100+ Free ABP Pediatric Endocrinology Practice Questions

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Question 1

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A 9-year-old presents with polyuria, polydipsia, and 5 kg weight loss over 3 weeks. Glucose is 412 mg/dL, pH 7.18, HCO3 10, ketones large, and islet autoantibodies are positive for GAD65, IA2, and ZnT8. Which statement best characterizes the immunologic basis of this disease?

Amyloid deposition within islets impairing insulin secretion

Autoantibody-mediated complement lysis of beta cells

T-cell mediated autoimmune destruction of pancreatic beta cells, with autoantibodies serving as disease markers rather than the primary effectors

Congenital agenesis of the dorsal pancreatic anlage

to track

2026 Statistics

Key Facts: ABP Pediatric Endocrinology Exam

~200

Total MCQ Items

4 timed sections, single-best-answer multiple-choice

~7 hrs

Total Exam Time

1-day CBT at Pearson VUE with scheduled breaks

25%

Diabetes Weight

Largest domain on 2026 content outline

$2,290

2026 Exam Fee

ABP initial certification fee

3 yrs

Required Fellowship

ACGME Pediatric Endocrinology fellowship

10 yr

Certification Validity

Time-limited; Continuing Certification (MOC) required

The ABP Pediatric Endocrinology exam is a 1-day ~200-question computer-based test from the American Board of Pediatrics administered at Pearson VUE. The 2026 content outline weights diabetes ~25%, adrenal ~15%, thyroid ~12%, growth ~12%, puberty ~10%, pituitary/posterior pituitary ~8%, calcium/bone ~8%, DSD/reproductive ~5%, and hypoglycemia/metabolic ~5%. The 2026 fee is $2,290 for initial certification. Eligibility requires ABP General Pediatrics certification plus a 3-year ACGME-accredited Pediatric Endocrinology fellowship.

Sample ABP Pediatric Endocrinology Practice Questions

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

1A 9-year-old presents with polyuria, polydipsia, and 5 kg weight loss over 3 weeks. Glucose is 412 mg/dL, pH 7.18, HCO3 10, ketones large, and islet autoantibodies are positive for GAD65, IA2, and ZnT8. Which statement best characterizes the immunologic basis of this disease?

A.Amyloid deposition within islets impairing insulin secretion

B.Autoantibody-mediated complement lysis of beta cells

C.T-cell mediated autoimmune destruction of pancreatic beta cells, with autoantibodies serving as disease markers rather than the primary effectors

D.Congenital agenesis of the dorsal pancreatic anlage

Explanation: Type 1 diabetes is a T-cell mediated autoimmune disease in which CD8+ cytotoxic T cells destroy pancreatic beta cells. Islet autoantibodies (GAD65, IA2, ZnT8, insulin) are markers of the autoimmune process used for diagnosis and prediction but are not themselves the primary mediators of beta-cell destruction.

2A 12-year-old with newly diagnosed T1DM is discharged on a basal-bolus regimen. Which insulin pairing correctly represents a modern MDI regimen?

A.Detemir plus regular insulin as needed for hyperglycemia only

B.NPH twice daily plus regular insulin at meals

C.Glargine plus NPH at bedtime

D.Glargine or detemir once/twice daily plus aspart, lispro, or glulisine at meals

Explanation: Modern basal-bolus MDI uses a long-acting analog (glargine, detemir, or degludec) for basal coverage and a rapid-acting analog (aspart, lispro, glulisine) for meals and corrections. This approach better mimics physiologic insulin secretion than older NPH/regular regimens and reduces hypoglycemia.

3Which statement about the 'honeymoon phase' of type 1 diabetes is most accurate?

A.It represents transient partial beta-cell recovery after diagnosis, during which insulin requirements fall below 0.5 U/kg/day

B.It is permanent and indicates spontaneous cure of T1DM

C.It occurs only in adults with latent autoimmune diabetes

D.It is characterized by complete loss of endogenous C-peptide

Explanation: The honeymoon (partial remission) phase typically occurs within weeks of diagnosis as residual beta cells recover after relief of glucose toxicity. Insulin needs fall, often <0.5 U/kg/day with A1c <7%. It lasts weeks to months. Families should be counseled this is temporary and insulin should be continued, not stopped.

4A 7-year-old in DKA presents with glucose 520 mg/dL, pH 7.05, HCO3 6, Na 132, K 5.4, and BUN 28. Per ISPAD/PES guidelines, which initial fluid strategy is most appropriate?

