Exam 3 Material Flashcards
atopic dermatitis
chronic skin disease characterized by itchy, inflamed skin
more common in males, white, higher socioecon class, and urban areas
strong genetic link
signs and symptoms of atopic dermatitis
red to brownish-gray colored patches that look like chapping
pruritus
small, raised vesicles which may leak fluid and crust over
thickened, cracked or scaly skin
raw, sensitive skin from scratching
secondary bacterial infections are common
Adults: hands/feet
Children: face/scalp
exacerbating factors of atopic dermatitis
exposure to allergens
long, hot baths or showers (dries skin out)
dry skin
stress
sweating
rapid changes in temp or low humidity
solvents, cleaners, soaps, or detergents
wool
pathophysiology of atopic dermatitis
genetic component:
1) genes encoding for epidermal or other epithelial structural proteins
2) genes encoding for the major elements of the immune system
FLG atopic dermatitis
encodes for profilaggrin->degrades to filaggrins-terminal differentiation of epidermis and formation of the skin barrier; natural moisturizers
FLG variants/deficiency
results in permeability barrier dysfunction: penetration of high MW allergens in pollens, microbes, food, etc
have more persistent disease, higher incidence of eczema herpeticum, greater risk of multiple allergies
-not exactly a pure correlation btwn FLG deficiency and eczema
genes for cytokines (AD)
TH1-suppress IgE
TH2-increase IgE->causes blood eosinophilia, increased total serum IgE, and increased growth and development of mast cells
features of AD pathophysiology
skin barrier dysfunction
immune deviation toward TH2
subsequent increased IgE
medication classes for treating AD
corticosteroids
calcineurin inhibitors
PDE-4 inhibitors
IL-4ra antagonist
psoriasis
chronic disease with recurrent exacerbations/remissions of thickened, red, scaly plaques
keratinocyte hyperproliferation and incomplete differentiation caused by cytokines released from infiltrating activated T cells
pathophysiology of psoriasis
T cell mediated systemic inflammatory disease
interaction btwn genetics and environmental influences
comorbidities are consequence of chronic inflammation
defects in epidermal cell cycle
genetic predisposition
immunologic disorder
psoriasis defects in epidermal cell cycle
normal: 13 days to divide skin cells and 26 to mature
Psoriasis: 1.5 days to divide and 4 days to mature
T cells contribute to the hyperproliferation of the epidermis
altered maturation of the epidermis occurs
immunologic disorder psoriasis pathophysio
keratinocytes encounter an antigen or undergo trauma
inflammatory triggers results in recruitment of T cells to site
histocompatibility complex->release of T cell cytokines->vasodilation and new capillary formation
T cell cytokines also cause further inflammation
contributing factors of psoriasis
climate
stress
infections
trauma
-koebner response
medications: lithium, Beta blockers
koebner response
lesions begin at previous clear sites on skin as a result of trauma
trauma=friction, venipuncture, bites, surgery, or pressure
medication classes for treating psoriasis
corticosteroids
calcineurin inhibitors
cytotoxic agents
T cell and cytokine suppressors
monoclonal antibodies: T cell inhibitor, TNFa inhibitor, IL-12/IL-13 inhibitor, IL-23 inhibitor, IL-17A inhibitor, JAK inhibitor
retinoids
Vit D analogs
PDE-4 inhibitor
phototherapy
pathophys of acne
increased androgen production both sexes (puberty)->follicular hyperkeratinization, increased sebum production, proliferation of P. acnes
follicular hyperkeratinization
causes skin cells to stick together
sebum production
sebaceous gland size/# and sebum production increases with an androgen surge at puberty
P. acnes
produces lipase->glyceride from sebum into free fatty acids, which irritate follicular walls
have an antigenic effect
formation of acne
skin cells stick together and are NOT shed
channel is plugged by a combo of skin cells and sebum
normal flow of sebum is blocked
exacerbating factors of acne
environmental and physical factors:
-high humidity or sweating
-acne mechanica
-occupational acne
-acne cosmetica
stress/emotions
hormones
acne medica mentosa
genetics
high glycemic index diet
acne mechanica
anything the occludes the skin or irritates it
occupational acne
excessive dirt, vaporized cooking oil, exposure to some industrial chemicals