Board Pearls

By Board Pearls

The most complete gastroenterology board-review podcast on the web, and it is entirely free. This is the GI series from Board Pearls: board review built around clinical reasoning, not recall. Every ep... more

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How many episodes does Board Pearls have?

The podcast currently has 153 episodes available.

Board Pearls episodes:

July 16, 2026Chapter 20, Ep 1 of 3: Sorting the Immune Liver Diseases and Autoimmune Hepatitis
Episode one of the Autoimmune and Cholestatic Liver Diseases chapter builds the sorting framework for the three immune liver diseases and then works autoimmune hepatitis in depth. The organizing idea: pattern plus demographics plus antibodies place a patient into autoimmune hepatitis, primary biliary cholangitis, or primary sclerosing cholangitis within the first two sentences of the vignette. Autoimmune hepatitis is then the ANA and smooth-muscle-antibody interface hepatitis of the middle-aged woman with elevated IgG, confirmed on biopsy. The second half is treatment: steroid induction plus a steroid-sparing agent, the type one versus type two split, the simplified score, and why withdrawal is cautious because relapse is the rule.

Topics covered
Sorting framework: target cell sets the biochemical pattern
Demographics and IBD association across the three diseases
Antibody panel and IgG profile as the discriminator
Autoimmune hepatitis pathogenesis and two clinical faces
Type one versus type two serologic subtypes
Simplified scoring system and its blind spots
Interface hepatitis and ancillary histology
Steroid induction, azathioprine, and budesonide
Remission endpoints and cautious withdrawal

Key decisions
Sort the three immune liver diseases by pattern plus demographics plus antibodies: hepatocellular with ANA or smooth-muscle antibody and high IgG is autoimmune hepatitis, cholestatic with anti-mitochondrial antibody is primary biliary cholangitis, and cholestatic in a man with ulcerative colitis needing MRCP is primary sclerosing cholangitis.
Check a TPMT level before starting azathioprine, because TPMT-deficient patients metabolize it to toxic levels and develop severe myelosuppression; induce a non-cirrhotic adult with prednisone thirty to sixty milligrams daily plus azathioprine fifty to one hundred fifty milligrams daily.
Budesonide at nine milligrams daily is an alternative induction agent for non-cirrhotic patients but must not be used in cirrhosis, because portosystemic shunting bypasses first-pass metabolism, lowering efficacy and raising systemic exposure.
Treat acute severe autoimmune hepatitis with high-dose prednisone or IV methylprednisolone without azathioprine or budesonide, reassess every one to two weeks, and refer for transplant on failure to respond rather than escalating the dose.
Maintain biochemical remission (normal transaminases and normal IgG) for at least two years before considering withdrawal, ideally after a confirmatory biopsy, because most patients relapse within a few years of stopping.
Drug-induced autoimmune-like hepatitis from nitrofurantoin, minocycline, methyldopa, hydralazine, statins, or checkpoint inhibitors is the exception to lifelong therapy: it remits with drug withdrawal and a steroid taper, so the medication history is the discriminator.
In pregnancy continue both prednisone and azathioprine, because the risk of a flare on withdrawal exceeds the fetal risk, and postpartum flare is common.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Autoimmune and Cholestatic Liver Disease
Read this episode: boardpearls.com/gi/episodes/autoimmune-and-cholestatic-liver-ep1
Questions or feedback: [email protected].
(00:00) - The sorting framework and its variable
(00:26) - Target cell sets the biochemical pattern
(01:22) - Demographics, IBD, and the antibody panel
(03:34) - Autoimmune hepatitis and its two faces
(04:57) - The simplified scoring system
(05:42) - Interface hepatitis on biopsy
(06:14) - Induction and steroid-sparing maintenance
(07:38) - Remission and cautious withdrawal
...more
12min
July 16, 2026Chapter 19, Ep 2 of 2: Acute Liver Failure and the King's College Criteria
Episode two shifts from the drug to the failing organ, asking whether the liver can still recover on its own, how much time you have to decide, and when a different liver is the only answer. It anchors on the four-criterion definition of acute liver failure, then shows how etiology maps directly to the probability of spontaneous recovery. Two special causes, Wilsonian and herpes acute liver failure, each carry a distinctive fingerprint that demands empiric therapy before the workup completes. The King's College Criteria then triage who gets listed, with separate acetaminophen and non-acetaminophen paths calibrated to that recovery probability.

