Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
14 Cards in this Set
- Front
- Back
|
What are the trichogenic agents?
What are they used for? |
Minoxidil Finasteride
Promoting hair growth |
|
|
What is the antitrichogenic agent?
What are they used for? |
Eflornithine
Preventing hair growth |
|
|
What are the two pigmentation therapies?
What are they used for? |
1. Hydroquinone/fluocinolone/tretinoin 2. Methoxsalen
Reducing skin hyperpigmentation |
|
|
How is minoxidil applied? Vasodilator or constrictor?
What is the mechanism of action?
Are systemic effects likely?
|
Same as oral antihypertensive lotion but applied topically!
Hair-regrowth
Systemic effects not likely because percutaneous absorption is poor. |
|
|
How is finasteride administered?
What is the MOA?
What obvious potential side effects? |
Oral
Blocks 5-alpha-reductase (testosterone analog) => decreased scalp and serum DHT concentrations (dihydrotestosterone)
Decreased libido, sexual dysfunction, feminization |
|
|
What drug should you worry about taking with finasteride because it has a similar mechanism and is used in benign prostatic hyperplasia? |
Saw palmetto (Serenoa repens) |
|
|
What is a topical drug used to reduce unwanted female facial hair?
What is the mechanism? |
Eflornithine
Decreased ornithin decarboxylase => decreased cell division and differentiation (trypanostatic action, used against sleeping sickness) |
|
|
In what areas of the body is eflornithin used?
Do skin adverse events occur? |
Facial and chin areas ONLY
Rarely |
|
|
Fluocinolone, hydroquinone, and tretinoin cause temporary relief of facial skin darkening by hormonal changes, pregnancy, OCs, and HRT. What is the mechanism of each?
Fluocinolone:
Hydroquinone:
Tretinoin: |
Fluocinolone = anti-inflammatory corticosteroid
Hydroquinone = Inhibitis melanin formation, blocks oxidation of tyrosine to 3,4 dihydroxyphenylalanine (DOPA)
Tretinoin = modulates skin growth and pigmentation (increased keratinocyte shedding from retinoid-treated epidermis => decreased epidermal melanin content) |
|
|
What is a side effect of the TRI treatment? |
Increased sensitivity to UV, need protection |
|
|
How is methoxsalen administered? How is it activated? What is the mechanism that leads to cell death? |
Oral and topical PIGMENTING agent
Activated by UV exposure
Conjugation and cross-linking of DNA leads to cell death => delayed erythema followed over several weeks by increased epidermal melanization and thickening of STRATUM CORNEUM |
|
|
What are some of the indications of methoxsalen? |
Vitiligo (melanocytes stimulated to move up the follicle and repopulate epidermis) Psoriaisis symptom relief Cutaneous T-cell lymphoma (mycosis fungoides) Alopecia areata Inflammatory dermatoses Eczema Lichen planus |
|
|
Chemotherapy-induced alopecia:
What does apoptotic cell death involve (increased and decrease enzymes)?
Regrowth of hair shaft occurs from stem cells located where? |
|
|
What is a problem with scalp cooling? |
PRESERVATION OF SCALP MICRO-METASTASES from vasoconstriction before giving chemotherapy => pharmacologic sanctuary |
