Pediatric derm Flashcards

1
Q

Physiologic processes of neonate skin

A
  • Physiologic desquamation: SC of neonates is thicker than adults and excess is shed in first few days
  • Vernix caseosa: moist, yellow coating on neonates (sebum, desquamated skin cells, lanugo hairs)
  • Preterm infants have immature hydrophobic barrier and are susceptible to dehydration, electrolyte imbalance, energy loss, percutaneous toxicity, mechanical injury, and infection
  • Birth resets hair growth cycle (anagen-> catagen-> telogen), thus babies have temporary hair loss at 3 months
  • Neonates have active sebaceous glands due to maternal steroids (and possible endogenous ones)
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2
Q

Skin barrier

A
  • Lamellar bodies formed in stratum spinosum and stratum granulosum
  • In stratum corneum they are broken down to FFA, ceramides, and cholesterol
  • Forms permeability barrier
  • Corneocytes held together by corneodesmosomes
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3
Q

Lines of blaschko

A
  • Reflects patterns of migration of skin cells during embryogenesis
  • Not the same as dermatomes
  • If a population of skin cells acquires a mutation, the pattern of disease may follow Blaschko’s lines
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4
Q

Cutis marmorata

A
  • Exaggerated vasomotor response to hypothermia
  • Disappears w/ rewarming
  • lasts weeks-months
  • Physiologic
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5
Q

Harlequin color change

A
  • Usually in premature infants
  • Sudden onset, lasts 30sec-20min
  • Occurs when lying on side, dependent side of body shows profound vasodilation, upper half is pale
  • Due to immaturity of hypothalamic centers controlling vasomotor tone
  • Physiologic
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6
Q

Neonatal acne

A
  • Not true acne
  • Pinpoint erythematous papules and pustules on cheeks, forehead, and chin
  • Associated w/ saprophytic yeast (malassezia sp.)
  • Around 3 weeks, self-resolves
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7
Q

Infantile acne

A
  • 3-6 months onset
  • Is true acne (comedones); papules, pustules, nodules
  • May last mos-yrs
  • can Rx w/ topicals or oral antibios if severe
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8
Q

Milia

A
  • Small keratin-filled cysts (white papules lacking erythema)
  • usually on nose, chin, cheeks, forehead
  • very common and physiologic
  • Can occur in oral epithelium: bohn’s nodules on gums, epstein’s pearls in midline of hard palate (both are very common)
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9
Q

Sebaceous hyperplasia

A
  • Many tiny white-yellow papules on the nose
  • Due to maternal androgen stimulation, very common and physiologic
  • Often accompanied by milia
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10
Q

Erythema toxic neonatorum

A
  • Starts as macules, progresses to ill defined erythematous papules and pustules on the trunk and arms (flea-bite appearance)
  • Appears a few days after birth, lasts up to 2 weeks
  • pustule content is eosinophils
  • Self-resolves, physiologic
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11
Q

Miliaria

A
  • Obstruction of eccrine duct leads to rupture of duct and sweating into skin
  • Related to immaturity of skin, warmer climates, over bundling, febrile infants
  • Miliaria crystallina: obstruction at stratum corneum
  • Miliaria rubra: intraepidermal obstruction
  • Miliaria profunda: obstruction at derma-epidermal junction (rare)
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12
Q

Transient neonatal pustular melanosis

A
  • Vesicopustules that rupture w/ scaling, leaving hyper pigmented macules
  • Rare, more common in dark-skinned
  • Diffuse, usually on chin, forehead, lower back, shins
  • Pustules (containing neutrophils) usually disappear in 24-48 hrs
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13
Q

Neonatal HSV

A
  • Erythematous macules that transition to individual and grouped vesicles on erythematous base
  • Dx: unroof, swab base for viral culture, DFA, or PCR
  • Mostly HSV2, usually from delivery
  • Sequelae: mucocutaneous, dissemination, CNS infection, death
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14
Q

Nevus simplex (salmon patch)

A
  • Most common vascular lesion of infancy
  • Problem in fetal circulation, not malformation
  • central facial distribution, forehead, nape of neck, upper eyelids
  • Usually disappears in 1-2 yrs (except for nape)
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15
Q

Port-wine stain

A
  • Capillary malformation, persistent and present at birth

- usually unilateral (how to distinguish from nevus simplex)

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16
Q

Sturge-weber syndrome

A
  • Triad of port-wine stain, seizures, and glaucoma
  • Based on dermatomes of cranial nerves
  • Use CT to Dx by looking for “tram track” calcifications
17
Q