Topics covered
The four-criterion definition of acute liver failure
Distinction from acute-on-chronic failure and cerebral edema
Encephalopathy grading one through four
Etiology distribution and its link to prognosis
Non-cerebral and cerebral edema management
Wilsonian acute liver failure and its fingerprint
Herpes acute liver failure and empiric acyclovir
N-acetylcysteine in non-acetaminophen failure
King's College Criteria and transplant listing

Key decisions
Acute liver failure requires all four criteria: an INR of at least one and a half, hepatic encephalopathy of any grade, total illness duration under twenty-six weeks, and no pre-existing cirrhosis.
Cerebral edema risk rises sharply at grade three or four encephalopathy, and arterial ammonia above roughly a hundred fifty to two hundred marks the threshold where herniation risk climbs, managed with head-of-bed elevation, hypertonic saline, mannitol, and continuous renal replacement.
The Wilsonian fingerprint is Coombs-negative hemolysis with high indirect bilirubin, an alkaline-phosphatase-to-bilirubin ratio under four, an AST-to-ALT ratio over two, low uric acid, and Kayser-Fleischer rings, treated with urgent transplant and bridged by plasmapheresis while avoiding penicillamine.
Herpes acute liver failure shows very high transaminases with a normal or low bilirubin, the anicteric pattern, so empiric intravenous acyclovir at five to ten milligrams per kilogram every eight hours is started in any pregnant or immunocompromised patient with indeterminate failure.
N-acetylcysteine improves transplant-free survival in non-acetaminophen failure only with grade one or two encephalopathy, not grade three or four, so it is given empirically inside the early-grade window at the same dosing as for acetaminophen.
The acetaminophen King's College path is met by an arterial pH under seven point three after resuscitation, or by grade three or four encephalopathy plus an INR over six and a half plus a creatinine over three point four.
The non-acetaminophen path is met by an INR over six and a half alone, or by any three of five features: age under ten or over forty, indeterminate or drug-induced etiology, jaundice over seven days before encephalopathy, an INR over three and a half, and a bilirubin over seventeen and a half.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Drug-Induced Liver Injury and Acute Liver Failure
Read this episode: boardpearls.com/gi/episodes/dili-and-alf-ep2
Questions or feedback: [email protected].
(00:00) - Introduction: from the drug to the failing organ
(00:44) - The four-criterion definition
(02:13) - Acute-on-chronic distinction and grading
(03:15) - Etiology distribution and prognosis
(04:24) - Non-cerebral and cerebral edema management
(06:12) - Wilsonian acute liver failure
(08:21) - Herpes acute liver failure
(09:50) - N-acetylcysteine in non-acetaminophen failure
(10:51) - King's College Criteria and listing
...more
17min
July 16, 2026Chapter 19, Ep 1 of 2: Drug-Induced Liver Injury and Acetaminophen
Episode one of the Drug-Induced Liver Injury and Acute Liver Failure chapter builds drug injury from a single mechanism: cytochrome oxidation makes a reactive intermediate, phase-two conjugation quenches it or fails, and injury appears where phase one outpaces phase two. That frame makes the offender lists predictable, the histology readable, and the severity rules non-arbitrary. Hy's Law converts biochemistry into a triage decision, R value predicts trajectory, and histology patterns map backward to drug classes. Acetaminophen is the prototype that runs the whole sequence at speed, with the Rumack-Matthew nomogram, N-acetylcysteine, and time-to-treatment mortality all board-tested cold.

