SHANZ – PEDIA II 2.

01
PEDIA DERMATOLOGY

SKIN FUNCTION
• Protect underlying structures from environment and infection
• Sensory perception
• Fluid balance
• Temperature regulation
• Vitamin synthesis (D)

PRIMARY SKIN LESIONS

Flat + color change Elevated + varying colors Elevated + rounded Raised + clear-fluid Evanescent + edematous Elevated + purulent
Macule (<1 cm) Papule (<1 cm) Nodule (>1 cm) Vesicle (<1 cm) Comes & goes within 24hr material (yellow fluid)
!"#$% !"# $%& Plaque (>1 cm) Tumor (larger, CA) Bullae (>1 cm) WHEAL PUSTULE

SECONDARY SKIN LESION

• Scale: desquamating • Fissure: linear break in the • Purpura: red • Scar: end stage lesion • Atrophy: reduction in skin
stratum corneum epidermis & dermis purple, due to o thin, depressed, atrophic thickness
• Crust: matted, retained • Erosion: focal loss of bleeding into skin o raised and hypertrophic • Lichenification: skin
accumulation of blood, epidermis (healing without • Petechiae: small o flat and pliable thickening with accentuation
serum, pus and scarring) purpura (<2-3mm) • Excoriation: ulcerated lesion from of lines due to chronic
epithelial debris • Ulcer: extend into dermis, heal repeated scratching rubbing, scratching or
with scarring inflammation

DISEASES OF THE NEONATE

NOTE
• Evanescent lesion
• Transient, benign
• No intervention needed
SEBACEOUS GLAND HYPERPLASIA
• Minute yellow white papules
• Forehead, nose, cheeks, upper lip
• Term infant
• Diminishes in size and disappears within few
weeks
MILIA
• Superficial epidermal inclusion cysts containing keratinized
material
• Firm, 1-2mm, pearly, opalescent white
• Neonates: face, gingivae, midline palate (epstein pearls)
• Spontaneously disappears

Cutis Marmorata Harlequin Color Change Mongolian spots Salmon Patch

• Evanescent, lacy, reticular red, • Place infant on 1 side (body is bisected • Dermal melanocytosis • Nevus simplex
blue cutaneous vascular longitudinally): pale upper half, deep red • Blue slate gray macules or • Erythematous macule or patch
pattern dependent half patches • Mostly spontaneously involute
• Due to exposure to low • Temporary imbalance in autonomic • Pre-sacral area • Localized vascular ectasia
environmental temp vascular regulatory • Deposition of melanocytes in • Symmetric, crosses midline
• Accentuated physiologic • Common in low birthweight infants dermis (arrested in migration • Glabella, eyelids, upper lip, nuchal
vasomotor response • Color change lasts few minutes to epidermis) area
• Disappear with age, maybe • Reversible by change in position • Common in Asians and • More visible during crying or change
discernible in older children • Muscular activity: generalized flushing and Hispanics in environmental temperature
obliteration of color differential • Fade during 1st year of life • Persisting lesion: nape, occipital area

VASCULAR CHILHOOD LESIONS

CAPILLARY MALFORMATION (PORT-WINE STAIN)
NOTE • Vascular malformation: developmental error in BV
• Do not regress, but slowly enlarge
• Present at birth
• Common on the head and neck
MORPHOLOGY • Mature, dilated dermal capillaries
• Unilateral, does not cross midline
COURSE • No spontaneous involution, Darker with age
• May develop papules or nodules in erythematous patch
COMPLICATION • Ulceration, bleeding
MANAGEMENT • Pulse dye laser
o Targeted to Hb, Avoid thermal injury to surrounding • Complicated:
o Result: No scarring, normal pigmentation & texture
INFANTILE HEMANGIOMA
• Exhibit endothelial cell hyperplasia and proliferation
• Most common tumor of infancy
• Present at birth, apparent in 1st 2 months of life
• Face, scalp, back, anterior chest
• Superficial: bright red, protuberant, compressible, sharply demarcated
• Deep: bluish, more diffused, less defined, cystic, firm, compressible
• Unpredictable, spontaneous involution seen in 60% 5 yo, 90-95% 9 yo
• Vital organ impairment (eyes, nose, airways, urethra)
• Ulceration, bleeding, disfigurement
• Uncomplicated: observation, reassurance
o Oral propranolol (1st line for disfiguring, life/vision threatening,
ulcerated lesion)
o Systemic corticosteroids: for those who can’t tolerate propranolol
o Topical, timolol solution: small, superficial, non ulcerating
o Intralesional corticosteroid: localized infantile hemangioma, with
risk of ulceration and atrophy

