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SMLE Pediatrics Syllabus

The Pediatrics syllabus for SMLE in full: 2 chapters and 6 topics, every one listed below, plus 50 Pediatrics flashcards with answers.

2Chapters
6Topics
50Flashcards

Pediatrics syllabus: all 2 chapters

Expand any chapter to see its topics and sub-topics.

  1. Neonatology

    3 topics
    • Neonatal Resuscitation
    • Neonatal Jaundice
    • Neonatal Sepsis
  2. Growth and Development

    3 topics
    • Milestones
    • Growth Disorders
    • Developmental Disorders

SMLE Pediatrics flashcards — 50 questions with answers

  1. During neonatal resuscitation, what is the correct compression-to-ventilation ratio and combined rate for a newborn requiring chest compressions?

    A ratio of $3:1$ (3 compressions to 1 breath), giving 90 compressions and 30 breaths per minute, for a total of $120$ events per minute.

  2. In the initial steps of neonatal resuscitation, what three questions determine whether a newborn stays with the mother or requires intervention?

    Is the baby term? Is there good muscle tone? Is the baby breathing or crying? If all three are 'yes,' routine care with the mother; if any is 'no,' begin the initial steps (warm, dry, stimulate, position airway).

  3. What heart rate threshold during neonatal resuscitation indicates the need to begin positive pressure ventilation (PPV)?

    A heart rate below $100$ beats/min (or apnea/gasping) after the initial steps mandates starting PPV.

  4. At what heart rate during neonatal resuscitation should chest compressions be initiated?

    When the heart rate remains below $60$ beats/min despite $30$ seconds of effective PPV (ideally with an endotracheal tube and $100\%$ oxygen).

  5. What is the recommended dose and preferred route of epinephrine in neonatal resuscitation?

    Intravenous/intraosseous epinephrine $0.01$–$0.03$ mg/kg (of $1{:}10{,}000$ concentration); the preferred route is the umbilical vein. Endotracheal dosing is higher at $0.05$–$0.1$ mg/kg if no IV access.

  6. What are the five components of the APGAR score, and when is it assessed?

    Appearance (color), Pulse (heart rate), Grimace (reflex irritability), Activity (muscle tone), and Respiration; each scored $0$–$2$ for a max of $10$, assessed at $1$ and $5$ minutes (and every 5 min up to 20 if low).

  7. What preductal oxygen saturation target is expected at 5 minutes and at 10 minutes of life during neonatal resuscitation?

    About $80$–$85\%$ at 5 minutes and $85$–$95\%$ at 10 minutes, measured by a right-hand (preductal) pulse oximeter.

  8. For term newborns, what initial oxygen concentration is recommended when starting PPV, versus preterm infants?

    Term and late-preterm ($\geq 35$ weeks) start with $21\%$ oxygen (room air); preterm infants ($<35$ weeks) start with $21$–$30\%$, then titrate to target saturations.

  9. What defines pathologic (versus physiologic) neonatal jaundice by timing of onset?

    Jaundice appearing in the first $24$ hours of life is always pathologic; physiologic jaundice appears after $24$ hours, peaks around days $3$–$5$, and resolves within $1$–$2$ weeks.

  10. What is the most common cause of severe early (first 24 hours) neonatal hyperbilirubinemia due to hemolysis?

    Isoimmune hemolytic disease from blood group incompatibility—Rh incompatibility (most severe) and ABO incompatibility (most common), producing unconjugated hyperbilirubinemia with a positive direct Coombs test.

  11. Distinguish unconjugated from conjugated neonatal hyperbilirubinemia by the conjugated (direct) bilirubin threshold.

    Conjugated hyperbilirubinemia is defined by a direct bilirubin $>1$ mg/dL (or $>20\%$ of total). Conjugated jaundice is always pathologic and suggests cholestasis (e.g., biliary atresia).