Topics covered
Drug injury as the diagnosis for any new abnormal liver tests
Intrinsic versus idiosyncratic versus indirect hepatotoxicity
Epidemiology and environmental plus genetic risk factors
Herbal and dietary supplement injury
Metabolic activation and the phase-one, phase-two two-step
Agent-specific patterns from isoniazid to amiodarone
Hy's Law, R value, and causality assessment
Histology patterns mapped to drug classes
Acetaminophen toxicity, the nomogram, and N-acetylcysteine

Key decisions
Hy's Law is met when transaminases exceed three times normal, total bilirubin exceeds two times normal, alkaline phosphatase is under two times normal, and no other cause explains it, at which point mortality is about ten percent and the drug is stopped with transplant-center awareness.
The R value classifies pattern, hepatocellular over five, cholestatic under two, mixed between, with hepatocellular injury more likely to evolve to acute failure and cholestatic or mixed more likely to become chronic.
Acetaminophen toxicity occurs when NAPQI production exceeds glutathione capacity, so a chronic alcohol user with CYP2E1 induction and glutathione depletion can develop fulminant injury on therapeutic-range dosing without ever taking an overdose.
An acute single ingestion of seven and a half grams or more in an adult, or over a hundred fifty milligrams per kilogram in a child, puts the patient in the toxic window.
The Rumack-Matthew treatment line runs from a hundred fifty micrograms per milliliter at four hours down to about five at twenty-four hours, and a level above that line within the four-to-twenty-four-hour window indicates N-acetylcysteine.
Intravenous N-acetylcysteine is dosed as a hundred fifty milligrams per kilogram over sixty minutes, then fifty over four hours, then a hundred over sixteen hours, totaling three hundred over twenty-one hours, and started the moment the diagnosis is suspected because mortality roughly doubles with each block of delay.
Drug-induced autoimmune-like hepatitis from nitrofurantoin, minocycline, hydralazine, or methyldopa usually remits when the drug stops and does not need long-term immunosuppression, unlike idiopathic autoimmune hepatitis which flares on steroid taper.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Drug-Induced Liver Injury and Acute Liver Failure
Read this episode: boardpearls.com/gi/episodes/dili-and-alf-ep1
Questions or feedback: [email protected].
(00:00) - Introduction and the mechanistic frame
(01:13) - Intrinsic, idiosyncratic, and indirect injury
(02:02) - Epidemiology and risk factors
(04:12) - Herbal and dietary supplements
(05:12) - Metabolic activation: the hepatic two-step
(07:11) - Agent-specific patterns
(09:45) - Hy's Law, R value, and causality
(12:31) - Histology patterns by drug class
(17:18) - Acetaminophen: nomogram and antidote
...more
22min
July 16, 2026Chapter 18, Ep 3 of 3: Hepatitis C
Episode three covers hepatitis C, now a curable disease, and tests the entire workflow of cure: identify the virus, confirm replication, stage the liver, pick the regimen, document cure, then ask the one remaining cancer question. It runs the reflex antibody-then-RNA diagnosis, the two pangenotypic direct-acting antiviral regimens plus the salvage regimen, and a special-populations set built on a few absolute rules. Decompensated cirrhosis forbids protease inhibitors; advanced kidney disease no longer forbids sofosbuvir. It closes on the highest-yield post-cure point: cancer surveillance continues forever in F4 cirrhosis but stops in F3 fibrosis short of cirrhosis.

Topics covered
Hepatitis C as a curable disease and the drug classes
The reflex antibody-then-RNA diagnostic algorithm
Universal screening and the pre-treatment workup
The two pangenotypic regimens and the salvage regimen
Sustained virologic response and what cure buys
Decompensated cirrhosis and the protease-inhibitor rule
Kidney disease, transplant, and pregnancy
Post-cure cancer surveillance by fibrosis stage

