exam 1 - derm Flashcards

1
Q

mottling/cutis marmorata

A

-Lace-like pattern of bluish, reticular discoloration (dilated cutaneous vessels)
-Response to lowered room temperatures, resolved on rewarming

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2
Q

milia

A

-Tiny (1-2 mm) epidermal cysts filled with keratinous material predominantly on face in 40% of newborns
-Spontaneously rupture and exfoliate their contents

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3
Q

miliaria/heat rash

A

-Obstruction of eccrine sweat ducts
Superficial: Tiny (1-2 mm), superficial grouped vesicles without erythema over intertriginous areas and adjacent skin (neck/upper chest)
-Deep: Erythematous grouped papules called miliaria rubra
-Cooling is tx of choice

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4
Q

erythema toxicum

A

-Up to 50% of newborns at 24-48 hours of age
-Blotchy, erythematous macules 2-3 cm in diameter – chest, back, face, and extremities
-Macules fade within 1-2 days or progress to urticarial wheals/pustules; lesions disappear completely within 5-7 days
-Smears of lesions reveal numerous eosinophils without organisms

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5
Q

sebaceous gland hyperplasia

A

-White-yellow papules at opening of pilosebaceous follicles without surrounding erythema (nasal region)
-Response to maternal androgens
-Occurs in > 50% of newborns and spontaneously regresses in the first few months of life

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6
Q

neonatal acne

A

-Inflammatory papules and pustules with occasional comedones on the face
-Most often occurs at 2-4 weeks of age with spontaneous resolution over 6 months-1 year

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7
Q

transient neonatal pustular melanosis

A

-Pustular eruption in African American newborns
-Pustules rupture leaving a collarette of scale surrounding a macular hyperpigmentation
-Lesions contain neutrophils and involve the palms and soles

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8
Q

harlequin color change

A

-Cutaneous, vascular phenomenon unique to neonates in the first week of life when infant is placed on one side
-Dependent half develops an erythematous flush with a sharp demarcation of the midlines/upper half of the body becomes pale
-Subsides on its own over 20 minutes

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9
Q

sucking blisters

A

-Bullae without inflammatory borders over the forearms, wrists, thumbs, or upper lip from vigorous sucking in utero
-Resolve without complications

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10
Q

dermal melanocytosis

A

Blue-black macule found over the lumbosacral area in 90% of darker-skinned infants; lesions fade with time

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11
Q

cafe au lait macule

A

-Light-brown, oval macule may be found anywhere on body
-Persist throughout life and may increase in number with age
-6+ lesions > 0.5 cm/> 1.5 cm (based on age) is a major diagnostic criterion for NF-1

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12
Q

vascular birthmarks

A

Excess of capillaries in localized areas of skin; light red-pink to dark red
-hemangiomas
-nevus simplexes
-port wine stains

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13
Q

vascular birthmarks: nevus simplexes

A

-Light red macules over nape of neck, upper eyelids, and glabella of newborns
-Fade completely x 1 year (especially eyelid/glabella)

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14
Q

vascular birthmarks: hemangiomas

A

-Red, rubbery vascular plaque or nodule
-Benign tumors of capillary endothelial cells
-50% reach maximal regression by 5 years, 70% by age 7 years, and 90% by age 9 years
-Treatment
-Immediate intervention for visual obstruction, airway obstruction, cardiac decompensation, ulceration, association with underlying anomalies
-Topical timolol (gel-forming solution) for small, superficial hemangiomas
-Oral propranolol (2 mg/kg/d divided BID)
-Ulcerated/bleeding – wound care and pulsed dye laser

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15
Q

vascular birthmarks: port-wine stains

A

-Dark red macules appearing anywhere on the body
-Bilateral facial port-wine stain or one covering the entire half of the face may be a clue to Sturge-Weber Syndrome (seizures, mental retardation, glaucoma, and hemiplegia)
-Treatment: Pulsed dye laser

