100+ Free ABP Transplant Hepatology Practice Questions

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Which serum protein synthesized by the liver has the LONGEST half-life and is therefore a poor marker of acute hepatic synthetic function?

Prothrombin (factor II)

Factor VII

Albumin

Fibrinogen

to track

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2026 Statistics

Key Facts: ABP Transplant Hepatology Exam

100

Total MCQ Items

Single-best-answer ABP sub-subspecialty exam

8 hr

Exam Time

ABP-administered CBT

~$2,200

2026 Exam Fee

Confirm current fee on abp.org

1 yr

Required Fellowship

ACGME-accredited Pediatric Transplant Hepatology fellowship

<60 d

Optimal Kasai Timing

>70% jaundice clearance if performed before 60 days

MOCA-Peds

Continuing Certification

5-year longitudinal assessment plus 10-year MOC cycle

The ABP Pediatric Transplant Hepatology sub-subspecialty certifying exam is an 8-hour computer-based test of approximately 100 single-best-answer MCQs administered by the American Board of Pediatrics. Pre-requisites: ABP Pediatric Gastroenterology certification plus a 1-year ACGME-accredited Pediatric Transplant Hepatology fellowship (or 2-year combined training). 2026 fee is approximately $2,200. Highest-yield domains: pediatric LT listing (~20%, biliary atresia first indication, PELD/MELD, living donor lateral segment, split grafts), cholestatic liver disease (~20%, biliary atresia Kasai HPE <60d, Alagille JAG1 with maralixibat, PFIC1-3 with odevixibat), metabolic liver disease (~15%, Wilson, A1AT, tyrosinemia/NTBC, urea cycle), post-transplant care (~15%, tacrolimus + Banff RAI rejection, CMV D+/R-, EBV/PTLD), and acute liver failure (~10%, PALF criteria, GALD, Wilsonian crisis). MOC every 10 years plus MOCA-Peds longitudinal assessment.

Sample ABP Transplant Hepatology Practice Questions

Try these sample questions to test your ABP Transplant Hepatology exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Which serum protein synthesized by the liver has the LONGEST half-life and is therefore a poor marker of acute hepatic synthetic function?

A.Prothrombin (factor II)

B.Factor VII

C.Albumin

D.Fibrinogen

Explanation: Albumin has a half-life of approximately 21 days, so it lags behind acute changes in hepatic synthetic function. Coagulation factors (especially factor VII with a half-life of 4-6 hours) change within hours-to-days; INR is therefore the most sensitive marker of acute hepatic dysfunction.

2A previously healthy 4-year-old presents with acute liver failure. Which laboratory pattern best reflects RAPID-onset hepatic synthetic dysfunction?

A.Marked drop in serum albumin within 24 hours

B.Marked rise in INR within 24 hours despite vitamin K administration

C.Falling serum cholesterol over 24 hours

D.Falling ceruloplasmin within 24 hours

Explanation: Vitamin K-dependent factors (especially factor VII, t1/2 ~4-6 hours) drop quickly when the liver fails, producing a rapidly rising INR that does not correct with parenteral vitamin K. Albumin (t1/2 ~21 days), cholesterol, and ceruloplasmin all change too slowly to reflect acute hepatocyte loss.

3A 3-week-old breastfed infant has total bilirubin 12 mg/dL with direct bilirubin 0.4 mg/dL, normal stools, and normal urine. What is the MOST appropriate next step?

A.Urgent HIDA scan to evaluate for biliary atresia

B.Reassurance — this is consistent with breast milk jaundice

C.Liver biopsy

D.Start ursodeoxycholic acid

Explanation: Indirect (unconjugated) hyperbilirubinemia in a thriving breastfed infant with pigmented stools and a direct fraction <1 mg/dL (and <20% of total) is consistent with breast-milk jaundice, which can persist to 8-12 weeks. Direct hyperbilirubinemia (>1 mg/dL) is ALWAYS pathologic and would mandate urgent evaluation for biliary atresia.

4A 5-week-old has total bilirubin 7 mg/dL with direct fraction 3.5 mg/dL, acholic stools, and dark urine. What does this presentation MANDATE?

A.Reassurance and follow-up in 2 weeks

B.Urgent evaluation for biliary atresia and other cholestatic liver disease

C.Phototherapy only

D.Trial of phenobarbital alone

Explanation: Conjugated (direct) bilirubin >1 mg/dL or >20% of total is ALWAYS pathologic in an infant. Acholic stools and dark urine are classic for biliary obstruction. Workup must proceed urgently because Kasai hepatoportoenterostomy outcomes for biliary atresia are best when performed before 60 days of age.

