylaxis risk.
Ask about supplements by name in unexplained cirrhosis, because chronic vitamin A intake of 50,000 units a day or more causes stellate cell fibrosis, and stop the vitamin A.
Diagnose essential fatty acid deficiency with a triene-to-tetraene ratio above 0.2 and treat with intravenous long-chain lipid, since MCT oil cannot prevent or treat it.
Confirm a borderline serum B12 of 200 to 400 pg/mL with methylmalonic acid and homocysteine, check B12 before ever starting folate, and replace with intramuscular cyanocobalamin 1,000 micrograms weekly for one to two months and then monthly.
Look for and treat small intestinal bacterial overgrowth when B12 is low and folate is high, and give B12 for life when the terminal ileum has been resected because oral B12 fails.
Give thiamine before any glucose and treat suspected Wernicke encephalopathy empirically with 500 mg intravenously three times daily for two to three days, then 250 mg daily for five to seven days.
Treat pellagra with nicotinamide 250 to 500 mg daily and give pyridoxine 25 to 50 mg daily with long-term isoniazid.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(01:03) - Cholestasis and fat-soluble deficiencies
(03:04) - Vitamin D repletion and bone
(04:56) - Vitamin K, warfarin, and antibiotics
(05:55) - Vitamin A excess and cirrhosis
(07:12) - Essential fatty acids and MCT oil
(09:02) - B12 deficiency, folate, and SIBO
(13:32) - Pellagra and pyridoxine
(15:21) - Thiamine, vitamin C, and biotin
(17:46) - Board traps and episode summary

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

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

Each mineral and trace element has a specific biochemical job and a typical exposure or disease that tips it into deficiency or excess, so the exposure is asked about first. The episode starts with a man whose denture cream gives him zinc excess and copper deficiency that mimics B12 myeloneuropathy, then covers zinc deficiency and why zinc replacement is monitored. It moves to PPI-induced hypomagnesemia, manganese buildup in cholestasis on parenteral nutrition, and selenium and chromium deficiency from an unsupplemented bag. It then covers selenosis from Brazil nuts, iron replacement after gastric bypass, and why dietary calcium is preferred over pills.

Topics covered

Zinc excess and copper deficiency
Copper deficiency myeloneuropathy versus B12
Zinc deficiency and replacement
PPI-induced hypomagnesemia
Manganese toxicity on parenteral nutrition
Selenium and chromium deficiency
Selenosis from Brazil nuts
Iron deficiency after gastric bypass
Dietary calcium versus supplements
Board traps for minerals

Key decisions

When a myeloneuropathy looks like subacute combined degeneration but B12, MMA, and folate are normal, check serum copper and ceruloplasmin, and ask by name about denture cream and zinc supplements.
Treat copper deficiency with oral copper, two milligrams daily, and remove the zinc source, such as switching to a zinc-free denture adhesive.
When zinc deficiency is suspected from periorificial dermatitis, poor wound healing, or taste change, check a zinc level and, if low, give zinc sulfate, two hundred twenty milligrams daily (fifty milligrams elemental zinc), with monitoring because excess zinc causes copper deficiency.
In a long-term PPI user with tetany, seizure, or arrhythmia and very low magnesium despite normal kidneys and no diuretic or alcohol use, stop the PPI where feasible, substitute an H2 blocker, and replace magnesium intravenously as magnesium sulfate if symptomatic and in hospital, or orally if an outpatient.
Remove manganese from parenteral nutrition once cholestasis develops or once T1 hyperintensity of the globus pallidus is seen on MRI, whichever comes first.
Consider selenium deficiency when a new cardiomyopathy appears on long-term unsupplemented parenteral nutrition, and chromium deficiency when unexplained glucose intolerance appears.
Replace iron with oral ferrous sulfate, move to intravenous iron if it is not tolerated or not absorbed, and expect reticulocytes to rise within seven to ten days.
Prefer dietary calcium over calcium supplements, taken with vitamin D, in patients whose bones are threatened.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Minerals and trace elements overview
(01:00) - Unsteady gait and denture cream
(02:10) - Copper deficiency mimics B12
(04:04) - Zinc deficiency and monitored replacement
(05:08) - PPI-induced hypomagnesemia
(06:43) - Manganese buildup on parenteral nutrition
(08:01) - Selenium and chromium deficiency
(08:46) - Selenosis from Brazil nuts
(09:27) - Iron replacement after gastric bypass
(10:11) - Calcium from food, not pills

Chapter 33, Ep 1 of 5: GI Infections: Diagnosis to Surgery

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

This episode follows one Clostridioides difficile infection from the first loose stool to the operating room. The organizing idea is that each step has a gate: test only the right patient, read a two-step result correctly, grade severity from two laboratory numbers, then match the drug and route to that grade. The order is the testing threshold, NAAT with toxin EIA, a second patient whose positive NAAT may be colonization, severity, first-line therapy with fidaxomicin or oral vancomycin, why metronidazole ranks last, fulminant disease with rectal vancomycin and early surgical consultation, the choice of operation, and why a recovered patient is not retested.

Topics covered

Risk factors and presentation of CDI
Cecal variant and pseudomembranous colitis
Testing threshold
Two-step testing with NAAT or GDH and toxin EIA
Colonization versus infection
Severity by white count and creatinine
Fidaxomicin and oral vancomycin
Why metronidazole ranks last
Fulminant disease and rectal vancomycin
Surgical indications and operations
No test of cure

Key decisions

Test only patients with three or more unexplained watery stools a day who are not taking laxatives and have classic risk factors, and do not test formed stool.
Screen with NAAT or GDH and confirm with toxin EIA, and treat a positive NAAT with a negative toxin as possible colonization that needs clinical correlation.
Stop laxatives and reassess stools before giving C. difficile therapy to a patient with a positive NAAT, negative toxin EIA, and laxative use.
Call disease severe when the white count is 15,000 or more or the creatinine is 1.5 or more, and fulminant when hypotension or shock, ileus, or megacolon is present.
Treat a first nonsevere or severe non-fulminant episode with fidaxomicin 200 mg twice daily for 10 days, or oral vancomycin 125 mg four times daily when fidaxomicin is unavailable, and reserve metronidazole 500 mg three times daily for the lowest-risk patients when neither is available.
Treat fulminant disease with oral vancomycin 500 mg every six hours plus intravenous metronidazole 500 mg every eight hours, add rectal vancomycin when ileus blocks oral delivery, consult surgery early, and never use intravenous vancomycin.
Operate for perforation, refractory hemorrhage, megacolon with progressive distention, or persistent sepsis, choosing subtotal colectomy with end ileostomy for unstable patients with necrosis and loop ileostomy with colonic lavage for selected stable patients.
Do not perform a test of cure after symptoms resolve, because nucleic acid often stays detectable and a positive result can be mistaken for recurrence.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode roadmap
(00:47) - Clindamycin patient with watery stools
(02:53) - Who meets the testing threshold
(03:28) - Two-step testing algorithm
(04:31) - Post-hip-surgery patient and colonization
(05:17) - Grading severity with two numbers
(06:02) - First-line drugs and metronidazole
(07:37) - Fulminant disease and rectal vancomycin
(08:29) - Surgery and choice of operation
(09:22) - No test of cure

Chapter 33, Ep 2 of 5: GI Infections: Recurrent Clostridioides difficile

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

Recurrent Clostridioides difficile infection is a problem of surviving spores, so every second-line plan aims to keep drug in the colon across several rounds of germination. The episode follows one woman through three steps. At her first recurrence, the drug that failed last time decides the next drug: fidaxomicin after metronidazole or vancomycin, and a vancomycin taper and pulse after fidaxomicin. Bezlotoxumab is no longer available. At her second recurrence, microbiota therapy replaces a third antibiotic course, as screened-donor FMT, rectal Rebyota, or oral Vowst. Her next antibiotic brings oral vancomycin prophylaxis, because she has prior CDI. Last, a recurrence is defined by symptoms before any testing, since post-infection irritable bowel syndrome can mimic it.