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16
Q

acne vulgaris: pathogenesis

A

-Obstruction of sebaceous follicle > formation of the microcomedo (precursor to all future lesions)
-This phenomenon is androgen-dependent in adolescent acne
-4 primary factors:
-1. Plugging of the sebaceous follicle
-2. Increased sebum production
-3. Proliferation of Cutibacterium acnes in the obstructed follicle
-4. Inflammation

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17
Q

acne vulgaris: clinical manifestations

A

-Open comedones are the predominant lesion in adolescent acne
-Black color from oxidized melanin within plug
-Closed comedones (whiteheads)
-Obstruction just beneath follicular opening in neck of sebaceous follicle > swelling of duct directly beneath epidermis
-Precursor to inflammatory acne lesions
-Cystic acne
-Severe, chronic, inflammatory lesions may occur as interconnecting, draining sinus tracts > scar formation

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18
Q

acne vulgaris: tx

A

-Topical Keratolytic Agents
-Address plugging of follicular opening with keratinocytes
-Retinoids, benzoyl peroxide, and azelaic acid
-Topical retinoid (tretinoin, adapalene, tazarotene) is the first-line treatment for comedonal and inflammatory acne
-Applied nightly with or without BPO/AA applied in AM
-Topical Antibiotics
-Less effective than systemic
-1% Clindamycin phosphate solution is most efficacious topical antibiotic
-Should never be used alone (several combination products exist)
-BPO has shown to minimize development of resistance
-Systemic Antibiotics
-Concentrated in sebum – tetracycline, minocycline, and doxycycline
-Anti-inflammatory effects and decrease C. acnes in follicle
-Reserved for moderate-severe inflammatory acne
-Should never be used alone and always for a finite time
-Oral Retinoids
-Isotretinoin is the most effective treatment for severe cystic acne
-Exact MOA is unknown (multifactorial)
-Side effects: Dry mucous membranes/skin, myalgias, mild/reversible hair loss, elevated LFTS/lipids (rare), acute depression/mood changes (no definitive causative relationship), teratogenic
-Oral contraceptives

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19
Q

acne vulgaris: education/follow up

A

-Wash face consistently, use only oil-free/noncomedogenic cosmetics/creams/hair sprays
-Therapy takes 8-12 weeks to produce improvement
-Follow-up every 3-4 months with objective documentation of improvement (photo)

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20
Q

atopic dermatitis

A

-Pathogenesis
-Interaction among susceptibility genes, host environment, skin barrier defects, pharmacologic abnormalities, and immunologic response
-3 clinical phases
-1. Infantile eczema: Onset 2-3 months, ends at 18 months – 2 years
-Dermatitis on cheeks and scalp, oval patches on trunk
-Later involves extensor surfaces of extremities
-2. Childhood/flexural eczema: Onset 2 years, lasts through adolescence
-3. Adolescent eczema: Continuation of flexural eczema with hand/foot dermatitis

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21
Q

discoid annular eczema

A

mimics ring worm

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22
Q

atopic dermatitis: tx

A

-Acute Stages
-Medium-potency topical glucocorticoids (under wet dressings) -> Low-potency only for face and intertriginous areas
-Wet dressings: Wet underwear, cotton socks (several days x 1 week)
-Relief of itching: Oral antihistamines (cetirizine in AM, hydroxyzine in PM)
-Chronic Stages
-Treatment aimed at avoiding irritants and restoring moisture
-No soaps or harsh shampoos
-Bathing minimized to every second or third day
-Lubrication of skin
-Medium-potency topical steroids
-Superinfection > systemic abx x 10-14 days
-Topical immunosuppressive agents (tacrolimus/pimecrolimus) -> > 2 years of age, unresponsive to medium-potency steroids
-Narrow-band UV-B, twice weekly
-Systemic immunosuppressive (dipilumab/Dupixent) is the first biological therapy approved in patients 12 years or greater

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23
Q

atopic dermatitis: complications

A

-Dry, itchy skin
-Cracks in epidermal barrier (inability to hold water within stratum corneum > shrinking of layer)
-Ineffective barrier to entry of irritants
-Secondary infections with S. aureus and S. pyogenes

