Skin conditions I and II Flashcards
how do cellulitis, erysipelas and abscesses normally present?
- erythema
- edema
- warmth
- d/t breach in skin barrier -> bacterial entry
where/who is erysipelas normally found
- upper dermis and superficial lymphatics
- kids and older adults
where/who is cellulitis normally found
- deeper dermis and subcutaneous fat
- middle aged and older adults
where are abscesses normally found
upper and deeper dermis
risk factors for cellulitis/ erysipelas
- skin barrier disruption
- preexisting skin conditions
- skin inflammation i.e. d/t radiation
- edema - lymphatic or venous insufficiency
- obesity
- immunosuppression
most common cause of erysipelas
- beta hemolytic strep
most common cause of cellulutis
- beta hemolytic strep
- staph aureus (including MRSA)
most common cause of skin abscess
- staph aureus (including MRSA)
clinical manifestations of cellulitis
- erythema, warmth, edema
- unilateral almost always
- common in lower extremities
- +/- purulence
- slower onset
- localized sx develop over days
- less distinct boarders
- +/- drainage
clinical manifestations of erysipelas
- erythema, warmth, edema
- unilateral almost always
- common in lower extremities
- nonpurulent
- acute onset sx
- clear demarcation- butterfly involvement on face
- systemic manifestations- fever/ chills
- raised above level of surrounding skin
what does induration mean
hard surrounding
what does fluctuant mean
soft and moveable
what is a skin abscess
- collection of pus
- in dermis or subcutaneous space
clinical presentation of skin abscess
- painful
- fluctuant
- erythematous nodule
- +/- cellulitis
- surroudning induration
- regional adenopathy
- systemic sx rare
furuncle
infection of hair follicle -> abscess
carbuncle
infection of multiple hair follicles -> abscess
what are common areas for skin abscesses to develop?
- neck
- face
- axillae
- buttocks
what is LRINEC score?
- lab risk indicator for necrotizing fasciitis
- distinguish NF from other soft tissue infections like cellulitis
when would you use the LRINEC score
- concerning hx and exam
- pain out of proportion to exam
- rapidly progressive cellulitis
- score >6 means NF
complications of cellulitis
- NF
- bacteremia and sepsis
- osteomyelitis
- septic joint
conditions that may be hard to distinguish from cellulitis
- gout
- DVT
- venus stasis dermatitis
management of cellulitis/ abscess/ erysipelas
- depends on severity
- should see improvement in 24- 48 hours
- tx duration of 7-10 days, up to 14
- if no improvement consider underlying abscess
where does impetigo most commonly occur
on face of kids 2-5
what is the most common form of impetigo
- non-bullous
- papules progress to vesicles surrounded by erythema
- dev into pustules which break down and form golden crust
ectyhma impetigo
- ulcerative
- extend deep into dermis
- “punched out ulcers” with yellow crust
possible consequences of impetigo
- post-strep glomerulonephritis
- rheumatic fever
sx of post-streph glomerulonephritis
- edema
- HTN
- hematuria
- occurs 1-2 weeks post infection
most common cause of impetigo?
- s. aureus
most common cause of bullous impetigo?
- s. aureus strain that produces toxin -> cleavage of superficial skin
most common cause of ecthyma impetigo?
- strep pyogenes
urticaria
- hives, welts, wheels
- common
- intensely pruritic
- usually no identifiable trigger
- sometimes accompanied by angioedema
- anyone can get it
acute urticaria
- less than 6 weeks
chronic urticaria
- recurrent
- signs and sx recur most days of week for more than 6 weeks
clinical manifestations of urticaria
- circumscribed, raised, erythematous plaque with central palor
- round/oval
- very itchy
- most severe at night
- any area of body
- transiently appearing
- can get angioedema in lips, extremities, genitals
pathophys of urticaria
- mediated by mast cells in dermis
- release histamine -> itching
- release vasodilatory mediators -> swelling
dx of urticaria
- mainly clinical exam and history
- signs and sx of allergic reaction
- any underlying disorders
- allergy test
management of urticaria
- focused on short term relief
- 2/3 spontaneously resolve and are self limited
- can use H1 and H2 antihistamines
- may use steroids
lipomas
- most common benign soft tissue neoplasm
- mature fat cells enclosed by fibrous capsule
- dx based on history and PE
where are lipomas usually found?