Topics covered

Definition and risk of recurrence
Spore germination and why CDI returns
Choosing the drug by prior therapy
Vancomycin taper and pulse
Extended-pulse fidaxomicin
Bezlotoxumab discontinuation
Fecal microbiota therapy
Rebyota and Vowst
Vancomycin prophylaxis
Recurrence versus post-infection IBS

Key decisions

After a first recurrence that followed fidaxomicin, give a vancomycin taper and pulse rather than repeating fidaxomicin.
After a first recurrence that followed metronidazole or vancomycin, give fidaxomicin, either 200 mg twice daily for ten days or the extended-pulse regimen of 200 mg twice daily for five days, then every other day on days seven through twenty-five.
Use the full vancomycin taper and pulse, 125 mg four times daily for ten to fourteen days, then twice daily for seven days, once daily for seven days, and every two to three days for two to eight weeks, rather than a short course.
After two or more recurrences following appropriate antibiotic courses, offer fecal microbiota therapy instead of a third antibiotic course, after controlling symptoms with vancomycin four times daily for ten to fourteen days and then tapering.
Give microbiota therapy only through a program using screened donors, by colonoscopy, capsule, or enema, or use rectal Rebyota or oral Vowst after a completed standard antibiotic course.
Give oral vancomycin prophylaxis during later antibiotic exposure in patients with prior CDI, and avoid clindamycin, fluoroquinolones, third-generation cephalosporins, and broad-spectrum penicillins when possible.
Do not give vancomycin prophylaxis to patients without prior CDI, and do not offer bezlotoxumab, which is discontinued in the United States.
Define recurrence by three or more unexplained watery stools a day off laxatives before testing, and do not retest after symptoms resolve.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and roadmap
(00:42) - The patient and first recurrence
(01:30) - Why spores cause recurrence
(02:02) - Choosing the drug and taper
(03:08) - Extended-pulse fidaxomicin and bezlotoxumab
(04:30) - Fecal microbiota therapy after recurrence
(05:43) - Rebyota and Vowst products
(06:38) - Prophylaxis during later antibiotics
(07:29) - Recurrence versus post-infection IBS
(07:58) - Board traps and summary

Chapter 33, Ep 3 of 5: GI Infections: Bacteria and Toxins

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

The organizing idea is that the right move in acute diarrhea depends on the organism, the host, and the clock. The episode starts with a traveler's bloody diarrhea and asks when to give an antibiotic, which one fits the region, why rifaximin fails in invasive disease, and when loperamide is safe. It then separates Campylobacter, Salmonella, Shigella, and Shiga toxin-producing E. coli, where one must get no antibiotic. Next come hosts at special risk, with Vibrio and Yersinia in iron overload and Listeria in pregnancy. It closes with preformed toxin syndromes recognized by onset time, and the sequelae that follow infection.

Topics covered

Travelers' diarrhea and when to treat
Azithromycin, ciprofloxacin, and rifaximin
Loperamide indications and contraindications
Campylobacter
Nontyphoidal Salmonella
Shigella
Shiga toxin-producing E. coli and hemolytic uremic syndrome
Vibrio and Yersinia in iron overload
Listeria in pregnancy
Preformed toxin syndromes and sequelae

Key decisions

Give an antibiotic for travelers' diarrhea with fever, dysentery, moderate-to-severe disease, or illness that stops travel or work, using azithromycin (one gram once or 500 mg daily for three days) for Southeast Asia and increasingly elsewhere, and ciprofloxacin 500 mg twice daily for one to three days where resistance is not high.
Avoid rifaximin in febrile or bloody diarrhea because it is unabsorbed and does not cover invasive Salmonella, Shigella, or Campylobacter, and give loperamide only for diarrhea without fever or blood.
Treat Campylobacter with azithromycin 500 mg daily for three days when there is high fever, bloody stools, bacteremia, or a risk of complications from older age, cirrhosis, pregnancy, or immunocompromise.
Withhold antibiotics in Salmonella gastroenteritis in a healthy adult, but treat severe disease, the extremes of age, immunocompromise, sickle cell disease, prosthetic vascular grafts, bacteremia, or typhoid fever.
Treat Shigella with a fluoroquinolone or azithromycin to shorten illness and shedding, but give Shiga toxin-producing E. coli neither antibiotics nor loperamide and monitor creatinine, platelets, and hemoglobin.
Treat Vibrio vulnificus immediately with doxycycline plus a third-generation cephalosporin, never a cephalosporin alone, and treat Yersinia in iron-overloaded or other special hosts, with a stool culture before calling terminal ileitis Crohn disease.
Treat invasive listeriosis with intravenous ampicillin, adding gentamicin for severe infection or meningitis, using trimethoprim-sulfamethoxazole for penicillin allergy, and never relying on a cephalosporin.
Give no antibiotics or stool studies for a preformed toxin syndrome that starts within hours without fever, and treat scombroid with H1 and sometimes H2 antihistamines.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and Roadmap
(01:20) - Travelers' Diarrhea Becomes Dysentery
(02:24) - Antibiotic Choice by Region
(03:53) - Campylobacter Culture and Treatment
(04:52) - Salmonella and Shigella Decisions
(07:30) - STEC After the Hamburger
(09:06) - Vibrio and Yersinia in Iron Overload
(12:03) - Listeria in Pregnancy
(13:54) - Preformed Toxin Syndromes
(16:57) - Post-Infectious Sequelae

Chapter 33, Ep 4 of 5: GI Infections: Gut Parasites and Drugs

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

Each gut parasite is matched to its own test and its own drug, and the episode works through that idea in two patients and a final case. A woman who drank stream water shows when to suspect a parasite, why antigen or PCR testing beats stool microscopy, and how Giardia, pregnancy, recurrence, and Cryptosporidium change management. A traveler with a liver abscess shows why amebiasis needs a tissue agent followed by a luminal agent. A man from rural Ecuador facing prednisone shows how Strongyloides is screened by serology and treated with ivermectin to prevent hyperinfection, and why hookworm needs one dose of albendazole. The episode ends with Anisakis, which is removed at endoscopy rather than treated with a drug.

Topics covered

When to suspect a parasite
Giardia testing with antigen or PCR
Tinidazole versus metronidazole
Lactose intolerance after Giardia
Giardia in pregnancy and recurrence
Cryptosporidium and HIV
Amebiasis and liver abscess
Strongyloides screening and ivermectin
Hookworm and single-dose albendazole
Anisakiasis and endoscopic removal

Key decisions

Test for Giardia with stool antigen enzyme immunoassay or stool PCR rather than a single ova-and-parasite exam, which misses a third to a half of infections.
Treat Giardia with tinidazole 2 g as a single dose, with metronidazole 250 mg three times daily for five to seven days as the alternative, and use paromomycin in pregnancy.
Do not retreat a patient whose Giardia antigen is negative but who has bloating after dairy, because lactose intolerance often persists for weeks; cut back on lactose instead.
Treat Cryptosporidium with nitazoxanide 500 mg twice daily for three days, but in HIV rely on antiretroviral therapy as the main treatment.
Treat invasive amebiasis with metronidazole 500 to 750 mg three times daily for seven to ten days or tinidazole 2 g daily for three to five days, followed by paromomycin for seven days to clear luminal cysts, and drain only large, rupture-prone peripheral, or unresponsive liver abscesses.
Check Strongyloides serology, not stool microscopy, before planned immunosuppression in anyone with past endemic exposure, and give ivermectin 200 micrograms per kilogram daily for one to two days, empirically if steroids cannot wait.
Treat hookworm with a single 400 mg dose of albendazole, because adult worms live in the gut lumen and there is no autoinfective cycle.
Remove Anisakis larvae endoscopically for severe epigastric pain hours after raw fish, since no antihelminthic is reliably effective and surgery is reserved for ulcer, perforation, or eosinophilic granuloma.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and parasite roadmap
(00:52) - Giardia case and when to suspect
(01:45) - Choosing the Giardia workup
(02:28) - Giardia drugs and post-infection symptoms
(03:54) - Cryptosporidium in healthy and HIV hosts
(04:48) - Amebiasis and the two-drug sequence
(06:50) - Strongyloides before immunosuppression
(09:05) - Hookworm and single-dose albendazole
(10:02) - Anisakiasis treated with a scope
(11:01) - Board traps and episode summary

Chapter 33, Ep 5 of 5: GI Infections: Opportunists and Norovirus

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

This final episode of the GI Infections chapter covers infections that a weakened immune system lets in, then the virus that needs no such help. It begins with CMV colitis in steroid-refractory ulcerative colitis, where the ulcer base is biopsied with immunohistochemistry and ganciclovir is given with immunosuppression reduced. A transplant recipient then shows how UL97 and UL54 mutations decide the next drug. Next comes advanced HIV: separating MAC from Whipple disease with an acid-fast stain, treating MAC with several drugs, and finding and treating microsporidia, Cyclospora, and Cystoisospora. The episode closes with a norovirus outbreak on a care-home floor, managed with supportive care, soap and water, and bleach.