  12. What is kernicterus, and which bilirubin fraction causes it?

    Kernicterus is bilirubin-induced neurologic dysfunction from deposition of free unconjugated (fat-soluble) bilirubin in the basal ganglia and brainstem, causing lethargy, hypertonia, opisthotonus, and later choreoathetoid cerebral palsy and hearing loss.

  13. Compare breastfeeding jaundice and breast milk jaundice by timing and mechanism.

    Breastfeeding (breastfeeding-failure) jaundice appears in the first week from inadequate intake and dehydration (increased enterohepatic circulation). Breast milk jaundice appears later (days $5$–$14$, persisting weeks) due to substances in milk that increase enterohepatic reabsorption.

  14. What is the first-line treatment for significant unconjugated neonatal hyperbilirubinemia, and how does it work?

    Phototherapy with blue light ($\sim 460$–$490$ nm), which converts unconjugated bilirubin into water-soluble photoisomers (lumirubin) that are excreted without conjugation.

  15. When is exchange transfusion indicated in neonatal jaundice?

    When total serum bilirubin exceeds the exchange threshold on the nomogram despite intensive phototherapy, or when there are signs of acute bilirubin encephalopathy; it rapidly removes bilirubin and antibody-coated red cells.

  16. What enzyme deficiency causes Crigler-Najjar and Gilbert syndromes, and how do they differ in severity?

    Deficiency of UDP-glucuronosyltransferase (UGT1A1). Crigler-Najjar type I has complete absence (severe, kernicterus risk); type II is partial; Gilbert syndrome is a mild reduction causing benign intermittent unconjugated hyperbilirubinemia with stress.

  17. How is early-onset neonatal sepsis defined by timing, and what is the classic causative organism?

    Early-onset sepsis occurs within the first $72$ hours (often $\leq 24$ h) of life, acquired vertically from the maternal genital tract; the classic pathogen is Group B Streptococcus (Streptococcus agalactiae), followed by E. coli.

  18. How does late-onset neonatal sepsis differ from early-onset in timing and typical organisms?

    Late-onset sepsis presents after $72$ hours (up to $\sim 90$ days), often nosocomial or community-acquired; common organisms include coagulase-negative Staphylococci, Staphylococcus aureus, E. coli, Klebsiella, and Listeria.

  19. What are the major maternal risk factors for early-onset neonatal sepsis?

    Maternal GBS colonization, prolonged rupture of membranes ($\geq 18$ hours), chorioamnionitis/maternal fever, preterm labor, and a previous infant with invasive GBS disease.

  20. What is the standard empiric antibiotic regimen for early-onset neonatal sepsis?

    Ampicillin plus an aminoglycoside (gentamicin). Cefotaxime is added if Gram-negative meningitis is suspected; ampicillin specifically covers Listeria and Enterococcus.

Show the other 30 Pediatrics flashcards
  1. What intrapartum prophylaxis prevents early-onset GBS neonatal sepsis, and who receives it?

    Intravenous penicillin G (or ampicillin) given intrapartum to mothers who are GBS-positive on $35$–$37$ week screening, have GBS bacteriuria, a prior GBS-affected infant, or unknown status with risk factors.

  2. What are common nonspecific clinical signs of neonatal sepsis?

    Temperature instability (hypo- or hyperthermia), respiratory distress/apnea, poor feeding, lethargy, hypotonia, tachycardia or bradycardia, hypoglycemia, jaundice, and poor perfusion. Signs are subtle and nonspecific ('not doing well').

  3. What is the gold-standard diagnostic test for neonatal sepsis, and what supportive labs are used?

    Blood culture is the gold standard. Supportive tests include CBC (neutropenia, elevated I:T ratio $>0.2$), C-reactive protein, procalcitonin, and lumbar puncture/CSF analysis if meningitis is suspected.

  4. By what age should a normally developing infant demonstrate social smile and head control?

    Social smile appears by about $2$ months; steady head control (no head lag) is achieved by around $4$ months.

