Board Pearls

Board Pearls
  • 4.8 (4)
  • Medicine
  • Series

The most complete gastroenterology board-review podcast on the web, and it is entirely free. This is the GI series from Board Pearls: board review built around clinical reasoning, not recall. Every episode takes one high-yield topic and works it the way you would on rounds: a case to anchor it, the framework that sorts the differential, and the specific decisions the exam rewards. No trivia, no textbook dictation, just the thinking that earns the point. Over 100 episodes span the full blueprint across nine modules (esophagus, stomach and duodenum, small bowel, colon, pelvic floor, liver, pancreas and biliary, endoscopy, and the cross-cutting topics), grouped by chapter and built from the guidelines and pivotal trials the boards are written from: ACG, AGA, AASLD, and ASGE. Pair it with the written curriculum, question bank, and AI tutor at boardpearls.com. Questions or feedback: hello@boardpearls.com.

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  1. Episode 1

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

    Episode one of the GI Emergencies chapter treats massive upper GI bleeding as a resuscitation problem before it is an endoscopic one. The organizing idea is a clock that starts when the patient arrives, where permissive hypotension protects the clot and the wrong decision made confidently is worse than none. It moves through the timeline the patient is actually on: restrictive transfusion, the balanced massive transfusion ratio and the calcium citrate chelates, anticoagulation reversal run in parallel rather than as a delay, and field-clearing erythromycin before endoscopy. It closes on the two recognition stems the boards reward, the herald bleed of an aortoenteric fistula and the two arteries where failed hemostasis sends you to interventional radiology.   Topics covered Upper GI bleeding as a resuscitation problem Restrictive transfusion target and its exceptions Massive transfusion protocol and calcium repletion Anticoagulation reversal in the first hour Pre-endoscopic erythromycin and why TXA fails Airway protection and endoscopy timing Aortoenteric fistula recognition Salvage angiography for failed hemostasis   Key decisions Transfuse to a restrictive hemoglobin trigger of seven with a target of seven to nine, raising the trigger to eight only in active acute coronary syndrome, and transfuse empirically in uncontrolled hemorrhage because the lab hemoglobin lags real-time loss by thirty to sixty minutes. Activate the massive transfusion protocol at anticipated need over ten units of red cells in twenty-four hours or four in one hour, delivering a balanced one-to-one-to-one ratio and repleting ionized calcium that citrate chelates. Reverse warfarin with four-factor prothrombin complex concentrate rather than fresh frozen plasma, reverse dabigatran with idarucizumab five grams and apixaban or rivaroxaban with andexanet alfa, and run reversal in parallel with endoscopy rather than letting the INR delay it. Give erythromycin two hundred fifty milligrams intravenously thirty to ninety minutes before endoscopy to clear the gastric field, but do not give tranexamic acid because it adds venous thromboembolism risk without benefit in arterial spurting. Scope non-variceal upper GI bleeding within twenty-four hours and variceal hemorrhage within twelve, reserving sub-six-hour endoscopy for uncontrollable hemorrhage or suspected aortoenteric fistula. Suspect aortoenteric fistula in a prior aortic graft patient with a herald bleed and image with CT angiography for periaortic gas before EGD, and send failed dual-therapy hemostasis to embolization of the gastroduodenal or left gastric artery.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Bleeding as a resuscitation problem (01:06) - The restrictive transfusion target (02:22) - Massive transfusion protocol and calcium (03:16) - Reversing anticoagulation in parallel (04:24) - Erythromycin, TXA, and airway (05:43) - Endoscopy timing by bleed type (06:31) - The aortoenteric fistula trap (07:03) - Salvage angiography when hemostasis fails

