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)
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
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
4
Q
Cutis marmorata
A
- Exaggerated vasomotor response to hypothermia
- Disappears w/ rewarming
- lasts weeks-months
- Physiologic
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
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
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
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)
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
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
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)
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
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
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)
15
Q
Port-wine stain
A
- Capillary malformation, persistent and present at birth
- usually unilateral (how to distinguish from nevus simplex)
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
Infections with AD
- 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
Pathomechanism of AD
- 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
Management of AD
- 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
Diaper rash
- 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
Irritant diaper dermatitis
- 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
Seborrheic dermatitis (SD)
- 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