  5. At what age does a typical infant sit without support and transfer objects hand to hand?

    Sitting without support and transferring objects between hands occur at around $6$ months.

  6. What gross-motor milestones are expected at 9 months and at 12 months?

    At $9$ months: sits well, crawls, and pulls to stand. At $12$ months: stands alone and may take first independent steps (walks).

  7. When does a child typically develop a pincer grasp and object permanence?

    A mature pincer grasp develops around $9$–$12$ months, and object permanence (looks for a hidden object) emerges around $9$ months.

  8. What are the expected language milestones from cooing to two-word phrases?

    Cooing at $\sim 2$ months, babbling at $\sim 6$ months, first words ('mama/dada' nonspecific) at $\sim 9$ months and specific at $\sim 12$ months, $\sim 5$–$10$ words at $15$–$18$ months, and two-word phrases by $24$ months.

  9. By what age should a child walk independently, and what is the red-flag age for failure to walk?

    Independent walking is expected by $12$–$15$ months; failure to walk by $18$ months is a red flag warranting evaluation (e.g., for cerebral palsy or myopathy such as Duchenne).

  10. What fine-motor/drawing milestones correspond to ages 2, 3, and 4 years?

    At $2$ years: copies a vertical line; at $3$ years: copies a circle (and builds a tower of ~8 cubes); at $4$ years: copies a cross/square. Rule of thumb: draws a person with a number of parts roughly equal to age.

  11. What is the formula-based rule of thumb for estimating expected height at ages 2, 3, and 4 years relative to birth length?

    Birth length ($\sim 50$ cm) roughly doubles by age $4$. Common rules: length increases $\sim 25$ cm in year one, $\sim 12$ cm in year two, then $\sim 6$–$8$ cm/year until puberty.

  12. What are the expected timelines for a newborn to double and triple its birth weight?

    Birth weight doubles by about $4$–$6$ months and triples by about $12$ months; it quadruples by roughly $24$ months.

  13. What is the mid-parental (target) height formula for a boy and for a girl?

    For a boy: $\dfrac{\text{father's height} + (\text{mother's height} + 13)}{2}$ cm. For a girl: $\dfrac{(\text{father's height} - 13) + \text{mother's height}}{2}$ cm, each $\pm 8.5$ cm.

  14. How do you distinguish constitutional growth delay from familial (genetic) short stature using bone age?

    In constitutional growth delay, bone age is delayed (less than chronologic age) with a 'late bloomer' family history and eventually normal final height. In familial short stature, bone age equals chronologic age and predicted final height is short.

  15. What pattern of growth suggests an acquired systemic or endocrine cause of short stature rather than a genetic one?

    A falling height velocity crossing percentiles downward (deceleration) after previously normal growth suggests an acquired pathologic cause (e.g., hypothyroidism, growth hormone deficiency, chronic disease, Cushing) rather than genetic/constitutional short stature.

  16. In growth hormone deficiency, what is the characteristic relationship between weight and height, and how is it confirmed?

    Height is more affected than weight (child appears short and relatively chubby with delayed bone age). Confirmed by low IGF-1/IGFBP-3 and a subnormal growth hormone response to two stimulation tests.

  17. What is failure to thrive, and how is it defined on the growth chart?

    Failure to thrive is inadequate weight gain/growth: weight (or weight-for-length) below the $3$rd–$5$th percentile, or a sustained drop crossing $\geq 2$ major percentile lines. Weight is typically affected first, then length, then head circumference.

  18. How does head circumference growth in the first year help distinguish causes of poor growth?

    In malnutrition/FTT, weight falls first and head circumference is relatively preserved (spared last). Early microcephaly with proportionate small size suggests a congenital/genetic or intrauterine cause rather than caloric deprivation.

  19. What defines microcephaly and macrocephaly by standard deviations of head circumference?

    Microcephaly is occipitofrontal circumference below $-2$ standard deviations (below the $2$nd–$3$rd percentile) for age/sex; macrocephaly is above $+2$ standard deviations (above the $97$th–$98$th percentile).