  2. Episode 2

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

    Episode two moves below the ligament of Treitz and then to the mesenteric vessels, carrying the same rule forward: pick the imaging that feeds the next intervention and recognize the pattern that flips the algorithm. Acute lower GI bleeding branches on hemodynamic stability, CT angiography for the unstable patient because it hands interventional radiology the anatomy and colonoscopy at twelve to twenty-four hours for the stable one, with the etiologies read by pattern. Colon ischemia separates from diverticular bleeding on pain before bleeding, and isolated right colon ischemia flips the workup toward mesenteric imaging. Acute mesenteric ischemia turns on recognizing pain out of proportion to exam and reaching for CT angiography before lactate rises, then matching intervention to each of four etiologies.   Topics covered Acute lower GI bleeding and the BUN-to-creatinine clue Hemodynamic split: CT angiography versus colonoscopy Diverticular, angiodysplastic, and post-polypectomy bleeding Endoscopic hemostasis and the no-serosa rule Colon ischemia and pain before bleeding Isolated right colon ischemia flipping the algorithm Four etiologies of acute mesenteric ischemia Etiology-specific intervention The lactate trap and initial bundle   Key decisions Send the hemodynamically unstable lower GI bleeder to CT angiography first because it images extravasation at about zero point three milliliters per minute and gives IR the anatomy for superselective embolization, and send the stable patient to colonoscopy at twelve to twenty-four hours after rapid polyethylene glycol prep. Suspect a brisk upper source in about fifteen percent of presumed lower GI bleeds and when the BUN-to-creatinine ratio exceeds thirty, and exclude anorectal sources by anoscopy before colonoscopy referral. Treat diverticular and post-polypectomy bleeding with clips or bands rather than deep thermal therapy because the diverticular wall and thinned resection base lack serosa and coagulate to perforation. Distinguish colon ischemia by cramping pain preceding hematochezia within twenty-four hours, treat mild disease supportively, and add antibiotics when the white count exceeds fifteen thousand, BUN exceeds twenty, or ulceration is severe. Image the mesenteric vessels in isolated right colon ischemia because that SMA watershed-equivalent territory can herald silent SMA occlusion, and anchor suspected acute mesenteric ischemia on pain out of proportion with CT angiography now, not lactate first. Match the mesenteric intervention to etiology: embolectomy for SMA embolus, revascularization with bypass or stenting for SMA thrombosis, intra-arterial papaverine with low-flow correction for NOMI, and systemic anticoagulation for mesenteric venous thrombosis, with peritoneal signs sending everyone to laparotomy.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Below the ligament of Treitz (00:49) - Defining the bleed and the BUN clue (01:47) - The hemodynamic split (02:56) - The stable patient and colonoscopy (03:42) - Etiologies by anatomy and pattern (06:11) - Colon ischemia and pain before bleeding (07:51) - Acute mesenteric ischemia (08:40) - Four etiologies, four interventions (13:20) - The lactate trap and management bundle