A.10 mL/kg isotonic saline bolus over 30-60 minutes if needed, then replace deficit over 24-48 hours with maintenance; avoid cumulative fluids >40 mL/kg in the first 4 hours

B.Aggressive 40 mL/kg bolus over 1 hour followed by D5 half-normal saline at 2x maintenance

C.Fluid restriction to two-thirds maintenance to prevent cerebral edema

D.Bolus with D10 half-normal saline to treat hyperglycemia

Explanation: Pediatric DKA fluid management: initial 10 mL/kg isotonic bolus (repeat if shock persists), then rehydrate evenly over 24-48 hours. The 2018 PECARN FLUID trial showed no difference in neurologic outcome between faster and slower rehydration, but ISPAD/PES still caution against >40 mL/kg cumulative in the first 4 hours as prudent practice.

5In pediatric DKA management, what is the recommended insulin infusion rate and the rationale for avoiding an initial insulin bolus?

A.0.01 U/kg/hr infusion with no dose adjustment until ketosis resolves

B.0.3 U/kg bolus followed by 0.3 U/kg/hr infusion to rapidly normalize glucose

C.0.05-0.1 U/kg/hr continuous; avoid bolus because it does not improve outcomes and increases risk of hypokalemia and rapid osmolar shifts

D.Subcutaneous rapid-acting insulin every 2 hours with no continuous infusion

Explanation: ISPAD and PES recommend continuous IV insulin at 0.05-0.1 U/kg/hr without an initial bolus. A bolus provides no additional benefit and may contribute to hypokalemia, rapid osmolar shifts, and cerebral edema risk. Infusion continues until acidosis resolves (pH >7.3, HCO3 >15, anion gap closed).

6Four hours into DKA treatment, a 6-year-old develops headache, bradycardia, rising blood pressure, and altered mental status. Which is the most appropriate immediate intervention?

A.Give a 20 mL/kg normal saline bolus to improve perfusion

B.Double the insulin infusion rate to clear ketones faster

C.Administer 3% hypertonic saline 5 mL/kg over 15 minutes (or mannitol 0.5-1 g/kg) and reduce IV fluid rate

D.Administer IV dexamethasone 0.6 mg/kg

Explanation: Cerebral edema in DKA (Muir criteria) is a medical emergency. First-line treatment is 3% hypertonic saline 2.5-5 mL/kg over 10-15 minutes, or mannitol 0.5-1 g/kg. Fluid rate should be reduced by about one-third. Bolusing more fluid would worsen cerebral edema; steroids have no role.

7A 14-year-old on an insulin pump with Dexcom G7 asks about 'time in range' (TIR). Which TIR target does ADA/ISPAD recommend for most children and adolescents with T1DM?

A.>70% TIR (70-180 mg/dL), with <4% time below 70 mg/dL and <1% below 54 mg/dL

B.>50% TIR with no limits on time below range

C.>95% TIR with any time below range acceptable

D.TIR is not recommended in pediatrics — use A1c alone

Explanation: ADA and ISPAD endorse TIR >70% (glucose 70-180 mg/dL) as the general target for most youth with T1DM, with time below 70 <4% and time below 54 <1%. TIR correlates with A1c and microvascular complications and is considered a key CGM-era metric.

8Which of the following is a characteristic of hybrid closed-loop insulin delivery systems (e.g., Tandem Control-IQ, Omnipod 5)?

A.Fully autonomous — user does not need to interact with the pump at all

B.Automated basal adjustment and correction boluses based on CGM input, with user still announcing meals for bolus calculation

C.Closed-loop delivery without any CGM input

D.Manual basal adjustment only; no automated corrections

Explanation: Hybrid closed-loop systems (Control-IQ, Omnipod 5, MiniMed 780G) automatically modulate basal insulin and deliver automatic correction boluses using CGM data, but users still must announce carbohydrate intake for meal boluses. They improve TIR and reduce hypoglycemia compared to open-loop pump or MDI therapy.

9A 10-year-old with T1DM becomes unconscious at home after missing dinner. He has an intact swallow reflex but cannot cooperate. What is the best out-of-hospital treatment the family should have available?

