SMLE Pediatrics Flashcards

24 sample cards from the Pediatrics deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. 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.

2. 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.

3. 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).

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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).

14. 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.

15. 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.

16. 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.

17. 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.

18. 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.

19. 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.

20. 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.

21. 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).

22. 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.

23. 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.

24. 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.

What this deck covers

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