5Which laboratory pattern is MOST characteristic of cholestasis in a child?

A.Marked elevation of AST/ALT with normal GGT and alkaline phosphatase

B.Elevation of conjugated bilirubin, GGT, alkaline phosphatase, and bile acids

C.Isolated unconjugated hyperbilirubinemia with normal liver enzymes

D.Isolated elevation of ammonia

Explanation: Cholestasis is defined by impaired bile flow and is characterized biochemically by elevated direct/conjugated bilirubin, GGT, alkaline phosphatase, total bile acids, and often cholesterol. Aminotransferases are variably elevated. Note that low GGT in the face of cholestasis is a clue to PFIC1, PFIC2, or bile acid synthesis defects.

6Which clinical scenario is the SINGLE most common indication for pediatric liver transplantation worldwide?

A.Wilson disease

B.Biliary atresia

C.Autoimmune hepatitis

D.Hepatoblastoma

Explanation: Biliary atresia is the most common indication for pediatric liver transplant globally and accounts for roughly 40-50% of all pediatric LT. Even with timely Kasai portoenterostomy, approximately 70-80% of patients will require liver transplantation by adolescence or young adulthood.

7Which is the MOST common anatomic subtype of biliary atresia (Kasai/Japanese classification)?

A.Type I (atresia at the common bile duct)

B.Type II (atresia at the common hepatic duct)

C.Type III (atresia at the porta hepatis)

D.Type IV (combined intra- and extrahepatic atresia)

Explanation: Type III biliary atresia, with obliteration extending up to the porta hepatis, accounts for approximately 90% of cases and is the most challenging surgically because no extrahepatic patent duct remains for anastomosis. Type I (CBD only) is least common but has the best prognosis after Kasai.

8A 6-week-old infant with cholestasis is undergoing biliary atresia workup. Which pretreatment maximizes the diagnostic accuracy of hepatobiliary scintigraphy (HIDA)?

A.5 days of phenobarbital prior to imaging

B.5 days of ursodeoxycholic acid prior to imaging

C.Single dose of cholestyramine

D.Single dose of vitamin K

Explanation: Phenobarbital 5 mg/kg/day for 5 days induces hepatic enzymes and bile flow, improving the sensitivity of HIDA scanning. Failure to demonstrate small-bowel tracer excretion at 24 hours after phenobarbital priming is suggestive of biliary atresia, prompting intraoperative cholangiography for definitive diagnosis.

9Which liver biopsy finding is MOST characteristic of biliary atresia in an infant?

A.Bridging fibrosis with regenerative nodules

B.Ballooning hepatocytes with Mallory-Denk bodies

C.Bile ductular proliferation, bile plugs in canaliculi, and portal fibrosis

D.Granulomas with caseous necrosis

Explanation: The classic biliary atresia biopsy shows expanded portal tracts with bile ductular proliferation, intracanalicular bile plugs, and portal fibrosis. Giant cell transformation may be present but is nonspecific. PAS-D inclusions would suggest A1AT deficiency.

10What is the MOST important determinant of long-term native-liver survival after Kasai hepatoportoenterostomy for biliary atresia?

A.Patient gender

B.Age at the time of Kasai operation

C.Use of postoperative antibiotics

D.Use of postoperative corticosteroids

Explanation: Earlier Kasai is consistently associated with better jaundice clearance and native-liver survival. Approximately 70% of infants achieve jaundice clearance when Kasai is done before 60 days of age, compared with ~30% if performed after 90 days. Postoperative steroid use has not been shown to improve outcomes in randomized trials (START trial).

About the ABP Transplant Hepatology Exam

The ABP Pediatric Transplant Hepatology sub-subspecialty exam validates expert-level knowledge of pediatric liver transplantation across cholestatic disease (biliary atresia/Kasai HPE, Alagille JAG1, PFIC 1-3 — odevixibat/maralixibat IBAT inhibitors), metabolic liver disease (Wilson ATP7B, A1AT PiZZ, tyrosinemia/NTBC, urea cycle disorders, GSD), pediatric acute liver failure (PALF criteria, GALD, Wilsonian crisis, NAC), liver transplant listing (PELD <12y, MELD ≥12y, UNOS Status 1A/1B, living-donor lateral segment, split LT), post-transplant immunosuppression (tacrolimus, MMF, mTOR inhibitors, basiliximab), rejection (Banff RAI), infections (CMV D+/R-, EBV/PTLD, PJP), recurrent disease (AIH, PSC), hepatic tumors (hepatoblastoma PRETEXT, fibrolamellar HCC, infantile hemangioma), and adolescent transition (Got Transition Six Core Elements). 8-hour CBT requiring ABP Pediatric Gastroenterology certification plus a 1-year (or 2-year track) Transplant Hepatology fellowship.