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24
Q

primary irritant contact dermatitis: diaper dermatitis

A

-Develops within several hours, peaks at 24 hours, then disappears
-Prolonged contact of skin with urine and feces (irritating chemicals – urea and intestinal enzymes)
-Erythema and scaling of the skin in the perineal area with sparing of inguinal folds
-In 80% of cases lasting > 3 days, affected area is colonized with C. albicans
-Beefy red, sharply demarcated dermatitis with satellite lesions
-Treatment
-Frequent diaper changes, washing area with clean cloth and water
-Air drying with diaper changes and prior to application of topicals
-Barrier creams with zinc oxide and imidazole cream BID

25
allergic contact dermatitis
-Delayed onset of 18 hours, peaks at 48-72 hours, lasts up to 2-3 weeks -Plants such as poison ivy, poison sumac, and poison oak cause most cases in children -Also, from nickel (earrings/belts), neomycin -Blisters (linear), oozing, crusting -Treatment: -Localized: Potent topical corticosteroid -Severe, generalized: Prednisone, 1-2 mg/kg/day, PO, x 10-14 days
26
sebhorrheic dermatitis/cradle cap
-Erythematous, scaly dermatitis accompanied by overproduction of sebum (face, scalp, and perineum) -Occurs predominantly in the newborn and at puberty (hormonal stimulation of sebum production is maximal) -Treatment: -Responds well to low-potency topical corticosteroids, antifungal shampoos (ketoconazole 1-2%), and anti-dandruff shampoos
27
viral exanthems: measles (rubeola)
-Highly contagious (droplet and airborne transmission), caused by single-stranded RNA paramyxovirus, with humans as only host -Infects URT/regional lymph nodes > spreads systemically; secondary viremia (5-7 days) spread to respiratory tract, skin, and other organs -Contagious from 1-2 days prior to onset of symptoms (5 days before – 4 days following appearance of rash) -dont need to know^^^ -4 phases: Incubation (8-12 days from exposure to onset), prodromal (catarrhal), exanthematous (rash), and recovery -3 day prodromal period: Cough, coryza, conjunctivitis and pathognomonic Koplik spots! (gray-white, sand-grain-sized dots on buccal mucosa, opposite lower molars) -Conjunctiva with possible Stimson line! (transverse line of inflammation along the eyelid margin) -Exanthematous phase: Sx + FEVER -Macular rash, spreading from HEAD TO TOE over 24 hours; rash fades in the same pattern -Generalized lymphadenopathy (cervical nodes most prominent) -AOM, PNA, and diarrhea common in infants
28
viral exanthems: measles (rubeola): dx and tx
-dx: -Serologic testing for IgM antibodies (appear 1-2 days into rash, persist for 1-2 months) -+/- genetic testing -> RT-PCR -Suspect cases reported immediately to local/state health department -Treatment: -Supportive care – fluids, antipyretics -WHO recommends routine administration of vitamin A x 2 days to children with acute measles
29
viral exanthems: rubella (german/3-day measles)
-Caused by single-stranded RNA togavirus, humans only host -Invades respiratory tract > dissemination (primary viremia) > replication in reticuloendothelial system > secondary viremia, virus present in peripheral blood monocytes, CSF, and urine -Spread through direct or droplet contact with NP secretions (2 days before or 5-7 days after rash onset) -dont need to know^^^ -Incubation period 16-18 days, mild catarrhal symptoms -Retroauricular, posterior cervical, and posterior occipital lymphadenopathy with erythematous, maculopapular, discrete rash -Rash spreads from head to toe, lasts for 3 days -Rose-colored spots (Forchheimer spots) on soft palate may appear before rash -Other symptoms: Pharyngitis, conjunctivitis, anorexia, headache, malaise, low-grade fever, polyarthritis, parasthesias, tendonitis -Dx: -Serologic testing for IgM antibodies (positive 5 days after onset) or by 4-fold or greater increase in specific IgG antibodies in acute/convalescent sera -Treatment: Supportive
