Skin Diseases Flashcards
Ehlers Danlos Presentation
collagen disorder, hyperextensible skin, skin fragility
Type I (classic) : hypermobile joints, xs stretching, fish mouth scars
Type IV: involves BVs- bruising, GI/arterial rupture
Pseudoxanthoma elasticum presentation
auto dominant
clumped elastic fibers
yellow papules of neck and axilla
ocular involvement, CV
marfan syndrome presentation/etiology
auto dominant
fibrillin mutation
skin, ocular, CV
tall, long limbs and digits, aortic dilation
Livedo reticularis presentation
net-like macular erythema cause by hypoperfusion, worse w/ cold weather, may be ass w/ autoimmmune or coagulation disorders
vasculitis presentation
BV inflammation, systemic problems: weight loss, fever, sinusitis, asthma, CMP
Leukocytoclastic vasculiltis presentation
inflamm of small cutaneous vessels, palpable purpura
Triggers: meds, infection, CT diseases, autoimmune
may affect renal vasc.
Scleroderma: morphea presentation
LOCALIZED, hypopigmented, depressed plaque, lilac-colored rim, most commonly on trunk
Scleroderma: limited systemic presentation
face and distal extremities, CREST - calcinosis cutis, Raynaud’s, Esophageal dysmotility, Scleroderma, Telangiectasis
Ehlers Danlos Tx
None
Advise type IV to avoid trauma and contact sports
Pseudoxanthoma elasticum Tx
Co-manage by cardio, derm, optho
Livedo reticularis Tx
None- benign
Leukocytoclastic vasculiltis Tx
Remove trigger
closely monitor renal fxn
pyogenic granuloma presentation
proliferative vasc lesion
bleeds easily
often at site of trauma
pyogenic granuloma Tx
must excise lesion
Scleroderma: morphea work up
W/U: biopsy (but will be identical to systematic scleroderma)
Scleroderma: limited systemic Tx
favorable prognosis
Diffuse scleroderma presentation
affects trunk, prox extremities, cutaneous fibroisis, Raynauds, pulm fibrosis, renal insuff, cardiac disease
Diffuse scleroderma Tx
Poor prognosis?
Photoaging presentation
atrophy, lentigines (large freckles), rhytides (wrinkles), dilated pores, yellow skin caused by repeated prolonged UV exposure
photoaging Tx
hard and expensive treatment, best to avoid sun
panniculitis presentation
tender, erythematous, non-ulcerated nodules w/ ill-defined borders, inflammation of subQ fat
Causes: meds (esp contraception, estrogens, penicillin, sulfa), infections(strep, HIV), sarcoidosis, IBS, idiopathic
panniculitis Tx
W/U: histo- inflamm of fibrous septae b/t fat lobules
Tx: eliminate offending agent, rest, elevation, compression, NSAIDS
Erythema nodosum presentation
Most common form of Panniculitis (inflamm of subQ fat),
Erythema nodosum Tx
remove trigger, rest, elevation, compression NSAIDS
Ichthyosis vulgaris presentation
itchy dry skin, white adherent scales, trunk and extremities favored, may demonstrate Keratosis pilaris, exacerbated in cold weather and low humidity
Disorder of cornification - failure to shed
Auto dominant
ichthyosis vulgaris Tx
consult on proper skin care, emollients, humectants
Keratosis pilaris presentation
follicular retention, hyperkeratosis, overlies hair follicles of extensor upper and lower extremities and buttocks
Palmoplantar keratoderma (general) etiology
hyperkeratosis of palms and soles, auto dominant recessive, keratin mutations result in abnormal pairings of type I and II keratins
palmoplantar keratoderma (general) Tx
pare (shave down) hyperkeratotic areas and use topical humectants to soften skin
Diffuse PPK presentation
thick yellow plaques of entire palms/soles
border may have erythema
hyperhidrosis (xs sweat)
focal PPK presentation
hyperkeratosis localized over pressure points
punctate PPK presentation
hyperkarotic papules/nodes
commonly misdiagnosed as warts
xerosis presentation
rough, dry skin
dec in intercelllular lipids and NMF, failure of adherent bonds of stratum corneum, corneocyte dehydration