CAPILLARY MALFORMATION (PORT-WINE STAIN)
• Sturge-weber syndrome
PWS is Lateral, localized to forehead and upper eyelid
Tissue hypertrophy, hemiparesis contralateral to PWS
Glaucoma, leptomeningeal serous angioma, seizures
• Klippel trenaunay syndrome
PWS, varicosities, hypertrophy of bone & soft tissue,
ophthalmic abnormalities
Beckwith-wiedemann syndrome
ASSOCIATED CONDITIONS
INFANTILE HEMANGIOMA
• Facial hemangioma: evaluate PHACES, CVS, midline abnormality
• Cutaneous hemangioma in beard distribution: evaluate airway hemangioma
• Periocular hemangioma: MRI of orbit, evaluate ophtha
• Paraspinal midline vascular lesion: UTZ, MRI for occult spinal dysraphism evaluation
• Hemangiomatosis (Multiple small cutaneous): evaluate parenchymal hemangioma
(hepatic, CNS), guaiac stool test
• Large hemangioma (hepatic): UTZ + doppler flow, MRI, Thyroid function study
• Thrill and/or bruit: CVS evaluation, ECG, rule out aortic problem, MRI
• Head tilting: evaluate specific site lesion, consider PT
• Delayed milestones: side effects of corticosteroids (myopathy, weight related), INF side effect
• LUMBAR syndrome: MRI of spine, kidneys

CUTANEOUS NEVI
Acquired Melanocytic Nevi Congenital Melanocytic Nevi
note • Common mole, • Nevus cells in reticular dermis
• Nest of melanocytes in epidermis, dermis • 1% of newborns
Morph • Flat (macule/patch), or elevated (papule/nodule) • Small or giant CMN
course • Gradually increase in number during childhood • Neurocutaneous
• Slow increase in number during adulthood (leptomeningeal) melanocytosis:
• Plateau in 3rd-4th decade o Located on head/midline on
• Greater number of nevi, greater risk of melanoma trunk with satellite
• Signs of malignancy: Asymmetry, uneven border, 2/more colors, >6mm diameter, change in nevi >20lesions
size/shape/color/trait o Manifestation:
JUNCTIONAL NEVUSU COMPOUND NEVUS INTRADERMAL NEVUS hydrocephalus, seizures,
• >90% • Slightly elevated • Dome shaped intellectual disability
• Flat, brown-black • Brown-light brown • Warty, sessile
• Found in junction of • Found in epidermis & • Light brown, flesh colored
epidermis and dermis dermis • Found in dermis
• Hair may come out of nevus
Tx • No intervention needed • Early excision and defect repair
• Malignant cases: do excision biopsy

TYPES OF CONGENITAL MELANOCYTIC NEVI

SMALL CMN GIANT CMN
Size <1.5 cm >20 cm or < 5% BSA
Areas of predilection Chest, Lower trunk Posterior trunk
Upper back, Proximal limbs Less extent: head & neck
Malignant potential Very rare 1-2%
Associated diseases None Neurocutaneous (leptomeningeal) melanocytosis:
Located on head/midline on trunk with satellite nevi >20lesions
Manifestation: hydrocephalus, seizures, intellectual disability
management None Early excision, grafts

CUTANEOUS NEVI
NEVUS of OTA NEVUS of ITO Epidermal Nevus
note • A hamartoma • Supraclavicle, scapula, deltoid • Birth- 1st few years of life
• Melanocytes in lower part of dermis region • Maybe associated with other organ system abnormalities:
• Unilateral on the face area supplied by CHILD (congenital hemidysplasia with ictbyosiform
CN V1, V2 erythroderma and limb defects)
• Common in asians and females Proteous syndrome:
• Sometimes present at birth • hemihypertrophy of the face, tongue, lips.
• Develop during 1st – 2nd decade of life • Skeletal overgrowth
• Tumor, cyst, vascular abnormality
Morph • Violaceous, confluent black-blue, • Bluish-black macule or patch • Hyperpigmented scaly patch
speckled patch • More diffused, less mottled • Verrucous, thick plaque
• More speckled > Mongolian spots compared to nevus of ota • Linear configuration
course • Does not disappear with age • Distribution:
• May enlarge or darken o Systematized (diffuse, extensive)
• Malignant degeneration is rare o Ichthyosis hystrix (extensive, bilateral)
Tx • Concealer • Keratolytic agents: retinoid acid, salicyclic acid to reduce
• Laser therapy: Q switched Nd:YAG, or Q switched alexandrite scaling and pruritus
• Excision: definitive treatment
 ECZEMATOUS DISORDERS
(ECZEMATOUS DERMATITIS)
ACUTE SUBACUTE CHRONIC
• Erythematous macules, papules • Days – weeks • >6 weeks
• Swelling/edema • Excoriations • Thickened, dry and scaly
• Vesicles, bullae • Crust, scabs, scales • With coarse markings (lichenification)
• Slight thickening of skin • Well defined lesion
• Scaly desquamation