Questions

100 scored questions

Time Limit

8 hours (CBT)

Passing Score

Scaled by ABP

Exam Fee

~$2,200 (American Board of Pediatrics (ABP))

ABP Transplant Hepatology Exam Content Outline

10%

Liver Anatomy, Physiology, and Pathophysiology in Children

Couinaud segmental anatomy (segments II/III for left lateral grafts), hepatic synthetic function (albumin half-life ~21 days; coagulation factors INR rapid response within hours-days; cholesterol; ceruloplasmin), metabolism (drug, urea cycle, ammonia), excretion (bile, bilirubin), storage (glycogen, fat-soluble vitamins ADEK, iron, copper). Bilirubin metabolism: unconjugated → UDP-glucuronyl transferase → conjugated → bile. Pediatric-specific portal anatomy and growth/age-related physiology.

20%

Pediatric Cholestatic Liver Disease

Direct hyperbilirubinemia >1 mg/dL (or >20% total) is ALWAYS pathologic in infants — mandates urgent biliary atresia evaluation. Biliary atresia (most common indication for pediatric LT, types 1/2/3 with type 3 porta hepatis ~90%, HIDA after 5-day phenobarbital, intraoperative cholangiography, Kasai HPE <60 days for >70% jaundice clearance, ~80% need LT despite Kasai). Alagille (JAG1/NOTCH2 AD; bile duct paucity, characteristic facies, butterfly vertebrae, posterior embryotoxon, peripheral pulmonary stenosis; maralixibat IBAT inhibitor 2021). PFIC1 (FIC1/ATP8B1 low GGT), PFIC2 (BSEP/ABCB11 low GGT, high HCC risk in childhood), PFIC3 (MDR3/ABCB4 high GGT); odevixibat (Bylvay 2021).

15%

Metabolic Liver Disease

A1AT deficiency (PiZZ, PAS-D globules), Wilson disease (ATP7B AR, KF rings on slit lamp, ceruloplasmin <20, 24-h urine Cu >100 mcg, liver Cu >250 mcg/g, Leipzig score, D-penicillamine/trientine plus zinc), tyrosinemia type 1 (FAH deficiency, succinylacetone in urine, NTBC/nitisinone since 1992 transformed prognosis), GSD type Ia (von Gierke, G6Pase) and GSD III (debrancher), hereditary fructose intolerance (ALDOB), galactosemia (GALT, E. coli sepsis risk), urea cycle disorders (OTC X-linked most common, hyperammonemia + respiratory alkalosis + low BUN, hemodialysis + Ammonul, Ravicti), Crigler-Najjar I/II, MAFLD/MASLD (2023 nomenclature), resmetirom (Rezdiffra 2024 first MASH-specific drug, adults only).

10%

Acute Liver Failure and Wilson's Crisis

PALF criteria: INR ≥2.0 (or ≥1.5 with HE) without prior chronic liver disease. Etiology age-dependent — neonatal: HLH, GALD (gestational alloimmune liver disease — extrahepatic iron, IVIG/exchange transfusion), mitochondrial; older: APAP (NAC), viral, indeterminate (largest single category), autoimmune, Wilson. King's College Criteria with pediatric modifications and PALF score for transplant decisions. New Wilson Index for pediatric Wilsonian ALF prognosis. Wilsonian crisis = ALF + Coombs-negative hemolysis + AKI; mortality without LT >95%, emergent transplant required. Hepatic encephalopathy grading I-IV; cerebral edema with hyperammonemia >150 mcmol/L.

20%

Pediatric Liver Transplantation: Indication, Listing, Allocation

Indication mix: cholestatic ~50% (biliary atresia leading), metabolic ~13%, ALF ~11%, malignancy ~5%. PELD score for <12 years (albumin, INR, total bilirubin, growth failure z-score, age <1); MELD for ≥12 years. UNOS Status 1A (ALF, primary nonfunction within 7 days post-LT, hepatic artery thrombosis within 14 days) > Status 1B (intractable variceal bleed, hepatoblastoma, severe decompensation in <18) > calculated PELD/MELD. Living donor LT — left lateral segment (II + III) for infants. Split LT — deceased adult liver split for pediatric (LL segment) + adult (extended right) recipients. Domino LT rare. Contraindications: uncontrolled extrahepatic infection, severe extrahepatic mitochondrial disease, irreversible MOF unrelated to liver.