Topics covered

CMV colitis in steroid-refractory ulcerative colitis
Ulcer-base biopsy and immunohistochemistry
Blood CMV PCR limits
Ganciclovir and valganciclovir treatment
UL97 and UL54 resistance
Foscarnet, maribavir, and letermovir
MAC versus Whipple disease
MAC regimen and duration
Microsporidia, Cyclospora, and Cystoisospora
Norovirus outbreak control

Key decisions

In steroid-refractory acute severe ulcerative colitis, look for CMV before escalating immunosuppression, because an adequate biopsy finds it in about a third of patients.
Biopsy the ulcer base rather than the edge or normal mucosa, and request CMV immunohistochemistry, since standard staining detects fewer than half of colonic cases.
Treat CMV colitis with intravenous ganciclovir 5 mg/kg every 12 hours, adjusted for kidney function, for 14 to 21 days, then valganciclovir 900 mg twice daily, while reducing immunosuppression where feasible.
For a UL97 mutation, switch to foscarnet or maribavir 400 mg twice daily, and remember that a UL54 mutation resists both ganciclovir and foscarnet, while letermovir is only for prophylaxis.
Use an acid-fast stain on PAS-positive macrophages to call MAC rather than Whipple disease, and treat MAC with a macrolide plus ethambutol, adding rifabutin in advanced disease, until the CD4 count has been above 100 for at least six months.
Order a trichrome stool stain or PCR for microsporidia, treating Encephalitozoon intestinalis with albendazole 400 mg twice daily for 21 days, and rely on antiretroviral therapy in HIV.
Treat Cyclospora and Cystoisospora with double-strength trimethoprim-sulfamethoxazole twice daily, not metronidazole or nitazoxanide, and give Cystoisospora prophylaxis below a CD4 count of 200.
In a norovirus outbreak, give supportive care without antibiotics, and use soap-and-water hand-washing and bleach cleaning rather than alcohol gel.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(01:34) - Who gets CMV colitis
(03:09) - Ulcer-base biopsy and stains
(04:42) - Ganciclovir and valganciclovir treatment
(05:22) - Resistance mutations choose the drug
(07:16) - MAC versus Whipple disease
(08:59) - MAC regimen and duration
(10:13) - Microsporidia diagnosis and treatment
(11:23) - Cyclospora and Cystoisospora
(13:15) - Norovirus outbreak control

Chapter 34, Ep 1 of 4: GI in the Immunocompromised Host: Organ Transplant

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

Every GI symptom in a solid organ transplant recipient is weighed against five causes: CMV, mycophenolate enteropathy, calcineurin inhibitor toxicity, EBV-driven post-transplant lymphoproliferative disorder, and C. difficile. Time since transplant narrows the list. The episode follows a kidney recipient with diarrhea, covering how CMV is prevented by serostatus and organ, how CMV colitis is diagnosed by biopsy and treated, how mycophenolate injury is separated from CMV and managed, and how a new azole drives tacrolimus toxicity. It closes with a liver recipient with a small bowel mass, showing when PTLD responds to less immunosuppression and rituximab and when it needs chemotherapy.

Topics covered

Five causes of GI symptoms after transplant
Time since transplant and the differential
CMV risk by donor and recipient serostatus
CMV prophylaxis duration by organ
CMV colitis diagnosis and treatment
Mycophenolate enteropathy
Tacrolimus toxicity and drug interactions
Calcineurin inhibitor toxicity and mTOR inhibitors
Post-transplant lymphoproliferative disorder
Board traps in transplant GI

Key decisions

Use time since transplant to narrow the differential, since months one to twelve are the peak window for CMV, mycophenolate enteropathy, and C. difficile.
Give valganciclovir prophylaxis at nine hundred milligrams daily for three months in kidney, three to six in liver, six in heart, and six to twelve in lung recipients, using the upper limit for D plus R minus patients.
Do not exclude CMV colitis on a negative blood PCR; perform colonoscopy with biopsies from the ulcer base and CMV immunohistochemistry.
Treat CMV colitis with intravenous ganciclovir at five milligrams per kilogram every twelve hours, adjusted for kidney function, then oral valganciclovir, and reduce immunosuppression as far as the graft allows.
Treat mycophenolate enteropathy by cutting the dose by twenty-five to fifty percent or switching to enteric-coated mycophenolic acid, reserving azathioprine for refractory cases, and do not treat it as Crohn disease with a biologic.
When a recipient on tacrolimus has tremor and a rising creatinine, look first for a new CYP3A4 inhibitor such as an azole or macrolide, and remember that rifampin lowers levels.
Substitute sirolimus or everolimus for the calcineurin inhibitor when kidney function declines.
Treat PTLD by reducing immunosuppression first, then giving rituximab at three hundred seventy-five milligrams per square meter weekly for four doses for CD20-positive disease, followed by four more rituximab cycles for complete responders or four cycles of R-CHOP for incomplete responders.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Five causes at every symptom
(01:55) - Time since transplant narrows the list
(03:01) - CMV risk and prophylaxis duration
(04:19) - Diagnosing and treating CMV colitis
(06:00) - Mycophenolate enteropathy and its management
(07:47) - Tacrolimus toxicity from drug interactions
(09:56) - Switching to mTOR inhibitors
(11:06) - Post-transplant lymphoproliferative disorder
(12:02) - Staged PTLD treatment by response
(13:21) - Board traps and summary

Chapter 34, Ep 2 of 4: GI in the Immunocompromised Host: Gut in Leukemia

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

The episode follows one woman with acute myeloid leukemia, and the organizing idea is that timing and the failed barrier of the gut decide the diagnosis and the treatment. During induction chemotherapy, neutropenic enterocolitis is confirmed with CT rather than colonoscopy, treated with bowel rest and antibiotics that cover gram-negatives, anaerobes, and Pseudomonas, then widened to antifungals after seventy-two hours of fever, with surgery reserved for complications. After allogeneic transplant, days since transplant narrow the cause of diarrhea. Gut graft-versus-host disease is staged by stool volume, proven by rectosigmoid biopsy with CMV excluded, treated with methylprednisolone, and escalated to ruxolitinib if steroids fail.