30
viral exanthems: erythema infectiosum (5th ds)
-Caused by single-stranded DNA virus, parvovirus B19!! -Viral affinity for RBC progenitor cells -> aplastic crisis in pts with hemolytic anemias (SCD, spherocytosis, and thalassemia)!!! -Incubation period typically 4-14 days -Begins with mild illness characterized by fever, malaise, myalgias, and headache > rash 7-10 days later -3 stages of rash: -1. Initially: “Slapped cheek” rash with circumoral pallor -2. 1-4 days later: Erythematous, symmetric, maculopapular, truncal rash -3. Central clearing of rash takes place, distinct lacy!, reticulated! rash -Rash may be pruritic, does not desquamate -Adolescents/adults may experience myalgia, significant athralgias/arthritis, headache, pharyngitis, coryza, and GI upset -May cause hepatitis, myocarditis, and papular-purpuric gloves and socks syndrome -Transient aplastic crisis (SCD): Fever, lethargy, malaise, pallor, headache, GI symptoms, respiratory symptoms -Extremely low reticulocyte count, low hemoglobin, transient neutropenia/thrombocytopenia
31
viral exanthems: erythema infectiosum (5ths ds): dx and tx
-Diagnosis -Hematologic abnormalities: Reticulocytopenia x 7-10 days, mild anemia, thrombocytopenia, lymphopenia, and neutropenia -Detected by PCR and electron microscopy of erythroid precursors in bone marrow -Serologic testing (IgM antibodies) is diagnostic (detects infection within prior 2-4 months) -Treatment: Supportive care, transfusion (aplastic crisis), IVIG for immunocompromised
32
viral exanthems: roseola infantum (exanthem subitum, 6th ds)
-Caused by double-stranded DNA virus, human herpesvirus type 6 (HHV-6) in most cases (HHV-7 in 10-30% of cases) -Major cause of acute febrile illnesses in infants and may be responsible for up to 20% of ER visits for children 6-18 months of age -High fever!!! (> 40C) with abrupt onset, lasts 3-5 days > giving way to maculopapular, rose-colored rash (lasts 1-3 days) -URI symptoms, erythematous TMs, and cough -Dx: PCR for detection of HHV-6 in blood (does not differentiate latent, reactivation, or primary infections) Treatment: Supportive
33
viral exanthems: varicella-zoster (chickenpox/zoster)
-Caused by double-stranded DNA virus, varicella-zoster virus (VZV) -Chickenpox (varicella) is primary infection -Transmission via direct contact, droplet, and air -Infects via conjunctivae or respiratory tract and replicates in NP and URT -Primary viremia -> infects regional lymph nodes, liver, spleen, and other organs -Secondary viremia -> cutaneous infection with typical vesicular rash -Communicability from 2 days prior to 7 days after onset of rash (when all lesions are crusted) -Resolution of chickenpox -> virus persists in dorsal root ganglia -Zoster (shingles) is reactivated latent infection -Transmission via direct contact
34
varicella-zoster sx
-Incubation period is generally 14-16 days -Prodromal symptoms of fever, malaise, and anorexia may precede rash by 1 day -Rash progression: -Small red papules -> nonumbilicated, oval, tear-drop-like vesicles on an erythematous base -> vesicles ulcerate, crust, and heal -New crops appear for 3-4 days -Usually begins on trunk followed by the head, face, and extremities (rare) -All forms of lesions are present at same time -Marked pruritis -Pre-eruption phase: Intense, localized, burning pain and tenderness (acute neuritis) along a dermatome, accompanied by malaise and fever -Rash progression: -Several days later, eruption of papules -> vesiculation (in dermatomal distribution/unilateral) -> crusting/healing -Thoracic and lumbar regions MC -CN V involvement: Corneal/intraoral lesions -CN VII involvement: Ramsay Hunt Syndrome –facial paralysis and ear canal vesicles -Postherpetic neuralgia: Pain persisting > 1 month is uncommon
35
