100+ Free ABPath Pediatric Pathology Practice Questions

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Question 1

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A placenta from a preterm delivery shows neutrophilic infiltration of the chorionic plate and chorioamniotic membranes, with neutrophils within the fetal umbilical vein wall and Wharton jelly. Which Amsterdam consensus diagnosis best fits?

Acute chorioamnionitis with fetal inflammatory response (funisitis)

Chronic villitis of unknown etiology

Maternal vascular malperfusion

Massive perivillous fibrin deposition

to track

2026 Statistics

Key Facts: ABPath Pediatric Pathology Exam

235

Total MCQ Items

170 Written/Practical + 65 Virtual Microscopy

6h 23m

Total Exam Time

3h 8m W/P + 3h 15m VM

22%

Perinatal/Placenta Weight

Largest combined domain on 2026 blueprint

$2,100

2026 Exam Fee

Includes $200 admin fee

12 mo

Required Fellowship

ACGME Pediatric Pathology fellowship

10 yr

Certification Validity

Time-limited; CC/MOC required

The ABPath Pediatric Pathology exam is a 1-day 235-question computer-based test from the American Board of Pathology — 170 Written/Practical items (3h 8m) + 65 Virtual Microscopy items (3h 15m). The 2026 blueprint weights Perinatal/Placenta 22% W/P, Fetal/Neonatal pathophysiology 15%, Alimentary Tract 7%, Hematopoietic 6%, Respiratory 6%, Hepatobiliary 6%, Cardiovascular 6%, CNS 5%, Kidney 5%, Soft Tissue 4%, and other organ systems. The 2026 fee is $2,100 (includes $200 nonrefundable administrative fee). Testing window: September 8-28, 2026.

Sample ABPath Pediatric Pathology Practice Questions

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

1A placenta from a preterm delivery shows neutrophilic infiltration of the chorionic plate and chorioamniotic membranes, with neutrophils within the fetal umbilical vein wall and Wharton jelly. Which Amsterdam consensus diagnosis best fits?

A.Acute chorioamnionitis with fetal inflammatory response (funisitis)

B.Chronic villitis of unknown etiology

C.Maternal vascular malperfusion

D.Massive perivillous fibrin deposition

Explanation: Acute chorioamnionitis (maternal inflammatory response, MIR) is defined by neutrophils in chorionic plate/membranes and is staged 1-3 and graded 1-2 per Amsterdam criteria. When neutrophils involve umbilical vessels (phlebitis → arteritis → funisitis) this is fetal inflammatory response (FIR) and is clinically more significant for neonatal morbidity. Associated with ascending infection.

2A term placenta is markedly small for gestational age. Histology shows accelerated villous maturation, distal villous hypoplasia, infarcts, and decidual arteriopathy with atherosis. Which diagnosis?

A.Maternal vascular malperfusion (MVM)

B.Fetal vascular malperfusion (FVM)

C.Villitis of unknown etiology

D.Chronic histiocytic intervillositis

Explanation: Maternal vascular malperfusion (MVM) — small placenta, infarcts, accelerated villous maturation, distal villous hypoplasia, and decidual arteriopathy (atherosis, fibrinoid necrosis, failure of physiologic conversion) — is the Amsterdam consensus pattern associated with preeclampsia, FGR, and stillbirth. It reflects inadequate trophoblast invasion and uteroplacental insufficiency.

3Fetal vascular malperfusion (FVM) of the placenta is characterized histologically by which findings?

A.Avascular villi, intramural thrombi of large fetal vessels, and villous stromal-vascular karyorrhexis

B.Neutrophilic villitis with bacterial colonies

C.Decidual atherosis and accelerated villous maturation

D.Massive perivillous fibrin deposition

Explanation: Fetal vascular malperfusion (FVM) shows avascular villi (groups of ≥3 in segmental or diffuse patterns), thrombotic vasculopathy of chorionic plate/stem villous vessels, and villous stromal-vascular karyorrhexis — reflecting obstruction of fetal circulation. Associated with umbilical cord anomalies (hypercoiling, long cord, knots), fetal thrombophilias, and stillbirth/FGR. Amsterdam consensus defines low- vs high-grade FVM.