Topics covered

Neutropenic enterocolitis (typhlitis)
CT instead of colonoscopy
Antibiotic coverage for cecal flora
Empiric antifungals and surgical indications
Calendar of post-transplant GI complications
Acute graft-versus-host disease risk factors
Glucksberg-Seattle staging by stool volume
MAGIC biomarkers
Rectosigmoid biopsy and CMV exclusion
Steroids and ruxolitinib for refractory disease

Key decisions

Image a febrile neutropenic patient with right lower quadrant pain using contrast CT, looking for cecal wall thickening over four millimeters, and avoid colonoscopy because the friable bowel can perforate.
Treat typhlitis with bowel rest, fluids, and piperacillin-tazobactam or a carbapenem to cover gram-negatives, anaerobes, and Pseudomonas, adding vancomycin when gram-positive coverage is needed.
Add an echinocandin or liposomal amphotericin B when fever or sepsis persists seventy-two hours after the first antibacterial dose, and give granulocyte colony-stimulating factor for prolonged neutropenia.
Operate for perforation, hemorrhage that persists despite correction of clotting, full-thickness necrosis, persistent sepsis, or an abscess that fails percutaneous drainage.
Use the days since transplant to narrow the cause of diarrhea: conditioning toxicity in the first twenty-one days is not treated as graft-versus-host disease, while classical acute disease presents from day fifteen to one hundred.
Stage gut graft-versus-host disease by measured daily stool volume, with one thousand five hundred to two thousand milliliters a day being stage three.
Confirm the diagnosis with a rectosigmoid biopsy showing crypt apoptosis, and exclude CMV with PCR and tissue immunohistochemistry, plus C. difficile, before starting steroids.
Start intravenous methylprednisolone two milligrams per kilogram per day, using budesonide alone only for mild upper-gut disease, and call steroid-refractory disease at day five to seven and start ruxolitinib five to ten milligrams twice daily.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Patient and episode overview
(01:54) - Typhlitis: scan, not scope
(02:29) - Antibiotics for typhlitis
(03:33) - Antifungals and surgery
(04:57) - Timing after transplant
(07:10) - Staging gut GVHD by stool volume
(08:18) - Biopsy and excluding CMV
(09:56) - First-line steroid treatment
(10:45) - Steroid-refractory disease and ruxolitinib
(12:21) - Board traps and summary

Chapter 34, Ep 3 of 4: GI in the Immunocompromised Host: HIV as a Host

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

The organizing idea is that in HIV the CD4 count, more than any single organism, sets the GI differential, and antiretroviral therapy is the main treatment for most of what follows. The episode follows a newly diagnosed man with a CD4 count of forty. It starts with the CD4 tiers and the workup they dictate, then AIDS cholangiopathy, where papillary stenosis still needs a sphincterotomy. Next is Kaposi sarcoma, recognized by appearance and confirmed with LANA-1 staining when pinch biopsies are normal. It then covers when to start antiretroviral therapy, how to handle immune reconstitution inflammatory syndrome with MAC, and why routine MAC prophylaxis is not given when effective therapy is starting.

Topics covered

CD4 count tiers and the GI differential
Workup of diarrhea at a CD4 count of forty
AIDS cholangiopathy causes and ERCP patterns
Papillary stenosis and sphincterotomy
Kaposi sarcoma and human herpesvirus eight
LANA-1 staining after a normal biopsy
Antiretroviral therapy as main treatment
Timing of antiretroviral therapy and cryptococcal meningitis
Immune reconstitution inflammatory syndrome and MAC
MAC prophylaxis and board traps

Key decisions

Use the CD4 count to set the workup: thrush at 200 to 500, herpes simplex, esophageal Candida, and Cystoisospora below 200, Cryptosporidium, microsporidia, and CMV below 100, and disseminated CMV and MAC below 50.
Give secondary prophylaxis after treating Cystoisospora when the CD4 count is below 200.
Do not dismiss AIDS cholangiopathy because fever and jaundice are absent; pain plus diarrhea with a dilated duct and high alkaline phosphatase should prompt ERCP.
Treat cholangiopathy with antiretroviral therapy plus pathogen-specific treatment, and add ERCP sphincterotomy for symptomatic papillary stenosis because the scarring does not reverse with antiretrovirals.
Do not exclude Kaposi sarcoma on a negative pinch biopsy; confirm with LANA-1 immunohistochemistry for human herpesvirus eight, taking deeper samples if needed.
Treat Kaposi sarcoma with antiretroviral therapy, and give liposomal doxorubicin only if lesions grow despite immune recovery or advanced disease does not regress.
Start antiretroviral therapy within two weeks of an opportunistic infection diagnosis, but delay it four to six weeks in cryptococcal meningitis.
Continue antiretroviral therapy through IRIS, treat the infection (a macrolide plus ethambutol for MAC), add corticosteroids if severe, and do not give routine MAC prophylaxis to a patient starting effective therapy.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Introduction to HIV as a host
(00:52) - The patient with a CD4 of forty
(01:49) - CD4 tiers and the workup
(03:01) - AIDS cholangiopathy
(04:09) - Treating cholangiopathy and stenosis
(04:40) - Kaposi sarcoma of the stomach
(05:05) - Normal biopsies and LANA-1
(06:10) - When to start antiretroviral therapy
(06:42) - Worsening after treatment: IRIS
(07:47) - MAC prophylaxis and board traps

Chapter 34, Ep 4 of 4: GI in the Immunocompromised Host: Checkpoint Drugs

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

Checkpoint inhibitors release T cells against tumor and also against the gut and liver, so the episode asks which drug, which organ, and which grade. For colitis, it moves from regimen and timing to excluding C. difficile, and CMV after steroids, then endoscopy, stool-frequency grading, steroids, and the seventy-two hour decision to add infliximab or vedolizumab. It then covers restarting by drug class and microscopic colitis. For hepatitis, it covers workup, biopsy versus autoimmune hepatitis, grading by ALT and bilirubin, steroid taper, mycophenolate instead of infliximab, and re-challenge. It closes with the cholangitic variant, pancreatic, gastric, and endocrine events, and board traps.

Topics covered

Checkpoint inhibitor classes and colitis risk
Excluding infection before steroids
Endoscopy and biopsy findings
Stool-frequency grading and treatment
Seventy-two hour biologic decision
Re-challenge by drug class
Microscopic colitis pattern
Checkpoint hepatitis workup and grading
Mycophenolate and second-line liver therapy
Cholangitic variant, pancreatitis, gastritis, endocrine events

Key decisions

Test every patient for C. difficile before escalating steroids, and add CMV PCR in blood and tissue once steroids or biologics have been given.
Grade colitis by stool frequency above baseline: loperamide and continued drug for grade one, hold the drug and give budesonide nine milligrams or prednisone one milligram per kilogram for grade two, and intravenous methylprednisolone one to two milligrams per kilogram with permanent anti-CTLA-4 discontinuation for grade three to four.
If colitis has not responded by seventy-two hours of steroids, add infliximab five to ten milligrams per kilogram or vedolizumab three hundred milligrams, choosing vedolizumab when the liver is also injured or anti-TNF should be avoided.
After grade three to four colitis never restart anti-CTLA-4, but consider anti-PD-1 alone once the patient has recovered with a normal fecal calprotectin and careful counseling.
Grade checkpoint hepatitis by the worse of ALT and bilirubin, and for grade three or four stop the inhibitor permanently and give intravenous methylprednisolone, tapering over four to six weeks.
For steroid-refractory checkpoint hepatitis use mycophenolate one gram twice daily, with tocilizumab eight milligrams per kilogram third-line, and never infliximab.
Add ursodeoxycholic acid to steroids when a cholangitic pattern appears with beaded ducts on MRCP.
Leave an asymptomatic lipase rise without imaging changes untreated, reserving steroids for symptomatic pancreatitis with an imaging correlate.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two cases
(00:59) - Melanoma case and infection workup
(04:12) - Grading and treating colitis
(05:11) - Seventy-two hours and biologic choice
(07:13) - Restarting immunotherapy after colitis
(09:16) - Checkpoint hepatitis presentation and workup
(11:52) - Grading hepatitis and steroid dosing
(13:04) - Mycophenolate instead of infliximab
(14:46) - Cholestatic variant and ursodeoxycholic acid
(15:45) - Pancreatic, gastric, and endocrine events

Chapter 35, Ep 1 of 6: GI in Pregnancy: Hyperemesis and Normal Labs

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

Any lab change that pregnancy itself does not cause is pathologic, and this episode applies that rule to a woman with twins at nine weeks who has hyperemesis gravidarum. It first defines hyperemesis and its risk factors. It then covers normal changes in blood count, creatinine, alkaline phosphatase, GGT, and the exam, and shows why a creatinine of 1.0 and an ALT of 240 are abnormal. Next come the usual causes of abnormal liver tests and the hyperemesis pattern, then imaging chosen for fetal safety. Treatment steps up from pyridoxine with doxylamine to ondansetron, then fluids with thiamine before glucose, then steroids after ten weeks.