varicella-zoster: dx and tx
-dx- PCR of vesicular fluid is method of choice -Treatment (Varicella) -Symptomatic: Anti-pyretics, cool baths, and careful hygiene -Acyclovir (all age groups), valacyclovir (2 years and older) -Not recommended in otherwise healthy children -Early (within 24 hours of rash onset) in immunocompromised patients is effective in preventing PNA, encephalitis, and death -Treatment (Zoster) -Acyclovir, valacyclovir, famciclovir (adults) -Accelerates cutaneous healing, hastens resolution of acute neuritis, and reduces risk of postherpetic neuralgia
36
viral exanthems: coxsackie (hand-foot-mouth ds)
-Caused by coxsackieviruses, especially types A5, A10, and A16 -Mild fever, sore throat, and malaise -Rash: -Vesicles/red papules found on pharyngeal pillars, tongue, oral mucosa, hands (palms), and feet (soles) -Lesions may last 1-2 weeks -soft palate tiny red spots -nails are peeling 1-2 months after -swab for strep jic -Treatment: Supportive
37
bacterial infections: impetigo
-Erosions covered by honey-colored crusts -Staphylococci and group A streptococci -Treatment: Topical (mupirocin, polymyxin, gentamycin, erythromycin) and/or PO -> if widespread (B-lactamase- resistant PCN, cephalosporins, clindamycin, amoxicillin-clavulanate) x 7-10 days -hand, feet, mouth -Bullous impetigo: Border filled with clear fluid; treatment with PO abx x 7-10 days -Ecthyma: Firm, dry crust, surrounded by erythema that exudes purulent material (deeper form of impetigo affecting the superficial dermis); treatment with systemic PCN
38
bacterial infections: cellulitis
-Erythematous, hot, tender, ill-defined, edematous plaques accompanied by regional lymphadenopathy -Invasion of microorganisms into lower dermis/beyond -GABHS and coagulase-positive staphylococci are the MC causes -Treatment with systemic antibiotic
39
bacterial infection: folliculitis
-Pustule at a follicular opening -Staphylococcal and streptococcal infections MC -Treatment: Warm, wet compresses x 24 hours, topical keratolytics, topical/PO antibiotics
40
bacterial infections: abscess
-Erythematous, firm, acutely tender nodule with ill-defined borders -Staphylococci are MC infections -paronychia -Treatment: I&D alone/with adjuvant antibiotics -bactrim
41
bacterial: scalded skin syndrome
-Sudden onset of bright red, acutely painful skin (perioral, periorbital, flexural areas) -Slightest pressure on skin results in severe pain and separation of epidermis (Nikolsky sign) -Commonly from staph infection -Treatment: Systemic anti-staphylococcal antibiotics
42
dermatophyte infections: tinea capitis
-Caused by Microsporum canis and Trichophyton tonsurans -Thickened, broken-off hairs with erythema and scaling of underlying scalp -Hairs broken off at surface of scalp, leaving a “black dot” appearance -Boggy, fluctuance mass (kerion) may be seen -Fungal cultures for all suspected cases -Treatment: -Systemic therapy: Griseofulvin, terbinafine -Eat with fatty meal to enhance absorption -Dosing 20 mg/kg/day divided BID x 4 weeks > re-culture > continued for 4 weeks past negative result -Terbinafine dosing is weight dependent
43
dermatophytes: tinea corporis, cruris, pedis
-Tinea corporis -Caused by M. canis, Trichophyton mentagrophytes, and Trichophytan rubrum -Annular, marginated plaques, thin scale at periphery and clear center -Diagnosis via skin scraping > dissolving in 20% KOH, examining for hyphae -Tinea cruris -Caused by T. mentagrophytes, T. rubrum, and Epidermophyton floccosum -Symmetrical, sharply demarcated lesions in inguinal areas -Tinea pedis -Caused by T. mentagrophytes and T. rubrum -Red, scaly soles; blisters on instep of foot, fissuring between toes -Treatment for above infections: -Topical anti-fungal: Imidazoles, allylamines, benzylamines, or ciclopirox BID x 3-4 weeks
44
dermatophyte: tinea unguium (onychomyocosis)
