burns & chronic skin disorders Flashcards
causes/types of burns
thermal Scolding (most common) corrosive (chemical) electrical (extensive damage but not visable) classification of burn: depth/extent/complications
superficial burn
reddend skin
painful
superficial partial thickness burn
burned epidermis/papillary dermis
blistering
dermis is red/moist
painful
deep partial thickness burns
damage to epidermis/papillary dermis
reticular layer of dermis
injury to hair follicles
blistering
full thickness burns
damage to epidermis/dermis/subQ (maybe even muscle/bone)
skin is scarred/pale
painless
leathery skin
greater than 20% surface bone
produces major systemic effect (inflamm, coagulation, firbrinolysis)
life-threatening hypovolemia
thermal injuries
extent of injury relative to body surface area (BSA) trunk 36% arm 9% leg 18% total rule of nines does not apply for electrical burns
complications of large burns
vascular prermeability and edema (hypopreteinemia caused by increased capillary permeability)
altered hemodynamics (fluid shifts, decreased CO)
hypermetabolism (catecholamine, glucagon, glucocorticoids release, increased gluconeogenesis, muscle catbolism)
decreased renal blood flow
immunosuppression
complications of smoke inhalation
carbon monoxide poisoning
cynaide poisoning
airway obstruction or chemical injury to lungs
carbon monoxide poisoning s/s
HA weakness N/V confusion decreased LOC "cherry-red" skin loss of short-term memory seizures DX: ABG/serum CO
carbon monoxide poisoning TX
100% FiO2 (half-life is 75-80 min)
hyperbaric oxygen therapy
carbon monoxide poisoning complications
acidosis (r/t cellular respiration)
loss of consciousness
death
CO has a higher affinity to bind to RBC than CO2
ABC TX
asses airway = early intubation
watch for burns that prevent chest movement
TX hypovolemia (aggressive fluid replacement)
assess for distal pulses (some burns are like tourniquet)
urine output should be .5ml/kg/hour or greater
eschartomy
incision in eschar down to subQ fat layer
allows for expansion w/ swelling
5Ps of compartment syndrome (pain, paresthesia, pallor, pulselessness, paralysis)
burn TX
depends on classification pain management fluid resuscitation infection prevention (PPE/clean/sterile sheets/ABX) wound care (w/ mild soap/water) continuous enteral feeding surgical debridement
chemical burns
direct contact
inhalation
ingestion
chemical burn s/s
pain erythema burning sensation numbness blisters necrotic tissue visual impairment/blindness coughing/dyspnea hypotension HA dizziness
chemical burns TX
depends decontamination irrigation ABCDE fluid resuscitation sterile dressings analgesics debridement
electrical injuries
electricity/lightening lowvoltage <1000 volts high voltage >1000 can have low evidence of external damage risk for compartment syndrome extravasation of fluids
electrical injuries heart/neuro injury s/s
shortness of breath
chest pain
palpitation
loss of consciousness
electrical injuries tx
electrical: LR, cardiac monitor, wound care
lightning: burn center, CPR, exit wound care
Herpes simplex virus 1
labialis (lips/cold sores) keratitis (eye) whitlow (hands/fingers) gladiatorum (torso of wrestlers) sycosis (beard follicles) usually contracted during childhood
herpes simplex virus 2
most sexually-transmitted anogenital herpes
lesions on genitals/perineum/anus
may cause cold sores
likely to be contracted during sexual contact (typically younger)
5th most common STI
HSV 1/2
herpesvirus family
covered by glycopreotein coat
helps virus attach to host sell
vesicular rash
dermatome eruption
localized skin region
innervated by single sensory spinal nerve
pattern may lead to misdiagnosis
HSV 1/2 s/s
may be asymptomatic or mild fever
prodrome (early): fever/flu-like symptoms (primary) pain, itching, tingling, burning, paresthesia (recurrent)
red/swollen area of skin/mucous membrane
painful vesicles
regional lymph nodes swell
vesicles open (painful ulcer then crusts)
primary genital herpes: dysuria/urinary retention, especially in women)
