Vesiculobullous Diseases
Direct Immunoflourescence
Bullous Pemphigoid
IgG and C3 at the BM, roof of
blister on salt split skin
Herpes Gestationis
Only C3 at the BM
Pemphigus vulgaris
IgG intercellular
Pemphigus foliaceous
IgG subcorneal
Epidermolysis Bullosa
IgG at BM
Indirect Immunoflourescence
positive IgG
Epidermolysis Bullosa Aquisita IgG and C3 at BM, base of
blister on salt split skin
Dermatitis Herpiformis
IgA in papillae
Erythema multiform
None
None
Psoriasis
Subtypes
Chronic plaque-type (most common)
Guttate (rain drop lesions, strep inf)
Erythrodermic
Pustular
Palmo-plantar
Triggers
Endocrine: Pregnancy, hypocalcemia
Withdrawal from steroids
Streptococcal pharyngitis infection
HIV
Stress
Drugs (beta blockers, lithium, interferon)
Trauma (Koebner phenomena)
Mechanical injury, sunburn
Genetics
Multifactorial
Polygenic - PSORS1 gene on chromosome 6p, PSORS2, 3, 4, 5
Strong association between Crohn's disease and plaque psoriasis
Treatments
Topical (emollients, corticosteroids, tars, vitamin A and D derivatives)
Phototherapy
Oral (methotrexate, cyclosporine)
Injection
anti-TNF
etanercept = synthetic TNF receptor protein, soaks up TNF
adalimumab = human anti-TNF antibody
inflixumab = chimeric (human + mouse) anti-TNF antibody
anti-Tcell (alefacept, efalizumab)
blocks T-cell activation and diapedesis
Melanoma
Biopsy = Excisional with 1-2 mm margins
Risk factors
UV light
Phenotype (fair skin)
Upper socioeconomic status
Family History
Immunosuppresion
DNA repair defect
Large congenital nevi
Prior history
Multiple dysplastic nevi
Acral Lentiginous Melanoma most common type in African Americans and Asians
Superficial Spreading Malignant Melanoma most common type
Photomedicine
UVB damage
direct, forms pyrimidine dimers
repaired by excision of DNA strand and synthesis/gap closure by DNA ligase
UVA damage
indirect, absorption by chromophores --> reacts with guanine -->
forms 8-oxo-guanosine
repaired by base excision and replacement of single base by DNA glycosylase
60% of UVB light falls between 10am and 2pm
longer wavelength lights penetrate deeper into skin – UVA deeper than UVB
Photodermatoses
Polymorphous light eruption (most common)
early spring, hours to days after exposure, seen in young adults
Chronic Actinic Dermatitis
abnormal response to UVB/UVA/visible light
lymphohistiocytic infiltrates
associated with HIV and atopic dermatitis
Solar Urticaria
Phototoxicity
blisters, hyperpigmentation, necrotic keratocytes, minutes to days
Photoallergy
erythema, edema, spongiotic dermis, 24-48 hours
Photocarcinogenesis
SCC – chronic sun exposure
Basal cell, melanoma – intermittent sun exposure
Photoaging
Activation of AP-1 transcription factor – upregulates MMP's
Degradation of dermal matrix + imperfect repair
Solar scar = wrinkling
Papulosquamous diseases
Psoriasis
Extensor surfaces, scalp, nails
Lichen Planus
wrists, mucous membranes
Pityriasis Rosea
* must do VRDL to differentiate from 2dary syphilis
Secondary Syphilis
VRDL always positive
Tinea Corporis and Versicolor
Seborrheic Dermatitis
Drug Eruption
Disorders of skin color
Vitiligo
absence of melanocytes leading to depigmented white patches and macules
associated with thyroid disease, pernicious anemia, Addison's disease
usually begins in childhood/young adulthood, progresses
Light penetration
Red – into the dermis
Brown – mid epidermis
Black – epidermal-dermal junction
Dermatitis/Eczema
Atopic Dermatitis
Chronic and relapsing, pruritic condition
children – face and extensor surfaces
adults – flexor surfaces
overabundance of Th2 CD4+ T cells
atopy triad – eczema, allergic rhinitis, asthma
tx: tepid showers, non-alkali soaps, emollients, topical steroids, phototherapy
3 stages
acute – vesicles, blisters
subacute – plaques with indistinct borders, scales, fissuring
chronic – thickened skin (lichenification)
Contact Dermatitis
inflammatory process due to external agent
irritant – occurs in most people after exposure to particular amount of substance
allergic – occurs in subset of people after exposure to small quantity of allergen
3 stages
acute – erythema, vesicles
subacute – erythemetous scaly plaques
chronic – lichenified scaly plaques
Granulomatous diseases
disorders of macrophages and monocytes in the dermis
Granuloma annulare
associated with diabetes, usually self-limiting (no tx needed)
Sarcoidosis
systemic granulomatous diseases
involves variety of different organs, including the lung (order chest X-ray)
non-caseating granulomas without identifiable cause
treat with topical or intralesional steroids
Panniculitis
inflammation of subcutaneous fat
erythema nodosum
rapid onset of erythematous, painful, poorly demarcated plaques
associated with malaise and fever
inflammation of connective tissue between fat lobules
reactive condition due to infection, OCDs, malignancy
associated with Crohn's disease, ulcerative colitis, sarcoidosis
Vasculitis
inflammation and necrosis of blood vessels
Henoch-Schonlein Purpura
neutrophilic inflammation around small blood vessels
acute onset of purpuric rash, abdominal cramping, hematuria
