Arab Board Pediatrics Part 1 study materials
Arab Board Pediatrics Part 1 study resources

Arab Board Pediatrics Part 1: Pediatric Endocrinology and Metabolism

Arab Board Pediatrics Part 1 · Work through your exam, one topic at a time.

All guide sections

Pediatric Endocrinology and Metabolism

What to master

Know growth hormone and thyroid physiology, including congenital hypothyroidism (screening, jaundice, constipation, large fontanelle) and the importance of early treatment for neurodevelopment. Understand diabetes mellitus types: type 1 (autoimmune, ketosis-prone) versus type 2 (obesity, insulin resistance, acanthosis nigricans). Master diabetic ketoacidosis management-fluids, insulin, potassium, and cerebral edema risk. Know adrenal disorders: congenital adrenal hyperplasia (21-hydroxylase deficiency, virilization, salt wasting) and Addison disease. Understand puberty timing and the difference between central (GnRH-dependent) and peripheral precocious puberty.

Concepts that recur

Hypoglycemia in a neonate or child requires a critical sample (insulin, cortisol, growth hormone, ketones, lactate, ammonia) before correction. Metabolic disorders present with acidosis, hyperammonemia, or hypoglycemia; the fasting-versus-feeding clue is key. Vitamin D deficiency causes rickets-know biochemical pattern (low calcium, low phosphate, high alkaline phosphatase, high PTH). Obesity complications include insulin resistance, hypertension, and sleep apnea. Thyroid nodules in children have higher malignancy risk than in adults.

Traps

Examiners test DKA fluid strategy-rapid fluid shifts can precipitate cerebral edema; use isotonic fluids and gradual correction. Another trap is congenital hypothyroidism presenting late because screening was missed; do not rely on clinical signs alone. Beware precocious puberty questions that confuse central with peripheral-GnRH stimulation testing distinguishes them.

Rule of thumb

In DKA, treat dehydration first, add insulin after fluids, and always check potassium before insulin-insulin drives potassium intracellularly and can cause fatal hypokalemia.