GI board review podcast episodes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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

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

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

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

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

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

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

The organizing idea is that a hereditary cancer syndrome is found by testing tumors, not by relying on pedigree, and that a confirmed diagnosis becomes work for a whole family. The episode begins with universal mismatch repair immunohistochemistry on every colorectal and endometrial cancer. It then shows how the pattern of lost proteins chooses the next test: BRAF and methylation testing for MLH1 and PMS2 loss, germline testing for the other patterns, and EPCAM when MSH2 and MSH6 are lost together. It goes on to panel testing after counseling, coordinated surveillance across organs, cascade testing of first-degree relatives, the limits of GINA, handling a variant of uncertain significance, and risk-reducing surgery.

Lynch syndrome is a mismatch repair defect, and every part of a carrier's program follows from what that defect breaks. The episode follows a 24-year-old MSH2 carrier found by cascade testing. It starts with microsatellite instability and why MSI-high tumors respond to checkpoint inhibitors, then shows how each gene sets organ-specific risk. Next come colonoscopy timing and interval, extended colectomy and pembrolizumab, then urinary tract, stomach, pancreas, prostate and skin surveillance. Aspirin and the gynecologic program with risk-reducing surgery follow. The episode ends with Muir-Torre, Turcot, constitutional mismatch repair deficiency, familial colon cancer syndrome X, and the common board traps.

The episode is organized around the idea that one gene defect, or one repair defect, can produce hundreds of adenomas, and the care that follows is largely about what happens after the colon is removed. It follows a young woman with classic FAP: how the diagnosis is made, including findings outside the colon, when colonoscopy starts, when colectomy is indicated, and which operation fits her rectum. It then turns to duodenal surveillance by Spigelman stage, desmoid tumors, thyroid ultrasound, and reproductive counseling. A second patient shows how recessive MUTYH polyposis hides in a family, and the episode closes with the common board traps.

This episode covers the two hamartomatous polyposis syndromes through two patients. A young man with an intussusception and buccal pigmentation has Peutz-Jeghers syndrome from STK11. His main danger is obstruction and short bowel rather than cancer, so large or growing small bowel polyps come out and surveillance starts at eight to ten. Cancer surveillance outside the gut follows, with breast, pancreatic, gynecologic, and testicular programs. A woman with macrocephaly, facial papules, diffuse glycogenic acanthosis, and mixed polyps has Cowden syndrome from PTEN. Her main cancers are breast, thyroid, endometrial, and renal, so she enters multi-organ surveillance, with endoscopy from thirty-five.

Both cancers are hard to find early, so management rests on the gene and the family history rather than on a normal test. A CDH1 carrier is offered prophylactic total gastrectomy in her twenties because diffuse signet-ring cancer grows beneath normal-looking mucosa. Cambridge protocol endoscopy is the fallback, and breast MRI starts at thirty. GAPPS is told apart from hereditary diffuse gastric cancer and FAP by where the disease sits. Pancreatic surveillance is offered above about five percent lifetime risk. Some genes qualify alone and others need an affected relative. The episode then covers start age, test choice, PRSS1, and germline testing for every pancreatic cancer.