Key decisions
Diagnose in two tests in fixed order, the hepatitis C antibody then a reflex RNA, because the antibody persists for life and cannot distinguish active from resolved infection.
A high-suspicion patient with a negative antibody is not cleared, because the antibody lags viremia by a couple of months, so the RNA confirms acute hepatitis C.
The two preferred first-line regimens are pangenotypic: sofosbuvir-velpatasvir for twelve weeks and glecaprevir-pibrentasvir for eight weeks, the eight weeks holding even in treatment-naive compensated cirrhosis.
Sustained virologic response means undetectable RNA twelve weeks after the end of treatment, not twelve weeks of treatment, and that is the trap.
Protease inhibitors are unsafe in decompensated Child-Pugh B or C cirrhosis, so the regimen there is sofosbuvir-velpatasvir with ribavirin for twelve weeks or without for twenty-four.
Advanced kidney disease no longer forbids sofosbuvir, but glecaprevir-pibrentasvir is the simplest choice in renal impairment or dialysis when liver function is preserved.
Post-cure cancer surveillance continues every six months indefinitely in patients who had F4 cirrhosis at cure, while patients with F3 fibrosis short of cirrhosis stop surveillance after clearance.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Viral Hepatitis
Read this episode: boardpearls.com/gi/episodes/viral-hepatitis-ep3
Questions or feedback: [email protected].
(00:00) - Introduction: hepatitis C is curable
(00:27) - The cure framework and drug classes
(01:23) - The reflex antibody-then-RNA diagnosis
(03:04) - Screening and the pre-treatment workup
(03:31) - The two pangenotypic regimens and salvage
(05:20) - Sustained virologic response and what cure buys
(06:37) - Special populations and decompensated cirrhosis
(08:05) - Kidney disease, transplant, and pregnancy
(10:01) - Post-cure cancer surveillance by fibrosis stage
...more
15min
July 16, 2026Chapter 18, Ep 2 of 3: Hepatitis B and D
Episode two steps inside hepatitis B, where the serologic panel is not just diagnostic but a phase grid that determines treatment, the pregnancy strategy, the reactivation rule, and the hepatitis D testing decision. It reads two grids: the serologic grid of surface antigen, core antibody, and surface antibody that places the patient, and the phase grid of e-antigen, DNA, and ALT that decides whether to treat. From there it covers the nucleoside analogs, the three-pillar pregnancy bundle, the preemptive reactivation prophylaxis rule under immunosuppression, and hepatitis D with its new entry inhibitor bulevirtide. Every threshold, drug, and cutoff is named as the boards test it.

Topics covered
The six hepatitis B markers and what each means
The serologic grid and the isolated core antibody
The phase grid of chronic infection
Treatment principles, thresholds, and the drug menu
Reactivation under immunosuppression and prophylaxis
Pregnancy: the three-pillar vertical-transmission bundle
Hepatitis D: coinfection versus superinfection
Hepatitis D treatment and bulevirtide

Key decisions
Read the serologic grid of surface antigen, core antibody, and surface antibody to place the patient, with isolated core antibody positivity worked up by viral DNA and a repeat panel.
The phase grid of e-antigen status, viral DNA, and ALT decides treatment: immune-tolerant and inactive-carrier phases are not treated, while both immune-active phases are.
Treat with entecavir or a tenofovir prodrug indefinitely, choosing alafenamide for renal or bone protection and tenofovir disoproxil in pregnancy.
Reactivation is prevented preemptively, not rescued: surface-antigen-negative core-antibody-positive patients starting rituximab or transplant get prophylaxis because their risk approaches the surface-antigen-positive group.
The pregnancy bundle is universal surface-antigen screening, infant immunoglobulin plus vaccine within twelve hours regardless of viral load, and maternal tenofovir disoproxil from twenty-eight to thirty-two weeks when DNA exceeds two hundred thousand.
Tell coinfection from superinfection by the core antibody: coinfection shows core IgM with acute B and D, while superinfection shows total core without IgM because the underlying B is chronic.
Test for hepatitis D when a chronic hepatitis B patient has an ALT flare with low DNA, because hepatitis D drives injury using circulating surface antigen without needing active B replication.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Viral Hepatitis
Read this episode: boardpearls.com/gi/episodes/viral-hepatitis-ep2
Questions or feedback: [email protected].
(00:00) - Introduction and the phase-grid idea
(00:43) - The six hepatitis B markers
(01:57) - The serologic grid and isolated core antibody
(03:07) - The phase grid of chronic infection
(05:31) - Treatment principles and the drug menu
(07:30) - Reactivation under immunosuppression
(09:41) - Pregnancy: the three-pillar bundle
(11:58) - Hepatitis D: coinfection versus superinfection
(14:00) - Hepatitis D treatment and bulevirtide
...more
18min
July 16, 2026Chapter 18, Ep 1 of 3: Acute Viral Hepatitis and the Fecal-Oral Viruses
Episode one of the Viral Hepatitis chapter builds the acute-hepatitis framework and covers the two fecal-oral viruses, hepatitis A and hepatitis E. The organizing idea: acute viral hepatitis looks the same no matter which virus caused it, so you read the virus off the serology, not the symptoms. It walks the four clinical phases, the four-test acute panel with its two named traps, and then hepatitis A as a post-exposure-prophylaxis decision that splits by age and host. Hepatitis E closes it with its two high-yield scenarios: twenty to thirty percent mortality in third-trimester pregnancy and chronic infection in the immunocompromised.