erythematous macules, urticarial plaques, non-blanching papules
located on buttocks and knees
recurrent cases are associated with streptococcal infection
treatment: topical steroids and NSAIDs, oral steroids is kidney involved
Non-melanoma skin cancer
Indications for Mohs surgery
incompletely excised tumors, recurrent tumors, large tumors, poor margins
perineural invasion, immunosuppressed, difficult closures, high recurrence areas
aggressive tumors, embryonic fusion planes
BCC, SCC, Bowen's disease, and keratoacanthomas most commonly treated
Basal cell carcinoma
pearly flesh colored plaques with telangiectasias, central ulcer, rolled border
nodular is most common form
superficial more common on back/chest, non-blanching erythematous plaques
micronodular, infiltrative, morpheaform are more aggressive
Squamous cell carcinoma
UV, radiation, arsenic, scars, ulcers, HPV, immunosuppression, nitrogen mustard
keratotic, indurated plaque, usually with exophytic growth and central ulcer
metastasis more likely with mucosal surfaces, de novo, deep/large, perineural
can arise from actinic keratosis or Bowen's disease
Fungal Infections
KOH preparations
scrape lesion to remove scales
place scale on glass slide and add KOH solution
Candidiasis
predisposing factors: antibiotics, steroids, malignancy, AIDS, immunosuppresion
yeast and pseudohyphae
Candida albicans is most common causes
Tinea versicolor
caused by Malassezia furfur (pityrosporum ovale)
spaghetti and meatball pattern
lesions on upper chest, back, neck
Dermatophytes
Tinea capitis
Trichophyton tonsurans
alopecia, scaling, cervical lymphadenopathy
endothrix infection (fungi grow in inner root sheath)
Tinea pedis
caused by T. rubrum, T. mentagrophytes, E. floccosum
interdigital, moccasin-type, vesiculobullous
two feet and one hand syndrome
Tinea corporis
fungal infection of skin
known as ringworm
Onychomycosis
fungal infection of the nail, usually T. rubrum, incidence increases with age
distal subungal – most common type
affects distal underside of nail plate, usually toenails
hyperkeratosis, thickening, yellowing from onycholysis
proximal subungal
fungi penetrate proximal nail and invade distally
sign of HIV infection
white superficial
well defined opaque whit islands on the external nail plate, can be scraped
caused by T. mentagrophytes
Candida onychomychosis
usually in dishwashers, housekeepers
erythema and tenderness around nail
total dystrophic
end stage nail disease, entire nail bed affected, thickened, dystrophic
Scabies
severe pruritis that's worse at night
burrows, vesicles and nodules, usually on hands/wrists, axillae, feet, ankles, waist
men affected on penis and scrotum, women on breasts and nipples
infants, elderly and immunocompromised can develop scalp lesions
type IV immuno reaction – incubation from few days to few weeks
treat with permethrin, avoid use of lindane because of neurotoxicity
Acne and Rosacea
Acne associated with Propionibacterium acnes – gram +, nonmotile, anaerobic rods
Acne vulgaris
multifactorial, centered around pilosebaceous unit
microcomedone formed, then PMN inflammatory response forms pustule
Acne fulminans
most severe form of cystic acne, usually teenage men, abrupt onset
may have ulcer formation, severe scarring, systemic symptoms
Acne conglobata
abrupt onset of nodulocystic acne, without systemic symptoms
follicular occlusion triad with dissecting cellulitis and hidradenitis suppurativa
Acne mechanica
result of mechanical and frictional obstruction of pilosebaceous unit
seen with use of helmets, chin straps, violinists
Acne excoriee
usually young women, OCD, anxiety disorder
Drug induced
monomorphous eruption of inflammatory papules, caused by steroids, lithium
Occupational
cutting oils, petroleum products, coal tar derivatives, chlorinated hydrocarbons
Neonatal
appears at 1-2 weeks, resolves at 3 months, due to M. furfur
Side effects of systemic antibiotics: nausea, vomiting, epigastric burning
Rosacea
erythema and telangiectasias with centrofacial distribution, lateral areas spared
no comedones present, can progress to papules and pustules
aggravated by sun exposure, hot liquids, caffeine, alcohol, spicy foods, stress
Hair and Nail abnormalities
Nail psoriasis - random pitting, oil spotting, yellowing, onycholysis
Alopecia areata – nonrandom pitting, all same depth and size
Onychomycosis treatment: oral terbinafine
Non scarring alopecias
*Androgenic alopecia – male pattern baldness, increased type II alpha reductase and
DHT
*telogen effluvium – diffuse hair shedding 2-4 months after major life stressor
*anagen effluvium – due to chemotherapy drugs
*alopecia areata – autoimmune disease targeting hair/nails, T cells swarm around follicles
*tinea capitis – T. tonsurans endothrix infection, prepubertal children
Scarring alopecias
*lichen planopilaris – patchy, perifollicular erythema, follicular spines, footprints in snow
*pseudopelade of Brocq – noninflammatory, progressive, adult women, starts at vertex
*dissecting cellulitis – part of follicular occlusion triad, granulomatous response, fibrosis