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
Kasabach-Merritt phenomenon
Vascular anomalies + thrombocytopenia + coagulopathy

Examples of vascular tumors
Kaposiform hemangioendothelioma
Tufted angioma
Multifocal lymphangioendotheliomatosis with thrombocytopenia
Cutis aplasia
Focal congenital defects of skin
Involve dermis and epidermis
Reepithilialize over several months without intervention
Tuberous sclerosis
Autosomal dominant Cutaneous, cardiac, neuro anomalies Hypomelanocytic macules or patches (ash leaf spots) are earliest sign, seen in 90% of patients <3 maybe a normal variant May need woods lamp if fair skin
Waardenburg syndrome
Autosomal dominant Depigmented patches of skin and hair Heterochromia iridis Congenital nerve deafness Craniofacial anomalies
Café au lait macules
Round/oval, tan to brown macules
Can be a normal variant
>6 bigger than 5mm concerning for neurofibromatosis type 1
McCune–Albright syndrome: large Café au lait spots, polyostotic fibrous dysplasia, endocrine dysfunction
Urachus
Remnant of regressed allantois that runs from baldder to umbilicus
Omphalomesenteric duct
Connects ileum to umbilicus
Regresses between 5-9 weeks GA
Umbilical granuloma
Small bright red papules
Due to umbilicus not re-epitheliazing
Treat with silver nitrate
No discharge
Peutz-Jeghers Syndrome
Autosomal dominant
Mucocutaneous pigmentation and G.I. polyps
Has been a/w bowel obstruction in the neonate
Develop hamartomatous polyps later in life
Harlequin color change
Dependent 1/2 of body turns red, other 1/2 pale
Due to temporary inbalance of autonomic regulatory mechanism of cutaneous vessels
Eosinophils on Wright stain
Erythema toxicum
Inclusion cysts with keratinized stratum corneum
Milia
Miliaria profunda
Occlusion at or below dermoepidermal junction
Rare in newborns
Miliaria rubra
Heat rash
Erythematous papules/pustules on head/neck/trunk
Intraepidermal eccrine duct obstruction
Miliaria crystallina
Subcorneal or intercorneal ductile obstruction
Due to overheating
Leads to sweat-producing, small, clear vesicles
Neutrophils on Wright stain
Transient pustular neonatal melanosis
Skin infection with a negative culture
SSSS
Four stages of incontinentia pigmenti
- Vesicular
- Verrucous
- Hyperpigmented
- Atrophic
Autosomal recessive forms ofichthyosis
Lamellar ichthyosis
CIE
Forms of ichthyosis with no flexural involvement
X-linked ichthyosis
Ichthyosis vulgaris
X-linked ichthyosis
X-linked recessive
A/W cryptorchidism in 25% of males
Benign neonatal hemangiomatosis
Multiple hemangiomas
Cutaneous only, no visceral involvement
Diffuse neonatal hemangiomatosis
Multiple hemangiomas
Both cutaneous and visceral lesions present
Treatment of Kasabach Merritt phenomenon
Medical emergency Treat with: - steroids - vincristine - interferon-alpha - ticlopidine - aspirin - embolization
Patent urachus from bladder to umbilicus
Urachal fistula
Urine can leak
Partially patent urachus
Urachal cyst
Urachus only patent at umbilicus
Urachal sinus
Failure of normal obliteration of omphalomesenteric duct
Omphalomesenteric fistula
Partially patent omphalomesenteric duct
Omphalomesenteric cyst
Omphalomesenteric duct patent only at umbilicus
Umbilical polyp
Conditions associated with cutis aplasia
Epidermolysis bullosa Opitz syndrome Adams–Oliver syndrome Oculocerebrocutaneous syndrome Trisomy 13–15 4p- syndrome Johanson–Blizzard syndrome Xp22 microdeletion syndrome Chromosome 16–18 defect
Symptoms of Sturge-Weber syndrome
Port wine stains (usually in trigeminal nerve distribution)
Leptomeningeal capillary venous malformation
Mental deficiency
Seizures
Hemiparesis contralateral to facial lesion
Glaucoma
Ipsilateral cortical calcifications (tramline)

Anomalies associated with incontinentia pigmenti
Teeth (delayed, hypodontia)
Hair (alopecia, wiry hair)
Nails (dystrophy)
Retina (retinal vascular proliferation)
Finding on Tzanck smear in incontinentia pigmenti
Eosinophils 
What do infantile hemangiomas over express during their proliferative phase?
Type 3 iodothyronine deiodinase
Leads to a consumptive hypothyroid state