Endogenous: atopy, IV, renal insuff, statins, malnutrition
xerosis Tx
consult on proper skin care, emollients, humectants
Atopic dermatitis (eczema) presentation
ITCHY rash (may become lichenified), ill-defined borders, papules, placques, scales
Adults: flex surfaces, face
Infants: face, extensor surfaces
May see 2* infection w/ s. aureus
Atopic dermatitis etiology
part of atopic triad, inc inflamm (TH2 predominance)
Fillagrin defects = predisposition (genetic)
positive feedback of inflamm b/c barrier is leaky
Atopic dermatitis W/U, Tx
W/U: get family or personal history of atopy
Tx: topical steroids
psoriasis presentation
erethymetous plaques, thick adherent scale, nail changes (oil spots), may be itchy, but much less so than ACT
favors extensor surfaces
Koebner phenomenon - more itch = more inflamm
psoriasis etiology
inflammatory disease overgrowth of epidermis shortened cell turnover (4 days) Interplay b/t Th1, Th17, and keratinocytes Char by large amt of neutrophils
psoriasis Tx
topical steroids reduce inflamm
very severe: chemo drugs that target T cells
Staphylococcal scalded skin syndrome presentation
malaise, irritable, fever, SKIN PAIN
flaccid bullae -> widespread desquamation
Staphylococcal scalded skin syndrome etiology
exotoxin targets desmoglein 1 –> loss of cell adhesion
at risk:
Staphylococcal scalded skin syndrome W/U and Tx
culture from nasopharynx, conjunctivae, purulent lesions (NOT from bullae)
hospital admission, close monitoring, IV antibiotics
Pemphigus vulgaris presentation
Flaccid bullae (+N sign), easily ruptured
ORAL erosions + pain
crusting scalp
Pemphigus vulgaris etiology
autoimmune –> Desmoglein 3
Pemphigus vulgaris W/U and Tx
W/U tombstone appearance on histo, DIF - intercellular staining to IgG against Dsg3 throughout epidermis
Tx: long term steroids and immunosuppresants
Poor prognosis - used to be lethal
Bullous pemphigoid presentation
> 60 y/o
Tense bullae on trunk and extremities (-N sign)
typically not painful or oral
Bullous pemphigoid etiology
Antibodies against BPAG1/2 -> split at hemidesmosome
Bullous pemphigoid W/U and Tx
biopsy: subepidermal blister
DIF shows linear staining of BMZ with IgG against BPAG1/2
Tx: Better prognosis, may remit spontaneously
mild: high potency topical steroids, antibiotics
severe: oral steroids/immunosuppress - TAPER SLOWLY
Cicatrical pemphigoid presentation
rare and aggressive favors mucosal surfaces scarring ORAL, ocular, maybe skin Tense bullae
Cicatrical pemphigoid etiology
antibodies for BPAG2 and laminin5
Cicatrical pemphigoid W/U and Tx
biopsy resembles BP (subepidermal blister)
advanced: fibroids and scarring
DIF: linear IgG at lamina lucida
Tx: mild: topical corticosteroids + monitor for scarring
Severe: oral immunosuppressants
routine eye exams
Epidermolysis bullosa (general) presentation
mechanobullous disease congenital absence/mutation of BMZ component Char by: skin fragility painful blistering scarring non-dermal manifestations
EB simplex present/etiology
auto dominant
blisters on feet
absence of epidermal keratins
Junctional EB present/etiology
auto recessive
Laminin and BPAG2 mutations in lamina densa
can be very severe
inc squamous cell carcinoma
dystrophic EB present/etiology
auto dom and recessive
collagen VII absent/abnormal
can present with mitten hands
Dermatitis Herpetiformis presentation
intensely pruritic disease
occipital scalp, extensor upper and lower extremities, buttocks
cutaneous lesions - papules, vesicles, urticarial plaques
Ass. w/ celiac
Dermatitis Herpetiformis W/U and Tx
biopsy vesicle- subepidermal blister w/ neutrophils
perilesional biopsy DIF - granular deposits of IgA in dermal papillae
Serum anti-endomysial antibodies
Tx: GF diet
psoriatic arthritis
destructive arthritis ass. with psoriasis
Guttate psoriasis
small round papules and plaques
Strep infection may cause it -> swab throat!