- most common in upper extremities and trunk
- can be found anywhere
- range in size
pathophys of lipomas
- > 50% develop in subcutaneous tissue
- cause unknown but associated with gene rearrangement of chromosome 12
clinical manifestations of lipomas
- superficial
- soft
- painless
- round, oval, multilobulated
- pt may confuse them for enlarged lymph nodes
management of lipomas
- if stable/asymptomatic then no tx
- can surgically excise
epidermal inclusion cyst
- most common cutaneous cyst
- skin colored dermal nodules
- visible central punctum
- usually small in size
where are epidermal inclusion cysts usually found
- face
- scalp
- neck
- trunk
- can occur anywhere
- 2X more common in men
what disease is epidermal inclusion cysts associated with?
gardener syndrome- predisposition to colon polyps
pathophys of epidermal inclusion cysts
- d/t trauma
- implantation and proliferation of epithelial elements into dermis
- spontaneous rupture can occur
- cheesy material
clinical manifestations of epidermal inclusion cysts
- firm
- asymptomatic
- overlyting a punctum (where hair follicle comes out)
management of epidermal inclusion cysts
- asymptomatic- none
- excesion of cyst or incision and drainage
- intralesional injection with triamcinolone
tetanus cause
- clostridium tetani
- found in soil
- rarely seen in US d/t vaccine
- incidence increases after natural disasters
pathophys of tetanus
- c. tetani produces matalloprotease tetanospasmin (toxin)
- toxin released in brain stem -> blocks neurotransmission that modulates muscle contraction
- result- increased muscle tone, painful spasm, widespread autonomic instability
what is the incubation period for tetanus?
- 8 days
- further the inoculation site is from CNS the longer the incubation pd
clinical manifestations of tetanus
- trismus (lock jaw)
- massester muscle reflex . spasm
- tonic contractions of skeletal muscles
- no impairment in consciousness
when does acne typically resolve?
- 3rd decade
- post adolescent usually impacts women
pathogenesis of acne
- inflammation of pilosebaceous follicles
- follicular hyperkeratinization
- increased sebum production
- cutibacterium acnes
- inflammation
sebaceous gland changes in ance
- gland enlarges
- sebum production increases during puberty -> medium for c. acne
- micromedones = enviornment for bacteria
closed comedone
- white head
- accumulation of sebum and keratinous material
open comedone
- black head
- keratinocytes
- oxidized lipids
- melanin
pathogenesis of inflammatory acne
- follicle ruptures -> proinflammatory lipids and keratin released into surrounding dermis
- family history has 3X risk
- stress doesnt appear to be associated
androgens and acne
- stimulates growth of secretory fn of sebaceous glands
- high levels at birth -> acne until about 2 y/o
- acne onset correlated to DHEA-s levels
- most pts with acne have normal androgen levels*
external factors that cause acne
- soaps/ detergents/ astrigents
- repetitive mechanical trauma like scrubbing
- bra straps, shoulder pads, helmets
milk and acne
- milk can exacerbate acne d/t increased levels of IGF
insulin resistance and acne
- stimulates androgen production
- associated with increased IGF-1
- increased facial sebum production
- normal rise in insulin resistance and IGF-1 in puberty
BMI and acne
- possible that low BMI reduces risk of acne in males
- increased risk of high BMI and acne only in women
ways to classify acne
- comedonal acne- noninflammatory
- inflammatory acne- papules, pustules
- nodular acne- aka cystic acne
dx of acne
- PE
- type and location
- medication hx
- endocrine fn
- DHEA-S, total testosterone, free testosterone
counseling points for acne tx
- no cure
- 4-6 weeks for improvement
- may get worse before better
Rosacea
- chronic disorder
- relapses
- primarily in central face
- 4 main subtypes
- more common in fair skinned and adults (F) >30
main subtypes of rosacea
- erythematotelangiectatic
- papulopustular
- phymatous
- ocular
pathogenesis of rosacea
- abnormalities in innate immunity
- inflammatory reactions to cutaneous microorganisms
- UV damage
- vascular dysfunction
erythematotelangiectatic rosacea
- presistant central erythma
- flushing
- rough and scaling
- enlarged cutaneous BV
- skin sensitivity
- erythema congestivum
erythema congestivum
after exacerbation of facial redness in rosacea, return to baseline is slow
papulopustular rosacea
- papules and pustules in central face
- can be mistaken for acne
- comedones dont occur
- inflammation extends beyond follicle
phymatous rosacea
- tissue hypertrophy
- irregular contours
- usually on nose
- can occur on chin, cheeks, forehead
- most common in men
ocular rosacea
- happens in more than 50% of pts
- conjunctival hyperemia
- blepharitis
- keratitis
- lid margin teleangiecstasis
- abnormal tearing
- chalazion
- refer to ophthalmologist
rosacea exacerbating factors
- extreme temps
- sun exposure
- hot drinks
- spicy food
- alcohol
- exercise
- irritation from topical products
- emotions
- drugs
- skin barrier disruption
dx for rosacea
- clinical assessment
- no biopsy or serologic studies
management of erythematotelangiectatic rosacea
- first line- behavioral changes/ avoid triggers
