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atopic dermatitis (eczema) - etiology
personal or family hx of atopy (AD, asthma, allergic rhinitis)
childhood onset most common
genetic, environmental, immunological factors
atopic dermatitis (eczema) - s/s
pruritic, xerotic (dry), exudative, lichenified eruption
ill-defined, scaly, red plaques, loss of pigmentation
darker skin - follicular accentuation, post-inflammatory hyperpigmentation
atopic dermatitis (eczema) - dx
clinical presentation - need 3 major criteria = itchy, eczematous, relapse, personal or family hx
atopic dermatitis (eczema) - tx
emollients or bleach bathing
high potency topical corticosteroids for a short period of time depending on severity
irritant contact dermatitis - etiology
80% of contact dermatitis cases
localized to area of direct contact
develops within 24 hours of contact with irritant
irritant contact dermatitis - s/s
erythematous rash with well defined borders localized to area of direct contact
burning sensation
chronic - scaling, erythema, and thickened skin
irritants - acids, plastics, detergents, food, water, plants, bodily fluids
allergic contact dermatitis - etiology
20% of contact dermatitis cases
extends beyond area of contact with allergen
delayed response - may take 24 to 72 hours to develop
type IV hypersensitivity - requires prior sensitization
common occupations - textile workers, cashiers, shoemakers, hairdressers, medical , masseuse
allergic contact dermatitis - s/s
pruritic, erythematous rash with ill-defined borders extending past area of direct contact
itchy
contact dermatitis - dx
clinical presentation
localized vs. widespread
burning vs. itching
contact dermatitis - tx
avoidance of irritants
topical corticosteroids
antihistamines
severe - prednisone
dishidrotic eczema (pompholyx) - etiology
not an independent disease - linked with AD, ICD, ACD
hyperhidrosis (excessive sweating)
stress
dishidrotic eczema (pompholyx) - s/s
extremely pruritic “tapioca” vesicles on lateral and medial aspects of fingers, palms, and soles
dishidrotic eczema (pompholyx) - dx
clinical presentation
don’t need skin biopsy or KOH unless trying to rule out other pathologies
dishidrotic eczema (pompholyx) - tx
high potency topical corticosteroids
stasis dermatitis - etiology
venous hypertension due to incompetent valves
chronic venous insufficiency
stasis dermatitis - s/s
occurs in lower extremities around the ankle area
pruritus, discoloration, hyperpigmentation, edema, scaly dry skin
stasis dermatitis - dx
venous doppler
clinical presentation
stasis dermatitis - tx
compression stockings
vein ablations
wet to damp gauze dressings
lichen planus - etiology
idiopathic
systemic drugs and HepC
lichen planus - s/s
very itchy!
5 P’s - pruritic, purple, polygonal, papules, and plaques with fine white streaks (Wickham striae)
flexor surfaces, mucous membranes
lichen planus - dx
clinical presentation - cardinal findings = typical skin lesions, mucosal lesions, and histopathological features of band-like infiltration of lymphocytes in upper dermis
lichen planus - tx
super potent topical corticosteroids
candidiasis - etiology
Candida albicans
common normal flora but opportunistic pathogen
common in diabetic patients, pregnancy, obese, immunocompromised
can be secondary to abx, oral corticosteroids, oral contraceptives, or hormone therapy
candidiasis - s/s
beefy redness and itching primarily in bold fold areas or moist areas
burning around the affected vulva or anus
candidiasis - dx
clinical presentation - moist, erythematous plaques usually in body fold areas
KOH positive for cluster of buddying yeast and pseudohyphae
candidiasis - tx
keep area dry
mild = antifungal topical or ointment
vaginal - fluconazole
drug eruptions - etiology
delayed T-cell mediated hypersensitivity
morbilliform (most common)
fixed
immediate-type hypersensitivity
urticarial
morbilliform drug eruption - s/s
maculopapular
erythematous macules that sometimes become slightly palpable and confluent
symmetrical distribution beginning on trunk and spreading to extremities
fixed drug eruption - s/s
solitary dusky erythematous plaque that may be edematous or bullous
urticarial drug eruption - s/s
wheals that usually resolve within 24 hours
drug eruptions - dx
clinical presentation with precise medication hx prior to rash onset
drug eruptions - tx
discontinue suspected medication triggers
topical corticosteroids
photosensitivity disorders - etiology
UV radiation
phototoxic (most common)
medication becomes activated by UV exposure causing damage to skin that looks like rash or sunburn
happens within minutes - timing is important
photoallergic
UV rays interact with ingredients of meds applied direct to skin
body recognizes changes caused by UV exposure as foreign threat
production of antibodies and attacks = rxn
takes a couple days, not immediate
photosensitivity disorders - s/s