-MC cause is T. rubrum -Loosening of nail plate from nail bed (onycholysis), giving a yellow discoloration > thickening of distal nail plate > scaling/crumbly appearance of entire nail plate surface -Diagnosis confirmed by KOH exam and culture -Treatment: -Topical ciclopirox 8% (Penlac nail lacquer) daily – low success rates (20%) -Terbinafine x 6-12 weeks or pulsed-dose itraconazole (three, 1-week pulses, each separated by 3 weeks)
45
insect infestation: pediculosis (lice)
-Presence of excoriated papules and pustules and a hx of severe itching at night -gelatinous nits of head louse adhere tightly to hair shaft -Pubic louse may be found crawling among hairs, eyelashes of newborns -Treatment: -OTC pyrethrin/permethrin product -> More effective if nits are manually removed (hand or lice comb) -Malathion 0.5% is ovicidal and highly effective (but toxic and flammable) -Used if OTC products do not eradicate after 2 applications, 7 days apart -Other ovicidal agents include topical ivermectin and spinosad -Clean all clothing (stuffed animals, bedding…etc.) and wash at high temperature
46
insect infestations: scabies
-Suggested by linear burrows about the wrists, finger webs, areolas, anterior axillary folds, genitalia, or face -Excoriations, honey-colored crusts, and pustules (secondary infections) -Dx confirmed by identification of female mite, her eggs/feces -Skin scraping > mineral oil > microscopic evaluation -Treatment: -Permethrin 5% -Applied as a single overnight application and repeat in 7 days to patient and household contacts -< 2 years entire body (including face); older children/adults (neck down) -Resistant cases – PO ivermectin x 1, repeat in 7 days
47
irritant dermatits vs candidal/fungal dermatitis -> diaper rash
-if aquaphor doesnt work after 2-3 days -> go back to office -> prob fungal -irritant- spares creases/skinfolds -candidal/fungal- satelittle lesions, beefy -doesnt spares the creases and folds
48
papulosquamous eruptions: pityriasis rosea
-Common in school-aged children and adolescents -Presumed to be viral in origin -Pink to red oval plaques with fine scales that tend to align with long axis parallel to skin tension lines (“Christmas tree pattern” on the back) -Usually proceeded by 30 days of a solitary, larger, scaling plaque with central clearing and scaly border (herald patch) -Lasts 6-12 weeks -Treatment: -Usually, no treatment warranted -Exposure to natural sunlight -PO anti-histamines/steroids for pruritic lesions -Rash lasting > 12 weeks – dermatologist
49
papulosquamous eruptions: psoriasis
-Immune-mediated inflammation, familial, multiple psoriasis susceptibility genes -Increased epidermal turnover (3-4 days versus 28 days for normal skin) -> excessive stratum corneum -> thick, opaque scales -Erythematous papules covered by thick, white scales -MC form in children is guttate (drop-like) psoriasis, usually following a streptococcal infection (2-3 weeks later) -Sudden onset of small papules (3-8 mm) over the trunk, quickly covered by white scales -> usually wide spread rather than just extensors -Chronic psoriasis is marked by thick, large, scaly plaques (5-10 cm) over elbows, knees, scalp, and other sites of trauma
50
psoriasis tx
-Topical steroids are initial tx of choice – high potency, BID (fluocinonide 0.05%/Lidex, clobetasol 0.05%/Temovate) -Second line is topical vitamin D, BID (calcipotriene/Dovonex, calcitriol (Vectical) -Or a combo of the two -Severe cases -> dermatologist -Narrow band UVB phototherapy, systemic medications, biologic agents -Methotrexate, retinoids, cyclosporine
51
virus-induced tumors: molluscum contagiosum
-Caused by poxvirus -> induces epidermis to proliferate, forming a pale papule -umbilicated, flesh-colored papules in groups anywhere on body -Common in infants, preschool children, and sexually active adolescents -secondary infections are common -Treatment: -Observational: Resolve over months to years -Immunological: Topical imiquimod, PO cimetidine, intralesional Candida antigen injection (like a wart) -Cytodestructive: Topical cantharidin, cryotherapy with liquid nitrogen, and curettage