15%

Post-Transplant Care: Immunosuppression, Rejection, Infection, Recurrence

Induction: no induction common in peds, basiliximab (IL-2R antagonist) frequent; ATG for high-risk. Maintenance: tacrolimus backbone (early trough 8-12, late 4-8 ng/mL) + MMF + steroid taper over 3-6 months; mTOR inhibitors (sirolimus, everolimus) for renal sparing or PTLD/CMV. Operational tolerance trials (~20% successful). Rejection: ACR with Banff RAI 0-9 (portal inflammation + bile duct injury + venular endothelialitis each 0-3); pulse methylprednisolone first-line; chronic ductopenic rejection. CMV (D+/R- highest risk; valganciclovir 100-200 days; preemptive PCR; IV ganciclovir for tissue-invasive disease). EBV/PTLD (peds higher risk especially primary EBV; reduce IS + rituximab for CD20+ B-cell PTLD). PJP prophylaxis with TMP-SMX 6-12 months. Live vaccines contraindicated post-LT — complete pre-LT. Tacrolimus drug interactions (azoles, macrolides via CYP3A4). Recurrent AIH, PSC, de novo AIH.

Hepatic Tumors

Hepatoblastoma — most common pediatric primary liver malignancy; peak 1-3 years; AFP markedly elevated; PRETEXT staging; COG/SIOPEL cisplatin-based chemotherapy with sodium thiosulfate (Pedmark 2022) to reduce ototoxicity; surgical resection or LT for unresectable PRETEXT IV. HCC less common in peds, often arising in chronic liver disease (tyrosinemia, BSEP/PFIC2, hepatitis B). Fibrolamellar HCC — adolescent/young adult, normal AFP, DNAJB1-PRKACA fusion. Focal nodular hyperplasia (central scar, no malignant potential, follow). Hepatocellular adenoma (estrogen, GSD Ia, resect if >5 cm). Infantile hepatic hemangioma — multifocal lesions can cause high-output cardiac failure and severe consumptive hypothyroidism (D3 deiodinase); first-line propranolol.

Adolescent Transition to Adult Care

Got Transition (gottransition.org) Six Core Elements: transition policy, tracking/monitoring, readiness, planning, transfer, transfer completion. Begin structured transition by age 12-14; formal transfer typically 18-22. Increased graft loss in late adolescence/young adulthood (peak 17-24 years) from non-adherence — leading cause of late graft loss in pediatric LT. Joint or co-located pediatric/adult transition clinics improve outcomes. Late mortality drivers beyond 5 years: malignancy (PTLD, skin), CKD from chronic CNI, infection.

How to Pass the ABP Transplant Hepatology Exam

What You Need to Know

Passing score: Scaled by ABP
Exam length: 100 questions
Time limit: 8 hours (CBT)
Exam fee: ~$2,200

Keys to Passing

Complete 500+ practice questions
Score 80%+ consistently before scheduling
Focus on highest-weighted sections
Use our AI tutor for tough concepts

ABP Transplant Hepatology Study Tips from Top Performers

1Anchor the cholestasis section on ONE rule: in any infant, a direct (conjugated) bilirubin >1 mg/dL or >20% of total is ALWAYS pathologic and mandates urgent biliary atresia workup. Master the BA workflow: ultrasound (triangular cord sign, absent/contracted gallbladder), HIDA after 5-day phenobarbital priming (no small bowel excretion suggests BA), liver biopsy (bile ductular proliferation, bile plugs, portal fibrosis), then intraoperative cholangiography. Kasai HPE before 60 days yields >70% jaundice clearance vs ~30% if delayed past 90 days; despite Kasai, ~80% require LT by adolescence.

2Make the PFIC table second nature for the exam: PFIC1 (FIC1/ATP8B1 — low GGT, post-LT diarrhea/steatohepatitis because FIC1 is also intestinal); PFIC2 (BSEP/ABCB11 — low GGT, high childhood HCC risk — surveillance); PFIC3 (MDR3/ABCB4 — HIGH GGT due to detergent bile injuring ducts). IBAT inhibitors (FDA 2021): odevixibat (Bylvay) for PFIC pruritus, maralixibat (Livmarli) for Alagille pruritus — both expanded since approval. Alagille = JAG1/NOTCH2 AD with paucity of bile ducts + facies + butterfly vertebrae + posterior embryotoxon + peripheral pulmonary stenosis.