painful or prurutic erythema, edema, or vesciulation on sun-exposed surfaces
peeling of epidermis and pigmentary changes
photosensitivity disorders - dx
clinical presentation - localization of rash to sun exposed areas
photosensitivity disorders - tx
sunscreen
severe = systemic corticosteroids
pityriasis rosea - etiology
idiopathic
healthy adolescents and young adults
pityriasis rosea - s/s
initial herald patch - skin-to-pink-to-salmon colored patch or plaque with slightly raised advancing margin
single herald patch will progress to christmas tree pattern on posterior trunk
darker skin - lesions are more papular and hyperpigmented
pityriasis rosea - dx
clinical presentation
histopathology to nonspecifically rule out tinea vs. psoriasis
definitive = KOH or skin biopsy
pityriasis rosea - tx
no treatment required
low to medium topical corticosteroids
psoriasis - etiology
immune-mediated disease
usually leads to psoriatic arthritis in 5-30% of patients
genetic and environmental triggers
psoriasis - s/s
symmetric distribution of sharply defined plaques covered with silvery scales
mild to moderate = usually asymptomatic
severe or widespread = severe pruritus
present on elbows, knees, scalp, and lower back and legs
if symptomatic to nail and scalp, more likely to develop into psoriatic arthritis
psoriasis - dx
clinical presentation
definitive = biopsy
psoriasis - tx
based on BSA involvement and presence of secondary diseases like arthritis
vitamin D3 - inhibit epidermal proliferation
topical corticosteroids or retinoids
erythema multiforme (EM) - etiology
does not usually progress to SJS/TEN
rarely caused by drugs
HSV = most common cause
erythema multiforme (EM) - s/s
acute, self limited
symmetrical, fixed, erythematous papules
true targetoid appearance
minor - extensor surfaces, face, mild to no mucosal, no systemic sx
major - all minor locations, but severe mucosal and systemic sx
erythema multiforme (EM) - dx
clinical presentation - good H&P
skin biopsy
erythema multiforme (EM) - tx
oral variant - oral and topical corticosteroids
widespread and severe lesions - systemic prednisone
oral prophylaxis for HSV
SJS/TEN - etiology
always drug related
usually abx, antiepileptic, neurological meds
1-3 weeks after initiating drug therapy
SJS/TEN - s/s
SJS - <10% BSA detachment
SJS/TEN 10-30% BSA
TEN - >30% BSA detachment
initial sx - fever, stinging eyes, pain upon swallowing
progresses to erythema and erosions of buccal, ocular, and genital mucosae and increased epidermal involvement
full-thickness necrosis, dusky red macular lesions
detaching of epidermis
SJS/TEN - tx
discontinue all meds
burn care/ICU
bullous pemphigoid - etiology
primarily affects the elderly
drugs such as furosemide
autoimmune
bullous pemphigoid - s/s
subepidermal blistering in flexural areas
starts as pruritic urticarial and edematous lesions that progress to blistering
symmetrical distribution
does not happen in the mouth!!
bullous pemphigoid - dx
biopsy with direct immunofluorescence exam and serum antibody testing
punch biopsy = closer to lesion, DIE = further away from lesion
bullous pemphigoid - tx
mild/localized disease - superpotent topical corticosteroid
extensive/persistent - superpotent TCS and oral corticosteroid
pemphigus vulgaris - etiology
autoimmune
happens in the mouth!!
pemphigus vulgaris - s/s
relapsing crops of bullae that are fragile leading to rupturing and erosions
lesions usually appear first on oral mucous membrane, skin, or on erythematous base
Nikolsky sign - intact epidermis shears away from underlying dermis leaving a moist surface
Asboe-Hansen sign - bulla-spread phenomenon = pressure on intact bulla gently forces fluid to spread to adjacent skin
GI involvement
pemphigus vulgaris - dx
Light microscopy, direct (skin) and indirect (serum and blood) immunofluorescence (IIF) microscopy, and ELISA to detect autoantibodies to desmoglien 3 and 1
pemphigus vulgaris - tx
severe = hospitalized at bed rest with IV abx
mild = topical corticosteroids, systemic or local abx
rosacea - etiology
idiopathic
possible factors
immune factors
vascular hyperreactivity or neurogenic inflammation
demodex folliculorum
genetics
UV exposure
rosacea - s/s
gradual onset of facial redness, flushing, or “pimples” on central face
no comodones are seen
erythematotelangiectatic (vascular) - flushing and persistent central facial erythema with or without telangiectasia
papulopustular (inflammatory) - persistent central facial erythema with transient papules and/or pustules
phymatous - thickening skin, irregular surface nodularities and enlargement (nose, chin, forehead, cheeks or ears)
ocular - FB sensation in eye, burning or stinging, dryness, itching, ocular photosensitivity, telangiectasia of sclera, periorbital edema
rosacea - dx
clinical presentation
biopsy only for severe cases
rosacea - tx
avoid triggers (EtOH, spicy foods)
topical abx or benzyl peroxide
oral abx if topical doesn’t work
do not give topical steroids!!