Topics covered
The acute-hepatitis mechanism and its four phases
The four-test first-line serologic panel
Serology interpretation rules and two named traps
Differential, alarm features, and treatment by virus
Hepatitis A course, risk factors, and atypical variants
Hepatitis A vaccine and post-exposure prophylaxis
Hepatitis E genotypes and when to test
Hepatitis E in pregnancy and chronic infection with ribavirin

Key decisions
The first move on any acute hepatitis stem is the serologic panel, not the history, because the clinical phases are identical across viruses.
The first-line acute panel is four tests, hepatitis B surface antigen, hepatitis B core IgM, hepatitis C antibody with reflex to RNA, and hepatitis A IgM, adding hepatitis E IgM in the returning traveler or when the panel is negative.
Surface antigen positive with core IgM positive is acute hepatitis B, while surface antigen positive with core IgM negative but total core positive is chronic hepatitis B.
A high-suspicion hepatitis C patient with a negative antibody is not cleared, because the antibody lags viremia by a couple of months, so the RNA closes the question.
Post-exposure prophylaxis splits by host: immunocompetent persons aged twelve months to forty get a single vaccine dose within two weeks, while those over forty, the immunocompromised, chronic liver disease patients, and infants under twelve months get immunoglobulin.
Vaccinate all patients with chronic liver disease of any cause against hepatitis A, because a superimposed acute hepatitis A decompensates them at a much higher rate.
Chronic hepatitis E is defined by persistent RNA beyond three to six months in an immunocompromised host, diagnosed by RNA not IgM, and treated by reducing immunosuppression first, then ribavirin for three months.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Viral Hepatitis
Read this episode: boardpearls.com/gi/episodes/viral-hepatitis-ep1
Questions or feedback: [email protected].
(00:00) - Introduction and the organizing idea
(00:27) - Mechanism and the four phases of acute hepatitis
(02:14) - The serologic panel and its two named traps
(04:13) - Differential, alarm features, and treatment by virus
(05:34) - Hepatitis A: course and atypical variants
(07:00) - Hepatitis A vaccine and post-exposure prophylaxis
(08:07) - Hepatitis E: genotypes and when to test
(10:12) - Hepatitis E treatment by host
...more
13min
July 16, 2026Chapter 17, Ep 2 of 2: Isolated Abnormalities, Imaging, and Biopsy
Episode two of the Liver Test Interpretation chapter covers what to do when a single value is up with everything else normal, or when the labs aren't the bottleneck and imaging and fibrosis assessment are. Each case forces the same question in a different form: what's the next reflex test, and does it commit you to an invasive workup or excuse you from it? Isolated bilirubin splits on direct versus indirect, isolated alkaline phosphatase splits on GGT, and the fibrosis workup runs FIB-4 before elastography before biopsy. Thresholds, mimic vignettes, and the percutaneous-versus-transjugular decision throughout.

