11

Question 1

Polysomnography (PSG)

Answer 1

A comprehensive recording of the biophysiological changes that occur during sleep.
monitors the brain (electroencephalogram [EEG]), eye movements (electrooculography [EOG]), muscle activity or skeletal muscle activation (electromyography [EMG]) and heart rhythm (electrocardiography [ECG]). Testing allows for the quantification of the severity of OSAS via the apnea-hypopnea index (AHI).

Question 2

if high suspicion for OSAS, next diagnostic step

Answer 2

nocturnal PSG, if positive, referral to otolaryngologist

Question 3

most common cause of OSAS thus, the primary treatment is ?

Answer 3

adenotonsillar hypertrophy
adenotonsillectomy (AT)
Others: adenoidectomy, partial tonsillectomy, and nasal CPAP, ntranasal steroids and montelukast for mild OSAS, maxillary expansion

Question 4

Untreated OSAS can lead to comorbidities such as

Answer 4

behavioral, cognitive, cardiovascular, and growth problems

Question 5

Screening tests for growth delay might include ?

Answer 5

CBC, ESR, electrolytes and general health chemistry panel; urinalysis; serum for thyroid function studies, IGF-1, IGF-BP3; bone age radiograph; and, if this were a girl, possibly chromosomal karyotype.

Question 6

constitutional growth delay

Answer 6

healthy child’s growth is slower than expected but for whom one or more parents demonstrated a pubertal development delay and ultimately normal adult height. In this case, the “bone age” equals the “height age.”

Question 7

height age

Answer 7

age at which a child’s measured height is at the 50th percentile.

Question 8

In the first year of life, children grow at a rate of approximately ? per year
drops to approximately ? per year for children aged 1 to 3 years
Until puberty, they grow approximately ? per year
At puberty, growth increases to ? per year for girls and to ? per year for boys

Answer 8

23 to 28 cm
7.5 to 13 cm
4.5 to 7 cm
8 to 9 cm, 10 to 11 cm

Question 9

constitutional growth delay vs GH deficiency vs familial short stature

Answer 9

constitutional: normal growth rate +fam hx for 1+ parent with pubertal development delays (“late bloomers”) who developed normal adult height
GH def: slow growth rate, may “fall off the curve”
familial: short parents, growth parallel to a growth line at or just below 3-5%

Question 10

bone ages in constitutional growth delay vs GH deficiency vs familial short stature

Answer 10

consti: shows potential for growth
familial: bone age = chronological age (no “room for growth)
GH def: delayed bone age

Question 11

GH screening tests

Answer 11

serum IGF-1 or somatomedin C and IGF-BP3
GH level is of little diagnostic value because secretion is pulsatile and difficult to interpret.
Confirmation often requires GH stimulation testing and interpretation by a peds endo

Question 12

GH def. tx

Answer 12

Replacement therapy involves recombinant GH injections several times per week until the child reaches full adult height.

Question 13

constitutional delay tx

Answer 13

Monthly testosterone injections “jump start” the pubertal process without altering final growth potential; a pediatric endocrinologist might be required to assist

Question 14

delayed puberty

Answer 14

No signs of puberty in girls by the age of 13 years or in boys by the age of 14 years. May be caused by gonadal failure, chromosomal abnormalities (Turner syndrome, Klinefelter syndrome), hypopituitarism, chronic disease, or malnutrition

Question 15

precocious puberty

Answer 15

Onset of secondary sexual development before the age of 8 years in girls and 9 years in boys (2.5-3 standard deviations below the mean of 10.5 years in girls and 11.5 years in boys). Categorized as central or noncentral

Question 16

precocious (noncentral) pseudopuberty

Answer 16

Gonadotropin independent. No hypothalamic-pituitary-gonadal activation. Hormones usually are either exogenous (birth control pills, estrogen, testosterone cream) or from adrenal/ovarian tumors.

Question 17

incomplete precocious puberty

Answer 17

Early breast development (typically in girls ages 1-4 years),
no pubic/axillary hair development or linear growth acceleration (premature thelarche), or early activation of adrenal androgens (typically in girls ages 6-8 years),
with gradually increasing pubic/axillary hair development and body odor (premature adrenarche).