  3. Episode 3

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

    Episode three works two mechanical emergencies that each hand you a recognition cue and a defined intervention with a clock embedded in it. For foreign bodies the urgency of removal follows the mechanism of injury, not the politeness of the object, sorting into three timing tiers from two-hour disc batteries to blunt objects that never come out. The food bolus doubles as the eosinophilic esophagitis biopsy opportunity that closes if you do not take it at the same procedure. For caustic ingestion, substance category drives the injury pattern, the airway is the first priority, and the Zargar grade at endoscopy drives short-term feeding and monitoring while late stricture and squamous cell carcinoma risk drive long-term surveillance.   Topics covered Urgency follows mechanism, not the object Three timing tiers for removal Disc batteries, sharps, and magnets Drug packers versus stuffers Food bolus and the eosinophilic esophagitis gateway Alkali versus acid injury patterns Airway priority and contraindicated interventions Zargar grading and feeding safety Late strictures and cancer surveillance   Key decisions Remove an esophageal disc battery within two hours because hydroxide drives alkaline liquefactive necrosis within two hours and can perforate, and remove esophageal obstruction with unmanageable secretions or a sharp esophageal object within six hours. Remove food bolus without complete obstruction, non-sharp esophageal objects, gastric or duodenal sharps, objects longer than six centimeters, and reachable high-power magnets within twenty-four hours, while managing blunt asymptomatic post-duodenal objects expectantly. Do not endoscope body packers or stuffers because rupture during retrieval risks a fatal toxic dose, reserving laparotomy for symptoms of leak. Take at least four biopsies from proximal and distal esophagus at the same procedure when no eosinophilic esophagitis diagnosis exists, since roughly half of adult food bolus impactions trace to it and the histologic threshold is fifteen eosinophils per high-power field. Prioritize the airway in caustic ingestion because alkali can cause supraglottic edema, and avoid induced emesis, activated charcoal, chemical neutralization, and acute nasogastric intubation. Endoscope caustic ingestion within twelve to twenty-four hours and let the Zargar grade decide: grades zero through two-A feed and observe, two-B and three delay feeding with ICU monitoring and surgical consult, and grade four operate, with dilation in one-to-two-millimeter increments toward fourteen to fifteen millimeters for late strictures.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Cue, mechanism, threshold, act (00:42) - Urgency follows the mechanism (01:05) - The three timing tiers (02:44) - The twenty-four hour list (04:06) - Food bolus and the EoE biopsy (05:50) - Caustic ingestion by substance (07:22) - Airway first, contraindicated moves (08:54) - The Zargar grade drives management (10:15) - Late strictures and cancer risk

  4. Episode 4

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

    Episode four closes the chapter with two emergencies that run on the same cue-plus-threshold-plus-intervention shape, where the threshold is a mechanism in disguise. For esophageal perforation the clock starts when the wall tears, and the twenty-four hour window separates clean primary closure from sealed stent and drainage because the mediastinal tissue planes change from friend to enemy. For acute colonic pseudo-obstruction the clock starts when the colon stops moving, and a four-step algorithm anchored by a cecal-diameter threshold and a neostigmine-with-cardiac-monitoring decision moves the patient from the conservative bundle to pharmacology to decompression to surgery. Laplace's law explains why the cecum fails first and the neostigmine contraindication list explains why every dose comes with atropine at the bedside.   Topics covered Causes of esophageal perforation and Boerhaave The Mackler triad and recognition stem Perforation site and left-sided effusion Water-soluble contrast imaging and antibiotics The twenty-four hour repair-versus-stent window Ogilvie syndrome and autonomic imbalance Ruling out mechanical obstruction Neostigmine and cardiac monitoring Colonoscopic decompression and surgery   Key decisions Image suspected esophageal perforation with CT chest and oral water-soluble contrast looking for pneumomediastinum, avoiding barium initially because barium granulomatous mediastinitis is a feared complication, since a normal chest radiograph does not exclude the diagnosis. Cover both mediastinal compartments with piperacillin-tazobactam or a meropenem-based regimen plus antifungal coverage in severe disease, and place nasogastric decompression under fluoroscopic guidance to avoid the leak. Repair Boerhaave and large iatrogenic perforations primarily within twenty-four hours while tissue planes hold, shift beyond twenty-four hours to covered self-expanding metal stents with drainage, and clip small iatrogenic perforations caught at the index endoscopy. Rule out mechanical obstruction and volvulus first in suspected Ogilvie syndrome with CT showing a dilated colon without a transition point, because a mechanical cause will not respond to neostigmine and may perforate during conservative management. Manage the first forty-eight to seventy-two hours conservatively with decompression, electrolyte correction, and stopping opioids and anticholinergics, then escalate at cecal diameter over twelve centimeters, persistent distension, or impending perforation because Laplace's law makes the cecum fail first. Give neostigmine two milligrams intravenously over three to five minutes with mandatory cardiac monitoring and atropine at the bedside, honor the contraindication list, and move to colonoscopic decompression then surgery when it fails or is contraindicated.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Two tears, one shape (00:42) - Causes of esophageal perforation (01:16) - The Mackler triad and recognition (02:14) - Imaging and antibiotic coverage (03:42) - The twenty-four hour threshold (05:14) - Ogilvie syndrome and autonomic imbalance (06:46) - Ruling out mechanical obstruction (09:19) - Neostigmine with atropine at the bedside (10:40) - Decompression and surgery

