Ped Derm Flashcards
Congenital melanocytic nevi CMN presentation
macules, paules, or plaques at birth
+/- hair
appearance may change with time
lesions grow in proportion to individuals size
congenital melanocytic nevus risk of malignancy
small/medium- less than 1%
large/giant 0-7.6% with most estimated risk of 2%
mongolian spots presentation
-patch of bluish-grey pigmentation with IRREGULAR BOARDER and normal skin texture
commonly buttocks and lower back
asian>black>hispanic
evident at birth
mongolian spot clinical diagnosis
none additional required
affected areas fade by age 2 and often disappear by age 10
nevus sebaceous clinical presentation
mostly on scalp or face
waxy, smooth, yellow-orange hairless patch, often oval or linear in shape
becomes MORE PRONOUNCED in adolescence
may become bumpy, warty, or scaly
nevus sebaceous treatment
intermittent interval follow up is recommended
refer to dermatologist if concerning changes are observed
aplasia cutis congenita ACC presentation
most commonly found midline posterior scalp
tuft of hair may surround defect which may indicate neural tube defect
may be associated with bulla
possible other developmental abnormalities
lesions well demarcated
aplasia cutis congenita ACC treatment
depends on size, depth and location
gentle cleansing and ointment
hypertrophic scar
refer to neurosurgery
cafe au lait macules CALM presentation
discrete uniformly pigmented macules or patches
present at birth and early childhood
conditions such as mccune albright syndrom
or neurofibromatosis type 1 NF1 (lisch nodules eye, bone defects, scoliosis, neurofibromas, optic nerve glioma) (autosomal dominant, 50% new mutations) get yearly opthalmology exams at year 1
vascular tumor classification
hemangiomas -infantile hemangioma -congenital hemangioma tufted angioma pyogenic granuloma
Vascular malformations
capillary malformations
port-wine stain
nevus simplex
port-wine stain clinical presentation
presents at birth and DOES NOT REGRESS
pink or dark red patches
soft tissue or bony overgrowth
sturge weber syndrome in the V1 distribution
congenital glaucoma concerns if patch affects eyelid
infantile hemangiomas
common benign vascular tumor
risk factors: low birth wt, famle, twin gestation, and fair skin
not present at birth but shortly after
superficial, deep, or mixed
superficial: bright red and minimally elevated
deep: larger with a bluish color
ulceration is a common complication
Proliferative:
early RAPID GROWTH during first 3 months of age
max growth 5-7w of age
Late: less rapid but still ongoing completed typically by 9 m
Involution phase:
color darkens and tumors soften
ultimate residual skin changes
nevus simplex (salmon patch) clinical presentation
faint, transient capillary malformation
-flat, pink/red patch
-typically midline of forehead, scalp, upper eyelids, posterior neck and back
commonly called a “STORK BITE”at the nape of the neck
and “ANGEL KISS” on the eyelid
LESIONS TYPICALLY FADE WITHIN 1-2y
pyogenic granuloma
common ACQUIRED lobular vascular tumor occurs at any age *affects skin particularly prone to trauma (hands finger face and mucous membranes) *extremely friable can recur despite treatment
pyogenic granuloma treatment
biopsy to confirm (may mimic malignant lesions)
- preferred: surgical excision with primary closure
- curettage or shave removal with electrodessication of base
- pulsed-dye laser
risk of recurrence is high
Diaper dermatitis (diaper rash) causes and pathogenesis
most cases CONTACT/IRRITANT DERMATITIS
may be caused by seborrheic dermatitis, atopic dermatitis, or other underlying skin conditions
excessive moisture, friction, increased ph causing localized skin breakdown
-macerated skin makes susceptible for infection from urine and feces
diaper dermatitis presentation
episodic symptoms with varying severity
persistent symptoms: secondary infections with C. ALBICANS or other microorganisms
CANDIDAL SUPERINFECTION: beffy red plaques
dx: clinical or KOH prep/fungal culture
IMPETIGO: secondary infection S. AUREUS or S. Pyrogenes
**halmark: fragile PUSTULES and HONEY CRUSTED erosions
diaper dermatitis therapeutic options
barrier preperations: OTC pastes and ointment
Low-potency topical corticosteroids if more severe and NOT resolving
-breast milk: anti-inflammatory and intimicrobial
Topical antifungals: secondary Candida infection
Topical vs oral antibiotics: bacterial superinfection (Mupirocin)
*avoid powder: respiratory risk
lice scientific name
pediculosis capitus
lice clinical presentation
asymptomatic
itching if allergic to saliva
cervical lymphadenopathy
febrile if secondary staph infection
diagnosis of lice
visualize live lice
nits may persist for months and does not indicate active infection
lice treatment
topical pediculicides: pyrethroids, malathion, benzy alcohol, spinosad
wet combing 15-60 min every 3-4 days for several weeks
neonatal acne: neonatal cephalic pustulosis
not true acne
inflammatory reaction possibly due to malassezia colonization
self limiting
presents in first 2-3w of life and resolved by 6-12m
neonatal acne clinical presentation
inflammatory papules and pustules on forehead nose and cheeks
*no true comedones
neonatal acne treatment
self limiting
mild: cleansing with soap and water
if persisitant: may use ketoconazole or hydrocortisone to expedite clearance
typically resolves by 4 months without scarring
infantile acne
presents at 3-4 months of age and commonly resolves by 2-3 years of age
hyperplasia of sebaceous glands
androgenic stimulation
M>F
inflammatory papules, COMEDONES, and pustules
infantile acne management
often required to prevent scarring
benzoyl peroxide, topical antibiotics, topical retinoids
oral treatment only needed in severe cases
