Dermatology Flashcards
Erythema toxicum
Most common pustular rash
Onset 1 to 2 days, lasts <1 week
Wright staining - eosinophils
Milia
Tiny, white, smooth-surfaced papules on face and scalp
Inclusion cysts in epidermidis with layers of trapped keratinized stratum corneum
Resolves spontaneously
Sebaceous hyperplasia
Follicular, smooth yellow-white papules grouped into plaques
No surrounding erythema
Due to androgen stimulation from mom
Miliaria
Obstruction of eccrine duct
Transient neonatal pustular melanosis
Three phases
- Superficial vesicopustules at Birth, very fragile
- Fine collarette of scale around resolving pustule
- Hyperpigmented brown macules, may take months to fade
Neonatal acne
Appears by 2-3 weeks Inflammatory, erythematous papules/pustules mostly on cheeks No comedones Resolves spontaneously Not infantile acne
Congenital melanocytic nevi
Pigmented proliferations seen at birth
Benign, tumor-like malformations due to faulty development of melanocyte precursors
Composed of abnormal mixture of skin elements
Risk for malignant melanoma transformation later in life
Epidermolysis bullosa
Inherited disorders
Fagility of skin in response to minor trauma
Mutation in genes for basement membrane proteins
May present in neonate as congenital localized absence of skin/large ulcers
Three major types
Epidermolysis bullosa simplex
Most common/mild
Autosomal dominant
Usually just skin involvement
Junctional epidermolysis bullosa
Least common Autosomal recessive Poor outcome due to extracutaneous complications Nail dystrophy is common Specific subtype with pyloric atresia
Dystrophic epidermolysis bullosa
Milder
Autosomal recessive and dominant
Extracutaneous complications can occur
Bullous impetigo
Infection with S. aureus phage group 2 Release of toxins -> epidermolysis/blister formation
Localized to diaper area and abdomen
Gram stain with gram-positive cocci in clusters
Treat with IV antibiotics (not mupirocin)
Staph scalded skin syndrome (SSSS)
Due to staph aureus phage 2
Bright erythema of face-> severe bolus eruptions
Fever, irritability, tender skin, conjunctivitis, nasal congestion
Positive Nikolsky sign
Cultures from bullae are sterile
Can culture nasopharynx, blood, or conjunctiva
Treatment IV antibiotics
Nevus sebaceous (of Jadassohn)
Organoid hamartoma of a appendageal structures
Pink/yellow or yellow/orange plaque on scalp or face
Some with cerebriform or papillomatous morphology
May develop neoplastic growths -> observe
Incontinentia pigmenti
Newborns present with small clustered blisters on an erythematous base (along Blaschko lines)
Ichthyosis vulgaris
Autosomal dominant Appear normal at birth Presents at three months with mild scales, no flexural involvement Maximum symptoms by puberty A/W atopic dermatitis
Epidermolytic hyperkeratosis
Autosomal dominant
Seen at birth, looks similar to SSSS
Wide spread bullae with possible bad odor 2/2 infection
Ichthyosis
Can present as collodion infant at birth
Congenital hemangiomas
Fully formed at birth
Do not proliferate
Two types: rapidly involuting, non-involuting
Infantile hemangiomas
Most common vascular tumor of infancy
Rapid growth followed by spontaneous involution
Three types - Superficial, combined, deep
Complications of hemangiomas
Ulceration
Structural deformity and airway involvement
Congestive heart failure
When to treat hemangiomas
Life or function threatening Located where permanent deformity may occur (nose, lip, ear) Large facial lesions Ulcerated Pedunculated
Multiple hemangiomas
10 to 25%
Visceral involvement - screen for liver/other lesions if >5 hemangiomas noted, echo to rule out heart failure