ENDOGENOUS ECZEMA
Atopic dermatitis Seborrheic dermatitis Nummular eczema Dyshidrotic eczema
note • Skin asthma/ atopic eczema • Lower legs • Adult: usually lesion is on
• Most common chronic, relapsing skin disease • buttocks the palm where skin is
• Onset: infancy, 50% starts in 1st year of life • shoulders very thick
• Area of predilection • lateral digits of hands,
o Infant & children: face/cheek, extensor surface (elbow, feet, palm and soles
knee), diaper area spared
o Adolescent: flexural area (popliteal fossa, antecubital
fossa)
Etio • IgE sensitization • Malassezia furfur • Xerosis Unknown pathogenesis
• T helper 2 cell abnormality (upregulation) • Stress • Irritants
• Defective skin barrier • Allergens
• Defective thermoregulation • Staphylococcal
• Increased transepidermal water loss infection
• Skin is inherently dry
• Reduced skin innate immune response
• Exaggerated t cell responses to allergens and microbes
• Genetic mutation in filaggrin: epidermal protein
• Personal/Family history of atopic disease (allergic rhinitis,
bronchial asthma)
morph • Hallmark: severe dryness of skin • Greasy, scaly plaque on • Coin-shaped • Pruritic vesicles
• Very pruritic dermatitis scalp (cradle cap), face • Erythematous
• Acute: erythematous, intensely pruritic papules & plaques (nasolabial fold, glabellar plaques
• Subacute: erythematous, excoriated, scaling plaques area), chest, diaper area
• Chronic: lichenification and fibrotic plaques • Adult: dandruff

ASSOCIATED WITH ATOPIC DERMATITIS COURSE & PROGNOSIS OF ATOPIC DERMATITIS
• Dry skin (xerosis) • Young children: more severe and persistent
• Cutaneous infections (s.aureus, group A strep, HSV, coxsackie virus, vaccinia, • Remission increases with age
molluscum, warts) • Resolves in 20% monitored children
• Nonspecific dermatitis of hands or feet • Relapses occur with age
• Icthyosis, palmar hyperlinearity, keratosis pilaris
• Nipple eczema POOR PROGNOSIS PREDICTOR:
• White dermatographism and delayed blanch response • Widespread AD in childhood
• Anterior subscapular cataracts, keratocinus • Filaggrin gene null mutation
• Elevated IgE • Concomitant allergic rhinitis and asthma
• (+) immediate allergy skin test • Family history in parents, sibling
• Early age at onset • Early onset
• Dennie lines (dennie morgan infraorbital folds) • Being only child
o Hyperpigmented discoloration around eyes • Very high serum IgE
o Due to persistent rubbing of eyes secondary to pruritus
• Facial erythema or pallor: Peri-orofacial pallor/sparing
• Course influenced by environmental or emotional stress

