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

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Key decisions

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Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Small Bowel Mucosal Disease

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• (00:00) - When celiac is excluded

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

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Key decisions

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Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Celiac Disease and Sprue Spectrum

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• (00:00) - The non-responsive celiac differential

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

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Key decisions

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Celiac Disease and Sprue Spectrum

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• (00:00) - Mechanism: gluten to villous atrophy

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

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Upper GI Bleeding

Read this episode: boardpearls.com/gi/episodes/upper-gi-bleeding-ep2

Questions or feedback: [email protected].

• (00:00) - Introduction

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

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Key decisions

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Upper GI Bleeding

Read this episode: boardpearls.com/gi/episodes/upper-gi-bleeding-ep1

Questions or feedback: [email protected].

• (00:00) - The fixed sequence: perfusion, diagnosis, endoscopy

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

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Gastric and Small Bowel Motility

Read this episode: boardpearls.com/gi/episodes/gastric-and-small-bowel-motility-ep2

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• (00:00) - Introduction: the clean structural workup

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

Topics covered

Key decisions

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Gastric and Small Bowel Motility

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• (00:00) - Three failure points

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

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Gastritis, Gastric Cancers, and Submucosal Tumors

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• (00:00) - Introduction: histology and driver as discriminator

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

Topics covered

Key decisions

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Gastritis, Gastric Cancers, and Submucosal Tumors

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• (00:00) - Introduction: gastrin ties it together

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

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Key decisions

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Peptic Ulcer Disease and H. pylori

Read this episode: boardpearls.com/gi/episodes/pud-and-h-pylori-ep2

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• (00:00) - Introduction: the non-H. pylori ulcers