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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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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

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: [email protected]. (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