  5. Episode 5

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

    Episode one of the GI Nutrition chapter builds the inpatient nutrition framework and the enteral access decisions. The organizing idea is that the labs lie and the instinct to feed faster is usually wrong. Refeeding syndrome is what happens when a starvation-adapted patient meets a carbohydrate load, so the active intervention is restraint with thiamine before glucose. Hospital malnutrition is not what a low albumin says it is, so GLIM separates the phenotypic deficit from the etiologic cause. And the route of nutrition follows the gut's functional state, with a functional gut winning every time.   Topics covered Refeeding syndrome and the electrolyte shift Thiamine before glucose and Wernicke NICE high-risk criteria Restrained calorie reintroduction Albumin as an inflammatory marker GLIM phenotypic plus etiologic criteria Functional gut and enteral access selection PEG techniques and complications Tube-feed diarrhea and the medication list   Key decisions Refeeding calories start at ten to twenty kilocalories per kilogram per day and advance over four to seven days, with thiamine two hundred to three hundred milligrams given before any glucose load and continued daily for five to seven days. Any single NICE criterion, a BMI below sixteen, weight loss above fifteen percent, more than ten days of negligible intake, or pre-feeding hypokalemia, hypophosphatemia, or hypomagnesemia, makes a patient high risk for refeeding. Albumin and prealbumin are negative acute-phase reactants suppressed by IL-six and TNF-alpha, so they are excluded from GLIM criteria and should never be treated as nutrition markers in an inflamed patient. GLIM malnutrition requires one phenotypic criterion, weight loss, low BMI, or reduced muscle mass, plus one etiologic criterion, reduced intake or assimilation or inflammation. A functional gut wins, so short-term feeds under four to six weeks use nasogastric or nasojejunal tubes and longer-term feeds use percutaneous endoscopic gastrostomy. PEG does not prevent aspiration or extend survival in advanced dementia and is not standard of care, so families should be counseled against it. Tube-feed diarrhea is worked up by reviewing the medication list for sorbitol vehicles, checking recent antibiotics, and sending a stool C. diff test before any formula change.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - The framework and the organizing idea (00:31) - Refeeding syndrome and the electrolyte crash (03:01) - NICE high-risk criteria and restrained feeding (05:00) - Malnutrition versus catabolism, and the albumin trap (06:30) - GLIM phenotypic and etiologic criteria (09:19) - A functional gut wins: enteral access (10:05) - PEG techniques and complications (13:00) - Tube-feed diarrhea and the medication list

