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Pathophysiology and Pharmacology 2 > burns & chronic skin disorders > Flashcards

burns & chronic skin disorders Flashcards

1
Q

causes/types of burns

A 
thermal 
Scolding (most common)
corrosive (chemical)
electrical (extensive damage but not visable)
classification of burn: 
depth/extent/complications
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2
Q

superficial burn

A

reddend skin

painful

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3
Q

superficial partial thickness burn

A

burned epidermis/papillary dermis
blistering
dermis is red/moist
painful

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4
Q

deep partial thickness burns

A

damage to epidermis/papillary dermis
reticular layer of dermis
injury to hair follicles
blistering

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5
Q

full thickness burns

A

damage to epidermis/dermis/subQ (maybe even muscle/bone)
skin is scarred/pale
painless
leathery skin

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6
Q

greater than 20% surface bone

A

produces major systemic effect (inflamm, coagulation, firbrinolysis)
life-threatening hypovolemia

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7
Q

thermal injuries

A 
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
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8
Q

complications of large burns

A

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

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9
Q

complications of smoke inhalation

A

carbon monoxide poisoning
cynaide poisoning
airway obstruction or chemical injury to lungs

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10
Q

carbon monoxide poisoning s/s

A 
HA
weakness
N/V
confusion
decreased LOC
"cherry-red" skin
loss of short-term memory
seizures
DX: ABG/serum CO
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11
Q

carbon monoxide poisoning TX

A

100% FiO2 (half-life is 75-80 min)

hyperbaric oxygen therapy

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12
Q

carbon monoxide poisoning complications

A

acidosis (r/t cellular respiration)
loss of consciousness
death
CO has a higher affinity to bind to RBC than CO2

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13
Q

ABC TX

A

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

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14
Q

eschartomy

A

incision in eschar down to subQ fat layer
allows for expansion w/ swelling
5Ps of compartment syndrome (pain, paresthesia, pallor, pulselessness, paralysis)

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15
Q

burn TX

A 
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
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16
Q

chemical burns

A

direct contact
inhalation
ingestion

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17
Q

chemical burn s/s

A 
pain erythema
burning sensation
numbness
blisters
necrotic tissue
visual impairment/blindness
coughing/dyspnea
hypotension
HA
dizziness
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18
Q

chemical burns TX

A 
depends
decontamination 
irrigation
ABCDE
fluid resuscitation
sterile dressings
analgesics
debridement
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19
Q

electrical injuries

A 
electricity/lightening
lowvoltage <1000 volts
high voltage >1000
can have low evidence of external damage
risk for compartment syndrome 
extravasation of fluids
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20
Q

electrical injuries heart/neuro injury s/s

A

shortness of breath
chest pain
palpitation
loss of consciousness

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21
Q

electrical injuries tx

A

electrical: LR, cardiac monitor, wound care
lightning: burn center, CPR, exit wound care

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22
Q

Herpes simplex virus 1

A 
labialis (lips/cold sores)
keratitis (eye)
whitlow (hands/fingers)
gladiatorum (torso of wrestlers)
sycosis (beard follicles)
usually contracted during childhood
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23
Q

herpes simplex virus 2

A

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

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24
Q

HSV 1/2

A

herpesvirus family
covered by glycopreotein coat
helps virus attach to host sell

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25
Q

vesicular rash

A

dermatome eruption
localized skin region
innervated by single sensory spinal nerve
pattern may lead to misdiagnosis

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26
Q

HSV 1/2 s/s

A

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)

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27
Q

HSV 1/2 DX

A 
viral culture (PCR)
serologic testing
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28
Q

HSV 1/2 TX

A

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)

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29
Q

acyclovir, valacyclovir, famciclovir

A

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

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30
Q

herpes zoster

A

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+

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31
Q

herpes zoster pathogenesis

A

latent varicella-zoster virus reactivated
spreads
panful rash develops
usually preceded by a prodrome
onset: malaise, fever, chills, myalgia, HA, nausea

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32
Q

herpes zoster s/s

A

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

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33
Q

herpes zoster opthalmicus

A

involves opthalmic division of trigeminal nerve
may cause visual impairment
retinal necrosis
requires emergent treatment by opthalmologist
complication of shingles

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34
Q

ramsay-hunt syndrome/herpes zoster oticus

A

involves facial nerve CN7
risk of hearing loss or permanent facial weakness
emergent treatment required
complication of shingles