HSV 1/2 DX
viral culture (PCR) serologic testing
HSV 1/2 TX
antiviral meds (acyclovir, valacyclovir, famciclovir)
not curative, control s/s and shorten outbreak, supress recurrent episodes
anagesiccs (acetominopehn, ibuprofen)
cool compress
sitz bath (for genital herpes/dysuria, dilute urine, decreases burning)
acyclovir, valacyclovir, famciclovir
antivirals
selectively inhibit replication of viruses
short-half life (admin PO up to 5x a day)
SE: few, nephro/neuro toxic if IV, resistance can develop
interx: concurrent use w/ nephrotoxic agents
C
herpes zoster
shingles
chronic viral skin condition
caused by reactivation of varicella-zoster virus
first VZV infection causes chickenpox then viral particles travel to other structures and become dormant
cell-mediated immunity prevents virus reactivation but that decreases with age
zostavax vaccine recommended 60+
herpes zoster pathogenesis
latent varicella-zoster virus reactivated
spreads
panful rash develops
usually preceded by a prodrome
onset: malaise, fever, chills, myalgia, HA, nausea
herpes zoster s/s
typically affects one dermatone (tingling, itching, burning, numbness, pain, increased sensitivity to touch)
initial: macuales and papules on red base, vesicles spread over the dermatome, vesicles open and crusts form, painful skin lesions persist, rash 10 days - month
herpes zoster opthalmicus
involves opthalmic division of trigeminal nerve
may cause visual impairment
retinal necrosis
requires emergent treatment by opthalmologist
complication of shingles
ramsay-hunt syndrome/herpes zoster oticus
involves facial nerve CN7
risk of hearing loss or permanent facial weakness
emergent treatment required
complication of shingles
posterherpetic neuralgia PHN
most common complication of shingles
burning, itching pain w/ periods of lancinating pain
other herpes zoster complications
encephalitis/aseptic meningitis
bacterial superinfection of lesions
cranial or peripheral nerve palsies
pneumonitis hepatitis
herpes zoster TX
antiviral meds
if initiated w/in 72hrs of first lesions: shortens duration/severity
antivirals started later may benefit those (50+, complications)
glucocorticoids (may decrease pain/hasten healing in patients over 50 w/ no other contras)
post-herpatic neuralgia TX
gabapentin (analog of GABA, binds and modulates influx of calcium = decreased neurotransmitter release)
TCA ex amitriptyline/doxepin/imipramine (inhibit reuptake of serotonin/norepinephrine)
human papillomavirus (HPV)
warts in skin
occur anywhere on skin or mucous membranes
most lesions = benign
some HPV (genital) linked to dysplasia/cancer
specific to humans
HPV patho
enters skin via small openings, infects epidermal basal layer
viral replication in cell nuclei
causes structural abnormalities
triggers epidermal cell changes = wart
HPVs/s
lesion presentation varies due to selectivity of HPV
specific serotypes affect specific areas
ex: flat, papular, pedunculated
HPV (warts) TX
treats cutaneous warts
doens’t eradicate HPV or prevent HPV transmission
HPV does not respond to antiviral meds
50% resolve w/out TX w/in 1 year
HPV TX
salicylic acid (topical kertolytic agent, chemically destroys wart) antiproliferative topical agents (podophyllin) chemodestructive agents (trichloroacetic acid) second line: cryotherapy surgical intervention (electrosurgery, excision)
atopic dermatitis
eczema
genetic component of FLG gene
chronic recurring itchy inflammatory disorder
associated w/ increased IgE
affected individuals often have other atopic disorders (asthma, allergic rhinitis)
most often in children may persist into adulthood
environmental factors (extreme heat/cold, low humidity)
atopic dermatitis & immune system
increased IgE (increased IgE sensitization)
imbalance of T-cell subsets
predominance of T-helper 2 cells (produce inflamm cytokines)
increased eosinophils/mast cells
reduction in antimicrobial peptides
less movement of neutrophils to skin
toll-like receptor defects
high-risk for bacterial/viral/fungal infections