acne vulgaris - etiology
Cutibacterium acnes or Propionibacterium acnes
inc sebum production, cohesion, and hyperproliferation of keratinocytes —> inflammation —> rupture
acne vulgaris - s/s
comedomal
closed - white head
open - black head
papulopustular - papules, pustules, small cysts
nodular - severe cystic acne
acne vulgaris - dx
clinical presentation - comedones
acne vulgaris - tx
mild comodonal - topical retinoid
mild papular/pustular - topical retinoid and topical abx
mod papular/pustular - oral abx, topical retinoid, BPO
severe - isotretinoin
seborrheic dermatitis - etiology
Malassezia species - lipid dependent fungi
occur in areas rich in oil glands (head, neck, chest, back)
seborrheic dermatitis - s/s
sharply demarcated patches or thin plaques that may be flaky but not itchy
pink-yellow to dull red to red brown in color
crusting may occur
areas rich in sebacous glands
usually associated with HIV, mood disorders and neuroleptic drugs, Parkinson’s, stroke, DM, obesity
seborrheic dermatitis - dx
clinical presentation - distribution and involvement
skin biopsy may be needed with exfoliative erythroderma
fungal culture to r/o tinea
seborrheic dermatitis - tx
topical azoles
low potency topical corticosteroids and emollients
tinea - etiology
Trichophyton rubrum - most common dermatophyte worldwide
tinea corporis - s/s
rings of erythema that have an advancing scaly border and central clearing
pruritus and burning
tinea corporis - dx
KOH - hyphae
tinea corporis - tx
topical antifungals
never give topical corticosteroids —> tinea incognitio
tinea pedis - etiology
most common dermatophyte infection
acquired going barefoot (locker rooms, gyms, public facilities)
moccasin, interdigital, inflammatory (vesicular), ulcerative
tinea pedis - s/s
scaling, peeling, itchiness, redness
moccasin - soles of feet
interdigital - interdigital web spaces
tinea pedis - tx
topical antifungals
refractory - oral antifungals for diabetics, immunocompromised, and moccasin type
tinea versicolor - etiology
Malassezia furfur
tropical climates with high humidity
sebum-rich areas
tinea versicolor - s/s
multiple oval to round patches or thin plaques with mild scale
upper trunk and shoulders favored
common colors - brown (hyperpigmented), tan (hypopigmented)
sometimes mild inflammation with pink color
usually asymptomatic, only appearance
tinea versicolor - dx
KOH - pseudohyphae
ziti and meatballs
tinea versicolor - tx
ketoconazole
selenium sulfide shampoo
paronychia - etiology
chronic immersion of hands in water or trauma to the nail fold
acute = Staphylococcus aureus
chronic = Candida albicans
paronychia - s/s
erythema, swelling, and pain of nail fold along with retraction of cuticle
acute - painful and purulent
chronic - without fluctuance
paronychia - dx
clinical presentation showing soft tissue infection of lateral or proximal nail folds
paronychia - tx
I&D of abscess and topical abx
black widow bite - etiology
Lactrodectus mactans - release of neurotoxin Ach
found in the outdoors, usually in wood piles or shoes
black widow bite - s/s
muscular pain
muscle spasms
muscle rigidity
black widow bite - tx
Lactrodectus antivenom
parenteral opioids or muscle relaxants
brown recluse spider bite - etiology
Loxosceles reclusa - release cytotoxin
inside tiny dark spots or in bed sheets or clothing
brown recluse spider bite - s/s
local progressive necrosis of tissue
brown recluse spider bite - dx
enzyme immunoassay to detect venom in skin biopsy
brown recluse spider bite - tx
excision of necrotic tissue
oral corticosteroids
anecdotes (dapsone, colchicine)
verrucae - etiology
direct person to person contact
common warts by HPVs
verrucae - s/s
<1cm hyperkeratotic, exophytic and dome-shaped papules or nodules
usually asymptomatic unless on plantar (painful with pressure) or anogenital (itchy)
usuallyfound on fingrs, dorsum of hand, palmar and plantar
verrucae - dx
clinical presentation
definitive = punch biopsy
verrucae - tx
cryotherapy with liquid nitrogen
OTC salicylic acid
Herpes (Varicella) Zoster - etiology
primary varicella (chicken pox)
reactivation of latent varicella infection (Shingles)
Herpes (Varicella) Zoster - s/s
shingles - painful grouped vesicles on an erythematous base within a single unilateral dermatome
chicken pox - dew drops on rose petal = vesicle on erythematous base; very pruritic
Herpes (Varicella) Zoster - dx
clinical presentation of dermatomal rash or dew drops on rose petal