(guttate = rain drops)
Allergic Contact Dermatitis etiology
Classic Th1 hypersensitivity (delayed type/type IV)
Allergens are “haptens”- sm. molecules that bond native proteins
Common allergens: nickel, fragrances, preservatives, topical antibiotics
7-14 days for sensitization
2-7 days for re-exposure
Allergic contact dermatitis presentation
Itchy
Erythematous papilla and vesicles
Shapes/distribution suggestive of external cause
2-7 days after re-exposure
Atopic dermatitis (eczema) etiology
Genetic predisposition
Fillagrin defect/barrier dysfunction.
Repeated exposure to allergens (dust mites) from poor barrier leads to Imbalance of immune sys. with TH2 predominance
Colonization with staph aureus leads to more inflammation
Immune imbalance predisposes body to viral infection
Atopic dermatitis (eczema) presentation
Scaly, Ill-defined erythematous patches
May be lichenified
Distribution (adults): face, neck, flexors
Distribution (infants): face, extensor arms, legs, buttocks
Psoriasis pathogenesis
Complex interplay between keratinocytes, TH1 cells, TH17 cells that lead to keratinocyte proliferation.
Trauma to the skin leads to more inflammation (Koebner phenomenon)
Skin becomes thick with layers of scale
Psoriasis presentation
Well-demarcated, erythematous plaques with silvery, “micaceous” scale.
Koebner phenomenon may partially explain distribution.
Urticaria (hives) pathogenesis
Many immunologic and non-immunologic stimuli.
Mediated by mast cells and histamine release.
This leads to vasodilation and fluid accumulation -> urticaria within minutes
Urticaria (hives) presentation
Itchy annular edematous pink plaques “wheals”
Hallmark is evanescence - lesions come and go within 24 hours
Dermatographism (urticaria)
“To write on the skin”.
Scratching or writing on skin leaves hives in the same pattern
Angioedema (urticaria)
Deep form of urticaria
Exanthematous drug eruptions etiology
Systemic equivalent of contact dermatitis
TH1 hypersensitivity
Medications metabolized/deposited in the skin
4-14 days after medication started
May persist or worsen for 1-2 wks after drug is stopped.
Exanthematous drug eruption presentation
Identical clinical and biopsy findings to a viral rash.
Itchy, but not harmful.
Morbilliform eruption = measles-like. Erythematous macules and papules on the central body and extremities.
Urticarial drug eruption etiology
Widespread urticaria within minutes to hours following ingestion.
Direct mast cell stimulation or IgE related hypersensitivity.
ACE inhibitor associated angioedema occurs through a different mechanism.
SJS/TEN etiology
7-21 days after drug started, massive cell death. Mechanism not fully understood.
Does not evolve from drug exanthems.
High mortality and morbidity
SJS/TEN presentation
Sheets of sloughed skin. Severe skin pain. Dusky erythematous macules. Bullae and sheets of denuded skin (+Nikolsky sign) Mucosal erosions.
Colonization
Presence of microorganisms in numbers insufficient to cause disease.
Infection
Presence of microorganisms in numbers that interrupt normal cellular functioning
Non-bullous impetigo etiology
Staph aureus -> strep pyogenes
Non-healing wound (impetiginization)
Bullous impetigo etiology
Localized form of SSSS
staph aureus page II, type 71.
ET-A/ET-B causes desmoglein 1 to separate
Impetigo presentation
Honey-colored crusting Bullous impetigo - prodrome of malaise, fever, diarrhea. Flaccid bullae Children may appear healthy Rapid resolution
Impetigo W/U and Tx
Clinical presentation and culture from superficial wound or fluid from bullae.
Tx - cover affected site.
Topical antibiotics (mupirocin 2% ointment)
Oral antibiotics (high risk patients or generalized disease)
Ecthyma etiology
Onset following trauma.
Strep pyrogenes or staph aureus.
Ecthyma presentation
Deeper infection with associated ulceration and thick crust.