Topics covered
Isolated hyperbilirubinemia and the direct versus indirect split
Separating hemolysis from Gilbert on the indirect side
Direct hyperbilirubinemia: Dubin-Johnson and Rotor
Isolated alkaline phosphatase and the GGT discriminator
Imaging modalities: structure versus fibrosis
Transient and MR elastography cutoffs by etiology
Serum fibrosis biomarkers and the FIB-4 sequence
Liver biopsy indications and technique
Percutaneous versus transjugular and the pressure gradient

Key decisions
Split isolated hyperbilirubinemia at the first line of the panel into indirect versus direct, because the two branches share almost nothing and both are mostly benign.
On the indirect side, run a five-value hemolysis screen (haptoglobin, reticulocyte count, smear, LDH, direct Coombs); a clean screen in the right stem is Gilbert, and G6PD hemolysis after trimethoprim-sulfamethoxazole shows bite cells and Heinz bodies.
Truly isolated direct hyperbilirubinemia with a normal biliary tree narrows to Dubin-Johnson (black liver, inverted urinary coproporphyrin ratio) or Rotor, both benign, so the answer is reassurance, not biopsy.
For isolated alkaline phosphatase, order GGT: elevated GGT confirms a hepatic source, while a normal GGT points to bone and triggers calcium, phosphorus, vitamin D, and a bone fraction or scan.
In the fibrosis workup, reach for FIB-4 first (under one point three rules out advanced fibrosis, over two point six seven supports it, with the lower cutoff shifting to two point zero over age sixty-five), then elastography, then biopsy, and anchor elastography cutoffs to etiology.
Diagnose hepatocellular carcinoma in a cirrhotic by multiphase MRI or CT showing arterial enhancement, washout, capsule, and threshold growth without biopsy, since biopsy of a definite cancer risks needle-tract seeding.
Choose transjugular biopsy over percutaneous for tense ascites, uncorrectable coagulopathy, morbid obesity, or when the hepatic venous pressure gradient is needed, where a gradient of ten or more marks clinically significant portal hypertension and twelve or more correlates with variceal hemorrhage risk.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Liver Test Interpretation and Workup
Read this episode: boardpearls.com/gi/episodes/liver-test-interpretation-ep2
Questions or feedback: [email protected].
(00:00) - The reflex-test framing
(00:49) - Isolated hyperbilirubinemia: the first split
(01:42) - Hemolysis versus Gilbert on the indirect side
(03:47) - Direct hyperbilirubinemia: Dubin-Johnson and Rotor
(05:08) - Isolated alkaline phosphatase and GGT
(07:43) - Imaging: structure versus fibrosis
(09:15) - Elastography and etiology-specific cutoffs
(10:52) - Serum biomarkers and the FIB-4 sequence
(12:27) - Biopsy indications and the transjugular decision
...more
19min
July 16, 2026Chapter 17, Ep 1 of 2: The R Ratio and the Two Workup Tracks
Episode one of the Liver Test Interpretation chapter turns abnormal liver enzymes into a workup by computing the R ratio and committing to a track before ordering another test. The organizing idea: which enzyme dominates and by how many multiples of normal it sits at frames the entire differential, because hepatocellular and cholestatic patterns share almost nothing. The hepatocellular track runs five layers in order (viral, autoimmune, metabolic, ischemic, drug); the cholestatic track branches on a single ultrasound finding, dilated tree or not. Thresholds, magnitude anchors, and reflex panels throughout.

Topics covered
The R ratio and sorting hepatocellular from cholestatic
Hepatocellular injury and magnitude-based differential
AST-to-ALT ratio and the redefined normal range
Hepatocellular workup: viral, autoimmune, metabolic layers
Ischemic (shock liver) and drug-induced injury with Hy's Law
Cholestatic workup and the ultrasound branch point
Intrahepatic cholestasis: PBC, PSC, and IgG4 disease
The mixed pattern and the synthesis