4A second-trimester placenta shows hydropic villi of markedly variable size with trophoblast hyperplasia and cistern formation. IHC for p57 (CDKN1C) shows no staining in cytotrophoblast or villous stromal cells. Which diagnosis?

A.Complete hydatidiform mole

B.Partial hydatidiform mole

C.Placental mesenchymal dysplasia

D.Spontaneous abortion with hydropic change

Explanation: Complete hydatidiform mole is androgenetic diploid (usually 46,XX from duplication of a single paternal haploid set); p57 (paternally imprinted, maternally expressed) IHC is NEGATIVE in villous cytotrophoblast and stromal cells. Partial mole is triploid (69,XXX/XXY) with maternal genome present — p57 IS positive. Complete moles have higher risk of gestational trophoblastic neoplasia.

5Villitis of unknown etiology (VUE) differs from infectious villitis in that VUE:

A.Shows lymphohistiocytic (T-cell, CD4/CD8) villitis without identifiable organisms; high-grade VUE is associated with recurrence risk and FGR

B.Shows neutrophilic villous infiltration

C.Is caused by CMV with owl-eye inclusions

D.Is always associated with complete absence of villi

Explanation: VUE is lymphohistiocytic (T-cell predominant, maternal origin) villitis without identifiable pathogens by stains, IHC, or cultures. High-grade VUE (≥10 contiguous villi affected) is associated with FGR, preeclampsia, stillbirth, and ~25-50% recurrence. Infectious villitis typically shows plasma cells and specific findings (CMV owl-eye inclusions, Listeria microabscesses, syphilis, toxoplasma).

6Placenta accreta spectrum is defined by:

A.Abnormal adherence/invasion of placental villi into the myometrium due to absence of decidua

B.Premature separation of placenta

C.Chronic histiocytic intervillositis

D.Massive perivillous fibrin

Explanation: Placenta accreta spectrum (PAS) — placenta accreta (adherence to myometrium), increta (invasion into myometrium), and percreta (through serosa) — results from decidual deficiency, commonly at prior cesarean scar sites. Placenta previa + prior C-section is the major risk factor. Pathologic diagnosis confirms villi abutting myometrium without intervening decidua. Can cause severe peripartum hemorrhage.

7In monochorionic-diamniotic twin placentation, twin-to-twin transfusion syndrome (TTTS) results from:

A.Unbalanced deep AV vascular anastomoses between twins on a shared placenta

B.Two completely separate placentas

C.Absence of amniotic fluid in both sacs

D.Chronic histiocytic intervillositis

Explanation: TTTS occurs in monochorionic (shared placenta) twin pregnancies from unbalanced deep arteriovenous (AV) vascular anastomoses — a donor twin shunts blood via an unpaired artery into a cotyledon drained by a vein into the recipient. Donor becomes anemic/oliguric (stuck twin); recipient becomes plethoric/polyhydramnios. Fetoscopic laser ablation of anastomoses is therapeutic. Monochorionicity requires placental examination to identify.

8A hydropic fetus at 20 weeks gestation has anemia, hepatosplenomegaly, and placentomegaly. Fetal erythrocytes show intranuclear inclusions ('lantern cells') with IHC positivity for a viral capsid protein. Which infection?

A.Parvovirus B19

B.CMV

C.Toxoplasma

D.Syphilis

Explanation: Parvovirus B19 infects erythroid progenitors in fetal liver, causing aplastic anemia, high-output cardiac failure, and nonimmune hydrops. Characteristic 'lantern cells' (enlarged erythroid precursors with intranuclear inclusions) are pathognomonic. Parvovirus B19 IHC or in situ hybridization confirms. Maternal IgM testing and ultrasound-guided intrauterine transfusion are management options.