Heals with scarring.
Ecthyma Dx and Tx
Dx - culture
Tx - oral abx
Abscess etiology
Staph aureus most common. May involve many types of organisms.
Risk factors - diabetes, being old, immunosuppression, obese, poor hygeine
Abscess presentation
Collection of pus with surrounding fibrous reaction.
Abscess Dx and Tx
Ddx - ruptured epidermoid cyst
Tx - warm compress, incision and drainage (I&D), oral antibiotics (perinasal location, large and recurrent lesions, cellulitis, failure to respond to warm compresses and I&D)
Erysipelas etiology
Strep pyogenes. Commonly affects elderly patients.
Erysipelas presentation
Sharply demarcated border.
Fever, chills, malaise. May be recurrent.
Erysipelas Tx
Oral antibiotics
Erythrasma etiology
Corynebacterium minutissimum
Erythrasma presentation
Typically asymptomatic. Coral red glow under Wood’s lamp. Occurs in skin folds
Erythrasma Dx/Tx
Dx- Wood’s lamp exam
Tx - Topical antibiotics (clindamycin, benzoyl peroxide) or Topical antigungal agents (clotrimazole, ketoconazole)
Tinea Dx
KOH examination - long strings. No clusters of spores
Tinea etiology
Dermatophytes
- Trichophyton
- Epidermophyton
- Microsporum
Tinea Tx
Topical antifungals (focal) (clotrimazole, terbinafine) Oral antifungals for widespread or involving hair follicles
Pityriasis (Tinea) Versicolor presentatoin
Onset after puberty. Common in young adults.
Malassezia furfur. Transmitted via direct contact. Recurrances common
macules and patches w/ fine, white, superficial scale (gentle scraping makes scaling more apparent)
-asymptomatic
-recurrences common
-pink in winter, hypopigmented in summer (doesn’t tan)
-often across upper trunk
Pityriasis (Tinea) Versicolor Dx
KOH exam - spaghetti and meatballs- malassezia furfur
Pityriasis (Tinea) Versicolor Tx
Topical antifungals (focal) Oral antifungals (widespread) -Ketoconazole 200 mg and exercise Prevention -Selenium sulfide shampoo (Selson blue) -Wash skin 1-2 times monthly
Seborrheic Dermatitis etiology
Unknown. Possible role for Pityrosporum yeast infection. 3-5% of US population is affected. Infants
Seborrheic dermatitis presentation
Red, itchy rash on scalp/face with flaky scales
Seborrheic dermatitis Tx
Topical antifungals (clotrimazole, terbinafine)
Can add low potency topical steroid if no improvement (HCT 1% cream)
Anti-seborrheic shampoo
(Selenium sulfide, ketoconazole)
Response is typically rapid.
Recurrence common
Cutaneous Candidiasis etiology
Candida (albicans) yeast
Humid weather
Affects skin folds
Cutaneous candidiasis presentation
- Involves scrotum, satellite papules and pustules.
- Intertrigo
- diaper dermatitis
Cutaneous candidiasis Tx
Topical antifungals (clotrimazole, nystatin, DO NOT use terbinafine) Barrier pastes (zinc oxide)
Herpes Simplex Virus (HSV) Infection Pathogenesis
HSV 1 - oral
HSV 2 - genital
Transmission from direct contact or fomites.
High incidence of subclinical infection.
Possible transmission among asymptomatic carriers
HSV Presentation
Prodrome of tingling Pain Vesicles Hemorrhagic crust Scalloped border Palpable lymph nodes
HSV Dx
Clinical presentation Tzanck prep Serologic HSV 1 and 2 A/b's Culture PCR
HSV Tx
Topical antivirals (limited efficacy) Oral antivirals -Initiate tx as first sign of outbreak -Daily suppressive dosing (>6 outbreaks/year)
Erythema multiforme presentation
Reaction pattern to HSV. Affects skin and/or oral mucosa. Targetoid lesions. Self-limited Recurrent
Varicella Zoster Virus (VZV) etiology
Prior history of primary varicella (chicken pox)
More common among elderly and immunosuppressed.