 TREATMENT FOR ENDOGENOUS ECZEMA
Atopic dermatitis Seborrheic Nummular Dyshidrotic
dermatitis eczema eczema
NON MEDICAL • Infant: mild • Topical • Aluminum
• Avoid triggers (food allergy, aeroallergens, infection, reduced humidity, excessive shampoo, baby oil corticosteroids salt
sweating, irritants) to remove scales, • Saline soaks
MEDICAL emollients for dry • Topical
• Moisturizer (1st line): bathe <15-20 min the apply occlusive emollient to retain moisture area, topical corticosteroid
• Wet wraps: transepidermal penetration of topical medication, effective against steroid, topical anti • Adult: potent
scratching fungal topical
• Topical corticosteroid: cornerstone of anti inflammatory treatment for acute • Children & corticosteroid
exacerbation of atopic dermatitis (ointment > creams) (ointment: less drying, less irritant) adolescent 1st line:
(lotion prep for large surface area) antifungal
• Systemic corticosteroid: rarely indicated, severe rebound flare after discontinuation shampoo
• Antihistamine: reduces histamine-induced pruritus, sedation given at bedtime • 2nd line: topical
• Topical calcineurin inhibitors: calcineurin
o Pimecrolimus, tacrolimus ointment inhibitors,
o Short term, intermittent long term of > 2 years old keratolytics
o Steroid sparing agents
• Tar prep: anti pruritic, anti inflammatory
• Phototherapy: for chronic, refractory, severe, generalized AD
o Emits narrow band UVB by downregulating immune cells in the skin

STEROIDS CLASS GROUP INDICATIONS

Clobetasol, Betamethasone, Fluocinonide Superpotent 1 Adult
Mometasone furoate… Not on face/intertriginous area
Fluticasone proprionate For thick skin lesion (palms, soles)
Flucinolone acetonide Short period only
Hydrocortisone Avoid in infant and thin skin
Midpotent 2-6 For chronic AD
Trunk & extremities
May be used for longer periods
Least potent 7 Thin skin areas (face, neck)
Flexural areas

ANTIHISTAMINES
1st generation 2nd generation 3rd generation
• Brompheniramine • cetirizine • azelastine
• Chlorpheniramine • loratadine • olopatadine
• Clemastine • fexofenadine
• Diphenhydramine • desloratadine
• hyroxyzine • levocetrizine

EXOGENOUS ECZEMA (contact dermatitis: appear on thin skin, dorsum of hand)

Allergic contact dermatitis Irritant contact dermatitis
note • no clinical signs at first exposure • Clinical signs at first exposure
etio • T cell delayed hypersensitivity • Prolonged, repetitive contact with physical, chemical or mechanical irritants (saliva, urine, feces,
• Antigen sensitization detergents, dyes, henna, plants)
morph • Erythematous patches or • LIP-Licking contact dermatitis: (saliva is acidic)
plaques o erythematous patches /plaque on skin around lips or oral commissure
• Shape: allergen/object • IRRITANT-diaper dermatitis:
o due to elevated pH, urinary and fecal enzymes, friction, occlusion
o Erythematous patches or thin plaques in crural area, sparing inguinal folds
Tx • Identification and avoidance • Patch test for diagnosis
• Tx: avoidance of contact, topical corticosteroids

BACTERIAL DISORDERS
IMPETIGO CELLULITIS
NON-BULLOUS BULLOUS
note • >70% more common • Infant, young children
• Children & adult • Face, buttocks, trunk, extremities,
• Face: perinasal, perioral intact skin
• Traumatized skin
• Little/no pain
Etio • Staph aureus, GABHS • Staph aureus w/ exfoliative toxins • Infection & inflammation of loose CT
• Epidermis spared
• Limited dermis involvement
• S.aureus, Strep pyogenes
• Portal of entry: break in skin
morph • Erythematous, Honey colored • Flaccid bullae à erosion • Erythematous, edematous patch or plaque
crusted plaques • (-) adenopathy • Warm, tender to touch
• Regional adenopathy in 90% children • Indistinct border (deep skin process)
course • Can spread to other body areas • S.aureus: cellulitis (more localized, suppurative)
• Localized, self limiting with proper management • S. pyogenes: cellulitis (rapid spread, lymphangitis)
compli • Rare, osteomyelitis, septic arthritis, pneumonia (when left untreated) •
• APGN
DX • • Clinically and 25% isolation from aspirate for G/S
TX • Depends on severity & localization • Depends on age, immune status, etiologic agent
• Topical: for localized lesion • UNCOMPLICATED CASE: Oral antibiotic
o Mupirocin 2% 2-3x 10-14days o Cloxacillin 50-100 mg/kg/day for 7 d
o Retapamulin 1% 2-3x 10-14 days o Cephalosporin
• Systemic therapy: widespread disease, lesion near mouth, deep involvement • Severe disease, fever, lymphadenopathy, neonates:
o Cephalexin 25-50 mg/kg/day 3-4x for 7 days PARENTERAL Antibiotic
• MRSA:
o Clindamycin, Doxycycline, Sul-Trim

