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82 Cards in this Set

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  • Back
In allergic contact dermatitis the allergen binds w/a protein to form what?
An antigenic molecule
In allergic contact dermatitis when does
Sensitization &
Manifestions occur?
First exposure &

Reexposure to the allergen.
In allergic contact dermatitis, what initiates an inflammatory response?
Activation of the antigenic complex in the cutaneous tissue.
In allergic contact dermatitis what does the inflammatory response lead to?
Swelling & vesicle formation.
In Irritant contact dermatitis what allows the allergen to be absorbed into the skin?
Damage to the stratum corneum.
Are the manisfestations of allergic contact dermatitis the same as those for Irritant contact dermatitis?
What causes stasis dermatitis?
Impaired venous circulation.
What does stasis dermatitis look like?
Erythema & scaling of the lower extremities.
What is stasis dermatitis secondary to?
What population is stasis dermatitis usually seen in?
Older women
What are early signs of stasis dermatitis?
Dusky-red deposits of hemosiderin in the skin, w/itching & dimpling of subcutaneous tissue.
What are late signs of stasis dermatitis?
Edema, redness & scaling of large area of legs. Possible fissures crusts, & ulcers.
What is hemosiderin?
An iron-containing pigment derived from hemoglobin from disintegration of red blood cells. It is one form in which iron is stored until it is needed for making hemoglobin.
What is seborrheic dermatitis?
A chronic inflammatory, scaling eruption; lesion occurs chiefly on the scalp, face, upper trunk & skin folds.
What is seborrheic dermatitis characterized by?
Periodic remissions & exerbations.
What is seborrheic dermatitis of the scalp called?
In infants cradle cap.

In adults dandruff.
seborrheic dermatitis etiology;
Associated w/a genetic predisposition that is exacerbated by px or emotional stress.
What population is seborrheic dermatitis more common in?
Middle aged or older adults.
Describe plaque type psoriasis;
(most common type)
Clearly demarcated lesions most common on the elbows, knees & scalp.
Describe guttae psoriasis;
Tear drop shaped, pink to salmon, scaly lesions usually limitied to upper trunk & extremities.
Guttae psoriasis Patho & Manifestations;
Common in children & young adults, brought on by UR strep infection, responds to UVB phototherapy, recurrence is is common w/UR strep infection.
Pustular psoriasis Pathophysiology & Manfiestations;
Characterized by papules or plaques studded w/pustules.
More general involvement w/systemic sx (Malise,fatigue, fever, aneorexia)
Erythorodermic psoriasis Pathophysiology & Manfiestations;
Rare form, involves all body surfaces, lesions scale→confluent→bright red body surface, severe itching & pain, severe complications related to loss of body fluids, proteins, & electrolytes & temp regulation disturbances, results in death w/out tx.
What is Lichen Planus?
Chronic Papulosquamous disorder of the skin & mucus membranes.
Lichen Planus etiology;
Cause unknown, exacerbation is associated w/certain drugs & chemicals, has been associated w/hep C, abnormal immune mechanisms w/altered T-cells may be causitive factor, affects adults most often.
Lichen Planus Pathophysiology & Manfiestations;
A inflammatory process w/in the dermis is initiated, Lymphocytic infiltration & hyperkeratosis occur→vacuolation & cell degeneration, Lesions are prurtic papules w/a reddish, purple coloration, Whitish grey lines (Wickham's striae) may be present, Larger scaly plaques may eventually develop.
Lichen Planus Tx;
Usually is self-limiting, d/c all meds & follow tx w/topical corticosteroids & occlusive dressings. Antipruritic agents, systemic corticosteroids, cyclosporine, tacrolimus & other immunosuppressive agents.
What is Acne?
Inflammatory dz of the (sebaceous glands) pilosebaceous unit. Is characterized by papules, comedones, & pustules. Lesions are both inflammatory & noninflammatory.
In Acne what do noninflammatory lesions consist of?
Whiteheads (closed comedones) & Black heads (open comedones).
In Acne what do inflammatory lesions consist of?
Papules, pustules, nodules & in severe cases cysts.
What are the different pathologic types of Acne?
Acne vulgaris
Acne conglobata
Acne rosacea
Manfiestations of Acne Vulgaris?
Common in adolescents, lesions may consist of white heads & blackheads or inflammatory lesions.
Pathophysiolgic Processes & Manfiestations of Acne Conglobata?
Chronic form occurring in older adults characterized by comedones, papules, pustules, nodules, abscesses, & cysts resulting in scarring.
Manfiestations of Acne Rosacea?