  20. What are the core diagnostic features (DSM-5 domains) of autism spectrum disorder?

    Two domains: (1) persistent deficits in social communication and social interaction, and (2) restricted, repetitive patterns of behavior, interests, or activities (including stereotypies, insistence on sameness, and sensory abnormalities), with onset in early development.

  21. What are the developmental red flags for autism that warrant referral?

    No babbling or gestures by $12$ months, no single words by $16$ months, no two-word phrases by $24$ months, loss of previously acquired language/social skills at any age, and lack of eye contact, joint attention, or response to name.

  22. What are the three core symptom clusters of ADHD, and what is the minimum age-of-onset and duration criterion?

    Inattention, hyperactivity, and impulsivity. Several symptoms must be present before age $12$, persist $\geq 6$ months, occur in $\geq 2$ settings, and impair functioning; presentation may be predominantly inattentive, hyperactive-impulsive, or combined.

  23. What is the first-line pharmacologic treatment for ADHD, and a common non-stimulant alternative?

    Stimulants—methylphenidate or amphetamine derivatives—are first-line. Non-stimulant alternatives include atomoxetine (a selective norepinephrine reuptake inhibitor) and alpha-2 agonists such as guanfacine or clonidine.

  24. What is developmental (global) delay, and how many domains must be affected for the 'global' designation?

    Global developmental delay is significant delay ($\geq 2$ standard deviations below the mean) in at least two of the major developmental domains: gross/fine motor, speech/language, cognition, social/personal, and activities of daily living, in a child under $5$ years.

  25. What is the difference between developmental delay and developmental regression, and why is regression alarming?

    Delay is slower-than-normal acquisition of skills; regression is loss of previously acquired milestones. Regression is a red flag suggesting a neurodegenerative or metabolic disorder (e.g., Rett syndrome, leukodystrophy, storage diseases) and warrants urgent workup.

  26. What is the most common inherited cause of intellectual disability, and its inheritance pattern?

    Fragile X syndrome, an X-linked disorder from CGG trinucleotide repeat expansion in the FMR1 gene, presenting with intellectual disability, long face, large ears, macroorchidism, and autistic features.

  27. What is cerebral palsy, and which type is most common?

    Cerebral palsy is a non-progressive disorder of movement and posture from an insult to the developing brain. The most common type is spastic CP (spastic diplegia especially in preterm infants due to periventricular leukomalacia).

  28. What is the classic clinical presentation and inheritance of Duchenne muscular dystrophy as a cause of motor delay?

    X-linked recessive dystrophin deficiency in boys, presenting around $3$–$5$ years with delayed walking, proximal weakness, Gower sign, calf pseudohypertrophy, and markedly elevated creatine kinase; confirmed by genetic testing/muscle biopsy.

  29. What screening tool is routinely used to monitor developmental milestones, and what is the recommended screening schedule?

    Standardized tools such as the Ages and Stages Questionnaire (ASQ) or Denver II. General developmental screening is recommended at $9$, $18$, and $30$ months, with autism-specific screening (M-CHAT) at $18$ and $24$ months.

  30. What are the classic features of Rett syndrome, and whom does it affect?

    Rett syndrome is an X-linked (MECP2 gene) disorder almost exclusively in girls, with normal early development then regression around $6$–$18$ months: loss of purposeful hand use, stereotypic hand-wringing, deceleration of head growth (acquired microcephaly), and loss of language.

SMLE Pediatrics FAQ

What is in the SMLE Pediatrics syllabus?

SMLE Pediatrics is split into 2 chapters: Neonatology and Growth and Development. Together they contain 6 topics.

How many chapters are in SMLE Pediatrics?

2 chapters, containing 6 topics. The largest chapter is Neonatology, with 3 topics.

Are there flashcards for SMLE Pediatrics?

Yes — a 50-card Pediatrics deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.