Key decisions
Compute the R ratio first on any liver vignette: R over five is hepatocellular, R under two is cholestatic, and two to five is mixed, and commit to that track before ordering another test.
Acetaminophen and ischemic hepatitis are the two causes that cross an ALT of five thousand; ischemia carries an LDH-to-ALT ratio over one and a half with a hypotensive precedent, while an AST-to-ALT ratio over two with AST under four hundred in a drinker is alcoholic hepatitis until proven otherwise.
Use the current normal ALT of under twenty-five for women and under thirty-three for men, because the old range was inflated by undiagnosed fatty liver and hepatitis C.
Run the hepatocellular workup in order: viral first (hepatitis B surface antigen and hepatitis C antibody with reflex RNA), autoimmune second (ANA, smooth-muscle, anti-LKM-one, quantitative IgG), metabolic third (transferrin saturation over forty-five percent before HFE testing, ceruloplasmin in anyone under fifty-five).
Hy's Law is the drug-injury prognostic anchor: an ALT over three times normal with bilirubin over two without obstruction carries about ten percent mortality even after stopping the drug.
In the cholestatic track, get a right-upper-quadrant ultrasound first; a dilated tree goes to MRCP then endoscopic ultrasound for a mass, with ERCP reserved for therapy, while a non-dilated tree triggers anti-mitochondrial antibody and IgM for primary biliary cholangitis.
A positive anti-mitochondrial antibody with an alkaline phosphatase over one and a half times normal and AST under five times normal allows a no-biopsy diagnosis of primary biliary cholangitis, and MRCP showing beaded multifocal strictures diagnoses sclerosing cholangitis without ERCP.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Liver Test Interpretation and Workup
Read this episode: boardpearls.com/gi/episodes/liver-test-interpretation-ep1
Questions or feedback: [email protected].
(00:00) - The organizing idea and the R ratio
(00:39) - Computing R at the front door
(01:14) - Hepatocellular injury and magnitude
(02:56) - Redefining the normal range
(03:31) - The hepatocellular workup, layered in order
(07:36) - Shock liver, drug injury, and Hy's Law
(09:48) - The cholestatic workup and the ultrasound branch
(10:57) - Intrahepatic cholestasis: PBC, PSC, IgG4
(14:31) - The mixed pattern and the synthesis
...more
16min
July 16, 2026Chapter 16, Ep 3 of 3: Fecal Incontinence and Benign Anorectal Disorders
Episode three covers fecal incontinence managed in a fixed sequence and the benign anorectal disorders anchored to the dentate line. Incontinence rarely fails for a single reason, so the workup canvasses the whole continence stack and the treatment runs from optimizing the modifiable factor through loperamide and biofeedback to sacral neuromodulation, which has displaced sphincteroplasty as first-line surgery for refractory disease. The benign disorders follow the anatomy: above the dentate line means painless bleeding, below it means sharp pain, and that landmark predicts management for hemorrhoids, anal fissure, and pruritus ani. Manometry, endoanal ultrasound, the seventy-two-hour rule, and the atypical-fissure workup throughout.

Topics covered
The continence stack and multifactorial failure
Etiologic grid: sphincter, rectal, neurologic, consistency, overflow
History and targeted testing with manometry and endoanal ultrasound
Fixed treatment sequence from modifiable factors to loperamide and biofeedback
Sacral neuromodulation versus sphincteroplasty
Internal and external hemorrhoids and the dentate line
Anal fissure mechanism and atypical-location workup
Pruritus ani as a symptom, not a diagnosis

Key decisions
Endoanal ultrasound is the test of choice for sphincter integrity, mapping anterior defects from obstetric trauma the exam misses, while anorectal manometry is the most informative single test and changes management in most cases.
Soluble fiber like psyllium is the counterintuitive first move in leakage of liquid stool because firm stool is easier to retain than soft stool even with a damaged sphincter, alongside treating impaction and any diarrheal disease.
Loperamide is the drug that follows, a peripheral opioid agonist that slows transit, raises internal sphincter tone, and inhibits the rectoanal inhibitory reflex, all three helping.
For refractory fecal incontinence, sacral nerve stimulation is the favored answer and has displaced sphincteroplasty; the staged trial requires at least fifty percent symptom improvement before permanent implantation.
Sphincteroplasty is reserved for the younger woman with an isolated external sphincter defect from obstetric injury, buying time because outcomes decline over years as pudendal neuropathy undoes the repair.
Thrombosed external hemorrhoids are excised within seventy-two hours of onset for faster pain relief, but after seventy-two hours conservative management is preferred, and the procedure is excision of the whole hemorrhoid, not incision and drainage.
A posterior or anterior midline anal fissure is idiopathic, but a lateral, multiple, or atypical fissure demands a Crohn's and infection workup before topical therapy; treatment layers topical calcium channel blockers, then botulinum toxin, then lateral internal sphincterotomy.