Topics covered

Hyperemesis gravidarum definition and risk factors
Normal hematologic and renal changes in pregnancy
Alkaline phosphatase, GGT, AST, and ALT in pregnancy
Physical exam findings that are normal in pregnancy
Causes of abnormal liver tests in pregnancy
Liver test pattern of hyperemesis
Imaging safety: ultrasound, MRI, CT
Procedures and elastography in pregnancy
Stepwise antiemetic therapy
Thiamine before glucose
Steroids and parenteral nutrition for refractory disease

Key decisions

Diagnose hyperemesis gravidarum when vomiting persists more than a week with weight loss over five percent of pre-pregnancy weight, ketonuria, and electrolyte abnormalities.
Treat a creatinine of 1.0 in pregnancy as abnormal, since creatinine normally falls below 0.8, and consider dehydration when the patient is vomiting.
Never attribute a raised AST or ALT to pregnancy itself, and look for a cause such as gallstones, preeclampsia or HELLP, or cholestasis of pregnancy.
Do not worry about an isolated rise in alkaline phosphatase without a rise in GGT, because it comes from the placenta.
Start imaging with ultrasound, use MRI without gadolinium next, and reserve CT for clinical necessity with pelvic shielding, keeping cumulative fetal dose under 50 milligray.
Start treatment with pyridoxine 10 to 25 milligrams three to four times daily, often with doxylamine, then add ondansetron 4 to 8 milligrams every eight hours or a dopamine antagonist if that fails.
Give thiamine 100 milligrams before or with glucose-containing fluids to prevent Wernicke encephalopathy.
Hold methylprednisolone 16 milligrams every eight hours for refractory vomiting until after ten weeks, and use parenteral nutrition only as a last resort.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Welcome and episode overview
(01:07) - Hyperemesis gravidarum defined
(01:52) - Normal lab changes in pregnancy
(02:28) - Liver tests and the exam
(04:13) - Causes of abnormal liver tests
(05:16) - Liver pattern of hyperemesis
(05:58) - Choosing safe imaging
(07:39) - Stepwise antiemetic treatment
(09:00) - Thiamine before glucose
(09:35) - Steroids for refractory vomiting

Chapter 35, Ep 2 of 6: GI in Pregnancy: Reflux and Gallstones

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

This episode follows one pregnant woman who first has heartburn and then gallstones. Pregnancy causes reflux through lower esophageal sphincter pressure, a larger uterus, and slow gastric emptying, yet estrogen protects against ulcers. Treatment climbs from lifestyle changes to calcium carbonate, alginates, or sucralfate, then famotidine, then a proton pump inhibitor, while misoprostol is never given. Endoscopy is kept for alarm features, ideally in the second trimester, and H. pylori waits until after delivery. The gallstone half separates a first mild colic episode, which is watched, from recurrent or complicated disease, which leads to second-trimester cholecystectomy. It then covers ERCP with minimal radiation and the antibiotics that are safe in pregnancy.

Topics covered

Why pregnancy causes reflux
Lifestyle measures first
Antacids, alginates, and sucralfate
Famotidine and proton pump inhibitors
Misoprostol is contraindicated
Ulcer protection and H. pylori timing
Endoscopy indications and sedation
Biliary colic management
Cholecystectomy in the second trimester
ERCP and antibiotic choice

Key decisions

Treat heartburn of pregnancy in steps: lifestyle changes first, then calcium carbonate, alginates, or sucralfate at one gram four times daily, then famotidine, then a proton pump inhibitor.
Stop sodium bicarbonate and aluminum antacids and use calcium carbonate or magnesium hydroxide, because of maternal alkalosis and sodium retention with bicarbonate and fetal exposure concern with aluminum.
Use proton pump inhibitors when needed, including omeprazole despite its old FDA letter category, and never give misoprostol because it causes uterine contractions.
Defer H. pylori testing and treatment until after delivery unless complicated ulcer disease forces the issue.
Reserve endoscopy for dysphagia, GI bleeding, anemia, weight loss out of proportion to nausea of pregnancy, or prolonged vomiting, and do it in the second trimester when possible.
Manage a first mild episode of biliary colic conservatively, and perform laparoscopic cholecystectomy in the second trimester for recurrent colic, complicated gallstone disease, or gallstone pancreatitis.
Reserve ERCP for cholangitis, persistent biliary obstruction, or a large stone with refractory symptoms, using pulsed fluoroscopy, lead shielding, a fetal dose under one millisievert, and propofol sedation.
Treat biliary infection with ampicillin-sulbactam, piperacillin-tazobactam, or a cephalosporin plus metronidazole, and avoid fluoroquinolones and tetracyclines.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(01:12) - Reflux of pregnancy and lifestyle
(01:52) - Antacids, alginates, and sucralfate
(02:55) - H2 blockers and proton pump inhibitors
(04:03) - Misoprostol is never given
(04:32) - Ulcers, H. pylori, and endoscopy
(06:01) - Gallstones and biliary colic
(06:46) - When the gallbladder comes out
(07:26) - ERCP with minimal radiation
(08:18) - Safe antibiotics for biliary infection

Chapter 35, Ep 3 of 6: GI in Pregnancy: Liver Diseases of Pregnancy

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

The organizing idea is that each liver disease unique to pregnancy is sorted by trimester and by a few decisive findings, and that the dangerous ones end only with delivery. The episode starts with intrahepatic cholestasis of pregnancy: how itching with raised total bile acids and a normal GGT confirms it, how the bile acid level sets fetal risk and delivery timing, and what ursodeoxycholic acid, vitamin K, and later follow-up involve. It then covers HELLP syndrome, its Tennessee grading, and its management. Next is acute fatty liver of pregnancy, diagnosed by the Swansea criteria and separated from HELLP. It ends with hepatic infarction and rupture.

Topics covered

Intrahepatic cholestasis of pregnancy presentation
Total bile acids and normal GGT
Transporter genes and hormonal mechanism
Bile acid levels and fetal risk
Ursodeoxycholic acid and vitamin K
Delivery timing by bile acid level
Recurrence, contraception, and follow-up
Preeclampsia and HELLP syndrome
Acute fatty liver of pregnancy and Swansea criteria
Hepatic infarction and rupture

Key decisions

Diagnose intrahepatic cholestasis of pregnancy when nocturnal palm and sole itching comes with total bile acids above 10 micromoles per liter and a normal GGT, after ultrasound excludes obstruction and hepatitis C serology is checked.
Repeat normal labs when itching persists, because itching can come before the labs turn abnormal.
Deliver at 36 to 37 weeks when bile acids are 100 or more, at 36 to 39 weeks for 40 to 99, and at 39 weeks below 40.
Start ursodeoxycholic acid at 10 to 15 milligrams per kilogram per day for maternal benefit, give vitamin K around delivery, and avoid estrogen-containing contraception afterward.
Define HELLP by the Tennessee criteria: LDH of 600 or more, AST of 70 or more, and platelets of 100 thousand or fewer, then grade it by platelet count.
Treat HELLP with delivery, ICU monitoring, blood pressure control, and magnesium sulfate, give antenatal steroids only if delivery is before 32 weeks, and transfuse platelets to above 40 thousand at delivery.
Diagnose acute fatty liver of pregnancy by the Swansea criteria of six or more features, favor it over HELLP when hypoglycemia, high INR, and AST above ALT are present, deliver promptly, and test mother and infant for LCHAD deficiency.
Treat sudden right shoulder pain, falling hemoglobin, and hypotension after delivery as hepatic rupture needing blood products and surgery or embolization, and manage a stable contained subcapsular hematoma conservatively.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases ahead
(02:01) - Confirming cholestasis with bile acids
(04:10) - Bile acid level and fetal risk
(04:58) - Ursodeoxycholic acid and vitamin K
(06:14) - Timing delivery by bile acids
(07:50) - Third trimester emergency: preeclampsia
(09:38) - HELLP definition, grading, and treatment
(12:10) - Acute fatty liver of pregnancy
(14:27) - Telling AFLP from HELLP
(16:29) - Hepatic rupture and shoulder pain

