derm Flashcards
erythema toxicum neonatorum
Effects 50% of infants, less in preterm.
Presents as yellow-white papules on erythemeatous area, happens at 1-3d of life, spontaneously resolves.
Dx: eosinophils on smear
transient neonatal pustular melanosis
Occurs in 5% of AA babies, 1% in caucasian.
Presents as small pustules that last ~ 48 hours (neutrophils on smear) that leave hyperpigmented area from inflammation once ruptured which can last months. Multiple lesions at once in different stages.
congenital milia
Affects 40% of term babies
Presents as 1-2mm white papules from tiny epidermal cysts arising from vellus hair, selfe resolve over months.
miliaria neonatorum
This is due to obstruction of immature eccrine ducts.
Tx: resolves with cooling and avoidance of occlusive clothing
4 types:
crystallina - superficial, clear vesicles within stratum corneum
rubra (pictured): erythematous grouped papules in skin folds
pustolosa: erythematous grouped pustules with possible infection
profunda: papular eruption deep within eccrine gland
acrodermatitis enteropathica
Due to zinc deficiency (often when switching to formula).
Presentation: red erosive hemorrhagic crusted patches/plaques and flaccid bullae
Dx: low zinc and alk phos levels.
Tx: zinc.
neonatal lupus
Presents with annular patches on face and telangectasia. 30% assc with heart block.
Tx: Consider short course of topical steroids because leads to mild scarring.
aplasia cutis congenita
Presents as absence of skin, usually on scalp with overlying thing membrane. Heals hairless over 3-6m. May be associated with lipoma.
Distinguish from hair collar sign (dark hair cicrumfrentially) wich may be connected to brain/bone –> MRI
Staphylococcus Scalded Skin Syndrome
Presents as blistering eruption due to S. aureus toxin with fever, generlized skin redness, facial swelling, conjunctivitis, and crusting around eyes/nose/mouth. Delicate bullae form followed by desquamation of skin within 2-3d.
Distinguish from toxic epidermal necrolysis (TEN) which causes full thickness tissue necrosis from drug reaction.
incontinentia pigmenti
X linked dominant (often fatal to male fetus)
Goes through 4 stages: initially at <6m vesicular along lines of blaschko –> warty papules from 2m to 2 yrs –> hyperpigmentation into adolescence –> hypopigmented into adultood.
May have seizures, dvpt delay and blindness. Get MRI and optho consoult, at risk for retinal detachment.
ichythyoses
There are multiple types of ichythyoses:
1) halrequin ichthyosis - most severe, thick scales, deep red fissures, extreme ectropion (inversion of eyes) + eclabium (inversion of lips), die of sepsis within days
2) congenital ichtyosiform erythroderma (CIE) - mc cause of collodion membrane which evolves into fine white scales
3) lamellar ichythosis: colloidon membrane at birth which evolves into thick generalized brown scale
4) steroid sulfatase deficiency, x linked ichthysosis: dark brown scales sparing flexures, assc with corneal opacities, cryptorchidism
5) ichythosis vulgaris: most benign, later in infancy
6) epidermolytic hyperkeratosis: blistering at birth –> generalized hyperkaratosis with mal-odor
epidermolysis bullosa
Presents as fragile blistering skin, painful and deforming. Assc with nail and teeth dysplasia. There are multiple types depending on where skin layers split.
Some are caused by PLEC gene mutation.
port wine stain
Assc with SW if over V1 distribution.
Assc with vascular malformation of meninges (leptomeningeal vessels –> hemiparesis, seizures), and glaucoma.
Tx: with pulse dye laser. Most effective if started early, on smaller lesions, and most effective if lesions is on central forehead.
Nicolau syndrome
A hemmorhagic reaction and necrosis of skin after injection that is meant to be IM but accidentally given IV. It resolves over time with scar. Adverse events can include compartment syndrome.
Syphillis presentation
Lesions include papulosquamous plaques, erythematous macules, hemorrhagic vesicles and bullae (pemphigus syphiliticus), annular lesions, and polymorphous rashes. The palms, plantar surfaces of the feet, perioral skin, and anogenital region are common sites for lesions to be found
Ecthyma gangrenosum
the lesion usually begins as a painful red or purpuric macule that centrally vesiculates or becomes pustular. Bullae may also form. Surrounding tissues are pink or violaceous. The lesion quickly ulcerates, develops raised edges, and becomes necrotic in the center. A black, crusted eschar covers an erythematous base that microscopically is characterized by a vasculitis, especially the veins. The ecthyma gangrenosum lesions are caused by production of enzymes and proteases (especially elastase but also gelatinase, collagenase, lecithinase, neutral and alkaline protease, cytotoxin, and phospholipase C), endotoxin, and exotoxins A and S. The lesions are characteristically devoid of inflammatory Education Module Learner http://emb.aap.org/courseprodv2/Index.asp[4/6/2012 12:26:50 PM] cells. Pseudomonas organisms may be found in the adventitia and media of the dermal veins. Culture of the base of these lesions, not the exudate or eschar, is necessary to determine the microbial source of infection. The presence of ecthyma gangrenosum generally indicates treatment with anti-Pseudomonas antibiotic agents.