Bacterial Infection of the Hair Follicles

FOLLICULITIS FURUNCLES & CARBUNCLES
note • Superficial hair follicle infection • Face, neck, axilla, buttocks, groin
• Scalp, buttocks, extremities
Etio • S.aureus • S.aureus
• Poor hygiene • Obesity, hyperhidrosis
• Skin maceration, shaving, occlusive wraps • Maceration, dermatitis, friction
• Crowding, poor hygiene
morph • Erythematous papules / pustules FURUNCLE: 1 follicle
• Perifollicular pustules • Deep seated, tender, perifollicular nodule
CARBUNCLE: > 1 follicle
• Deep seated, bigger nodule, multiple drainage points
• Inflammation surrounding CT
• Fever, leukocytosis
DX • Clinically, G/S • G/S
TX • MILD: Clindamycin topical • Incision and drainage (if large and non responsive to Ab)
• Severe: Oral cloxacillin or cephalexin • Regular bathing, loose clothing
• Frequent hot moist compress

CUTANEOUS FUNGAL INFECTION

TINEA VERSICOLOR TINEA INFECTIONS
note • An-an • CAPITIS: Scalp, school children
• Chronic fungal infection of s.corneum • CORPORIS: GLABROUS SKIN, Except palms, soles, groin
• Adolescents, young adults • CRURIS: Groin/ crural area, Medial thigh
• Neck, upper chest, back, upper arms • PEDIS: Toes, feet, Toes: 3rd-4th interdigital spaces, Starts from toe webs
Etio • Yeast DERMATOPHYTOSES:
• Malassezia globose/ pityrosporum ovale • Filamentous fungi on Keratinized areas: hair, skin, nails
Predisposing • Warm, humidity • Trichophyton: skin, hair, nails
factors • Excessive sweating, moist area • Microsporum: hair
• Occlusion • Epidermophyton: intertriginous skin
• High plasma cortisol • Via direct skin contact
• Immunosuppression, malnourishment • Superficial skin infection, No systemic infection
morph • Hypopigmented macules/patches with fine scaling • erythematous scaly plaques with central clearing, elevated, well defined
• Adolescents: facial lesion is common borders
• Some have hyperpigmented lesions CAPITIS
• Black-dot ringworm
• Small patches of hair loss with broken off hairs
• Non inflammatory: scaly patches with/without alopecia
• Inflammatory: kerion (elevated, boggy, granulomatous masses, may
have pustules, lymphadenopathy, SCARRING ALOPECIA)
DX • 10-20% KOH: Spores and hyphae: spaghetti and meatball • KOH: Segmented hyphae
• Wood’s lamp: yellowish gold fluorescence

TX • Topical:
o 2% selenium sulfide shampoo = 10 mins for 2 weeks
o 2% ketoconazole shampoo – 3x/week for 1 month
o Antifungal cream & lotions
• Oral: (for severe or recurrent disease, and failed topical)
o Ketoconazole/fluconazole 400mg single dose
o Itraconazole 200 mg daily for 5-7 days
• CAPITIS
KOH stain: gold std:
• Spores surrounding or within hair strand
• Collect scales from periphery of lesion
Wood’s lamp exam:
• Ectothrix infection: blue green fluorescence
• Endothrix infection: no fluorescence
• Fungal culture: not done, 6-8 weeks for result
• Topical antifungal for 2-4 weeks:
o Azoles: ketoconazole, miconazole
o Allylamines: Terbinafine
• Oral antifungal
o Azoles, allylamines
• Wear loose clothing, Avoid tight footwear, Keep area dry
CAPITIS
GRISEOFULVIN: DOC 8-12 weeks, repeat KOH
• 20-25 mg/kg/d (microcrystalline)
• 10-15 mg/kg/d (ultramicrosize)
• Enhanced absorption by fatty meal
Terbinafine
Itraconazole

CANDIDA DIAPER DERMATITIS

CANDIDA DIAPER SEBORRHEIC IRRITANT
Etio • Candida albicans yeast
• Warm moist occluded skin of diaper
• Optimal for yeast growth
morph • Cutaneous erythematous, scaly patch or plaque with well defined border • Involves inguinal folds • Spares inguinal folds
• Satellite papules or pustules
• Perianal skin, inguinal folds, perineum, lower abdomen
DX • KOH Smear: budding yeast and pseudohyphae
TX • TOPICAL IMIDAZOLES: Ketoconazole BID 5 days
• ZN OXIDE CREAM: Protective skin barrier

