Exam #5- Integumentary Flashcards
aging changes of the skin
skin becomes thinner, drier, wrinkled, changes in pigmentation
of capillary loops shorten and decreases
less melanocytes and langerhans cells
sebaceous, eccrine, and apocrine glands atrophy
temp regulation is not as good
pressure/touch receptors decrease in number and decrease sensory perception
decreased protective functions
infections increase
delayed wound healing
neural innervation of the skin is the function of what?
the SYMPATHETIC nervous system by way of the ALPHA ADRENERGIC RECEPTORS
wheal
primary lesion
elevated, weird shaped area of cutaneous edema
solid and transient
diameter is varied
may last for a few hours
nodule
primary lesion
elevated, firm, circumscribed lesion
deeper than papule
tumor
primary lesion
elevated, solid lesion
deeper in dermis
vesicle
primary lesion
elevated, circumscribed, superficial lesion
does not extend into dermis
filled with SEROUS fluid (free fluid)
bulla
primary lesion
vesicle that measures >1cm
pustule
primary lesion
elevated, superficial lesion
like a vesicle but filled with PURULENT fluid (pus)
inflammatory cells
cyst
primary lesion
elevated, circumscribed, encapsulated lesion
is in dermis/subcutaneous layer
filled with liquid or semisolid
telangiectasia
primary lesion
irregular red lines
produced by capillary dilation
scale
secondary lesion
heaped up, keratinized cells
flaky skin and weird shape, can be thick or thin
dry or oily
lichenification
secondary lesion
rough, thickened epidermis caused by rubbing, itching, or irritation
keloid
secondary lesion
weird shaped, elevated progressively enlarging scar
grows beyond wound
caused by too much collagen formed during healing
scar
secondary lesion
think to thick fibrous tissue
replaces normal skin after injury/lacaration
excoriation
secondary lesion
loss of epidermis
linear, hollowed out, crusted area
fissure
secondary lesion
linear crack/break from epidermis to dermis
may be moist/dry
think of cracked feet
erosion
secondary lesion
loss of part of epidermis
depressed, moist, glistening
happens after rupture of vesicle or bulla
ulcer
secondary lesion
loss of epidermis/dermis
concave
atrophy
secondary lesion
thinning of skin surface
loss of skin markings
macule
circular flat discoloration <1cm
brown, blue, red or hypopigmented
patch
circumscribed flat discoloration >1cm
plaque
superficial elevated solid flat topped lesion >1cm
crust
dried serum or exudate on skin
pathophysiology of pressure ulcers
due to unrelieved pressure on skin (shearing forces, friction, moisture)
capillary blood flow occlusion
underlying tissue damage (like ischemia or necrosis)
decubitus ulcer
d/t lying/sitting in same position for too long on a bony prominence
stage 1 pressure ulcer
non-blanchable erythema of intact skin
intact skin with non blanchable redness of a localized area, usually over a bony prominence
the area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue
may be difficult to detect in individuals with dark skin tones
stage II pressure ulcer
partial-thickness skin loss
involves epidermis or dermis
presents as a shallow open ulcer with a red pink wound bed, without slough
may also present as an intact or open/ruptured serum-filled or serosanginous filled blister
stage III pressure ulcer
full-thickness skin loss
involves damage/loss of SUBQ TISSUE
subcutaneous fat may be visible but bone, tendon or muscle are not exposed.
slough may be present but does not obscure the depth of tissue loss
stage IV pressure ulcer
full thickness skin loss with damage to MUSCLE, BONE, or SUPPORTING STRUCTURES
slough or eschar may be present
often includes undermining and tunneling
category/stage IV ulcers can extend into muscle and/or supporting structures (fascia, tendon or joint capsule)
what is the outermost layer of the skin?
epidermis
pruritus
itching
most common s/s of primary skin disorders
itch
specific unmyelinated C nerve fibers
regulated by CNS
neuropathic pruritus
related to pathologic condition
psychogenic pruritus
psych problem
s/s of dermatitis eczema
pruritus, lesions w/indistinct borders, epidermal changes
chronic eczema- thickened, leathery, hyperpigmented skin from recurrent irritation/scratching
allergic contact dermatitis
t cell mediated or delayed hypersensitivity (TYPE IV)
allergen comes in contact with skin, binds to carrier protein
sensitizing antigen is formed
LANGERHAN CELLS process antigen
carry it to T cells
sensitization
which cells of the skin are important in immunity?