52
virus-induced tumors: verrucae (warts)
-Skin-colored papules with rough (verrucous) surfaces cause by infection with HPV -> stimulates proliferation of epidermal cells -Over 200 forms of HPV – Cause certain types and locations -Treatment: -30% of all warts will clear in 12 months, 60% in 24 months -Immunological: Topical imiquimod, PO cimetidine, intralesional Candida antigen injection, squaric acid contact therapy -Cytodestructive: 5-fluorouracil applied to warts under occlusive dressing (cut off O2) x 12 weeks (success rate in children ~ 80%) -Adjunctive therapy: Vascular pulsed dye lasers -Plantar warts: -40% salicyclic acid plaster -> placed over lesion daily x 5 days -> following 2 days soak in warm water x 30 minutes -> macerated tissue pared down with pumice stone/cuticle scissors/nail file -Repeat weekly with every 4-week follow-up -Resolution typically in 6-8 weeks
53
reactive erythemas: drug eruptions
-May produce urticarial, morbilliform, scarlatiniform, pustular, bullous, or fixed skin eruptions -Most reactions begin 7-14 days after drug first administered and may continue for days after discontinuation -Urticaria may appear within minutes -tends to involve the hands and feet -Treatment: Discontinuation of offending drug, anti-histamines prn
54
reactive erythemas: erythema multiforme
-Papules -> dark center -> lesions with central, bluish discoloration/blisters and characteristic target lesions (3 concentric circles of color change) -Most cases precipitated by HSV -wide spread targetoid rash -Treatment: -PO anti-histamines, systemic corticosteroids -Most lesions last no more than 2 weeks
55
reactive erythemas: steven johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)
-Severe, life-threatening disorders -Usually preceded by a prodrome of fever, malaise, and URI 1-14 days prior to onset of lesions -Red macules coalesce into large patches (face/trunk) -> evolve rapidly into bullae/areas of necrosis -SJS is epidermal detachment < 10% of body surface area; TEN > 30% -Any mucosal surface can be involved (oral, ocular, urogenital, GI, trachea) -MCC: NSAIDs, sulfonamides, anticonvulsants, and antibiotics -Dx is clinical -Mortality as high as 37% for severe TEN cases (sepsis) -Treatment: -Removal of offending agent -Controlled clinical trials: IVIG, cyclosporine, etanercept -Early interventions: Meticulous wound care, IV/NG feeding, monitoring I&Os and electrolyte status, early ophthalmology consult
56
alopecia
-Hair loss in children imposes emotional stress on the patient and the parent -A 60% hair loss in a single area is necessary before hair loss can be detected clinically -MC causes in children: Alopecia areata, tinea capitis, and hair pulling -Alopecia areata: -MCC of hair loss in children -Complete hair loss in a localized! area -Immunologic pathogenic mechanism suspected (lymphocytic infiltration) -50% of children completely regrow hair within 12 months (with possible relapse) -Alopecia totalis: Areata begins at occiput and proceeds along hair margins to frontal scalp; prognosis for regrowth is poor -Treatment: -Topical: Superpotent topical steroids, minoxidil (Rogaine), contact therapy, anthralin -Systemic corticosteroids (short course)
57
alopecia: hair pulling
-Traumatic hair pulling causes hair shafts to be broken off at !different lengths! -Ill-defined area of hair loss, petechiae at follicular openings, wrinkled hair shaft -Habitual, severe stress, trichotillomania, sign of another psychiatric disorder -Treatment: Psychiatric evaluation, cutting/oiling hair (behavior modification)
58
overview of viral
-dont need to know what causes it