Question 18

Sexual precocity is ? in more than 90% of girls, whereas a ? is present in 25% to 75% of boys

Answer 18

idiopathic

structural CNS abnormality

Question 19

good precocious puberty questions

Answer 19

rapid growth? increased appetite? body odor? exogenous hormones (OCPs, steroids)? age of sibling/parent puberty? fam hx of CAH?

Question 20

serum LH is undetectable in prepubertal children, but is detectable in 50% to 70% of girls (and an even higher percentage of boys) with ?

Answer 20

central precocious puberty

Question 21

? measures response time and peak values of LH and FSH after intravenous administration of GnRH and is a helpful diagnostic tool for dx central precocious puberty

Answer 21

GnRH stimulation test

Question 22

bone age in precocious puberty

Answer 22

advanced beyond chronologic age

Question 23

how to rule out organic CNS causes of central sexual precocity
who is this important in?
other imaging? indicate in who?

Answer 23

CT/MRI
girls younger than 6 years and in all boys
pelvic US indicated if gonadotropin-independent causes of precocious puberty (ovarian tumors/cysts, adrenal tumors) are suspected based on exam

Question 24

The goal of treating precocious puberty is to ?

treatment includes? how does it work?

Answer 24

prevent premature closure of the epiphyses, allowing the child to reach full adult growth potential
GnRH agonists (central), desensitizes the gonadotropic cells of the pituitary to the stimulatory effect of GnRH produced by the hypothalamus

Question 25

retropharyngeal space

Answer 25

Located posterior to the esophagus and extending inferiorly into the superior mediastinum; bordered by layers of the deep cervical fascia; contains lymphatics draining the middle ears, sinuses, and nasopharynx.

Question 26

parapharyngeal (lateral) space

Answer 26

Located lateral to the pharynx and bordered by muscles of the styloid process; comprises anterior and posterior compartments containing lymph nodes, cranial nerves, and carotid sheaths; infections in the lateral space can originate from the oropharynx, middle ears, and teeth.

Question 27

epiglottitis etiology

Answer 27

bacterial etiology historically Haemophilus influenzae type B (HiB) before widespread use of the HiB vaccine; most cases now involve Streptococcus pyogenes, Streptococcus pneumoniae, or Staphylococcus aureus

Question 28

rapid strep immunoassay

Answer 28

Detects GAS antigen by latex agglutination or ELISA; high specificity and variable sensitivity with false-negative results possible

Question 29

monospot test

Answer 29

Latex agglutination of heterophile antibodies to erythrocytes (sheep/horse RBCs) in EBV infection; high specificity and sensitivity in patients older than 3 years; infection may be confirmed by EBV immunoglobulin (Ig)M antibody if heterophile is negative.

Question 30

difficulty swallowing?
painful swallowing?
Inability to open the mouth secondary to pain or inflammation or mass effect involving facial neuromusculature?

Answer 30

dysphagia
odynophgia
trismus (more frequently in peritonsillar or parapharyngeal infection)

Question 31

typical pediatric patient with retropharyngeal abscess is a ?, why?

Answer 31

toddler younger than 4 years
coinciding with the time when retropharyngeal lymph nodes are prominent (which atrophy by puberty) and when the majority of URI and otitis cases are seen

Question 32

Peritonsillar abscess can be seen at any age, but prevalence is greater in ?

Answer 32

adolescents or young adults

-most common type in the pediatric population

Question 33

Cervical CT imaging is an excellent study for determining whether a patient has only ? or ?

Answer 33

cellulitis and edema surrounding a neck space, or hypodensity and rim enhancement consistent with an abscess

Question 34

An MRI is an alternative when there is a concern for ?

Answer 34

infection involving a compartment with neurovascular elements and more accurate visualization is desired

Question 35

Lymph chains draining the sinuses, nasopharynx, and oropharynx can seed the ?, with potential for spread to the ? where it could impact ?

Answer 35

retropharyngeal space
mediastinum, where impact on cardiorespiratory function (upper airway obstruction, aspiration pneumonia following abscess rupture), or mediastinitis could develop

Question 36

Bacterial etiologies for neck abscess

Answer 36

Streptococcus pyogenes (GAS), Staphylococcus sp, Haemophilus influenzae, Peptostreptococcus sp, Bacteroides sp, and Fusobacterium sp. 
may be polymicrobial

Question 37

viral etiologies for neck abscess

Answer 37

EBV, cytomegalovirus, adenovirus, and rhinovirus and may present similarly to bacterial infection

Question 38

neck abscess antibiotics
if anaerobes suspected?
mono therapy for PCN-allergic pt?