9Nonimmune hydrops fetalis has many causes. Which is a common chromosomal cause associated with cystic hygroma?

A.Turner syndrome (45,X)

B.Klinefelter syndrome (47,XXY)

C.Trisomy 21

D.Fragile X

Explanation: Turner syndrome (45,X) classically presents with cystic hygroma (cystic lymphangioma from failed lymphatic-venous communication) and nonimmune hydrops in affected fetuses. Most 45,X conceptions are lost in utero. Live-born Turner has short stature, gonadal dysgenesis, coarctation of aorta/bicuspid valve, and webbed neck. Alpha-thalassemia (Hb Barts) is another major cause of hydrops.

10Potter sequence (oligohydramnios sequence) results from:

A.Inadequate amniotic fluid causing pulmonary hypoplasia, limb contractures, and flattened facies

B.Excess amniotic fluid

C.Isolated chromosomal aneuploidy

D.Mitochondrial mutation

Explanation: Potter sequence results from severe oligohydramnios, which causes pulmonary hypoplasia (main cause of perinatal death), Potter facies (flattened nose, low-set ears, micrognathia), and limb deformities (contractures, talipes). Causes: bilateral renal agenesis (classic), ARPKD, severe obstructive uropathy (posterior urethral valves), or prolonged amniotic fluid leak.

About the ABPath Pediatric Pathology Exam

The ABPath Pediatric Pathology subspecialty certification validates expert-level diagnostic knowledge across perinatal and placental pathology, pediatric solid tumors (neuroblastoma, Wilms, rhabdomyosarcoma, Ewing, hepatoblastoma), pediatric CNS tumors (medulloblastoma, AT/RT), pediatric organ-system pathology (biliary atresia, Hirschsprung, CPAM, CHD, pediatric ALL), metabolic/storage disorders, and fetal/pediatric autopsy. The 1-day computer-based exam has 170 Written/Practical + 65 Virtual Microscopy items (235 total). Requires primary ABPath AP or AP/CP plus a 12-month ACGME-accredited Pediatric Pathology fellowship.

Questions

235 scored questions

Time Limit

1-day CBT (3h 8m Written/Practical + 3h 15m Virtual Microscopy)

Passing Score

Scaled criterion-referenced pass score (modified Angoff)

Exam Fee

$2,100 (includes $200 nonrefundable administrative fee) (American Board of Pathology (ABPath) / Pearson VUE)

ABPath Pediatric Pathology Exam Content Outline

15% W/P • 10% VM

Perinatal Pathology: Fetal/Neonatal

Fetal autopsy (organ weights by GA, maceration), IUFD workup, hydrops (parvovirus B19, α-thalassemia, Turner), chorioamnionitis/funisitis, TORCH, dysmorphology, malformation vs disruption vs deformation.

7% W/P • 10% VM

Perinatal Pathology: Placenta

Amsterdam consensus lesions — maternal vascular malperfusion (infarcts, decidual vasculopathy), fetal vascular malperfusion (thrombotic vasculopathy, avascular villi), acute/chronic chorioamnionitis, villitis of unknown etiology (VUE), placenta accreta, TTTS, hydatidiform mole (complete vs partial — p57/CDKN1C, androgenetic diploidy vs triploidy).

7% W/P • 8% VM

Alimentary Tract (GI)

Hirschsprung disease (calretinin, acetylcholinesterase, rectal biopsy), NEC, pyloric stenosis, meconium ileus (CFTR), intestinal atresia, malrotation, eosinophilic esophagitis, pediatric IBD, juvenile polyps.

7% W/P • 2% VM

Diagnostic/Technical Procedures

Frozen section, fetal/pediatric autopsy, placental examination, PAS-D, oil red O, Prussian blue, reticulin; FISH, chromosomal microarray, NGS, electron microscopy (ciliopathies, storage diseases).

