Dermatology Flashcards

1
Q

Erythema toxicum

A

Most common pustular rash
Onset 1 to 2 days, lasts <1 week
Wright staining - eosinophils

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2
Q

Milia

A

Tiny, white, smooth-surfaced papules on face and scalp
Inclusion cysts in epidermidis with layers of trapped keratinized stratum corneum
Resolves spontaneously

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3
Q

Sebaceous hyperplasia

A

Follicular, smooth yellow-white papules grouped into plaques
No surrounding erythema
Due to androgen stimulation from mom

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4
Q

Miliaria

A

Obstruction of eccrine duct

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5
Q

Transient neonatal pustular melanosis

A

Three phases

  1. Superficial vesicopustules at Birth, very fragile
  2. Fine collarette of scale around resolving pustule
  3. Hyperpigmented brown macules, may take months to fade
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6
Q

Neonatal acne

A
Appears by 2-3 weeks
Inflammatory, erythematous papules/pustules mostly on cheeks
No comedones
Resolves spontaneously
Not infantile acne
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7
Q

Congenital melanocytic nevi

A

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

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8
Q

Epidermolysis bullosa

A

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

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9
Q

Epidermolysis bullosa simplex

A

Most common/mild
Autosomal dominant
Usually just skin involvement

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10
Q

Junctional epidermolysis bullosa

A
Least common
Autosomal recessive
Poor outcome due to extracutaneous complications
Nail dystrophy is common
Specific subtype with pyloric atresia
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11
Q

Dystrophic epidermolysis bullosa

A

Milder
Autosomal recessive and dominant
Extracutaneous complications can occur

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12
Q

Bullous impetigo

A

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)

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13
Q

Staph scalded skin syndrome (SSSS)

A

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

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14
Q

Nevus sebaceous (of Jadassohn)

A

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

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15
Q

Incontinentia pigmenti

A

Newborns present with small clustered blisters on an erythematous base (along Blaschko lines)

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16
Q

Ichthyosis vulgaris

A
Autosomal dominant
Appear normal at birth
Presents at three months with mild scales, no flexural involvement
Maximum symptoms by puberty
A/W atopic dermatitis
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17
Q

Epidermolytic hyperkeratosis

A

Autosomal dominant
Seen at birth, looks similar to SSSS
Wide spread bullae with possible bad odor 2/2 infection

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18
Q

Ichthyosis

A

Can present as collodion infant at birth

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19
Q

Congenital hemangiomas

A

Fully formed at birth
Do not proliferate
Two types: rapidly involuting, non-involuting

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20
Q

Infantile hemangiomas

A

Most common vascular tumor of infancy
Rapid growth followed by spontaneous involution
Three types - Superficial, combined, deep

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21
Q

Complications of hemangiomas

A

Ulceration
Structural deformity and airway involvement
Congestive heart failure

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22
Q

When to treat hemangiomas

A
Life or function threatening
Located where permanent deformity may occur (nose, lip, ear)
Large facial lesions
Ulcerated
Pedunculated
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23
Q

Multiple hemangiomas

A

10 to 25%

Visceral involvement - screen for liver/other lesions if >5 hemangiomas noted, echo to rule out heart failure

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24
Q

Kasabach-Merritt phenomenon

A

Vascular anomalies + thrombocytopenia + coagulopathy



25
Q

Examples of vascular tumors

A

Kaposiform hemangioendothelioma
Tufted angioma
Multifocal lymphangioendotheliomatosis with thrombocytopenia

26
Q

Cutis aplasia

A

Focal congenital defects of skin
Involve dermis and epidermis
Reepithilialize over several months without intervention

27
Q

Tuberous sclerosis

A
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
28
Q

Waardenburg syndrome

A
Autosomal dominant
Depigmented patches of skin and hair
Heterochromia iridis
Congenital nerve deafness
Craniofacial anomalies
29
Q

Café au lait macules

A

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

30
Q

Urachus

A

Remnant of regressed allantois that runs from baldder to umbilicus

31
Q

Omphalomesenteric duct

A

Connects ileum to umbilicus

Regresses between 5-9 weeks GA

32
Q

Umbilical granuloma

A

Small bright red papules
Due to umbilicus not re-epitheliazing
Treat with silver nitrate
No discharge

33
Q

Peutz-Jeghers Syndrome

A

Autosomal dominant
Mucocutaneous pigmentation and G.I. polyps
Has been a/w bowel obstruction in the neonate
Develop hamartomatous polyps later in life

34
Q

Harlequin color change

A

Dependent 1/2 of body turns red, other 1/2 pale

Due to temporary inbalance of autonomic regulatory mechanism of cutaneous vessels

35
Q

Eosinophils on Wright stain

A

Erythema toxicum

36
Q

Inclusion cysts with keratinized stratum corneum

A

Milia

37
Q

Miliaria profunda

A

Occlusion at or below dermoepidermal junction

Rare in newborns

38
Q

Miliaria rubra

A

Heat rash
Erythematous papules/pustules on head/neck/trunk
Intraepidermal eccrine duct obstruction

39
Q

Miliaria crystallina

A

Subcorneal or intercorneal ductile obstruction
Due to overheating
Leads to sweat-producing, small, clear vesicles

40
Q

Neutrophils on Wright stain

A

Transient pustular neonatal melanosis

41
Q

Skin infection with a negative culture

A

SSSS

42
Q

Four stages of incontinentia pigmenti

A
  1. Vesicular
  2. Verrucous
  3. Hyperpigmented
  4. Atrophic
43
Q

Autosomal recessive forms ofichthyosis

A

Lamellar ichthyosis

CIE

44
Q

Forms of ichthyosis with no flexural involvement

A

X-linked ichthyosis

Ichthyosis vulgaris

45
Q

X-linked ichthyosis

A

X-linked recessive

A/W cryptorchidism in 25% of males

46
Q

Benign neonatal hemangiomatosis

A

Multiple hemangiomas

Cutaneous only, no visceral involvement

47
Q

Diffuse neonatal hemangiomatosis

A

Multiple hemangiomas

Both cutaneous and visceral lesions present

48
Q

Treatment of Kasabach Merritt phenomenon

A
Medical emergency
Treat with: 
- steroids
- vincristine
- interferon-alpha
- ticlopidine
- aspirin
- embolization
49
Q

Patent urachus from bladder to umbilicus

A

Urachal fistula

Urine can leak

50
Q

Partially patent urachus

A

Urachal cyst

51
Q

Urachus only patent at umbilicus

A

Urachal sinus

52
Q

Failure of normal obliteration of omphalomesenteric duct

A

Omphalomesenteric fistula

53
Q

Partially patent omphalomesenteric duct

A

Omphalomesenteric cyst

54
Q

Omphalomesenteric duct patent only at umbilicus

A

Umbilical polyp

55
Q

Conditions associated with cutis aplasia

A
Epidermolysis bullosa
Opitz syndrome
Adams–Oliver syndrome
Oculocerebrocutaneous syndrome
Trisomy 13–15
4p- syndrome
Johanson–Blizzard syndrome
Xp22 microdeletion syndrome
Chromosome 16–18 defect
56
Q

Symptoms of Sturge-Weber syndrome

A

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)

57
Q

Anomalies associated with incontinentia pigmenti

A

Teeth (delayed, hypodontia)
Hair (alopecia, wiry hair)
Nails (dystrophy)
Retina (retinal vascular proliferation)

58
Q

Finding on Tzanck smear in incontinentia pigmenti

A

Eosinophils 

59
Q

What do infantile hemangiomas over express during their proliferative phase?

A

Type 3 iodothyronine deiodinase

Leads to a consumptive hypothyroid state