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35
Q

posterherpetic neuralgia PHN

A

most common complication of shingles

burning, itching pain w/ periods of lancinating pain

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36
Q

other herpes zoster complications

A

encephalitis/aseptic meningitis
bacterial superinfection of lesions
cranial or peripheral nerve palsies
pneumonitis hepatitis

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37
Q

herpes zoster TX

A

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)

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38
Q

post-herpatic neuralgia TX

A

gabapentin (analog of GABA, binds and modulates influx of calcium = decreased neurotransmitter release)
TCA ex amitriptyline/doxepin/imipramine (inhibit reuptake of serotonin/norepinephrine)

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39
Q

human papillomavirus (HPV)

A

warts in skin
occur anywhere on skin or mucous membranes
most lesions = benign
some HPV (genital) linked to dysplasia/cancer
specific to humans

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40
Q

HPV patho

A

enters skin via small openings, infects epidermal basal layer
viral replication in cell nuclei
causes structural abnormalities
triggers epidermal cell changes = wart

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41
Q

HPVs/s

A

lesion presentation varies due to selectivity of HPV
specific serotypes affect specific areas
ex: flat, papular, pedunculated

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42
Q

HPV (warts) TX

A

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

43
Q

HPV TX

A 
salicylic acid (topical kertolytic agent, chemically destroys wart)
antiproliferative topical agents (podophyllin) chemodestructive agents (trichloroacetic acid)
second line: cryotherapy
surgical intervention (electrosurgery, excision)
44
Q

atopic dermatitis

A

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)

45
Q

atopic dermatitis & immune system

A

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

46
Q

atopic dermatitis s/s

A

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

47
Q

atopic dermatits DX

A

based on s/s

pruritius distribution chronic w/ recurring flare-ups

48
Q

atopic dermatitis TX

A

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)

49
Q

cyclosporine

A

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

50
Q

cyclosporine WBC/platelet levels

A

can’t be <4000 WBC
or
<75000 platelets

51
Q

psoriasis

A 
immune-mediated disease
noninfectious
hyperproliferation of keratinocytes
decreased epidermal cell turnover rate
inflamm
thickening of dermis &amp; epidermis (shed repidly 4-7 days)
52
Q

psoriasis s/s

A 
plaques (round/oval well-demarcated)
auspitz sign (removal of scale results in pinpoint bleeding)
53
Q

psoriasis TX

A

corticosteorids (betamethasone/hydrocortisone acetate
vitamin D analogs
topical retinoids calcieurin inhibitors
phototherapy biologic agents

54
Q

hidradenitis suppurativa

A

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

55
Q

hidradenitis suppurativa TX

A 
lifestyle changes (tobacco cessation)
diet (avoid diary &amp; eat low-glycemic diet)
stage III: extensive surgery is only permanent cure
56
Q

benign neoplasms

A

noncancerous types of tissue proliferation
may be mistaken for cancer
can be premalignant

57
Q

photodermatitis

A

photosensitivity (sun poisoning)

immune response to UV rays

58
Q

solar urticaria

A

skin cells may function as photoallergens

photodermatitis

59
Q

photoallergy

A

type IV cell-mediated response to sun

60
Q

phototoxicity

A

UV light generates free radicals & inflamm mediators

61
Q

photodermatitis s/s

A

urticaria in sun-exposed skin

acute: wheezing, dizziness, fainting, erythema, pruritis, papules, vsicles, eczema, skin pain, chills, HA, fever, N
chronic: skin thickening, scarring

62
Q

actinic keratosis

A

non inflamm skin disease
skin damage from sun/tanning-device
chronic UV exposure causes keratinocyte changes

63
Q

actinic keratosis s/s

A 
thick rough crusting or scaly areas
bald head
face
ears
lips
back of hands
forearms
shoulders
neck
64
Q

actinic keratosis TX

A 
cryotherapy
chemical peal
curettage
laser
5-fluorouracil cream 
diclofenac sodium gel
imiquimod cream
65
Q

hemangioma

A

strawberry mark
congenital (10-12% of infants)
collection of blood vessels in or beneath skin

66
Q

hemangioma s/s

A

bright red, slightly raised lesions
if beneath skin will appear bluish
50% on head/neck

67
Q

hemangioma TX

A

usually disappear w/out intervention

laser: if impairs vision or breathing
corticosteroids: shrink lesion prior to laser

68
Q

nevi (moles)

A

congenital or occur later in life
usually benign
may become cancerous
sun exposure can promote malignant changes
proliferation of altered melanocytes grow in clusters

69
Q

moles s/s

A

macules
papules
small plaques varying in color/size/shape
typical: symmetric/regular borders
atypical: multicolord, asymmetric, irregular shape, may evolve to melanoma