A.IV dextrose 25% — any family member can administer

B.Subcutaneous regular insulin

C.Oral glucose tablets forced into the cheek

D.Intramuscular or intranasal glucagon

Explanation: Severe hypoglycemia with altered mental status requires parenteral glucagon — either intramuscular/subcutaneous (traditional kits, dose 0.5 mg <25 kg, 1 mg ≥25 kg) or intranasal (Baqsimi, 3 mg fixed dose). Oral glucose is contraindicated when the child cannot protect the airway. Families cannot safely start IVs.

10A 13-year-old with T1DM develops gastroenteritis with vomiting. Home BG is 70 mg/dL. Which 'mini-dose glucagon' strategy is appropriate?

A.0.1 unit/kg SC regular insulin to stimulate glucagon release

B.1 full adult dose (1 mg) SC every 15 minutes until euglycemia

C.1 unit (10 μg) of glucagon per year of age SC (max 15 units), using an insulin syringe drawn from a glucagon kit, repeated once if needed

D.Oral glucagon tablets 50 mg

Explanation: Haymond's mini-dose glucagon protocol gives 10 μg (1 'unit' on an insulin syringe) per year of age, max 150 μg, SC, to treat impending hypoglycemia during illness when oral intake fails but the child is conscious. It avoids the nausea of a full dose and can be repeated once.

About the ABP Pediatric Endocrinology Exam

The ABP Pediatric Endocrinology subspecialty certification validates expert-level diagnostic and management knowledge across type 1 and type 2 diabetes, diabetic ketoacidosis, MODY and neonatal diabetes, thyroid disorders (Hashimoto, Graves, congenital hypothyroidism), adrenal disorders (congenital adrenal hyperplasia, Addison, Cushing, pheochromocytoma), growth (GH deficiency, Turner syndrome), puberty (precocious and delayed), pituitary (hypopituitarism, diabetes insipidus, SIADH), calcium/bone (rickets, hypocalcemia, PHP), disorders of sexual development, PCOS, obesity, hypoglycemia, and pediatric endocrine genetics. Requires ABP General Pediatrics certification plus a 3-year ACGME-accredited Pediatric Endocrinology fellowship.

Questions

200 scored questions

Time Limit

1-day CBT (~7 hours across 4 sections with breaks)

Passing Score

Scaled criterion-referenced pass score (~180 on 200-scale)

Exam Fee

$2,290 initial certification fee (2026) (American Board of Pediatrics (ABP) / Pearson VUE)

ABP Pediatric Endocrinology Exam Content Outline

~25%

Diabetes Mellitus

T1D autoantibodies (GAD65, IA2, ZnT8, insulin), honeymoon, MDI vs CSII, CGM, hypoglycemia unawareness; DKA (fluids 1.5x maintenance, insulin 0.05-0.1 U/kg/hr, avoid bicarbonate, cerebral edema risk, mannitol/hypertonic saline); T2D (metformin, GLP-1 — semaglutide/liraglutide); MODY (HNF1A/HNF4A sulfonylurea-responsive, GCK benign); neonatal diabetes (KCNJ11/ABCC8 K-ATP — transition to glyburide).

~15%

Adrenal Disorders

21-hydroxylase CAH (classic salt-wasting, simple-virilizing, nonclassic; 17-OHP newborn screen; glucocorticoid + fludrocortisone, stress-dose steroids), 11β-hydroxylase CAH (hypertension), 17α-hydroxylase, 3β-HSD; Addison (autoimmune, ALD ABCD1); Cushing (exogenous steroid, pituitary Cushing disease, ectopic ACTH, adrenal tumors); pheochromocytoma (VHL, RET/MEN2, SDHx).

~12%

Thyroid Disorders

Hashimoto (anti-TPO, anti-Tg), congenital hypothyroidism (newborn TSH screen, dysgenesis vs dyshormonogenesis, levothyroxine 10-15 mcg/kg/day), Graves (TSI/TRAb, methimazole first-line peds — PTU avoided for hepatotoxicity, RAI, thyroidectomy), neonatal Graves from maternal TRAb, pediatric papillary thyroid carcinoma, MEN2 RET prophylactic thyroidectomy.

~12%

Growth Disorders

GH deficiency (stim testing — arginine-clonidine, insulin tolerance, glucagon; low IGF-1/IGFBP-3; MRI; rhGH 0.15-0.3 mg/kg/week), constitutional delay vs familial short stature, Turner syndrome 45,X (GH + estrogen, coarctation and renal screening), Noonan syndrome, SHOX deficiency, SGA, idiopathic short stature, achondroplasia FGFR3 (vosoritide).

