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1

Polysomnography (PSG)

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).

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if high suspicion for OSAS, next diagnostic step

nocturnal PSG, if positive, referral to otolaryngologist

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

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

4

Untreated OSAS can lead to comorbidities such as

behavioral, cognitive, cardiovascular, and growth problems

5

Screening tests for growth delay might include ?

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.

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constitutional growth delay

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."

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height age

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

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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

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

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constitutional growth delay vs GH deficiency vs familial short stature

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%

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

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

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GH screening tests

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

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GH def. tx

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

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constitutional delay tx

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

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delayed puberty

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

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precocious puberty

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

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precocious (noncentral) pseudopuberty

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

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incomplete precocious puberty

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).

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

idiopathic
structural CNS abnormality

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good precocious puberty questions

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

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

central precocious puberty

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? 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

GnRH stimulation test

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bone age in precocious puberty

advanced beyond chronologic age

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

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

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The goal of treating precocious puberty is to ?
treatment includes? how does it work?

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

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retropharyngeal space

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.

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parapharyngeal (lateral) space

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.

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epiglottitis etiology

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

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rapid strep immunoassay

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

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monospot test

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.

30

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

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

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

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

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

adolescents or young adults
-most common type in the pediatric population

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

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

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

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

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

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

36

Bacterial etiologies for neck abscess

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

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viral etiologies for neck abscess

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

38

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

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

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in neck abscesses, must decide btw approaches

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

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

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

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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)

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

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neck lump that moves up with swallowing

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

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Slipped capital femoral epiphysis (SCFE)
common age groups?

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

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stable vs unstable SCFE

"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.

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chondrolysis

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

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risk factors for DDH

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.

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Legg-Calve-Perthes Disease (LCPD)
ages of onset?

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

48

LCPD imaging
treatment?

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.

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slippage in SCFE

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.

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Early MRI SCFE findings include

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

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Helpful features that differentiate DDH from SCFE include ?

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

52

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

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

53

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

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

54

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

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