  6. Episode 6

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

    Episode two takes the patient whose gut cannot do the work. Parenteral nutrition is a tool for a non-functional gut, with composition rules that follow from chemistry rather than biology and indication discipline that follows from trial data. Its long-term complications are driven by the loss of enteral stimulation, from gallbladder stasis and IFALD to manganese parkinsonism and catheter biofilm infection. Short bowel syndrome then turns on residual anatomy, where the colon's presence or absence determines both the rehabilitation trajectory and the complication pattern, and teduglutide's trophic effect explains both its efficacy and its surveillance burden.   Topics covered When parenteral nutrition is the answer Composition rules from chemistry Lipid emulsions and IFALD Indication discipline versus cachexia Cholelithiasis and manganese parkinsonism Catheter-related bloodstream infection Short bowel anatomic phenotypes Teduglutide and surveillance Enteric hyperoxaluria and D-lactic acidosis   Key decisions Dextrose in parenteral nutrition provides three and four-tenths kilocalories per gram, not four, because pharmaceutical dextrose is a monohydrate whose water contributes no calories, so calculating at four per gram overshoots. Calcium and phosphate cannot be co-administered freely because they precipitate, so compounding uses solubility tables or split bags, and acetate is the buffer of choice because it is metabolized to bicarbonate. Parenteral nutrition is reserved for a non-functional gut and is contraindicated or harmful in metastatic cancer cachexia and inferior to enteral feeding in mild-to-moderate acute pancreatitis. Even enteral feeding at twenty to thirty percent of caloric needs restores CCK-driven gallbladder contraction and reduces parenteral-nutrition-associated cholelithiasis. Manganese is removed from parenteral nutrition formulations once cholestasis develops or once globus pallidus T1 hyperintensity appears, since impaired biliary excretion drives basal ganglia accumulation and parkinsonism. Oral rehydration in short bowel uses sodium ninety milliequivalents per liter with glucose ninety to one hundred ten millimoles per liter to match SGLT-one stoichiometry, because plain water and most sports drinks produce net water loss. Teduglutide requires a baseline colonoscopy with polyp removal within six months before initiation, a follow-up at the end of year one, and surveillance every five years thereafter, and is contraindicated in active GI malignancy.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - The non-functional gut (00:26) - When the gut cannot do the work (01:01) - Composition rules from chemistry (02:05) - Lipid emulsions and IFALD (03:52) - Indication discipline and the bad uses (05:12) - Long-term complications and manganese (08:36) - Short bowel syndrome by anatomy (12:36) - Teduglutide and its surveillance (13:54) - Hyperoxaluria and D-lactic acidosis

  7. Episode 7

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

    Episode three reads the vitamins the way the boards test them, where every micronutrient produces a stereotyped phenotype that is the recognition cue on a stem. Behind each cue is a biochemical mechanism, and the same mechanism predicts the at-risk population and the replacement strategy. Memorizing the symptom list is the wrong frame; learning the mechanism lets the phenotype, the population, and the treatment fall out of it. The fat-soluble vitamins share a bile-salt absorption requirement, and the water-soluble vitamins carry the acute decisions, thiamine before glucose and B12 before folate.   Topics covered Bile-salt requirement for fat-soluble vitamins Vitamin A night blindness and toxicity Vitamin D metabolic bone disease Vitamin E neuropathy, hemolysis, and NASH Vitamin K, warfarin, and the NPO patient Essential fatty acid deficiency Thiamine and Wernicke encephalopathy B12 absorption steps and pernicious anemia B12-versus-folate masking trap   Key decisions Anything that disrupts the enterohepatic bile-acid cycle, cholestyramine, cholestasis, ileal disease, cystic fibrosis, or unsupplemented parenteral nutrition, deletes all four fat-soluble vitamins plus essential fatty acids. Chronic vitamin A intake above roughly fifty thousand international units per day activates hepatic stellate cells into myofibroblasts and produces perisinusoidal fibrosis and portal hypertension, while a single large dose instead causes pseudotumor cerebri. Vitamin E at eight hundred international units daily improves histology only in non-diabetic biopsy-proven NASH, and extension beyond that phenotype is unsupported given increased prostate cancer and hemorrhagic stroke risk at high doses. An NPO patient on warfarin started on broad-spectrum antibiotics spikes the INR within days because both dietary and colonic bacterial vitamin K sources are eliminated at once. Medium-chain triglyceride oil cannot prevent essential fatty acid deficiency because its eight-to-twelve-carbon chains lack the eighteen-carbon backbone, so intravenous lipid emulsion one to two times weekly is required. Thiamine must precede any glucose load in an at-risk patient, given empirically as five hundred milligrams intravenously three times daily, because glucose without thiamine precipitates Wernicke encephalopathy. Always check B12 before starting folate, because high-dose folate corrects the megaloblastic anemia while subacute combined degeneration of the cord progresses unchecked.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Deficiencies as recognition cues (01:02) - The fat-soluble bile-salt requirement (02:44) - Vitamin A: night blindness and toxicity (04:54) - Vitamin E: neuropathy, hemolysis, and NASH (06:23) - Vitamin K, warfarin, and the NPO patient (09:38) - Thiamine and Wernicke encephalopathy (11:33) - B12 absorption in four steps (13:52) - The B12-versus-folate masking trap