70
Q

moles TX

A

typical: none
atypical: surgical removal

71
Q

acrochordons (skin tags)

A

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

72
Q

skin tags s/s

A

pedunculated papules
flesh colored/dark pigmentation
usually painless

73
Q

skin tag TX

A

cryotherapy

excision

74
Q

lipomas

A

family tendency
arise from mesoerm
made up of mature adipose cells in fibrous sheath
grow under skin in subQ tissue

75
Q

lipomas s/s

A

may be single or multiple

smooth, soft, doughy, rubbery, painless

76
Q

lipomas TX

A

only needed if complications or changes
liposuction
surgical excision

77
Q

skin cancer

A 
most common cancer in US
1 in 5 
increased incidence past 30 years
most common: basal cell carcinoma / squamous cell carcinoma
most dangerous: melanoma
78
Q

basal cell carcinoma

A

UV rays damage DNA in cell nucleus

arises from bottom layer (base) cells of epidermis, hair follicles, sweat glands

79
Q

basal cell carcinoma causes/RF

A

repeated/prolonged UV exposure

chronic sun exposure, fair complexion, immunosuppression

80
Q

basal cell carcinoma s/s

A

most often in sun-exposed areas

81
Q

basal cell carcinoma TX

A 
requires biopsy then removal of lesion 
immune modulator (imiquimod)
82
Q

squamous cell carcinoma

A

arises from damaged, unrepared DNA in nucleus of squamous cells of epidermis
UV radiation triggers cancerous keratinocyte transformation
risk if sun exposure/fiar complexion

83
Q

squamous cell carcinoma s/s

A

firm, smooth, hyperkeratotic papules or plque w/ ulcer in center
non-healing sore that bleeds easily
sun-exposed areas

84
Q

squamous cell carcinoma TX

A

requires biopsy/removal of lesion
topical chemo
radiation or systemic chemo if metastasis present

85
Q

melanoma

A

not fully understood
linked to genetic mutations
least common, most dangerous
melanocytes mulitply rpaidly & form cancerous tumors

86
Q

melanoma s/s

A 
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
87
Q

melanoma TX

A 
biopsy and complete excision 
lymphadenectomy if metastasis
surgery
immunotherapy
chemo
radiation
88
Q

melanoma warning signs ABCDE

A

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)

89
Q

vitiligo

A

exact cause unknown

loss of functional melanocytes in skin/hair/mucous membranes

90
Q

vitiligo s/s

A

milky-white or chalk white hypopigmented

hands arms feet trunk & face most common

91
Q

vitiligo TX

A 
will never restore all skin color
phototherapy, laser therapy, steroid therapy, topical tacrolimus ointment 
depigmentation therapy
use higher SPF
cosmetic coverups
92
Q

cafe au lait spots

A

increased melanin spots on skin
neurofibromatosis type 1 commonly associated
usually benign

93
Q

cafe au lait spots s/s

A 
flat, light/dark brown lesions
irregular or smooth borders
vary in size
present at birth
darken with age
no TX required
94
Q

solar lentigo

A

cauesd by UV light exposure

UV light induces epidemral hyperplasia > increased pigmentation

95
Q

solar lentigo s/s

A 
tan, brown, black macules
well demarcated and surrounded by normal skin
variable in size 
irregular in shape
sun-exposed areas
96
Q

solar lentigo TX

A

usually benign
biopsy may be needed to r/o precancerous or melanoma
aimed at reducing appearance

97
Q

alopecia

A

various causes
hair growth cycle shortens
affected hair follicles stop replacing lost hair

98
Q

androgen alopecia

A

androgen receptors cause excess of androgen in hair follicles

99
Q

alopecias/s

A

androgen alopecia; starts around temples & progresses to top of scalp

100
Q

alopecia TX

A

males: minoxidil/finasteride
females: oral contraceptives/spironolactone (finasteride not used in women r/t teratogenic)

101
Q

alopecia areta

A

autoimmune, strong genetic connection
inflammatory cells attack hair follicles
hair shaft weakens and breaks at or near skin surface

102
Q

alopecia areata s/s

A

well-demarcated patches of hair loss
asymmetric
may progress to alopecia totalis (scalp) or alopecia universalis (entire body)

103
Q

alopecia areata TX

A

may spontaneously recover
topical steroids (minoxidil intralesional)
corticosteroid injections
topical immunotherapy

Pathophysiology and Pharmacology 2 (27 decks)

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