~10%

Puberty Disorders

Central precocious puberty (hypothalamic hamartoma, idiopathic in girls, CNS lesions in boys; GnRH agonists — leuprolide, histrelin); peripheral precocious puberty (McCune-Albright GNAS mosaic, familial male-limited LHCGR, CAH, ovarian/testicular/adrenal tumors, exogenous); delayed puberty — Turner, Klinefelter 47,XXY, Kallmann syndrome with anosmia (ANOS1/KAL1, FGFR1), CHARGE (CHD7).

~8%

Pituitary & Posterior Pituitary

Hypopituitarism (septo-optic dysplasia, PROP1/POU1F1, craniopharyngioma, germinoma, TBI, radiation), prolactinoma (cabergoline), central DI (desmopressin, water deprivation test), nephrogenic DI (AVPR2 X-linked, AQP2; thiazide + amiloride + indomethacin), SIADH, cerebral salt wasting (differentiate by volume status).

~8%

Calcium, Phosphate & Bone

Nutritional rickets (low 25-OH-D, high PTH, high alk phos), X-linked hypophosphatemic rickets (PHEX, elevated FGF23 — burosumab), VDDR type 1 (CYP27B1) and type 2 (VDR); DiGeorge 22q11.2 hypocalcemia, pseudohypoparathyroidism 1a Albright osteodystrophy GNAS; Williams syndrome ELN, familial hypocalciuric hypercalcemia CASR; osteogenesis imperfecta COL1A1/A2 (bisphosphonates).

~5%

DSD & Reproductive

46,XX DSD (CAH most common cause of virilization of XX newborn, aromatase deficiency CYP19A1), 46,XY DSD (complete/partial AIS AR, 5α-reductase deficiency SRD5A2, 17β-HSD3, Leydig hypoplasia LHCGR, gonadal dysgenesis), gonadoblastoma risk with Y chromosome, PCOS (Rotterdam, metformin/COCP), Kallmann (ANOS1, FGFR1, PROKR2).

~5%

Hypoglycemia & Metabolic

Critical sample panel at time of hypoglycemia (glucose, insulin, C-peptide, BHB, FFA, cortisol, GH, lactate, ammonia); congenital hyperinsulinism (focal vs diffuse, ABCC8/KCNJ11 diazoxide-unresponsive, GLUD1 HI/HA diazoxide-responsive); ketotic hypoglycemia; MCAD hypoketotic; GSD I (von Gierke — hepatomegaly, lactic acidosis).

How to Pass the ABP Pediatric Endocrinology Exam

What You Need to Know

Passing score: Scaled criterion-referenced pass score (~180 on 200-scale)
Exam length: 200 questions
Time limit: 1-day CBT (~7 hours across 4 sections with breaks)
Exam fee: $2,290 initial certification fee (2026)

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 Pediatric Endocrinology Study Tips from Top Performers

1DKA management pearls: IV fluids at 1.5x maintenance (not aggressive boluses unless shock), continuous insulin infusion 0.05-0.1 U/kg/hr starting 1 hour after fluids (no bolus), DO NOT give bicarbonate (increases cerebral edema risk), monitor Na (corrected Na should rise as glucose falls), watch for cerebral edema (headache, altered mental status, bradycardia, hypertension) → treat with mannitol 0.5-1 g/kg IV or 3% hypertonic saline 5-10 mL/kg

2CAH 21-hydroxylase (CYP21A2) — the classic vignette: virilized 46,XX newborn or salt-wasting crisis in a 2-week-old with hyponatremia, hyperkalemia, hypoglycemia and markedly elevated 17-OHP. Treat with hydrocortisone (glucocorticoid) + fludrocortisone (mineralocorticoid) + salt supplementation in infancy. Stress-dose steroids for illness/surgery. Nonclassic CAH presents in adolescence with hirsutism/oligomenorrhea

3MODY vs T1D vs T2D — MODY clues: strong autosomal dominant family history (3 generations), onset <25 y, negative autoantibodies, non-obese. HNF1A and HNF4A MODY are highly sulfonylurea-responsive (can transition off insulin). GCK-MODY causes mild fasting hyperglycemia with normal HbA1c trajectory — no treatment needed, excellent prognosis. Neonatal diabetes (<6 mo) from KCNJ11/ABCC8 K-ATP mutation → switch from insulin to oral sulfonylurea (glyburide)