CUTANEOUS VIRAL INFECTIONS

VERRUCA VULGARIS MOLLUSCUM CONTAGIOSUM
note • 5-10% children • 2-6 yo
• Immunocompromised
Etio • HPV 2,4 • Pox virus (ds DNA)
MOT • Skin-skin contact • Skin-skin contact
• Autoinoculation • Autoinoculation
• Sexual intercourse • Sexual intercourse
morph • Well-circumscribed hyperkeratotic papule • 1-5 mm pearly, skin colored
• Black dots on surface: thrombosed capillaries • Dome shaped papule with central umbilication
• Lesion along cutaneous trauma line • Plug of cheesy material expressed from umbilicus
• Anywhere in the body: mostly face, neck, axilla, thigh
• Genital area: STD associated
Course • 65%: spontaneous resolution • Self limiting
• Spontaneous resolution in 6-9 months
• Rapid spread in patients with atopic dermatitis/ immunodeficiency
TX • Salicylic acid IMMUNOTHERAPY
• Liquid nitrogen • Candida/ trichophyton antigen (most commonly used)
• Pulsed dye laser • Repeated every 4 weeks until resolution
• 25% podophyllin (genital warts) CRYOTHERAPY/ LIQUID NITROGEN
• 5% imiquimod (genital warts) • Depends on age, for limited lesion
• Cimetidine 30-40 mg/kg/day (multiple generalized warts CANTHARIDIN (BEETLE)
unresponsive to therapy) • For younger children
• Blister forms at site of application
• Molluscum will be removed with blister
AVOID SHARED BATHS AND TOWELS
 TYPES OF VERRUCA
HPV 2,4 Verruca vulgaris (common warts): fingers, dorsum of hands, face, knees, elbows
HPV 3,10 Verruca plana (flat warts): slightly elevated, hyperkeratotic papules/papules <3 mm, pink- brown
HPV 1,2,4 Verruca filiformis (filiform warts): base and verrucal outpouching
HPV 2,4 Periungal warts (around nails): often painful, may spread beneath nail palate, separate nail bed
HPV 1 Plantar warts (on the feet)
HPV 6,11 Condyloma acuminate (anogenital warts)
HPV 16, 18 Cervical CA

ARTHROPOD BITES & INFESTATIONS

NOTE BED BUGS FLEAS MOSQUITOS
• REACTION depends on: description • In uncovered areas • Legs and • anywhere
Species, age group, host reactivity buttocks
Lesion:
• Erythematous papules with central punctum (bite) morph • Pruritic in the • More pruritic • Non specific urticarial
• +/- excoriation morning during daytime papules
• Solitary, numerous, profuse • 3-4 bites in a • 3-4 bites in a • Timing: depends on
• Papular urticaria (bad reaction: edematous, red-brown line/curve line/curve causative agent
papule, 1st decade) TX • Identify and eradicate arthropod
PATIENT EDUCATION • Topical corticosteroid: clobetasol, betamethasone diproprionate
• Brown insect apple seed size on mattress/sofa/curtain • Oral antihistamines
• Pest management • Cool compress
• Wash clothes at 60C • Systemic steroid for severe reaction
• Examine secondhand furniture • Insect repellants