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

Study the full chapter on Board Pearls, with practice questions, tables and primary-guideline references: Pelvic Floor and Anorectal Disorders
Read this episode: boardpearls.com/gi/episodes/pelvic-floor-and-anorectal-ep3
Questions or feedback: [email protected].
(00:00) - Introduction and the continence stack
(01:18) - The etiologic grid of incontinence
(02:26) - History and targeted testing
(03:55) - The fixed treatment sequence
(05:05) - Sacral neuromodulation versus sphincteroplasty
(06:57) - Hemorrhoids and the dentate line
(08:43) - Thrombosed external hemorrhoids and the 72-hour rule
(09:39) - Anal fissure
(11:38) - Pruritus ani
...more
15min
July 16, 2026Chapter 16, Ep 2 of 3: Dyssynergia and Slow-Transit Constipation
Episode two covers the constipation phenotypes that need more than pharmacology: defecatory disorders diagnosed on anorectal manometry and balloon expulsion and treated with biofeedback, and slow-transit constipation documented on a marker or capsule study. The organizing discipline is to decide the mechanism before the next drug, because escalating laxatives in unrecognized outlet dysfunction produces overflow and urgency without relief. The central pitfall runs the whole episode: unrecognized outlet dysfunction falsifies the transit study and sends the wrong patient to colectomy, so check the outlet before you cut the colon. Testing thresholds, the two-of-three diagnostic rule, and precise colectomy criteria throughout.

Topics covered
Deciding phenotype before the next drug
Dyssynergic defecation mechanism and rectal exam clue
Balloon expulsion screening test
Anorectal manometry parameters and the rectoanal inhibitory reflex
Defecography and structural lesions
Two-of-three diagnostic rule and biofeedback
Slow-transit constipation and transit studies
Subtotal colectomy indications and disqualifiers

Key decisions
After empiric therapy fails, the first decision is which phenotype the patient has, not which drug comes next, because more laxative in outlet dysfunction produces urgency and overflow around a still-closed sphincter.
Balloon expulsion is the first-line screen: a rectal balloon is inflated with fifty milliliters of warm water and failure to expel within sixty seconds is abnormal and supports a defecatory disorder.
Anorectal manometry reads resting pressure, squeeze pressure, the push maneuver (dyssynergia is a paradoxical rise in anal pressure), and the rectoanal inhibitory reflex, whose absence is the hallmark of Hirschsprung disease.
The diagnosis of a defecatory disorder requires at least two of three positive studies among manometry, defecography, and balloon expulsion, because a paradoxical contraction on manometry alone is too soft.
Biofeedback is the treatment for a confirmed defecatory disorder and outperforms laxatives in this population, but it does not help slow transit without dyssynergia because that lesion is not mechanical at the outlet.
The radiopaque marker study retains twenty-four markers with a plain film on day five; more than five markers retained indicates slow transit, and rectosigmoid clustering points back to outlet dysfunction.
Subtotal colectomy with ileorectal anastomosis requires severe intractable symptoms, objectively confirmed slow transit, and a defecatory disorder excluded, disqualified by prominent abdominal pain, generalized dysmotility, or pseudo-obstruction.

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(00:00) - Introduction and the phenotype decision
(00:28) - Which phenotype, not which drug
(01:27) - Dyssynergic defecation and the rectal exam
(02:41) - Balloon expulsion, manometry, and defecography
(04:12) - Two-of-three rule and biofeedback
(05:55) - Sequencing and the central pitfall
(06:38) - Slow-transit constipation and transit studies
(08:08) - Colectomy criteria and disqualifiers
...more
12min

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