Common Dermatoses III and IV Flashcards
Mechanism of lichen planus
Unknown antigen, but cell-mediated immunity (tons of T cells found in the skin lesion biopsies)
What is the lichenoid reaction pattern on pathology?
Huge infiltration of lymphocytes lined up at the dermal-epidermal junction
2 known possible causes of lichen planus
- Hep C (especially in oral lichen planus)
- medication
What are the 4 P’s of lichen planus?
purple, papules, polygonal, pruritic
Most common sites for lichen planus
Wrist flexors (forearm surface), ankles, legs, genitalia
Lichen planus treatment
Self-limiting, usually goes away on its own in about 15 months
-topical steroids can be used if needed
What is tinea dermatophytosis?
(a) where does the infective organism live?
(b) how is it spread?
Tinea dermatophytosis = Ring worm
(a) Hangs in the stratum cornea => only in keratinized tissue (epidermis, hair, nails)
(b) Spread thru soil, animals, or other humans
Diagnostic tool for tinea dermatophytosis
See fungi w/ KOH prep
Septated, branching hyphae => tinea dermatophytosis (fungi causing ring worm)
Spaghetti and meatball’ appearance of hyphae and spores = yeast malassezia furfur = causes tinea versicolor
Treatment for tinea dermatophytosis
(a) Response to steroids
Treat ring worm w/ topical or oral (second line) antifungals
(a) Gets worse when given steroids
How to differentiate dysplastic nevi and malignant melanoma on appearance
Often very hard! => need to do biopsy
Dysplastic nevi often don’t fit the ABCDE pattern of benign lesions. Need to do skin exams very regularly (and w/ pictures) to see which lesions require biopsy
Why are dysplastic nevi dangerous?
6x higher risk of melanoma
-pts w/ sporadic dysplastic nevi + FHx of dysplastic nevi + FHx of melanoma = risk of melanoma approaches 100% by age 75
How to manage pts w/ dysplastic nevi
Very frequent skin checks, often use total body photographs to compare and note any changes
-biopsy the moles that you can’t clinically distinguish from melanoma => get pathologic confirmation that not cancerous
What is a woods lamp?
Distinguish hypopigmentation and depigmentation
What two things do you want to ask a pt w/ psoriasis
- joint pain (psoriatic arthritis)
- counsel on CVD (psoriasis pts have increased risk for CVD)
What is dyshydrotic eczema?
Not sweating! Recurrent, bilateral, symmetrical vesicular eruptions on hands and feet
- vesicles classically on side of fingers w/ deep seeded ‘tapioca pudding’ sppearance
- really itchy
Differentiate dyshydrotic eczema from herpetic vesicles
Herpetic vesicles
- erythematous base
- very easily to pop
Dyshydrotic Eczema
- not on a red base
- are deeper rooted in the skin => don’t burst very easily
- are itchy
- associated w/ topical exposures
How to treat dyshydrotic eczema
Assess for aggravating features: stress, topical exposure to soaps, detergents, irritating chemicals
- gloves
- topical steroids
Ephelides
= Freckles!
On sun exposed areas of red and blond haired children
-keratinocytes contain more melanin, not more melanocytes
Differentiate ephelides and lentigines
(a) Mechanism
(b) Reaction to lack of sun exposure
Ephelides (freckles) and lentigines
(a) Ephelides = normal number of melanocytes with increased amount of melanin. While lentigines is a hyperplasia of the melanocytes in the epidermis
(b) Freckles go away during the winter (when not in the sun) while lentigines stay the same color regardless of sun exposure
Gender disparity in prognosis for melanoma
Males have lower survival rates at all ages
Most common location for melanomas in
(a) males
(b) females
Melanoma most common locations
(a) Males- trunk
(b) Females- legs
What causes actinic keratosis?
Chronic UVB sun exposure in elderly pts
-sun damaged skin
Why do you treat actinic keratosis?
Not just for cosmetic reasons, but also so they don’t turn in squamous cell carcinoma