langerhan cells
a skin disorder that is the result of a type IV hypersensitivity reaction is known as what?
allergic contact dermatitis
irritant contact dermatitis
non immunologic inflammation
due to chemical irritation from acids/prolonged exposure to irritants
atopic dermatitis
d/t family history of allergies, hay fever, IgE
stasis dermatitis
happens in legs d/t venous stasis, edema, vascular trauma
seborrheic dermatitis
chronic skin inflammation that involves scalp, eyebrows, eyelids, nasolabial folds, axillae, chest, and back (cradle cap in babies)
greasy, scaly, white, or yellowish plaques
a skin lesion that is elevated, firm, rough, and has a flat top
plaque
psoriasis
chronic, relapsing, proliferative skin disorders
pathophysiology of psoriasis
t cell AUTOIMMUNE mediated skin disease
s/s of psoriasis
scaly, thick, silvery, elevated lesion, usually on scalp, elbows, or knees
pityriasis rosea
benign, self limiting inflammatory disorder
pathophysiology of pityriasis rosea
d/t a VIRUS
s/s of pityriasis rosea
herald patch- CIRCULAR, demarcated, salmon-pink
systemic complications of psoriasis
arthritis and heart disease
an autoimmune skin disorder that results in scaly, silvery lesions with evidence of dermal and epidermal thickening
psoriasis
pathophysiology of lichen planus
AUTO-INFLAMMATORY disorder of SKIN and MUCUS membranes
origin is unknown, but it involves t tubules, adhesion molecules, inflammatory cytokines, and antigen presenting cells
s/s of lichen planus
lesions are non-scaling popular VIOLET-colored with itching on wrists, ankles, lower legs, and genitals
a benign t cell mediated auto-inflammatory skin disorder that results in violet colored lesions is what?
lichen planus
acne vulgaris
inflammatory disease of pilosebaceous follicles
hypertrophy of sebaceous glands and telengiectasia
common during ADOLESCENCE
acne rosacea
skin inflammation of MIDDLE AGED ADULTS
lesions are erythematolangiectatic, papulopustular, phymateous, and ocular
related to chronic, inappropriate vasodilation
flushing and sun sensitivity
lupus erythematosus
inflammatory, autoimmune, systemic disease with cutaneous s/s
types: skin (discoid) and systemic (SLE)
discoid (cutaneous) lupus erythematosus
acute, subacute, chronic
restricted to skin
pathophysiology of discoid lupus
altered immune response with new T and B cells formed, decreased number of regulatory T cells, and increased pro inflammatory cytokines
tissue damage d/t autoantibodies and immune complexes
s/s of discoid lupus
photosensitivity, butterfly pattern, can lead to SLE
pathophysiology of erythema multiforme
immune complexes formed and deposited around dermal blood vessels, basement membranes, and keratinocytes
affects mouth, air passages, esophagus, urethra, and conjunctivae
s/s of erythema mutliforme
“bulls eye” or target lesion, erosions/crusts form when lesions rupture
steven johnson syndrome
cause is unknown but involves an immune mechanisms r/t drug administration
severe blistering
pathophysiology of pemphigus
AUTOIMMUNE, chronic, blister forming disease of skin and oral mucous membranes
caused by circulating IgG AUTOANTIBODIES that work against surface adhesion molecules in the epidermis
s/s of pemphigus
blisters can be deep or superficial to the epidermis
folliculitis
bacterial
infection of hair follicles from a staph infection
furuncles
bacterial
boils (inflammation of hair follicles) that develop from folliculitis from staph infection
carbuncles
bacterial
collection of infected hair follicles
painful, swollen, and red with systemic s/s
cellulitis
bacterial
infection of dermis and SQ tissue from staph or group B strep infection
necrotizing fasciitis
bacterial
inflammation that spreads quickly to fascia, muscles, and SQ fat to skin
erysipelas
bacterial
superficial form of cellulitis
impetigo
bacterial
superficial lesion from staph
HSV-1
virus
cold sores
HSV-2
virus
genital
herpes zoster (shingles)
virus
caused by varicella zoster virus
varicella chickenpox
virus
wart
virus
benign lesions caused by HPA
a child presents with lesions superficially on the skin. the provider knows that this disorder is caused by staph
impetigo
tinea
caused by dermatophytes tinea capitis, tinea pedis, tinea corporis, tinea cruris, tinea unguium
candidiasis
caused by candida albicans found on skin, GI, vagina
s/s of candidiasis
thin walled pustule that produces a whitish yellow curd-like substance
pathophysiology or urticaria (hives)
type I hypersensitivity reaction
histamine release
endothelial cells of skin to contract fluid leaks from vessels
s/s of urticaria
itchy area of raised erythema with central pallow
wheals
welts
urticaria is the result of which type of hypersensitivity reaction?