Answer 38

IV penicillins, advanced-generation cephalosporins, or carbapenems.
Clindamycin or metronidazole is added if anaerobes are suspected and broad coverage is desired.
Clindamycin often is a good choice for monotherapy in the patient with penicillin allergy

Question 39

in neck abscesses, must decide btw approaches

Answer 39

“watchful waiting” approach with a patient receiving antibiotics, or to proceed quickly with needle aspiration or incision and drainage

Question 40

Emergent surgical drainage may be required in the neck abscess patient with ?

Answer 40

respiratory distress (concerning for abscess-related airway obstruction), or with rapid, progressive deterioration (toxicity, persistent high fever) despite intravenous antibiotics.

Question 41

other conditions that may mimic deep neck infections as they (may present with sore throat, odynophagia, or swelling and pain of the oropharynx and neck)

Answer 41

thyroglossal duct cyst or second branchial cleft cyst
Thyroiditis and sialadenitis
thyroid nodule, goiter, or salivary gland tumor
extensive reactive lymphadenopathy

Question 42

neck lump that moves up with swallowing

Answer 42

Thyroglossal duct cyst
typically midline, often move on tongue protrusion, and often are noted after an URI
may become infected, remove surgically

Question 43

Slipped capital femoral epiphysis (SCFE)

common age groups?

Answer 43

displacement of the femoral head
11 to 13 years for girls and 13 to 15 years for boys.
Roughly 65% of affected individuals are above the 90th percentile for their weight for age

Question 44

stable vs unstable SCFE

Answer 44

“stable SCFE” characterized by an ability to bear weight or no displacement of the femoral epiphysis. An “unstable SCFE” is characterized as an inability to bear weight or displacement of the femoral epiphysis.

Question 45

chondrolysis

Answer 45

A breakdown of the femoroacetabular joint cartilage with no clear etiology, but more commonly seen in unstable slips

Question 46

risk factors for DDH

Answer 46

conditions that limit mobility of the hip joint whether in utero or after birth. These conditions include breech presentation, oligohydramnios, and large-for-gestational age infants.

Question 47

Legg-Calve-Perthes Disease (LCPD)

ages of onset?

Answer 47

idiopathic avascular necrosis of the femoral head. LCPD typically presents as thigh or knee pain with limp in a child. Similar to SCFE, the limp can be an antalgic with a Trendelenburg gait
between 3 and 12 years of age

Question 48

LCPD imaging

treatment?

Answer 48

radiographs of the hip in anteroposterior (AP) and frog leg views help differentiate the etiology. LCPD will show joint space widening due to loss (necrosis) of the femoral head height
casting the affected leg in an abducted and internally rotated fashion.

Question 49

slippage in SCFE

Answer 49

it is actually anterior superior displacement of femoral metaphysis? that in plain radiographs appears as posterior inferior displacement of the femoral epiphysis (ice-cream scoop slipping). The relationship between the femoral head and acetabulum is maintained.

Question 50

Early MRI SCFE findings include

Answer 50

haziness between the interface of the femoral epiphysis and metaphysis, widening of the joint angle, and effusion

Question 51

Helpful features that differentiate DDH from SCFE include ?

Answer 51

the lack of pain being a chief complaint in DDH, earlier onset of DDH (typically presents when the child first begins walking around 2 years of age), and toe walking in DDH on the affected side to compensate for the shortened leg length

Question 52

After confirmation of SCFE by radiographs, the patient will require ?

Answer 52

immediate orthopedic surgery evaluation to determine the timeframe for surgical pinning of the femoral head

Question 53

patients with a displaced SCFE, what is not performed due to increased risk of vascular compromise?

Answer 53

reduction is NOT performed during pinning of the femoral head. Reduction increases the risk of vascular compromise and subsequent avascular necrosis of the femoral head

Question 54

;some surgeons elect to simultaneously perform bilateral femoral pinning as prophylaxis, why?

Answer 54

in up to 30-60% of cases, SCFE eventually occurs on the contralateral hip