Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

20 Cards in this Set

  • Front
  • Back
How do we Dx contact dermatitis? What is the gold standard?
-No clinical or lab tests
-Use clinical morphology and course of rash, with appropriate negative patch tests
-Gold standard: patch testing
What are the characteristics of acute allergic contact dermatitis? chronic?
-Acute: edematous, erythematous papules and plaques
-Chronic: scaling, lichenification, fissuring, escoriations
What medications tend to cause contact dermatitis?
Neomycin (third most common allergy in country), benzocaine, additives and preservatives
How do contact dermatitis and urticaria differ immunologically?
Contact dermititis: Type IV rxn
Urticaria: Type I rxn
How do you differentiate acute and chronic urticaria?
Acute: outbreak lasts less than 6 wks; caused by meds, foods, or infxn
Chronic: outbreak lasts more than 6 wks; cause usually unknown
How do you treat contact dermatitis? urticaria?
Contact dermatitis: topical steroids
Urticaria: antihistamine
How would you define a morbilliform drug eruption?
diffuse blanching erythematous maculopapular
What kind of immunologic reaction is a morbilliform drug rxn?
Name four drugs inducing Stevens Johnson syndrome?
Allopurinol, antibiotics (ex: penicillins, sulfa), anticonvulsants (ex: phenytoin, carbamazepine, barbiturates), NSAIDS
SJS/TEN may present initially like a morbilliform drug eruption. What are the later stages of the dz?
macule/papules become purpuric or targetoid, skin tenderness indicated necrosis;. Vesicles and bullae develop. Mucous membranes (ex: hemorrhagic crusting) may become involved indicating severe dz.
What is follicular hyperkeratosis?
Overly "sticky" skin that encourages development of keratinous debris and thus acne. Retinoic acid combats acne by desquamating this sticky skin
Which anaerobic bacteria causes follicular inflammation in acne?
Propionibacterium acnes
Describe comedones.
Comedones are mxture of keratin, sebum, and vellus hairs obstructing pilosebaceous opening.
Differentiate a closed from an open comedone.
Open: blackhead, obstruction is superficial and oxidized
Closed: whitehead, obstruction is deep and pore is not open
What are 4 side effects of accutane?
teratogenicity, cheilitis, xerosis, hyperTG
What is the clinical presentation of rosacea?
central facial erythema, telangiectasia, papules and pustules, no comedones, eye involvement (keratitis, bepharitis, conjuctivitis), rhinophyma (bulbous nose)
What Tx should be avoided in rosacea?
Potent topical steroids
What is seborrheic dermatitis?
chronic inflammation of hairy body regions (esp scalp, eyebrows, face) possibly caused by yeast Pityrosporum
Severe acne in female with hirsutism and irregular menses may suggest...?
androgen excess (polycystic ovarian syndrome, androgen secreting tumor)
Aside form supportive therapy, what other therapy might be considered in SJS?
IVIg. Also consider an ophthalmology consult for these pts.