Chapter 35, Ep 4 of 6: GI in Pregnancy: Viral Hepatitis

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

Viral hepatitis in pregnancy is organized around decisions that belong to pregnancy itself. The first patient has chronic hepatitis B found by screening. Her viral load sets whether and when tenofovir starts, her newborn's protection is planned ahead, and the reason for treatment sets when it stops. Her negative hepatitis C test leads to how that infection is screened for, why it is not treated during pregnancy, and how infants are tested. The second patient has acute hepatitis with fever and very high enzymes in the third trimester. Herpes simplex is treated first, before confirmation, and hepatitis A and hepatitis E are weighed, with travel history deciding how dangerous hepatitis E would be.

Topics covered

Hepatitis B screening and viral load
Tenofovir timing in pregnancy
Newborn HBIG and vaccine
Cesarean and breastfeeding in hepatitis B
Stopping antiviral therapy after delivery
Hepatitis C screening and transmission
Why hepatitis C is not treated in pregnancy
Infant testing for hepatitis C
Herpes simplex hepatitis and acyclovir
Hepatitis A and hepatitis E in pregnancy

Key decisions

Treat a pregnant woman with HBV DNA above 200,000 international units per milliliter with tenofovir disoproxil fumarate, starting at 28 to 32 weeks so the viral load is low at delivery.
Give every exposed infant hepatitis B immunoglobulin and the first hepatitis B vaccine dose within 12 hours of birth.
Do not recommend cesarean delivery for hepatitis B or hepatitis C alone, and allow breastfeeding once the infant has had HBIG and vaccine.
When tenofovir was given only to prevent transmission, stop it at delivery or up to 6 weeks after, with ALT monitored for 6 months, and continue it in women with advanced fibrosis.
Screen all pregnant women for hepatitis C at the first prenatal visit, defer direct-acting antivirals until before conception or after delivery, and never use ribavirin.
Test an infant exposed to hepatitis C with HCV RNA at 2 to 6 months and HCV antibody after 18 months, not antibody at 6 weeks.
Start intravenous acyclovir immediately in a pregnant patient with acute hepatitis, especially with fever and upper respiratory symptoms, without waiting for a rash or PCR result.
Use travel history to judge hepatitis E risk, since genotypes 1 and 2 from endemic regions carry high third-trimester mortality, and treat it supportively because ribavirin and interferon are contraindicated.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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

Questions or feedback: hello@boardpearls.com.

(00:00) - Episode introduction and overview
(00:56) - Patient one: hepatitis B at prenatal visit
(01:48) - Viral load and tenofovir timing
(02:23) - Protecting the newborn
(03:01) - When antiviral therapy can stop
(03:30) - Hepatitis C screening and transmission
(04:41) - Hepatitis C treatment and infant testing
(05:36) - Patient two: herpes simplex hepatitis
(06:42) - Empirical acyclovir and hepatitis A
(07:56) - Hepatitis E and travel history

Chapter 35, Ep 5 of 6: GI in Pregnancy: Preexisting Liver Disease

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

The organizing idea is that a woman with chronic liver disease keeps her disease controlled with drugs that are safe for the fetus, and her risk is planned before and after delivery. The episode starts with autoimmune hepatitis, where mycophenolate stops six months before conception, azathioprine and prednisone continue, and flares are watched for after birth. The same principle is applied to PBC, PSC, and Wilson disease. It then turns to compensated cirrhosis, covering risk by MELD, variceal screening, propranolol over nadolol, avoiding vasopressin, splenic artery screening, and delivery planning. It ends with timing and drug choices for pregnancy after liver transplant.

Topics covered

Autoimmune hepatitis and pregnancy
Mycophenolate washout before conception
Azathioprine safety and postpartum monitoring
Primary biliary cholangitis and UDCA
Primary sclerosing cholangitis care
Wilson disease therapy and chelator dosing
Risk assessment in compensated cirrhosis
Variceal screening and treatment
Splenic artery aneurysm and delivery planning
Pregnancy after liver transplant

Key decisions

Continue prednisone and azathioprine through pregnancy in autoimmune hepatitis rather than withdrawing immunosuppression, and do not avoid azathioprine because of its old category D label.
Stop mycophenolate at least six months before conception, and have men taking it wait ninety days after stopping before fathering a child.
Check liver enzymes each trimester in autoimmune hepatitis, then every two to four weeks for six months after delivery, when flares are most likely.
In PBC, continue UDCA, check total bile acids as a first trimester baseline, and avoid obeticholic acid and fibrates.
In Wilson disease, never stop therapy, lower chelator doses by 25 to 50 percent in the third trimester, and prefer a levonorgestrel IUD over a copper IUD.
In cirrhosis, screen for varices within twelve months of conception or by early second trimester endoscopy, treat large varices with propranolol or banding rather than nadolol, and avoid vasopressin for bleeding.
Screen the splenic artery by ultrasound during pregnancy in cirrhosis, and deliver at a tertiary center with a plan for variceal, splenic artery, and uterine bleeding.
After liver transplant, delay pregnancy at least a year, check tacrolimus troughs every two to four weeks, avoid sirolimus and everolimus, and switch mycophenolate to azathioprine before conception.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:54) - Autoimmune hepatitis before conception
(01:52) - Mycophenolate and the washout
(02:23) - Azathioprine and postpartum monitoring
(03:27) - Primary biliary cholangitis in pregnancy
(04:29) - PSC and Wilson disease
(05:51) - Judging risk in compensated cirrhosis
(06:37) - Varices, beta blockers, and vasopressin
(08:19) - Pregnancy after liver transplant
(09:26) - Board traps and summary

Chapter 35, Ep 6 of 6: GI in Pregnancy: IBD and Gastric Bypass

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

The first case teaches that active disease, not active medicine, is the greatest risk in IBD pregnancy. A woman with Crohn disease in remission keeps her adalimumab and azathioprine, while methotrexate, JAK inhibitors, and ozanimod are the drugs to stop or avoid. The episode then covers how IgG anti-TNF drugs cross the placenta and certolizumab does not, how activity is monitored, how delivery is chosen, and how vaccines and breastfeeding follow from the drug. The second case is a woman with severe pain at thirty weeks after Roux-en-Y bypass. It covers internal hernia, why the glucose tolerance test is avoided, and the timing and nutrition that bypass requires.