atopic dermatitis s/s
exacerbation and remission of dry itchy red skin
begins in infancy
constant pruritus (prevailing symptom, preceds eczematous rash)
skin excoriations adn lichenification
xerosis and crusting lesions
negative impact on overall quality of life
atopic dermatits DX
based on s/s
pruritius distribution chronic w/ recurring flare-ups
atopic dermatitis TX
topical agents (moisturizers, oatmeal, corticosteroids, topical calcineurin inhibitors)
lukewarm water baths (for removal of scales, crusts, allergens, follow w/ moisturizer while wet)
cool-mist humidifiers (year-round)
wet-wrap therapy wet-to-dry (significant flare-ups, apply topical corticosteroid, wrap saline-soaked bandages/gauze, dry outside layer bandage/gauze)
cyclosporine
calcineurin inhibitors
immunosuppresant (binds to calcineurin & disrupt T cells)
less toxic to BM
SE: reduction in urine output, half will experience HTN/tremor, HA, gingival hyperplasia, elevated hepatic enzymres
BBW: only admin by those experienced in immunosuppressive therapy
interx: phenytoin phenobarbital carbamazepine rifampin (decrease elvels) antifungal drugs, ACE inhibitors, NSAIDS macrolids (^ levels) grapefruit juice can drastically raise cyclosporine levels
C
cyclosporine WBC/platelet levels
can’t be <4000 WBC
or
<75000 platelets
psoriasis
immune-mediated disease noninfectious hyperproliferation of keratinocytes decreased epidermal cell turnover rate inflamm thickening of dermis & epidermis (shed repidly 4-7 days)
psoriasis s/s
plaques (round/oval well-demarcated) auspitz sign (removal of scale results in pinpoint bleeding)
psoriasis TX
corticosteorids (betamethasone/hydrocortisone acetate
vitamin D analogs
topical retinoids calcieurin inhibitors
phototherapy biologic agents
hidradenitis suppurativa
genetic/immunologic/hormone/environment
occlusion of hair follicle > hyperplasia of follicular epithelium > collection of cellular wastes > cyst formation in sweat gland adjacent to follicle > abscess & tract formation > keloid-like scarring
lesions develop in skinfolds
hidradenitis suppurativa TX
lifestyle changes (tobacco cessation) diet (avoid diary & eat low-glycemic diet) stage III: extensive surgery is only permanent cure
benign neoplasms
noncancerous types of tissue proliferation
may be mistaken for cancer
can be premalignant
photodermatitis
photosensitivity (sun poisoning)
immune response to UV rays
solar urticaria
skin cells may function as photoallergens
photodermatitis
photoallergy
type IV cell-mediated response to sun
phototoxicity
UV light generates free radicals & inflamm mediators
photodermatitis s/s
urticaria in sun-exposed skin
acute: wheezing, dizziness, fainting, erythema, pruritis, papules, vsicles, eczema, skin pain, chills, HA, fever, N
chronic: skin thickening, scarring
actinic keratosis
non inflamm skin disease
skin damage from sun/tanning-device
chronic UV exposure causes keratinocyte changes
actinic keratosis s/s
thick rough crusting or scaly areas bald head face ears lips back of hands forearms shoulders neck
actinic keratosis TX
cryotherapy chemical peal curettage laser 5-fluorouracil cream diclofenac sodium gel imiquimod cream
hemangioma
strawberry mark
congenital (10-12% of infants)
collection of blood vessels in or beneath skin
hemangioma s/s
bright red, slightly raised lesions
if beneath skin will appear bluish
50% on head/neck
hemangioma TX
usually disappear w/out intervention
laser: if impairs vision or breathing
corticosteroids: shrink lesion prior to laser
nevi (moles)
congenital or occur later in life
usually benign
may become cancerous
sun exposure can promote malignant changes
proliferation of altered melanocytes grow in clusters
moles s/s
macules
papules
small plaques varying in color/size/shape
typical: symmetric/regular borders
atypical: multicolord, asymmetric, irregular shape, may evolve to melanoma
moles TX
typical: none
atypical: surgical removal
acrochordons (skin tags)
develop where skin rubs on skin (neck, axillae, groin)