Chronic form occurring in older adults & resulting in reddening of the nose & cheeks (nose can also develop hyperplasia)
Pathophysiology of Acne Rosacea?
Believed to be an inflammatory process, is often accompainied by GI symptoms; H.pylori has been implicated. Ocular problems occur in 50% of cases.
Causes of Acne Vulgaris?
(Multifactorial)Predisposing factors; Heredity, Androgen (sx more dramatic in males) stimulation, Certain drugs, Exposure to heavy oils, greases, tars, cosmetics. Trauma, Emotional stress etc.
Pathophysiologic Processes of Acne Vulgaris;
Adrogen stimulates sebaceous gland growth, sebum production, & shedding of the epithelial cells that line sebaceous follicles, these follicles dialte, & sebum & keratin from the epithelial cell form a plug that seals the follicle, creating a favorable environment for bacterial growth.
What are the bacteria of Acne Vulgaris?
Propionibacterium acne or staph. epidermis, are normal skin flora that secrete lipase, which interacts w/sebum to produce free fatty acids, which provoke inflammation & formation of comedones that may rupture, if d/c to the dermis occurs, a papular nodule or cyst may develop.(permanent scarring results eventually)
What is Lupus Erythematosis?
Chronic inflammatory disorder of the connective tissues.
What two forms does Lupus Erythematosis appear in?
Discoid(DLE)-affects only the skin.
Systemic(SLE)-affects multi-organ system as wells as the skin, & can be fatal.
SLE description;
Characterized by recurring remissions & exacerbations. 8 X more common in women as men & 15 X as often during childbearing age.
SLE etiology;
Direct cause unknown, Genetic predisposition, family hx of other autoimmune disorders, environmental & hormonal factors.
SLE Pathophysiology;
Autoimmune, formation of antibodies aganist body's own nucleic acids, phospholipids, WBC, RBC & coagulation components. Antigen-antibody complexes against host DNA form & deposit in a variety of tissues→diffuse damage, Neutrophills attempt to phagocytize the antigen-antibody complexes but are ineffective, Lysosomal enzymes are released, further promoting tissue damage.
DLE etiology;
More common in women 30-40yrs, abnormal immune reaction, 1 or more lesions appear on areas of the body or face exposed to light, usually a typical butterfly pattern develops over the nose & cheeks.
DLE Pathophysiology;
Leasion is a red plaque w/brown scale involving hair follicles, it heals & leaves scars & hypopigmentation, alopecia is common w/scalp lesions, telanglectasia occurs on the palm & fingers, Raynaud's phenomenon may be associated w/DLE.
What is Raynaud's phenomenon?
Intermittent attacks of pallor or cyanosis of the small arteries and arterioles of the fingers as the result of inadequate arterial blood flow.
What is Bullous Pemphigold?
(A Vestibullous skin disorder) A chronic blister-forming dz of the skin & oral muccous membranes. Auto immune caused by circulation of IgG autoantibodies directed against keratinocytes.
Name the forms of Bullous Pemphigold?
Pemphigus Vulgaris-most common
Pemphigus foliaceus-less common.
Pemphigus erythematosus-Severity of dz varies amoung individuals.
Bullous Pemphigold Pathophysiology;
Autoantibodies disrupt the cohesion between the epidermal cells→blister formation. Initially the lesions are either licalized erythema or pruritic plaques that ixtend & become edematous. The plaque then turns reddish purple in 2-3 wks. Vesicle & bulla appear on the surface. The blisters rupture w/in a week, followed by rapid healing.
Pemphigus Vulgaris Pathophysiology;
The epidermis separates above the basal layer, blisters form initially in the oral mucosa or scalp then spread over the face & trunk in the ensuing months (+ Nikolsky sign)The vesicles become large & tend to rupture, leaving large denuded areas of skin covered w/crusts, complicated by 2ndary infection.
What is Nikolsky Sign?
Pressure on a blister causes it to spread.
Pemphigus Foliaceus & Pemphigus Erythematosus Pathophysiology;
(More benign)Local development of erythema w/crusting, scaling & bullae, serum bound IgG present, blistering of subepidermal skin layer w/crusting & potential for spread, oral lesions usually absent.
What is Erythema Multiforme?
Acute eruption of macules, papules or subdermal vesicles, presentin a multiform appearance. Origin may bellergic, seasonal, drug sensitivity, or associated w/microorganisms, is relatively rare, most common 20-40yrs.
Erythema Multiforme Pathophysiology;
Formation of immune complex & deposition of C3, IgM & fibrinogen around the superficial dermal blood vessels, basement membrane & keratinocytes, edema develops in the superficial dermis→vesicles & bullae, healing occurs w/in 3-4wks, EM is a component of, & may develop into the life threatening Stevens-Johnson Syndrome.