6% W/P • 9% VM

Hematopoietic System

Pediatric B-ALL (Ph+, t(12;21) ETV6-RUNX1, MLL/KMT2A, hyperdiploid/hypodiploid), pediatric AML, LCH (BRAF V600E, CD1a, S100, langerin, Birbeck granules), Rosai-Dorfman, JXG, Burkitt MYC, HLH, XLP, neuroblastoma bone marrow involvement.

6% W/P • 6% VM

Respiratory & Mediastinum

CPAM types 1-4, bronchopulmonary sequestration, bronchogenic cyst, pulmonary hypoplasia, alveolar capillary dysplasia (FOXF1), surfactant disorders (SP-B, SP-C, ABCA3, NKX2.1), hyaline membrane disease, BPD, pleuropulmonary blastoma (DICER1), mediastinal germ cell tumors, thymic lesions.

6% W/P • 3% VM

Cardiovascular System

Congenital heart disease (conotruncal, septal defects, HLHS, coarctation, TGA, tetralogy of Fallot, Ebstein), cardiomyopathies (HCM, DCM, Barth, noncompaction), endocardial fibroelastosis, rhabdomyoma (TSC), Kawasaki vasculitis.

6% W/P • 8% VM

Hepatobiliary & Pancreas

Biliary atresia (Kasai), neonatal hepatitis, α1-antitrypsin (PAS-D globules), Alagille (JAG1/NOTCH2), PFIC 1-6, hepatoblastoma (fetal/embryonal/small cell undiff; β-catenin nuclear, AFP), fibrolamellar HCC (DNAJB1-PRKACA), mesenchymal hamartoma, undifferentiated embryonal sarcoma, solid pseudopapillary neoplasm.

5% W/P • 6% VM

Central Nervous System

Medulloblastoma (WHO 2021: WNT, SHH, Gp3, Gp4), pediatric-type diffuse gliomas (H3 K27-altered DMG, H3 G34), AT/RT (INI1/SMARCB1 loss), ependymoma (PFA/PFB, ZFTA fusion), pilocytic astrocytoma (KIAA1549-BRAF), choroid plexus tumors, HIE of newborn.

5% W/P • 6% VM

Kidney & Urinary System

Wilms tumor (triphasic; favorable vs anaplastic; WT1; nephrogenic rests ILNR/PLNR), clear cell sarcoma of kidney (BCOR ITD), malignant rhabdoid (SMARCB1/INI1 loss), mesoblastic nephroma (cellular type ETV6-NTRK3), cystic renal disease (ARPKD, ADPKD, MCDK), Denys-Drash, Beckwith-Wiedemann.

5% W/P • 5% VM

General Pathologic Principles & Syndromes

Cancer predisposition (Li-Fraumeni TP53, BWS, DICER1, NF1/2, TSC, VHL, Costello HRAS, Noonan, Gorlin PTCH1), storage disorders (MPS, Gaucher, Niemann-Pick, Pompe, Fabry), mitochondrial, dysmorphology, mosaicism.

4% W/P • 6% VM

Soft Tissue, Peripheral Nerve & Muscle

Rhabdomyosarcoma (embryonal — common in kids; alveolar PAX3/7-FOXO1 fusion), infantile fibromatosis, infantile fibrosarcoma (ETV6-NTRK3), lipoblastoma (PLAG1), Ewing sarcoma (EWSR1-FLI1/ERG, CD99), DSRCT (EWSR1-WT1), synovial sarcoma (SS18-SSX), MPNST.

3% W/P • 3% VM

Skeletal System

Osteosarcoma variants, Ewing of bone, osteochondroma, chondroblastoma, LCH of bone, aneurysmal bone cyst, fibrous dysplasia (GNAS), osteogenesis imperfecta (COL1A1/2), achondroplasia (FGFR3), rickets.