r/t insulin resistance, dyslipidemia, HTN, elevated c-reactive protein
friction leads to soft papules ons talk
skin tags s/s
pedunculated papules
flesh colored/dark pigmentation
usually painless
skin tag TX
cryotherapy
excision
lipomas
family tendency
arise from mesoerm
made up of mature adipose cells in fibrous sheath
grow under skin in subQ tissue
lipomas s/s
may be single or multiple
smooth, soft, doughy, rubbery, painless
lipomas TX
only needed if complications or changes
liposuction
surgical excision
skin cancer
most common cancer in US 1 in 5 increased incidence past 30 years most common: basal cell carcinoma / squamous cell carcinoma most dangerous: melanoma
basal cell carcinoma
UV rays damage DNA in cell nucleus
arises from bottom layer (base) cells of epidermis, hair follicles, sweat glands
basal cell carcinoma causes/RF
repeated/prolonged UV exposure
chronic sun exposure, fair complexion, immunosuppression
basal cell carcinoma s/s
most often in sun-exposed areas
basal cell carcinoma TX
requires biopsy then removal of lesion immune modulator (imiquimod)
squamous cell carcinoma
arises from damaged, unrepared DNA in nucleus of squamous cells of epidermis
UV radiation triggers cancerous keratinocyte transformation
risk if sun exposure/fiar complexion
squamous cell carcinoma s/s
firm, smooth, hyperkeratotic papules or plque w/ ulcer in center
non-healing sore that bleeds easily
sun-exposed areas
squamous cell carcinoma TX
requires biopsy/removal of lesion
topical chemo
radiation or systemic chemo if metastasis present
melanoma
not fully understood
linked to genetic mutations
least common, most dangerous
melanocytes mulitply rpaidly & form cancerous tumors
melanoma s/s
most often brown/black color asymmetrical irregular large diameter enlarging macule papule or nodule appears as sores, lumps, new moles after 30, color changes in skin, changes in existing mole
melanoma TX
biopsy and complete excision lymphadenectomy if metastasis surgery immunotherapy chemo radiation
melanoma warning signs ABCDE
asymmetry (two halves differ in shape)
borders (irregular, uneven, notched, scalloped)
diameter (more than 1/4 inch)
evolving (new mole if 30 +, changing mole or mole differs from others)
vitiligo
exact cause unknown
loss of functional melanocytes in skin/hair/mucous membranes
vitiligo s/s
milky-white or chalk white hypopigmented
hands arms feet trunk & face most common
vitiligo TX
will never restore all skin color phototherapy, laser therapy, steroid therapy, topical tacrolimus ointment depigmentation therapy use higher SPF cosmetic coverups
cafe au lait spots
increased melanin spots on skin
neurofibromatosis type 1 commonly associated
usually benign
cafe au lait spots s/s
flat, light/dark brown lesions irregular or smooth borders vary in size present at birth darken with age no TX required
solar lentigo
cauesd by UV light exposure
UV light induces epidemral hyperplasia > increased pigmentation
solar lentigo s/s
tan, brown, black macules well demarcated and surrounded by normal skin variable in size irregular in shape sun-exposed areas
solar lentigo TX
usually benign
biopsy may be needed to r/o precancerous or melanoma
aimed at reducing appearance
alopecia
various causes
hair growth cycle shortens
affected hair follicles stop replacing lost hair
androgen alopecia
androgen receptors cause excess of androgen in hair follicles
alopecias/s
androgen alopecia; starts around temples & progresses to top of scalp
alopecia TX
males: minoxidil/finasteride
females: oral contraceptives/spironolactone (finasteride not used in women r/t teratogenic)
alopecia areta
autoimmune, strong genetic connection
inflammatory cells attack hair follicles
hair shaft weakens and breaks at or near skin surface
alopecia areata s/s
well-demarcated patches of hair loss
asymmetric
may progress to alopecia totalis (scalp) or alopecia universalis (entire body)
alopecia areata TX
may spontaneously recover
topical steroids (minoxidil intralesional)
corticosteroid injections
topical immunotherapy