4Precocious puberty workup: bone age first, then LH (basal or after GnRH stim). Pubertal-range LH → central precocious puberty → brain MRI (always in boys; girls if <6 y or neurologic signs). Prepubertal LH with signs of puberty → peripheral (McCune-Albright — café-au-lait with irregular coast-of-Maine borders + polyostotic fibrous dysplasia + GNAS mosaic; CAH; ovarian/testicular/adrenal tumors; exogenous hormone). Central: GnRH agonist (leuprolide depot, histrelin implant)

5Turner syndrome (45,X) checklist: GH therapy starting early childhood for short stature, estrogen induction at 11-12 y with progressive escalation, ECHO for bicuspid aortic valve/coarctation, renal US for horseshoe kidney, audiology, thyroid screening (autoimmune), and fertility counseling (premature ovarian insufficiency). Avoid growth hormone if type A aortic dissection risk is elevated

Frequently Asked Questions

What is the ABP Pediatric Endocrinology subspecialty certification?

The ABP Pediatric Endocrinology subspecialty certification is awarded by the American Board of Pediatrics to pediatricians who demonstrate expert-level knowledge in pediatric diabetes (T1D, T2D, MODY, neonatal), thyroid disease, adrenal disorders (CAH, Addison, Cushing), growth and puberty, pituitary and posterior pituitary disorders, calcium and bone metabolism, disorders of sexual development, PCOS, obesity, and hypoglycemia. It qualifies physicians to lead pediatric endocrine services and consult on complex endocrine disorders in children and adolescents.

Who is eligible to take the ABP Pediatric Endocrinology exam?

Candidates must hold ABP General Pediatrics certification in good standing (or be eligible) and must have completed 3 years of full-time training in an ACGME-accredited Pediatric Endocrinology fellowship. A valid unrestricted medical license is required, and the fellowship program director must attest to satisfactory completion including the ABP Subboard Scholarly Activity requirement.

What is the format of the ABP Pediatric Endocrinology exam?

The exam is a 1-day computer-based examination delivered at Pearson VUE Professional Testing Centers. It consists of approximately 200 single-best-answer multiple-choice questions distributed across 4 timed sections, for roughly 7 hours of testing plus breaks. Questions are a mix of recall, case-based clinical vignettes, and interpretation of labs, genetic testing, imaging, and growth curves.

How much does the 2026 ABP Pediatric Endocrinology exam cost?

The 2026 initial certification fee is approximately $2,290. Fees are payable at the time of application and may be subject to cancellation or withdrawal policies per the ABP Booklet of Information. Subspecialty Continuing Certification (MOC) enrollment and question-of-the-week/MOCA-Peds assessment incur additional ongoing fees.

When is the 2026 exam administered?

The ABP Pediatric Endocrinology Subspecialty Certifying Examination is administered annually, typically in the fall, at Pearson VUE Professional Testing Centers. Application windows open in the spring; check the ABP Dates and Fees page for the exact 2026 application and testing dates.

How is the exam scored?

ABP uses criterion-referenced scoring with a cut score set in advance by subject-matter experts using the modified Angoff method. A candidate's pass/fail result depends on performance relative to the cut score (~180 on a 200-scale), not on other candidates. Scaled score reports include performance by content domain to guide future learning.

What are the highest-yield topics?

Diabetes is the single largest domain (~25%) — master DKA management (fluids, insulin infusion 0.05-0.1 U/kg/hr, avoid bicarbonate, recognize cerebral edema), T1D autoantibodies, MODY genotype-phenotype (HNF1A sulfonylurea-responsive, GCK benign mild hyperglycemia), and neonatal diabetes K-ATP mutations (glyburide). Master 21-hydroxylase CAH (classic salt-wasting, simple-virilizing, nonclassic; 17-OHP screen; glucocorticoid + mineralocorticoid replacement), Turner syndrome management, GH deficiency stim testing, precocious puberty workup (central vs peripheral; GnRH agonists), congenital hypothyroidism, and Graves disease (methimazole first-line in children).

How should I study for this exam?

Use a structured 6-12 month plan during the final fellowship year. Lead with diabetes and DKA (largest domain), then adrenal/CAH, then thyroid, then growth and puberty, then pituitary/calcium/DSD/hypoglycemia. Integrate the ABP content outline, ISPAD pediatric diabetes guidelines, Pediatric Endocrine Society (PES) board review courses, Sperling Pediatric Endocrinology textbook, and Pediatrics in Review. Use question banks heavily — complete at least 2,000 practice questions and take 2-3 timed full-length mock exams before test day.