Reactivation of latent infection from DRG.
Post-herpetic neuralgia is a rare complication.
VZV Tx
Oral antivirals
VZV presentation
Shingles or rash found along dermatomes
Human papilloma virus (HPV) etiology
Infects the basal keratinocyte
cancer high risk*** HPV 16,18,33,35
HPV presentation
Can affect skin (verucca vulgaris) or genital mucosa (condyloma acuminata)
- adults and kids
- skin-colored papules w/ rough surface +/- scale
- black dots = thrombosed bvs
- interruption of dermatoglyphs (fingerprints)
HPV Tx
Salicylic acid Cryotherapy Immunotherapy (topical irritant) Surgical removal (laser ablation or electrodessication [EDC] and currettage) Vaccine
Molluscum contagiosum presentation
asymptomatic skin colored umbilicated papule
- rarely puritic
- spontaneously resolves
- kids and adults (STI)
Molluscum contagiosum etiology
Pox virus transmitted via contact. Resolves spontaneously
Molluscum contagiosum tx
Destructive methods of removal. Resolves spontaneously
Erythema infectiosum etiology (Fifth disease)
Parvovirus B19
Children > adults
No seasonal predilection
Spread via respiratory secretions
Erythema infectiosum presentation
kids: low grade fever and malaise 1-2 days prior to rash, red cheeks (slapped cheeks), lacy, reticulate patches
- adults: headache, fever, abdominal pain, arthralgias, *risk of aplastic crisis (hemolytic anemia) , pregnant: risk of hydrops fetalis
Erythema infectiosum Tx
No effective treatment
Avoid contact w/ pregnant women
Scabies etiology
Sarcoptes scabei infect the stratum corneum. Eggs hatch after 1 week. Common among children and adults living in close contact
Scabies Dx and Tx
Dx - Scabies (mineral oil) prep.
Tx - Topical anti-scabetics (permethrin)
Oral anti-scabetics (ivermectin)
Environmental controls (wash bedding and clothing)
phototoxic rxn presentation
Photosensitivity that occurs based on chemical on skin or in body (drug)
- w/in hours , peaks at 24h
- redness, swelling, BURNING/STINGING
phototoxic rxn etiology
“UV light stimulates chemical –> toxic rxn + cell death
- NOT mediated by immune sys (no sensitization period) .. requires sun (not just caustic agent)
- common meds: amiodarone, doxy, furosemide, hydrocholorthiozide, methotrexane, naproxen “
phytophotodermatitis presentation
Type of phototoxic rxn caused by caustic plant (similar Sx: red, swelling, BURN/STING)
phytophotodermatitis etiology
wild parsnip, parsley, celery, lime, lemon, fig
-similar to ACD but with sun involvement
photoallergy presentation
Papular/papulovesicular lesions in sun-exposed areas
- ITCHING = hallmark
- onset 24-72h post exposure
photoallergy etiology
“delayed hypersensitivity rxn to chemical on skin or in body
- light alters chemical –> immune rxn
- requires sensitization
- most common cause: sulfa meds “
polymorphous light eruptions presentation
puritic, edema, pink papules coalescing into plaques and vesicles on sun-exposed skin areas (can spread to unexposed areas)
- onset in spring, gets better thru summer as skin adapts to UV light
- can be light thru glass windows
polymorphous light eruptions etiology + Tx
Delayed hypersensitivity rxn to unknown antigen
-skin exposure to UVA or UBV light (or both)
photoprotection, topical steriods, low dose phototherapy (skin “hardening” or adaptation), plaquenil
-may spontaneously remit over time
XP presentation
from early age, sunburn easily
- freckles and xerosis
- BCC and SCC starting at age 10
- severely high risk for skin cancers, brain,lung, renal carcinomas, neuro abnormalities
XP etiology + Tx
auto recessive
- defective DNA nucleotide excision repair pathway
- tx: strict UV avoidance
vitiligo presentation
Depigmentation (NO pigment)
- common sites: mouth, eyes, hands, genitals
- may kobnerize
- risk of sunburn
vitiligo etiology
autoimmune Inflammation caused by melanocyte destruction
-ass. with alopecia areata (focal hair loss), hypothyroidism, pernicious anemia