SCABIES PEDICULOUS CAPITIS

note • School age children (classmate/ playmates) • 3-12 yo children
• Trunk and face • Lice on lower scalp (occipital area)
• Infants: palms, soles, scalp
• Adults: interdigital webs, axillae, flexures, beltline, genitalia, buttocks
Etio • Sarcoptes scabiei (mite) • Pediculosis humanus Capitis (head louse)
• Burrowing and release of toxic /antigenic substance • Cannot survive beyond 2 days if taken away from host
• Secondary: s.aureus
MOT • Skin-skin contact • Head to head contact
• Isolated mite dies within 2-3 days • Infrequent: combs, accessories, bed, furniture
• Spreading factor: extent & duration of physical contact
morph • 2st sign: 1-2mm red papules, excoriated/crusted/ scaling • Intense scalp itchiness
• Threadlike burrows: classic lesion • Erythema and scaling of nape, scalp
• Intensely pruritic. (+) nocturnal pruritus • Nits on hair shaft
• Infants: generalized eczematous dermatitis
• CIRCLE OF HEBRA: Imaginary circle encompassing sites of predilection
TX • PERMETHRIN 5% cream: (not ovicidal) SCABICIDES: PERMETHRIN SHAMPOO (> 2 mon age)
DOC for > 2 months, once, 8-12hr, repeat after 1 week • Scabicidal but not ovicidal.
• Crotamiton 10% lotion • Leave on scalp 10 mins then rinse off,
• Lindane 1 % lotion • Repeat after 7 days
• Oral ivermectin 200 ug/kg, 2 doses, 2 weeks apart: Malathion 0.5%: treatment of choice (N/A in PH)
Severe & immunocompromised vermectin lotion 0.5%
• Pruritus: sedating antihistamines, topical corticosteroid Mechanical removal
• Bacterial: systemic antibiotics Supportive management
• Treat linen and towels: wash, boil, sun dry, iron,
• Sealed bag in 5 days
• Spray with insecticide
• Treat family members
 SLE
NOTE ETIOLOGY RISK FACTORS/ EPID PATHOLOGY
• CHRONIC autoimmune • GENETIC ABNORMALITIES • GENDER: • Hallmark: antibodies against self antigen (nucleic acid)
• Children, adults, • CONGENITAL DEFICIENCY: FEMALES • SLE: highly susceptible to damage from UV
ADOLESCENT (11-12 C1q, C2, C4 (reproductive, 90%), • Increased apoptosis or impaired ability to clear cell debris
YR) • Several polymorphisms ESTROGEN: B cell (B cell autoantibody, immune complex, tissue damage)
• Children, adolescent: (IFN-5, protein tyrosine autoreactivity • Ab to dsDNA : Glomerular deposit (glomerulonephritis)
more severe, more phosphatase N22) • Environmental: • Dysregulation of immune system
organ involvement • HLA B7M, DR2, DR3 EBV, UV light • Type 1 IFN: high level of IFN a by plasmacytoid dendritic cell:
• Most common organ: autoreactive B & T cells
skin, joints, kidney, • B cell: cytokines like BLyS: abnormality
blood forming cells, • T cell: increased memory t cells, decreased t regulatory t
blood vessels, CNS cells.

CLINICAL FEATURE DIAGNOSIS TREATMENT COMPLICATION/

4 CRITERIA (at least 1 for both clinical PROGNOSIS
and immunological)
• DISCOID RASH: hyperkeratosis, • Lupus band test: immunofluorescence • Sunscreen • Most common cause
follicular plugging, mononuclear cells of skin (immune complexes within • Avoid prolonged direct sun of death in 1st several
infiltration, dermal-epidermal junction dermal-epidermal jx) exposure years of diagnosis
• Diffuse proliferative • Acute cutaneous lupus: malar rash • Hydroxychloroquine 5-7 (infection &
glomerulonerphritis type IV: RENAL • Classic cutaneous lupus: discoid rash mg/kg/day (mild cases) complication of
morbidity • Oral/nasal ulcer • Corticosteroid: mainstay for glomerulonephritis
• Multiorgan system involvement • Nonscarring alopecia significant manifestation and neuropsychiatric
• Most common: fever, fatigue, • Synotivits > 2 JOINTS (monitor ADR) disease)
hematologic abnormalities, arthralgia, • Serositis: pleuritis, pericarditis, peritonitis • IV or oral cyclophosphamide • Long term:
arthritis (1st year of diagnosis), • Renal: proteinuria, renal casts (most severe) malignancy (immune
tenosynovitis • Seizure, psychosis • Atherosclerosis risk: chol level, dysregulation,
• Renal disease • Hematology: HA, leukopenia, smoking status, BMI, BP carcinogenic drug
• Adolescent: nephrotic syndrome/ lymphopenia, thrombocytopenia • Prevent future osteoporosis: exposure) or
renal failure • (+) anti dsDNA or antiSm (Specific) intake Ca and Vit D atherosclerosis
• Neuropsychiatric complication: • False positive RPR • Routine immunization: annual (chronic immune
adolescent with mood disorder • (+) lupus anticoagulant influenza and 23-valent dysregulation,
• Long term SLE complication: • Elevated anticardiolipin IgG or IgM pneumococcal inflammation)
accelerated atherosclerosis and • Worse prognosis in
• (+) ANA (Sensitive)
osteoporosis PEDIA
• Low complement C3,C4,CH50
• (+) DIRECT COOMBS w/O ha