Topics covered

Active disease as the greater risk in IBD pregnancy
Drugs that continue through pregnancy
Folic acid with sulfasalazine
Methotrexate, JAK inhibitors, and ozanimod
Placental transfer of anti-TNF agents
Monitoring with calprotectin and imaging
Aspirin and thromboembolism prophylaxis
Delivery, infant vaccines, and breastfeeding
Internal hernia and marginal ulcer after Roux-en-Y
Glucose testing and nutrition after bariatric surgery

Key decisions

Continue adalimumab and azathioprine through pregnancy in a patient in remission, because active disease harms pregnancy more than the drugs do.
Give folic acid two to three milligrams a day with sulfasalazine, and stop methotrexate at least three to six months before conception while confirming the new regimen holds remission.
Avoid tofacitinib, upadacitinib, ozanimod, thalidomide, and rifaximin in pregnancy.
Remember that infliximab, adalimumab, and golimumab cross the placenta after week twenty-two while certolizumab pegol does not, and consider timing the last biologic dose six to ten weeks before delivery.
Monitor activity with fecal calprotectin rather than CRP, test for C. difficile in any flare, and start aspirin eighty-one to one hundred fifty milligrams daily by week eleven.
Reserve cesarean for active perianal disease or a rectovaginal fistula, and delay live vaccines for six to twelve months in infants exposed to biologics, except after certolizumab.
Treat severe abdominal pain in pregnancy after Roux-en-Y as an internal hernia until proven otherwise, with CT using shielding and prompt surgical exploration.
Avoid the oral glucose tolerance test after Roux-en-Y and use fasting glucose with home monitoring, delay conception twelve to twenty-four months after surgery, and supplement micronutrients throughout pregnancy and breastfeeding.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and cases
(01:08) - Active disease is the greater risk
(01:59) - Drugs that continue in pregnancy
(02:57) - Drugs to stop before conception
(03:36) - Placental transfer and biologic dosing
(04:43) - Monitoring and preventive measures
(06:00) - Delivery, vaccines, and breastfeeding
(07:35) - Internal hernia after gastric bypass
(09:10) - Glucose testing and nutrition
(10:55) - Board traps in these patients

Chapter 36, Ep 1 of 5: Hereditary GI Cancer Syndromes: Finding Syndromes

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

The organizing idea is that a hereditary cancer syndrome is found by testing tumors, not by relying on pedigree, and that a confirmed diagnosis becomes work for a whole family. The episode begins with universal mismatch repair immunohistochemistry on every colorectal and endometrial cancer. It then shows how the pattern of lost proteins chooses the next test: BRAF and methylation testing for MLH1 and PMS2 loss, germline testing for the other patterns, and EPCAM when MSH2 and MSH6 are lost together. It goes on to panel testing after counseling, coordinated surveillance across organs, cascade testing of first-degree relatives, the limits of GINA, handling a variant of uncertain significance, and risk-reducing surgery.

Topics covered

Universal tumor screening for Lynch syndrome
Mismatch repair IHC versus microsatellite instability
Protein loss patterns and the next test
BRAF V600E and MLH1 methylation testing
Multigene germline panels and pre-test counseling
Coordinated multi-organ surveillance
Cascade testing of first-degree relatives
GINA coverage and its limits
Variant of uncertain significance
Risk-reducing surgery and reproductive counseling

Key decisions

Screen every newly diagnosed colorectal and endometrial cancer for mismatch repair loss by IHC or PCR microsatellite instability testing, whatever the family history, because pedigree alone misses thirty to fifty percent of carriers.
When MLH1 and PMS2 are lost together, test the tumor for BRAF V600E first, then MLH1 promoter methylation, and go to germline sequencing only if both are negative, because about seventy percent of these cancers are sporadic.
When MSH2, MSH6, or PMS2 is lost in isolation, go straight to germline testing without BRAF or methylation testing.
When MSH2 and MSH6 are lost together, include EPCAM on the germline panel, because three-prime EPCAM deletions silence the MSH2 promoter.
Order a multigene panel chosen by the dominant picture (GI cancer, polyposis, or comprehensive hereditary cancer) after pre-test counseling, rather than a single-gene test.
Give a confirmed Lynch carrier a surveillance plan that covers every organ at risk, each with a named owner, and offer hysterectomy with bilateral salpingo-oophorectomy once childbearing is complete.
Offer first-degree relatives single-site testing for the familial variant, and tell them before testing that GINA does not cover life, disability, or long-term care insurance.
Do not act on a variant of uncertain significance: do not test relatives or enter the patient into Lynch surveillance, manage on personal and family history, and recontact periodically for reclassification.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 first patient
(01:48) - Universal tumor screening, not pedigree
(02:44) - Protein loss pattern picks the test
(04:01) - Germline panel and counseling
(05:24) - Second patient: sporadic MLH1 loss
(06:06) - Coordinated surveillance across organs
(06:57) - Cascade testing of relatives
(07:41) - What GINA does not cover
(08:22) - Handling a variant of uncertain significance
(09:07) - Risk-reducing surgery and reproduction

Chapter 36, Ep 2 of 5: Hereditary GI Cancer Syndromes: Lynch Syndrome

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

Lynch syndrome is a mismatch repair defect, and every part of a carrier's program follows from what that defect breaks. The episode follows a 24-year-old MSH2 carrier found by cascade testing. It starts with microsatellite instability and why MSI-high tumors respond to checkpoint inhibitors, then shows how each gene sets organ-specific risk. Next come colonoscopy timing and interval, extended colectomy and pembrolizumab, then urinary tract, stomach, pancreas, prostate and skin surveillance. Aspirin and the gynecologic program with risk-reducing surgery follow. The episode ends with Muir-Torre, Turcot, constitutional mismatch repair deficiency, familial colon cancer syndrome X, and the common board traps.

Topics covered

Mismatch repair and microsatellite instability
Lynch tumor features and pedigree criteria
Gene-specific organ risk
Colonoscopy start age and interval
Extended colectomy and pembrolizumab
Urinary tract and gastric surveillance
Pancreatic, prostate and skin screening
Aspirin chemoprevention
Gynecologic surveillance and hysterectomy
Rare variants and familial colon cancer syndrome X

Key decisions

Start colonoscopy at 20 to 25 or five years before the youngest affected relative's diagnosis, whichever is younger, and repeat every one to two years rather than every ten.
Treat a Lynch colorectal cancer, particularly with MLH1 or MSH2, with extended colectomy (subtotal colectomy with ileorectal anastomosis) rather than segmental resection, then examine the rectum every year.
Use pembrolizumab first-line for advanced MSI-high or mismatch repair-deficient cancer.
In MSH2 carriers, do annual urinalysis with cytology from 30 to 35, and send positive cytology to CT urogram and ureteroscopy.
Offer baseline upper endoscopy with random gastric biopsies at 30 to 40, test for and eradicate H. pylori, and reserve capsule endoscopy or CT enterography for symptoms.
Enroll a carrier in pancreatic surveillance with EUS or pancreatic-protocol MRI only if a first- or second-degree relative had pancreatic cancer, starting at 50 or ten years before the earliest family case.
Offer long-term daily aspirin, anywhere from 81 to 600 mg, because the colorectal benefit appears only after about five years.
Offer hysterectomy with bilateral salpingo-oophorectomy once childbearing is complete, using endometrial biopsy and transvaginal ultrasound every one to two years from 30 to 35 only as a bridge.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and Case Setup
(00:41) - The Patient and Mismatch Repair
(03:14) - Gene-Specific Organ Risk
(04:12) - Colonoscopy Start and Interval
(04:45) - Extended Colectomy and Immunotherapy
(05:40) - Urinary Tract and Stomach
(07:10) - Pancreas, Prostate, and Skin
(08:35) - Aspirin Chemoprevention
(09:19) - Gynecologic Surveillance and Surgery
(10:36) - Rare Forms and Syndrome X

Chapter 36, Ep 3 of 5: Hereditary GI Cancer Syndromes: FAP and MUTYH

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

The episode is organized around the idea that one gene defect, or one repair defect, can produce hundreds of adenomas, and the care that follows is largely about what happens after the colon is removed. It follows a young woman with classic FAP: how the diagnosis is made, including findings outside the colon, when colonoscopy starts, when colectomy is indicated, and which operation fits her rectum. It then turns to duodenal surveillance by Spigelman stage, desmoid tumors, thyroid ultrasound, and reproductive counseling. A second patient shows how recessive MUTYH polyposis hides in a family, and the episode closes with the common board traps.