Klippel Trenaunay syndrome

A
  • Triad of vascular stain (usually port-wine), limb hypertrophy, venous vericosities
  • Often with capillary, venous, lymphatic malformations
  • Parkes weber syndrome: vascular stain, limb hypertrophy, arteriovenous malformation
18
Q

Segmental infantile hemangioma

A
  • Usually covers a territory over the face, darkens and thickens and may ulcerate
  • Associated w/ PHACES syndrome (brain and cardiac structures may be affected)
19
Q

Infantile hemangioma (IH)

A
  • Most common vascular tumor in neonates
  • Major associations: prematurity, female, multiple gestation, white non-hispanc
  • Erythematous vascular plaques, usually on head and neck but can be anywhere
  • Precursor lesion (at birth) usually not noticed, but looks like a red telangiectatic (vessels on surface), whitish, or bruise-like patch
  • Proliferation phase starts 1-2 weeks after birth, most growth by 3 months
  • Involution phase (apoptosis) takes years, but doesn’t always equal resolution (disfigurement)
20
Q

Types of IH

A
  • Can be superficial, mixed, or deep
  • Deep don’t show much erythema, superficial are very erythematous
  • Can be localized (one) or segmental (covers a territory)
21
Q

Pathogenesis of IH

A
  • Clonal proliferation of endothelial cells from vasculogenesis (new blood vessels from angioblasts), not from angiogenesis (new blood vessels from pre-existing ones)
  • Endothelial cells are derived from placenta, as demonstrated by the Ag GLUT1
  • This process can be triggered by hypoxia
22
Q

Rx of IH

A
  • Most only requires anticipatory guidance
  • Some do require Rx: ulcerations, impairment of vital function (breathing in beard hemangioma, liver involvement), risk for potential disfigurement
  • For ulcerations use antibacterial topicals
  • Other Rx: beta-blockers have become primary choice (oral propanolol)
23
Q

Lumbar segmental IH

A

-Associated w/ LUMBAR syndrome

24
Q

Atopic dermatitis (AD)

A
  • Begins around 6 months, manifests as itchy, scaly red skin (ill-defined) w/ weeping papules and plaques
  • Usually on cheeks, forehead, scalp, trunk, extensors as infants
  • Many with preceding seborrheic dermatitis in first 2-3 mos
  • Atopic triad: AD, asthmas, allergic rhinitis
  • In childhood, appears mostly in wrists, ankles, legs, face. is more dried, chronic, lichenified
25
Q

Infections with AD

A
  • Bacterial infections cause yellow crusting (staph), pustules, open weeping areas
  • Eczema herpeticum is HSV superinfection, presents as monomorphous punched out erosions
  • Swab base for viral culture, DFA, or PCR
26
Q

Pathomechanism of AD

A
  • Interaction btwn genetics, skin barrier dysfunction, immune regulation (TH2), and environment
  • Filaggrin dysfunction in families w/ heritable mutation
  • Skin barrier abnormality plays critical role in precipitating downstream immunologic abnormalities (elevated IgE)
27
Q

Management of AD

A
  • Repair skin barrier (bathe daily, soak and seal, cleanser and moisturizer w/ ointment)
  • Decrease inflammation (first try topical steroids, then calcineurin inhibitors, use wet wraps)
  • Treat/prevent infection (use topical antibios, bleach baths, oral antibios if needed)
  • Control pruritus (sedation via H1 antihistamines, wet wraps)
  • Avoid triggers (allergens)
28
Q

Diaper rash

A
  • Manifests as erythematous plaque
  • Often superinfected w/ candidia, involves the creases of the perineal area w/ peripheral scaling and satellite papules/pustules
  • Rx for candidiasis is topical antifungals
29
Q

Irritant diaper dermatitis

A
  • Presents as symmetric erythema along convex surfaces, folds relatively spared
  • Moist patches (from urine/feces) become eroded
  • Increased pH in urine activates fecal lipase’s and proteases
30
Q

Seborrheic dermatitis (SD)

A
  • Most common in first 3 mos
  • Due to inflammatory run against normal skin yeast (malassezia sp)
  • Causes erythematous moist patches along creases of diaper area
  • Can also affect scalp, eyebrows, other folds, and trunk
  • Can affect seborrheic areas (eyebrows, behind ears)
  • Can be yellow greasy scales