vitiligo w/u + Tx
clinical dx
-histopath shows complete absence of melanocytes
dilligent sun protection
topical steroids
nvUVB
grafing
Piebaldism presentation
white forelock of hair, depigmentation along midline
Piebaldism etiology
melanocytes fail to migrate all the way to midline b/c of defect in c-kit gene (leads to no steel factor)
-auto dominant
Piebaldism Tx
sunscreen cosmetic blends (just cover it up)
Pityriasis alba presentation
ill-defined, hypopigmented round patches
- may have overlying scale
- more common in kids
Pityriasis alba etiology
Melanocyte downregulation
-common among atopic dermatitis pts
Pityriasis alba tx
no tx
- sunscreen helps prevent accentuation
- moisturizing creams
Oculocutaneous albinism presentation
white, yellow, red or red-brown dyspigmentation
-may have ocular findings: nystagmus, photophobic, dec acuity
Oculocutaneous albinism etiology
altered melanin production due to tyrosinase enzyme defect
-auto recessive
Oculocutaneous albinism tx
sun protection vital -> they have inc risk of developing skin cancer
cosmetic blends
melasma presentation
“mask of pregnancy”
-photo-exposed areas affected
-women
light to medium brown patchy hyperpig., ill-def borders
melasma etiology
estrogen and progesterone -> inc melanin syn due to hormones (pregnancy or OCPs)
melasma tx
dilligent sunscreen use
stop OPCs
hydroquinone (bleaching agent)
Laser
Cafe-au-lait macules (CALMs) and NF1 presentation
increased epidermal melanin
-uniformly pigmented light brown patches w/ sharp borders
Cafe-au-lait macules (CALMs) and NF1 etiology
NF1 is auto dominant disorder
>6 CALMs, axillary freckling, neruofibromas, lisch nodules, optic gliomas, skeletal abnorm.
Cafe-au-lait macules (CALMs) and NF1 Tx
NF1- close monitoring for malignancies
addison’s presentation
bronze hyperpigmentation, generalized over body
especially in photoexposed and frictional areas
adrenal insuff may present w/ fatigue, nausea, hypotension, anorexia
addison’s etiology
Autoimmune destruction of adrenal cortex –> AP makes a ton of ACTH to compensate –> stim melanin synthesis
Basal cell nevus syndrome presentation and etiology
from young age, pts develop large number of basal cell cancers
inactivation of tumor suppressor gene
common melanocytic nevi- presentation
moles
Junctional (epidermis) - uniform, dark brown
compound (epi + dermis) - variable exophytic, lighter brown
Dermal (dermis) - more exophytic, lighter in color
common melanocytic nevi- etiology
"groups of melanocytes in skin -lighter skin -> more nevi -darker skin -> more nevi on acral sites (palm, sole, nail bed) # ass w. melanoma risk -nevi progress thru stages as peopl age -no new nevi after age 30 "
congenital nevi presentation/tx
“present at birth, darken over time
- range in size … giant > 20cm
- may surround hair follicles, bvs
- may develop cobbled surface
- color variation
- monitor for changes, giant have higher risk for melanoma
dysplastic nevi presentation
color variation irregular shape indistinct borders >5mm macular component always present -trunk = most common " risk factor for melanoma mildly dysplastic: monitor -mod-severe: excise
malignant melanoma - presentation and risk factors
“ABCDEs - asymm, border, color, diameter >6mm, evolution
-very hard to distinguish from dysplastic nevi “
malignant prolif of melanocytes at dermoepidermal junction
risk factors: numerous, large, dysplastic nevi, family/personal hx, UV radiation, childhood and intermittent burns, higher SES , immunosuppression
1/3 pre-existing, 2/3 de novo
malignant melanoma tx
“excision : .5cm for in situ, 1cm for 2mm
sentinel lymph node biopsy for 1-4mm depth
lymphaenectomy
chemo
regular skin exams “
malignant melanoma- superficial spreading
“in situ, long radial growth
most common
malignant melanoma- nodular
fastest growing, short radial growth, highest met risk
malignant melanoma- lentigo maligna