3PELD vs MELD: PELD applies to candidates <12 years (albumin, INR, total bilirubin, growth failure z-score, age <1 year); MELD is used for ≥12 years. UNOS Status 1A is highest priority — ALF (life expectancy <7 days), primary nonfunction within 7 days of LT, hepatic artery thrombosis within 14 days, decompensated Wilson disease. Status 1B includes hepatoblastoma, intractable variceal bleeding, and severe chronic decompensation in <18 yo. Living donor lateral segment (II + III) is the standard for infants/small children; split LT divides one deceased adult liver between a child (LL) and an adult (extended right).

4Build a quick post-LT immunosuppression mental model: induction (no induction common in peds; basiliximab IL-2R antagonist; ATG only if high risk) → maintenance (tacrolimus backbone, early trough 8-12 then 4-8 ng/mL; MMF; steroids taper over 3-6 months; mTOR inhibitors sirolimus/everolimus for renal sparing or CMV/PTLD). For ACR, Banff RAI sums portal inflammation + bile duct injury + venular endothelialitis (each 0-3) — pulse steroids for moderate-severe. Tacrolimus is a CYP3A4 substrate: azoles (especially voriconazole, posaconazole), macrolides, diltiazem, and grapefruit juice all sharply raise troughs.

5Learn the post-transplant infection timeline: weeks 0-1 (nosocomial bacterial — gram-negative biliary, line, MRSA, VRE), weeks 2-26 (opportunistic — CMV with D+/R- highest risk on valganciclovir 100-200 days, EBV/PTLD with EBV PCR surveillance, PJP on TMP-SMX 6-12 months, fungal in high-risk), >6 months (community-acquired, late CMV, recurrent disease). Live vaccines (MMR, varicella, rotavirus, BCG, oral polio, intranasal flu, yellow fever) are CONTRAINDICATED post-LT — complete pre-transplant. Non-adherence in ages 17-24 is the leading cause of late graft loss; structured transition (Got Transition Six Core Elements starting age 12-14) is essential.

Frequently Asked Questions

What is the ABP Pediatric Transplant Hepatology sub-subspecialty certification?

The ABP Pediatric Transplant Hepatology certification is awarded by the American Board of Pediatrics to pediatric gastroenterologists who complete additional training in liver transplantation and demonstrate expert knowledge in pre-transplant evaluation, listing, deceased and living donor pediatric LT, post-transplant immunosuppression, rejection management, infection prophylaxis, recurrent disease, hepatic tumors, and adolescent transition. It qualifies diplomates to lead pediatric liver transplant services.

Who is eligible for the ABP Pediatric Transplant Hepatology exam?

Candidates must hold ABP Pediatric Gastroenterology certification in good standing and have completed a 1-year ACGME-accredited Pediatric Transplant Hepatology fellowship (or an alternative 2-year combined training program). A valid unrestricted medical license is required. Training must include experience across the full continuum of pre-listing evaluation, perioperative LT management, post-LT immunosuppression, and complications.

What is the format of the exam?

The exam is an 8-hour computer-based test of approximately 100 single-best-answer multiple-choice questions delivered by the American Board of Pediatrics. Items emphasize clinical vignettes including liver biopsy histology (Banff RAI rejection), MRCP and ultrasound imaging, PELD/MELD calculations, immunosuppression pharmacology and drug interactions (tacrolimus CYP3A4), CMV/EBV monitoring, and longitudinal post-transplant decision making.

How much does the 2026 exam cost?

The 2026 fee is approximately $2,200. Always confirm current fees, application deadlines, and late-registration policies on the ABP transplant hepatology page (abp.org/content/transplant-hepatology) before applying, as ABP updates fees periodically.

What are the highest-yield topics?

Pediatric liver transplant listing and allocation (~20%) plus cholestatic disease (~20%) together cover ~40% of the exam. Master biliary atresia (Kasai HPE before 60 days), Alagille (JAG1, maralixibat), PFIC1-3 (odevixibat for PFIC; low- vs high-GGT split), Wilson disease (ATP7B, KF rings, ceruloplasmin, 24-h urine Cu, Wilsonian crisis), tyrosinemia (NTBC), PALF criteria (INR ≥2 or ≥1.5 with HE), GALD, PELD vs MELD, UNOS Status 1A/1B, living-donor lateral segment and split grafts, tacrolimus management with Banff RAI rejection, CMV D+/R-, EBV/PTLD, and infantile hepatic hemangioma with consumptive hypothyroidism.

What are the continuing certification requirements?

After initial certification, ABP diplomates maintain certification via the 5-year MOCA-Peds longitudinal assessment plus Part 2 (self-assessment CME) and Part 4 (improvement in medical practice) activities. Sub-subspecialty certificates renew every 10 years. Maintaining an unrestricted medical license is required throughout. Always check abp.org for current MOC/MOCA-Peds policies.