- second line- laser and light based therapy
psoriasis
- well demarcated plaques with silver scales
- associated with many comorbidities
- peak age onset: 30-39 and 50-69
risk factors for psoriasis
- genetics *
exacerbating factors for psoriasis
- smoking
- obesity
- drugs
- infection- post strep flaares and HIV
- alcohol
- vit D deficiency
- stress
pathophys of psoriasis
- immune mediated
- scaling, induration, erythema hyperproliferation
- abnormal differentiation of epidermis
- inflammatory cell infiltrates
- vascular dilitation
categories of psoriasis
- chronic plaque psoriasis
- guttate
- pustular
- erythrodermic
- inverse
- nail
chronic plaque psoriasis
- most common
- symmetrical distribution
- asymptomatic or pruritis
common places for plaque psoriasis
- scalp
- extensor elbows, knees
- gluteal cleft
guttate psoriasis
- multiple small papules and plaques
- trunk and proximal extremities common
- strong assoc with recent strep infection
- child or YA with no hx psoriasis
pustular psoriasis
- life threatening
- acute onset
- wide spread erythema, scaling, and sheets of superficial pustules
- maialse, fever, diarrhea, leukocytosis, hypocalcemia
causes of pustular psoriasis
- pregnancy
- infection
- withdrawal from glucocorticoids
erythrodermic psoriasis
- uncommon
- acute or chronic
- generalized erythema and scaling from head to toe
- complications d/t loss of adequate barrier
inverse psoriasis
- inguinal, perineal, genital, intergluteal, axillary and inframammory areas
- sometimes misdx as fungal or bacterial infections
nail psoriasis
- more common in pts with psoriatic arthritis
- nail pitting
dx of psoriasis
- family hx*
- clinical exam
- skin biopsy
management of psoriasis
- emollients
- topical corticosteroids
- vit D analogs
- Tar- T/gel
- topical retinoids
- UVB light therapy
- photochemothearpy
- excimer laser
- biologics
alopecia
- targets anagen hair follicles -> non-scarring hair loss
- usual onset before 30
- men and women equally affected
classifications of alopecia
- areata
- totalis
- universalis
alopecia areata
discrete patches
alopecia totalis
entire scalp
alopecia universalis
entire body
pathophys of alopecia
- T cell mediated inflammation disrupts normal hair cycle
- no destruction of hair follicle
- premature transition of active follicle to inactive
- collapse of immune privileged status
- inappropriate trigger of immune response vs follicular antigen
alopecia risk factors
- genetics
- severe stress
- drugs and vaccines
- infections
- vit D def
clinical manifestations of alopecia
- smooth, circular, discrete patches of hair loss
- dev over 2-3 weeks
- pruritis or burning may precede
- beard may be first site in men
- can spread in bizarre patterns
- nail abnormalities possible
onychorrhexis
- longitudinal fissuring of nail plate
- can occur in pts with alopecia
diseases associated with alopecia
- thyroid disease***
- lupus
- vitiligo
- atopic dermatitis
- allergic rhinitis
- psoriasis
- down syndrome
- polyglandular autoimmune syndrome type I
clinical course of alopecia
- 50% with limited patchy hair loss spontaneously recover in 1 yr
- some have multiple episodes
- 10% progress to totalis or universalis
dx of alopecia
- clinical exam
- exclamation point hair at margins
- skin biopsy only in uncertain cases- show inflammatory infiltrates surrounding follicles aka swarm of bees
management of alopecia
- topical or intralesional corticosteroids (caution skin atrophy and hypopigmentation)
- topical immunotherapy for severe
- rogaine
- phototherapy
- oral steroids or biologics as last line
hidradenitis supprativa
- chronic follicular occlusive skin condition
- aka acne inversa
- inertriginous area involvement
- onset usually puberty to 40, women more than men
pathogenesis of HS
- follicular occlusion, follicular rupture and associated immune response
- ductal keratinocyte proliferation
- ductal plugging then expansion -> rupture
- stim immune response leading to sinus tracts
risk factors and exacerbating factors of HS
- genetics*
- mechanical stress
- obesity
- smoking
- hormones- perimenstrual flares, goes away during pregnancy
- bacteria- staph and strep
- drugs
clinical manifestations of HS
- axilla most common site
- inguinal, inner thigh, perianal, inframammary, buttock, scrotum, vulva
- primary lesion is solitary, painful, deep seated inflamed nodule
- dev sinus tracts with chronic disease
- scarring
what is the staging system called for HS?
hurley staging
Stage I hurley manifestation and management
- abscess formation
- topical clindamycin
- intralesional corticosteroid
- punch debridement
- chemical peel
stage II hurley manifestation and management
- recurrent abscess
- sinus tract formation and scarring
- oral tetracyclines for several months
- clindamycin or rifampin
- oral retinoids
- antiadrenergics
- punch biopsy of fresh lesions
stage III hurley manifestation and management
- diffuse involvement
- multiple interconnected sinus tracts
- TNF alpha inhibitors
- systemic glucocorticoids
- cyclosporine
- surgery
dx of HS
- patient history
- clinical exam
- skin biopsy not necessary
prevention of HS
- avoid skin trauma
- stop smoking
- weight management
- antiseptics
- emollients
- management of comorbidities