> 70yo, longest radial growth phase, flat asymmetric, color variation, face = most common
malignant melanoma- acral lentiginous
“most common in darker skin types,
- palmar, plantar, subungual
- Huchinson sign - nail bed extends to skin
epidermoid cyst presentation
“Domed nodule
- mobile, compressible
- foul-smelling, pasty contents
- inflammation, but rarely infection”
epidermoid cyst etiology
“trapped epidermal cells, not sebaceous
- caused by injury or blocked hair follicle
- picket of macerated keratin
epidermoid cyst tx
“intralesional steroids or oral antibiotics if inflammed
-excision if recurrently inflamed (residual cyst wall can cause recurrence, don’t excise when inflammed )
seborrheic keratosis presentation
"Greasy horn on skin -looks like it could be flicked off, may fall off 40s or 50 yo -flesh, tan, brown or black colored -most common on trunk -pseudohorn cysts (white little indents)
seborrheic keratosis etiology
“Benign overgrowth of epidermis
-genetic predisposition “
seborrheic keratosis tx
“reassurance
curettage or cryotherapy for inflamed lesions
actinic keratoses presentation
actinic = sun induced
- pre-cancerous lesions of epidermis
- pink to red sandpapery papules
- better felt than seen
- photoexposed distribution
actinic keratoses risk factors
“risk factors: intense/frequent sun, fair skin, age, male, prior hx
DNA damage -> dysreg. of cell cycle “
actinic keratoses tx
Suspicious for SCC if: persists after tx, rapid growth, indurated, ulcerate
SCC presentation
“-in situ (Bowen’s) = limited to epidermis, well-demarcated, thin plaque, resembles superficial BCC, AK, eczema, psoriasis
-invasive: erythematous plaque/nodule, scaly, indurated(thick) base, may be ulcerated
“
SCC etiology
“second most common skin cancer
- DNA disruption, chronic inflamm
- 3x more common than BCC in immunocompromised
- sites lined w/ sq epi (skin, mouth, esophagus, penis, anal mucosa)
- high risk sites for mets: lips, ears, perianal/genital, hands
- may progress from SCC “
SCC tx
excision for low risk
Mohs for high risk sites
prognosis SCC + mets = very poor
BCC general etiology + tx
"malignant tumor of basal keritinocytes -most common cancer in US -90% head and neck (esp nose) -3x more common than SCC in immunocompetent pts" Tx: High rate of recurrence in mask area of face -rarely metastizizes -untreated --> local tissue destruction
BCC nodular presentation
‘Pearly’ or translucent papule
or nodule
– Telangectasias – ‘Rolled border’ – May have central erosion or ulceration – Friable, bleeds easily"
BCC nodular etiology
Nodules of basaloid cells in the dermis
BCC superficial presentation
“erythematous thin plaque w/ overlying scale
- slow growing
- may resemble dermatitis
- translucent, friable, crusting, rolled border “
BCC superficial etiology
“Basaloid tumor cells bud directly off epidermis
-favors trunk and extremities “
BCC morpheaform presentation
“depressed, atrophic scar-like hypopigmented papules
indistinct margins
*most aggressive
“
BCC morpheaform etiology + Tx
Infiltration of surrounding skin - > Mohns surgery indicated
acne vulgaris presentation
“closed (whiteheads) or open (blackheads- melanin detected at surface) comedones
along jawline/chin –> hormonal, women
**must have comedones to be acne”
acne vulgaris etiology
“4 stages, spurred by inc in 5a-DHT at puberty -> inc sebum production:
- mocrocomedones
- comedones
- inflammatory papule/pustule
- nodule/cyst “
acne vulgaris tx
“Topical retinoids to normalize follicular keratinization + prevent new lesions (adaptalene, tretinoin) - apply to entire face for PREVENTION, used for all acne
- topical anti-inflammatory (benzoyl peroxide, topical abx) - inhibit bacterial growth, apply just to lesion
- oral abx (tetra*, doxy, minocycline) for inflammatory acne papules, pustules, nodules, significant side effects
- OBC or spironolactone (inhibits T receptor) for women w/ hormonal causes