  8. Episode 8

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

    Episode four closes the chapter with the minerals and trace elements, which run on the same logic as the vitamins: each element has a specific biochemical role and a specific exposure or pathology context that produces its phenotype. The boards favor the pairs that turn on a single mechanism, zinc inducing metallothionein to trap copper, cholestasis blocking biliary manganese excretion, and Brazil nuts concentrating selenium. Each element pairs a recognition cue with a population and a replacement strategy, the same teaching unit used for the vitamins.   Topics covered Iron deficiency and malabsorptive anatomy PPI-induced hypomagnesemia and TRPM6 Zinc acrodermatitis and dysgeusia Copper myeloneuropathy from zinc excess Copper deficiency mimicking B12 Manganese toxicity in parenteral nutrition Selenium cardiomyopathy and selenosis Chromium and glucose intolerance D-lactic acidosis in short bowel   Key decisions PPI-induced hypomagnesemia works through impaired TRPM6 channel function, and the testable feature is kinetic asymmetry: magnesium normalizes within about a week of discontinuation but recurs within about two weeks of rechallenge. Vonoprazan or another potassium-competitive acid blocker is the alternative for the patient with recurrent PPI-induced hypomagnesemia because it does not lower magnesium. Zinc deficiency is repleted with oral zinc sulfate two hundred twenty milligrams, fifty milligrams elemental, daily, and refractory hepatic encephalopathy in cirrhosis can reflect zinc deficiency through its urea-cycle cofactor role. Chronic zinc excess from denture cream or supplements induces enterocyte metallothionein that traps copper, producing copper deficiency, so the treatment is copper two milligrams daily plus removing the zinc source. Copper deficiency mimics B12 subacute combined degeneration with myeloneuropathy, anemia, and neutropenia, and the discriminators are a normal B12 level and a zinc-excess history. Manganese is removed from parenteral nutrition once cholestasis develops or globus pallidus T1 hyperintensity appears, because impaired biliary excretion drives basal ganglia accumulation and levodopa-unresponsive parkinsonism. Selenium deficiency on long-term unsupplemented parenteral nutrition produces Keshan cardiomyopathy, while chronic Brazil nut overconsumption, more than three per day, produces selenosis with alopecia, brittle nails, and garlic breath.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: hello@boardpearls.com. (00:00) - Minerals as single-mechanism pairs (00:52) - Iron and the malabsorptive anatomies (01:22) - PPI-induced hypomagnesemia (02:32) - Zinc: acrodermatitis and altered taste (03:47) - Copper deficiency from zinc excess (05:35) - Manganese in parenteral nutrition (06:28) - Selenium cardiomyopathy and selenosis (07:44) - D-lactic acidosis in short bowel

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About

The most complete gastroenterology board-review podcast on the web, and it is entirely free. This is the GI series from Board Pearls: board review built around clinical reasoning, not recall. Every episode takes one high-yield topic and works it the way you would on rounds: a case to anchor it, the framework that sorts the differential, and the specific decisions the exam rewards. No trivia, no textbook dictation, just the thinking that earns the point. Over 100 episodes span the full blueprint across nine modules (esophagus, stomach and duodenum, small bowel, colon, pelvic floor, liver, pancreas and biliary, endoscopy, and the cross-cutting topics), grouped by chapter and built from the guidelines and pivotal trials the boards are written from: ACG, AGA, AASLD, and ASGE. Pair it with the written curriculum, question bank, and AI tutor at boardpearls.com. Questions or feedback: hello@boardpearls.com.

Information

  • Creator
    Board Pearls
  • Episodes
    116
  • Seasons
    9
  • Rating
    Clean
  • Copyright
    © 2025
  • Show Website
    Board Pearls