Board Pearls

By Board Pearls

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 ep... more

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How many episodes does Board Pearls have?

The podcast currently has 153 episodes available.

Board Pearls episodes:

July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Nutrition
Read this episode: boardpearls.com/gi/episodes/gi-nutrition-ep4
Questions or feedback: [email protected].
(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
...more
11min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Nutrition
Read this episode: boardpearls.com/gi/episodes/gi-nutrition-ep3
Questions or feedback: [email protected].
(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
...more
21min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Nutrition
Read this episode: boardpearls.com/gi/episodes/gi-nutrition-ep2
Questions or feedback: [email protected].
(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
...more
18min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Nutrition
Read this episode: boardpearls.com/gi/episodes/gi-nutrition-ep1
Questions or feedback: [email protected].
(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
...more
16min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Emergencies
Read this episode: boardpearls.com/gi/episodes/gi-emergencies-ep4
Questions or feedback: [email protected].
(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
...more
14min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Emergencies
Read this episode: boardpearls.com/gi/episodes/gi-emergencies-ep3
Questions or feedback: [email protected].
(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
...more
14min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Emergencies
Read this episode: boardpearls.com/gi/episodes/gi-emergencies-ep2
Questions or feedback: [email protected].
(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
...more
17min
July 16, 2026Chapter 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.

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: GI Emergencies
Read this episode: boardpearls.com/gi/episodes/gi-emergencies-ep1
Questions or feedback: [email protected].
(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
...more
10min
July 16, 2026Chapter 30, Ep 5 of 5: Serrated Pathway, Lynch, and Special Populations
Episode five closes the chapter on the other half of why colonoscopy quality matters, the serrated pathway where missed right-sided lesions become interval cancer. Sessile serrated lesions run through BRAF V600E, CIMP-high hypermethylation, MLH1 silencing, and microsatellite instability, which is why sessile serrated lesion detection rate is its own quality metric. That molecular route drives the Lynch reflex tree: mismatch repair immunohistochemistry, then BRAF and MLH1 methylation to triage sporadic disease, with the other loss patterns going straight to germline testing because sporadic biology cannot explain them. The special populations then bend the standard algorithm one mechanism at a time, as the kidneys forbid phosphate, the liver forbids morphine, the fetus forbids first-trimester benzodiazepines, and the IBD colon demands chromoendoscopy.

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

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

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: Colonoscopy Practice and Quality
Read this episode: boardpearls.com/gi/episodes/colonoscopy-practice-and-quality-ep5
Questions or feedback: [email protected].
(00:00) - Why serrated quality matters
(00:51) - Serrated pathway biology
(01:54) - Lynch reflex testing
(02:42) - BRAF as the discriminator
(03:50) - Other MMR loss patterns
(05:02) - Serrated polyposis syndrome
(06:47) - Special populations by physiology
(07:25) - Pregnancy, cirrhosis, and ESRD
(11:51) - IBD surveillance and antithrombotics
...more
17min
July 16, 2026Chapter 30, Ep 4 of 5: Post-Polypectomy Adverse Events
Episode four teaches the post-polypectomy adverse event set through mechanism, because each event has a distinct anatomic or thermal correlate that determines the next move. Immediate bleeding is treated at the visible vessel while delayed bleeding returns for endoscopic hemostasis on the still-recognizable scar, and the prophylactic-clip decision turns on proximal location and antithrombotic risk rather than reflex. Perforation forces a closure decision driven by defect age and size, while post-polypectomy electrocoagulation syndrome mimics perforation but lacks free air and resolves on bowel rest. The unifying frame is that the recognition cue tells you the mechanism and the mechanism tells you the response, so hematochezia, free air, focal peritonitis without free air, and left shoulder pain are not interchangeable.

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

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

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: Colonoscopy Practice and Quality
Read this episode: boardpearls.com/gi/episodes/colonoscopy-practice-and-quality-ep4
Questions or feedback: [email protected].
(00:00) - Reading events by mechanism
(00:33) - Post-polypectomy bleeding
(01:36) - The prophylactic clip question
(02:25) - Perforation and closure decisions
(03:44) - Electrocoagulation syndrome
(04:49) - Splenic injury
(05:27) - Cues, mechanisms, and responses
...more
7min

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