derm Flashcards
mottling/cutis marmorata
-Lace-like pattern of bluish, reticular discoloration (dilated cutaneous vessels)
-Response to lowered room temperatures, resolved on rewarming
milia
-Tiny (1-2 mm) epidermal cysts filled with keratinous material predominantly on face in 40% of newborns
-Spontaneously rupture and exfoliate their contents
miliaria/heat rash
-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
erythema toxicum
-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
sebaceous gland hyperplasia
-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
neonatal acne
-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
transient neonatal pustular melanosis
-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
harlequin color change
-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
sucking blisters
-Bullae without inflammatory borders over the forearms, wrists, thumbs, or upper lip from vigorous sucking in utero
-Resolve without complications
dermal melanocytosis
Blue-black macule found over the lumbosacral area in 90% of darker-skinned infants; lesions fade with time
cafe au lait macule
-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
vascular birthmarks
Excess of capillaries in localized areas of skin; light red-pink to dark red
-hemangiomas
-nevus simplexes
-port wine stains
vascular birthmarks: nevus simplexes
-Light red macules over nape of neck, upper eyelids, and glabella of newborns
-Fade completely x 1 year (especially eyelid/glabella)
vascular birthmarks: hemangiomas
-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
vascular birthmarks: port-wine stains
-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
acne vulgaris: pathogenesis
-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
acne vulgaris: clinical manifestations
-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
acne vulgaris: tx
-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
acne vulgaris: education/follow up
-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)
atopic dermatitis
-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
discoid annular eczema
mimics ring worm
atopic dermatitis: tx
-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
atopic dermatitis: complications
-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
primary irritant contact dermatitis: diaper dermatitis
-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
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
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
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
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
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
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
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
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
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
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
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
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
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
bacterial infections: cellulitis
-Erythematous, hot, tender, ill-defined, edematous plaques accompanied by regional lymphadenopathy
-Invasion of microorganisms into lower dermis/beyond
-GABHS (Group A beta-hemolytic streptococcal) and coagulase-positive staphylococci are the MC causes
-Treatment with systemic antibiotic
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
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
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
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
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
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)
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
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
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
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
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
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
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
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
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
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
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
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)
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)
overview of viral
-dont need to know what causes it