3% W/P • 5% VM

Skin

Infantile hemangioma (GLUT1+) vs vascular malformations (GLUT1-), congenital melanocytic nevi, pilomatrixoma (CTNNB1), JXG, Spitz/SAMPUS/STUMP, mastocytosis.

3% W/P • 3% VM

Endocrine (excluding ovary/testis)

Neuroblastoma (INRG stratification L1/L2/M/MS, INSS stage 1-4/4S, MYCN amplification = poor prognosis, Shimada histology classification, ploidy), ganglioneuroblastoma, ganglioneuroma, pheochromocytoma, adrenal cortical tumors, pediatric thyroid carcinoma, MEN syndromes, pituitary.

2% W/P • 2% VM

Female Reproductive / Male / DSD / Special Senses / Breast

Female: immature teratoma, dysgerminoma, yolk sac (Schiller-Duval, AFP), Sertoli-Leydig (DICER1), SCT. Male: prepubertal yolk sac testis, teratoma, gonadoblastoma (DSD with Y), paratesticular RMS. DSD: CAH, AIS, 5α-reductase, gonadal dysgenesis. Eye: retinoblastoma (RB1, Flexner-Wintersteiner, Fleurettes, Homer-Wright rosettes). Breast: juvenile fibroadenoma, gynecomastia.

2% + 2% W/P

Lab Management (Pediatric + Forensic)

Pediatric autopsy ethics, SUID/SIDS (triple risk), child abuse pathology (multiple fractures in various healing stages, retinal hemorrhages, subdural hematoma, bite marks), nonaccidental trauma, forensic interpretation.

How to Pass the ABPath Pediatric Pathology Exam

What You Need to Know

Passing score: Scaled criterion-referenced pass score (modified Angoff)
Exam length: 235 questions
Time limit: 1-day CBT (3h 8m Written/Practical + 3h 15m Virtual Microscopy)
Exam fee: $2,100 (includes $200 nonrefundable administrative fee)

Keys to Passing

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

ABPath Pediatric Pathology Study Tips from Top Performers

1Neuroblastoma prognostics rule: MYCN gene amplification (>10x copies) is an independent adverse prognostic factor regardless of stage or age. INRG Risk Stratification uses age (≥18 months higher risk), stage (L1/L2/M/MS), MYCN status, DNA ploidy, 11q aberration, and INPC Shimada histology (favorable vs unfavorable based on age + Schwannian stroma + mitosis-karyorrhexis index)

2Wilms tumor key facts: triphasic (blastemal, epithelial, stromal); favorable histology (no anaplasia) vs unfavorable (diffuse anaplasia — atypical tripolar mitoses, large hyperchromatic nuclei). WT1 gene (11p13). Nephrogenic rests are precursor lesions — perilobar (PLNR) vs intralobar (ILNR, associated with WT1 and Denys-Drash/WAGR)

3Rhabdomyosarcoma molecular rule: alveolar rhabdomyosarcoma (ARMS) harbors PAX3-FOXO1 (t(2;13), ~70%) or PAX7-FOXO1 (t(1;13)) fusions — worse prognosis; embryonal rhabdomyosarcoma (ERMS) is the most common pediatric variant, has loss of heterozygosity at 11p15, better prognosis. All rhabdos are myogenin (nuclear) + and MyoD1 + with desmin

4Placenta — p57/CDKN1C immunostain differentiates complete mole (androgenetic diploid, p57 NEGATIVE in villous stromal and cytotrophoblast nuclei) from partial mole (triploid 69,XXY/XXX, p57 POSITIVE). Complete mole has ~15-20% risk of persistent GTN vs ~5% in partial

5Ewing sarcoma: CD99 diffuse membranous positivity + EWSR1-FLI1 (t(11;22), ~85%) or EWSR1-ERG (t(21;22), ~10%). Small round blue cell differential includes neuroblastoma (PHOX2B, chromogranin/synapto +, CD99 −), alveolar RMS (myogenin +), DSRCT (desmin dot-like, EWSR1-WT1), lymphoma (CD45 +), and AT/RT (loss of INI1/SMARCB1)

Frequently Asked Questions

What is the ABPath Pediatric Pathology subspecialty certification?