- oral isotretinoin (acutane) - if all else fails, iPledge pregnancy promise
- surgical exfoliation/reduce inflammation”
acne fulminans presentation
“abrupt onset
deep lesions, may coalesce into oozing friable plaques w/ hemorrhagic crust
complicated by scarring
may be a/w: fever, arthralgias, lymphadenopathy, Hepatosplenomegaly”
acne fulminans etiology
“most common in boys 13-16
start w/ mild acne -> sudden eruption of severe “
acne conglobata presentation
“highly inflammatory
- comedones nodules, abscesses, draining sinuses
- absence of systemic sx “
acne conglobata etiology
part of follicular occlusion triad
acne mechanica presentation + etiology
linar or geometric distribution of involved areas
results from mech/frictional obstruction of pilosebaceous unit (helmets, chin straps, collars)
acne excoriee presentation/etiology
result of excoriation/manipulation
patients w/ anxiety, OCD, personality disorders pick at skin
drug induced acne presentation
“onset 2-4 wks after starting drug
- uniform morphology (not in diff stages like other acne forms)
- trunk/extremities “
drug induced acne common irritants
common irritants: glucocorticoids, anabolic steroids, topical steroids, hormones, lithium, iodides/bromides, isoniazid
neonatal acne etio+present
“superficial red papules on cheeks/nasal bridge
-2 weeks-3mos of age “
“>20% of healthy newborns
maternal hormones “
infantile acne etio
beyond 3-6 mos
hormonal influence of child (inc DHEA from immature adrenal gland)
rosacea present
“very common- affects nose bridge and cheeks
-variable severity
-absence of comedones**
-may have itching/burning in eyes
-easily flush
-may also have: xerosis, edema, burning/stinging, rhinophyma (overgrowth of sebaceous tissue on nose)
“
rosacea common triggers
Triggers: environment (wind, UV, heat, cold), hot liquids, spicy foods, alcohol, mites, emotional stress
rosacea tx
“topical abx (metronidazole, sulfur, BPO) to reduce erythema/inflamm
oral abx
laser and lights (surgical options) for telangiectasis (little bv’s), but doesn’t prevent future flares (tx needs to have succeeded first, laser for underlying redness)
perioral dermatitis presentation
“**spares vermillion border
small erythematous pap. in perioral areas “
perioral dermatitis etiology
rosacea exacerbated by topical steroids, cinnamon, mint flavorings
perioral dermatitis tx
“avoid mint/cinnamon
discontinue steroids”
pyoderma faciale/rosacea fulminans
acute eruption of inflamed papules and pustules
may occur in pts w/ mild rosacea
steroid rosacea
rosacea exacerbated by topical or systemic corticosteroids
hidradenitis suppurativa presentation
“chronic condition
- recurrent boils and draining sinuses -> scarring
- very painful and emotionally harmful
- may have foul odor “
hidradenitis suppurativa etio
“occlusion of follicular infundibulum of apocrine glands–> rupture of follicles
-more common in women “
hidradenitis suppurativa tx
“weight loss reduces friction
- topical abx, absorbent powder, AlCl
- prednisone, oral retinoids, abx, isotretinoin
- intralesional steroid injection, incision/drainage, laser”
acne inversa/follicular occlusion tetrad
series of 4 associated disorders: acne conglobata, dissecting cellulitis of scalp (perifollicular pustules, nodules, abscesses–> scarring alopecia/hair loss), HS, pilonidal cyst (cyst at top of gluteal cleft)
hyperhydrosis presentation
“axilla, palms, soles
-xs sweating from eccrine sweat glands “
hyperhydrosis etio
“sympathetic stim due to thermal or emotional stimuli
-secondary hyperhidrosis due to underlying disease or metabolic issue “
hyperhydrosis tx
“Aluminum chloride - plugs gland
oral anticholinergics (glycopyrrolate)- reduce sympathetic firing (side effects: blurred vision, dry mouth, urinary retention)
Botox -(axilla) inhibits ACh release at NMJ, works for 4-6 mos
-surgical sympathetectomy (only for hands)
-liposuction (axilla) - suck out glands “