type I
pathophysiology of scleroderma
SCLEROSIS (hardening) of skin
muscles, bones, and internal organs
T HELPER CELLS and their CYTOKINES: fibroblast proliferation and fibrosis due to multiple autoantibodies
s/s of scleroderma
skin is hard, hypopigmented, taut, shiny, and tightly connected to underlying tissue
pathophysiology of ticks
ticks embed their heads into pts skin so they can get blood
they gorge on blood and get huge
they they release their toxins/transmit microorganisms
pathophysiology of lyme disease
tick that spreads infection borrelia burgdorferi
stages of lyme disease
localized
disseminated infection
late persistent infection
localized lyme disease
3-32 days with erythema migrans with or without fever, fatigue, malaise, myalgia, arthralgia
dissmeninated infection of lyme disease
secondary erythema migrans, arthralgia, meningitis, neuritis, carditis
late persistent infection of lyme disease
years after
arthritis, encephalopathy, polyneuropathy, HF
seborrheic keratosis
benign
proliferation of cutaneous basal cells that produce smooth/warty elevated lesions
keratoaconthoma
benign
tumor of squamous cell that comes from hair follicles
actinic keratosis
benign
premalignant lesion made of aberrant proliferations of epidermal keratinocytes caused by too much UV light
nevi (moles)
benign
pigmented or not
lesions that form from melanocytes
can transition to malignant melanomas
basal cell CA
malignant
surface epithelial tumor
mutation of TP53 and PTCH1 genes
most common type of skin cancer
shiny “pearly” papule or nodule
grows slowly
usually occurs on sun-exposed areas
umbilicated center and telangiectasias
squamous cell cancer
malignant
tumor of epidermis: in situ or invasive
mutation of TP53 gene
more common in immunocompressed or transplant patients
hyperketatotic lesion with crusting and ulceration
can be more aggressive than basal cell cancer
usually occurs on sun-exposed areas
malignant melanoma
malignant
tumor of skin that comes from melanocytes
kaposi sarcoma
malignant
vascular malignancy
due to herpes virus
common in immunosuppressred pts (post transplant, AIDS)
a patient presents with a skin lesion with crusting and ulceration that is invading the epidermis. the provider would suspect which type of skin cancer?
squamous cell carcinoma
ABCDE rule
asymmetry
border irregularity
color variation
diameter >6mm
elevation that includes raised appearance/rapid enlargement
ABCD sign of melanoma
asymmetry- when half of the mole does not match the other half
border- when the border (edges) of the mole are ragged or irregular
color- when the color of the mole varies throughout
diameter- if the mole’s diameter is larger than a pencil’s eraser
cold injuries basics
injury from extreme cold that affects fingers, toes, ears, nose, cheeks
alternating cycles of vasoconstriction/vasodilation leads to burning reaction
s/s of cold injury
white/yellowish, waxy, firm to touch
partial thickness burn
ONLY epidermis
local pain with erythema
no blisters until 24 hours after injury
superficial partial thickness burn
thin walled, fluid filled blisters form minutes after injury
painful!
deep partial thickness burn
ENTIRE dermis
spares skin appendages like hair follicles and sweat glands
waxy, white skin
can distinguish after 7-10 days between deep partial and full when hair or skin buds reappear
full thickness burn
entire epidermis, dermis, and underlying SQ are destroyed
PAINLESS due to destroyed nerve endings
burn color is white, cherry red, or black
wound is dry or leathery
which type of burn is associated with injury to the epidermis and all skin barrier are intact?
partial thickness injury
burn shock
in immediate (acute) phase is d/t hypovolemia, heart issues, cellular issues
capillary seal
end of burn shock
ebb phase of burn shock
heart contractility is decreased during 1st 24 hours because blood is shunting away from liver, kidney, and gut