The ABPath Pediatric Pathology subspecialty certification is awarded by the American Board of Pathology to diplomates who demonstrate expert-level diagnostic knowledge in perinatal and pediatric pathology — placenta, fetal autopsy, pediatric solid tumors (neuroblastoma, Wilms, rhabdomyosarcoma, Ewing, hepatoblastoma), pediatric CNS tumors, pediatric ALL/AML, pediatric organ-system pathology, metabolic/storage disorders, and forensic pediatric pathology. It qualifies pathologists to lead pediatric pathology services at children's hospitals.

Who is eligible to take the ABPath Pediatric Pathology exam?

Candidates must hold primary ABPath certification in good standing in AP or AP/CP and have completed 12 months of full-time training in an ACGME-accredited Pediatric Pathology fellowship. A valid unrestricted medical license is required. The fellowship includes perinatal/placental pathology, pediatric surgical pathology, and pediatric autopsy experience with forensic elements.

What is the format of the ABPath Pediatric Pathology exam?

The exam is a 1-day computer-based examination administered at Pearson VUE. It consists of 170 Written/Practical items (3 hours 8 minutes) plus 65 Virtual Microscopy items (3 hours 15 minutes) for a total of 235 one-best-answer multiple-choice questions. No glass slides are used — all images are digital. The practical examination includes images of gross and microscopic specimens, cytogenetic preparations, and histochemical/molecular stains.

How much does the 2026 ABPath Pediatric Pathology exam cost?

The 2026 examination fee is $2,100, which includes a $200 nonrefundable administrative fee. Cancellations by June 15 forfeit $500; cancellations after June 15 forfeit the full fee. Retakes within the 7-year qualification window require re-registration and full fee payment.

When is the 2026 exam administered?

The 2026 ABPath Pediatric Pathology Subspecialty Certification Exam is offered September 8-28, 2026 at Pearson VUE Professional Testing Centers. Applications open February 16, 2026 and must be submitted by May 15, 2026 (11:59 PM EST). There are no late application deadlines. Scheduling with Pearson VUE opens in July after the application is complete.

How is the exam scored?

ABPath uses criterion-referenced scoring with a cut-score set in advance by subject-matter experts using the modified Angoff method. A candidate's result depends on performance relative to the cut-score, not on other candidates. Results are posted to the Board Correspondence tab in PATHway approximately 6 weeks after the final week of subspecialty exams.

What are the highest-yield topics?

Perinatal/placental pathology (22% W/P combined) and fetal/neonatal pathophysiology are core — master Amsterdam consensus placental lesions (MVM, FVM, chorioamnionitis, VUE), twin placentation/TTTS, and complete vs partial hydatidiform mole (p57 immunostain). For tumors, master neuroblastoma INRG staging + MYCN amplification (poor prognosis), Wilms tumor favorable vs anaplastic histology + WT1, rhabdomyosarcoma subtypes (embryonal common in kids vs alveolar PAX3/7-FOXO1 fusion with worse prognosis), Ewing sarcoma (EWSR1-FLI1, CD99), hepatoblastoma (AFP, β-catenin), LCH (BRAF V600E, CD1a, langerin), AT/RT (SMARCB1/INI1 loss).

How should I study for this exam?

Use a structured 6-12 month plan during or after fellowship. Lead with placental/perinatal pathology (high yield and frequently missed), then pediatric solid tumors with molecular genetics, then pediatric organ-system pathology, then CNS/skin/bone/soft tissue tumors. Complete heavy Virtual Microscopy practice (65 VM items in 3h 15m). Take 2-3 timed full-length mock exams. Integrate ABPath blueprint, WHO Classification of Pediatric Tumors, Amsterdam Placental Consensus, Gilbert-Barness, Stocker and Dehner, and SPP educational resources.