What is the characteristic lesion of Erythema Multiforme?
"Bull's eye" or "target" lesions on the skin surface w/a central dusky region surrounded by concentric rings or alternating edema & inflammation. Lesions usually occur in groups but there may also be single or multiple ones followed by pruritus & burning.
What is Stevens-Johnson Syndrome?
Widespread erythema multiforme w/oral, genital & conjunctival involvement, & widespread skin lesions, dz is common in pts w/mycoplasma pneumoniae infection.
Name another common form of EM;
TEN, toxic epidermal necrolysis.
Stevens-Johnson Syndrome etiology;
Most common in children & young adults, Numerous erythematous bullous lesions appear on skin & mucous membranes, cause is unknown,(may be autoimmune).
Stevens-Johnson Syndrome S/Sx;
Lesions form erosions & crusts when they rupture. Mouth, air passages, esophagus, urethra & conjunctiva may be involved.
What is Folliculitis?
A bacterial infection of a hair follicle that causes a pustule to form. It can be superficial or deep.
What is a furuncle?
(Another form of follicultiis)
AKA Boils, they are inflammations of hair follicles. They may develop p folliculitis that spreads through the follicular wall into the surrounding dermis.
What is a Carbuncle?
A group of interconnected furuncles.
Folliculitis Incidence & Prognosis;
Difficult to determine incidence of folliculitis in the general population, because most go untxd. W/appropriate tx prognosis is good.
Carbuncle Prognosis;
Prognosis depends on the severity of the infection, pt's px condition & ability to resist infection.
What are the causes of Folliculitis, Furuncle & Carbuncles?
Coagulase +staph aureus (Coagulase by product of staph a protein converts adrogen to fibrogen & makes a mesh) Other causes are; Klebsiella, Enterobacter or Proteus organisms.
What is the cause of Hot Tub Folliculitis?
Pseudomonas aeruginosa
What are the risk factors for folliculitis, furuncles & carbuncles?
Infected wound, poor personal hygiene, debilitation, tight clothes, friction, immunosuppressive therapy, exposure to certain solvents.
What is the general pathophysiology & manifestations of folliculitis, furuncles & carbuncles?
The infecting organism enters the body, usually through a break in the skin→inflammatory reaction w/in the hair follicle (infections have different S/Sx)
Folliculitis pathophysiology & manifestations;
Shows as pustules on the scalp, arms, & legs in children & adults on the trunk, buttocks & legs.
Furuncles pathophysiology & manifestations;
Hard, painful nodules, commonly on the neck, face, axillae & buttocks. Nodules enlarge for several days, rupture, discharging paus & necrotic material, following rupture, pain subsides, but erythema & edema persist for days or weeks.
Carbuncles pathophysiology & manifestations;
Extremely painful, deep abscesses draining through multiple openings onto the skin surface, usually around several hair follicles, fever & malaise follow.
What are the complications of carbuncles?
Scarring, bacteremia (bacteria in the blood), metastatic seeding of a cardiac valve defect, or arthritic joint.
How do you dx folliculitis, furuncles & carbuncles?
Pt hx showing preexisting Furuncles or Carbuncles, PE showing skin lesion, wound cultures, leukocytosis.
General tx of folliculitis, furuncles & carbuncles?
Cleaning the affected area w/antibacterial soap & H2O, Warm, wet compersses, topical ABX.
What is the specific tx of Folliculitis w/extensive infection?
Systemic ABX such as cephalosporin or dicloxacillin.
What is the specific tx of Furuncles;
I&D after warm wed compress, systemic ABX.
What is the specific tx of Carbuncles?
I&D & Systemic ABX.
What is cellulitis?
Acute spreading infection of the dermis or SubQ layers of the skin. It may follow damage to the skin (bite or wound) (cellulitis of lower extremity is more likely to develop into thrombophlebitis in a elderly pt)
Wha are the causes of cellulitis?
Bacterial infections, group A strep or staph aureus (uncommonly fungal infections)
Pathophysiology of cellulitis;
Organism invades the compromised area, overwhelms the normal defensive cells that normally contain & localize inflammation, cellular debris accumulates, as dz progresses the organisim invades tissue around the intial wound site.
What are the clinical manifestations of cellulitis?
Erythema & edema (classic signs) Pain at site, & possible surrounding area, fever & warmth.
Cellulitis Diagnostic tests;
WBC, ESR, gram stain & culture from fulid or abscess & bullae, culture of primary lesion by biopsy or aspiration, "Touch" prep-(KOH)