Topics covered

Classic FAP and APC biology
New mutations and unaffected parents
CHRPE and Gardner syndrome
Attenuated FAP and the I1307K variant
Colonoscopy start ages
Colectomy indications and choice of operation
Spigelman staging of duodenal adenomas
Desmoid tumors after colectomy
Thyroid cancer and reproductive counseling
MUTYH-associated polyposis

Key decisions

Diagnose classic FAP in a young patient with hundreds of adenomas, and do not exclude it because the parents are unaffected, since roughly a quarter of cases are new mutations.
Start annual colonoscopy at puberty, typically ten to twelve, for classic FAP, and at twenty to twenty-five for attenuated FAP or MUTYH polyposis.
Recommend prophylactic colectomy for a polyp larger than ten millimeters, high-grade dysplasia, a rising polyp count, a burden too high to clear endoscopically, or symptoms.
Choose total proctocolectomy with ileal pouch-anal anastomosis when the rectum has a substantial polyp burden, and ileorectal anastomosis with yearly rectal examination only when the rectum is sparse and can be cleared.
Do not use sulindac or celecoxib in place of colectomy, because they reduce polyp number but do not prevent colorectal cancer.
Survey the duodenum with a side-viewing duodenoscope and set the interval by Spigelman stage: every four years for stage zero, three for stage one, two for stage two, and yearly for stage three, with pancreaticoduodenectomy considered at stage four.
Treat a firm, growing mesenteric mass after colectomy as a desmoid until proven otherwise, and consider sulindac or tamoxifen.
Order annual thyroid ultrasound from diagnosis, and when APC testing is negative but siblings are affected and parents are not, test a panel that includes MUTYH.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 episode overview
(00:49) - Young woman with hundreds of adenomas
(02:31) - Eye and tooth clues, Gardner syndrome
(04:09) - Colonoscopy start and colectomy indications
(04:41) - Choosing the operation by rectum
(05:42) - Duodenal surveillance and Spigelman stage
(06:40) - Desmoid tumors after colectomy
(07:34) - Thyroid screening and family planning
(08:23) - Second patient: MUTYH-associated polyposis
(10:26) - Board traps and summary

Chapter 36, Ep 4 of 5: Hereditary GI Cancer Syndromes: Hamartoma Polyps

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

This episode covers the two hamartomatous polyposis syndromes through two patients. A young man with an intussusception and buccal pigmentation has Peutz-Jeghers syndrome from STK11. His main danger is obstruction and short bowel rather than cancer, so large or growing small bowel polyps come out and surveillance starts at eight to ten. Cancer surveillance outside the gut follows, with breast, pancreatic, gynecologic, and testicular programs. A woman with macrocephaly, facial papules, diffuse glycogenic acanthosis, and mixed polyps has Cowden syndrome from PTEN. Her main cancers are breast, thyroid, endometrial, and renal, so she enters multi-organ surveillance, with endoscopy from thirty-five.

Topics covered

Peutz-Jeghers syndrome and STK11
Buccal pigmentation versus freckles
Diagnostic criteria and polyp histology
Intussusception and short bowel risk
Which small bowel polyps to remove
GI and extraintestinal surveillance in Peutz-Jeghers
Cowden syndrome and PTEN
Glycogenic acanthosis and mixed polyps
Cowden cancer risks and surveillance
Board traps

Key decisions

Diagnose Peutz-Jeghers syndrome in a young patient with buccal pigmentation and hamartomatous polyps or intussusception without requiring a family history, and confirm it with germline STK11 testing.
Remove small bowel polyps larger than one centimeter, any symptomatic polyp, and any polyp that grows quickly between studies, using double-balloon enteroscopy, intraoperative enteroscopy, or surgical polypectomy.
Remove stomach and colon polyps once they exceed five millimeters.
Start upper endoscopy and colonoscopy at eight to ten, with small bowel capsule or MR enterography every one to three years, to prevent intussusception and short bowel.
In Peutz-Jeghers carriers, start breast MRI at twenty-five in women and annual pancreatic EUS or MRI from thirty to thirty-five.
Suspect Cowden syndrome from macrocephaly, facial trichilemmomas, diffuse glycogenic acanthosis, and polyps of mixed histology, and use a germline panel of PTEN, SMAD4, BMPR1A, and STK11 when histology is ambiguous.
Refer Cowden patients into multi-organ surveillance: breast exam from twenty-five, annual thyroid ultrasound from diagnosis, endometrial biopsy from thirty-five, and renal imaging from forty.
Start colonoscopy and upper endoscopy at thirty-five in Cowden syndrome, repeated every three to five years, or every one to three years when polyps are found.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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
(00:44) - Young man with intussusception
(01:50) - Recognizing and confirming Peutz-Jeghers
(03:36) - Obstruction as the main danger
(04:36) - Which polyps must come out
(05:34) - Intestinal surveillance schedule
(06:17) - Cancers outside the gut
(08:00) - Woman with esophageal clue: Cowden
(11:12) - Cowden cancer risks and surveillance
(13:29) - Board traps and summary

Chapter 36, Ep 5 of 5: Hereditary GI Cancer Syndromes: CDH1 and BRCA2

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

Both cancers are hard to find early, so management rests on the gene and the family history rather than on a normal test. A CDH1 carrier is offered prophylactic total gastrectomy in her twenties because diffuse signet-ring cancer grows beneath normal-looking mucosa. Cambridge protocol endoscopy is the fallback, and breast MRI starts at thirty. GAPPS is told apart from hereditary diffuse gastric cancer and FAP by where the disease sits. Pancreatic surveillance is offered above about five percent lifetime risk. Some genes qualify alone and others need an affected relative. The episode then covers start age, test choice, PRSS1, and germline testing for every pancreatic cancer.

Topics covered

Hereditary diffuse gastric cancer and CDH1
Testing criteria for CDH1
Why endoscopy misses diffuse gastric cancer
Prophylactic total gastrectomy and the Cambridge protocol
Breast surveillance in CDH1 carriers
GAPPS versus hereditary diffuse gastric cancer and FAP
Who qualifies for pancreatic surveillance
Start age and EUS or MRI surveillance
PRSS1 and hereditary pancreatitis
Germline testing, platinum, and PARP inhibitors

Key decisions

Offer a confirmed CDH1 carrier prophylactic total gastrectomy with Roux-en-Y reconstruction, typically between ages twenty and thirty, after multidisciplinary counseling, with lifelong vitamin B12 and iron afterward.
Do not trust a normal endoscopy in a CDH1 carrier, because diffuse signet-ring cancer lies beneath intact mucosa and random biopsies miss it.
If a carrier declines or delays surgery, do annual upper endoscopy under the Cambridge protocol with at least thirty to fifty random biopsies from every gastric region, and warn that a clean result is not a guarantee.
Start annual breast MRI plus mammography at age thirty in female CDH1 carriers for lobular breast cancer, and offer risk-reducing bilateral mastectomy as an option after counseling.
Offer pancreatic surveillance only above about five percent absolute lifetime risk: STK11, CDKN2A, and PRSS1 carriers qualify on the gene alone, while BRCA1, BRCA2, PALB2, ATM, and Lynch carriers need an affected relative.
Start pancreatic surveillance at fifty, or ten years before the earliest family case, for BRCA1, BRCA2, PALB2, ATM, Lynch, and familial kindreds; at forty for CDKN2A and PRSS1; and at thirty to thirty-five for STK11.
Use annual EUS or pancreatic-protocol MRI with MRCP, usually alternating them every twelve months, and send a new cyst, solid lesion, or main duct dilation for EUS-guided sampling and multidisciplinary review.
Send germline testing for every patient at the diagnosis of pancreatic cancer, because BRCA1, BRCA2, or PALB2 carriers with metastatic disease benefit from platinum chemotherapy and olaparib maintenance.

This is an AI-generated podcast, and some pronunciations may be imperfect. Thank you for your understanding, and we hope you enjoyed this content.

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 and two patients
(00:52) - CDH1 carrier and syndrome basics
(02:48) - Why endoscopy misses diffuse cancer
(03:48) - Gastrectomy and Cambridge fallback
(05:28) - Breast cancer risk in CDH1
(06:03) - GAPPS versus HDGC and FAP
(07:06) - BRCA2 carrier with affected father
(08:07) - Who qualifies for surveillance
(10:04) - Surveillance test and PRSS1
(12:09) - Germline testing and PARP inhibitors