Miscelaneous dermal drugs Flashcards

MOA; ADE; clinical uses; alopecia after CTX; ad/disad of concurrent scalp cooling

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1
Q

What are the trichogenic agents?

A

minoxidil; finasteride

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2
Q

What are the antitrichogenic agents?

A

eflornithine

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3
Q

what are the pigmentation therapies?

A

hydroquinone/fluocinolone/tretinoin; methoxsalen

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4
Q

What are proposed MOAs for minoxidil?

A

1) may activate hair follicle directly or stimulate microcirculation; 2) alter local androgen metabolism

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5
Q

What are the common ADEs of minoxidil?

A

skin irritations (excoriations, psoriasis, sunburn) can increase systemic absorption

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6
Q

T/F Minoxidil Tx must continue for maintenance of effects

A

true

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7
Q

What are the 2 uses for finasteride?

A

low dose for hair loss; high dose for BPH Tx

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8
Q

What is the MOA of finasteride?

A

Testosterone analog that blocks 5-a reductase activity

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9
Q

What does finasteride cause?

A

decrease in scalp and serum DHT concentrations

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10
Q

What are ADEs associated with finasteride?

A

loss of libido; sexual dysfxn; feminization

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11
Q

Why should finasteride and palmetto not be used together?

A

similar MOAs

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12
Q

Who would consider taking eflornithine?

A

women wanting to get rid of facial hair

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13
Q

What is the MOA of eflornithine?

A

decreases ornithine decarboxylase to decrease cell division and differentiation

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14
Q

How can eflornithine be used against sleeping sickness?

A

produces a trypanostatic action

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15
Q

Where should eflornithine be applied only?

A

facial and chin areas only

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16
Q

What are ADEs associated with eflornithine?

A

rare and if occur then mild

17
Q

What does the combination of fluocinolone; hydroquinone and tretinoin treat?

A

temp relief of facial skin darkening by hormonal changes, pregnancy, OCs or HRT

18
Q

What is the MOA of fluocinolone?

A

anti-inflam corticosteroid

19
Q

What is the MOA of hydroquinone?

A

inhibits melanin formation by blocking melanocyte enzymatic oxidation of tyr to 3,4 DOPA

20
Q

What is the MOA of tretinoin?

A

modulates skin growth and pigmentation

21
Q

How does tretinoin use result in decreased epidermal melanin content?

A

increased keratinocyte shedding

22
Q

What is the ADE associated with the combination of fluocinolone; hydroquinone and tretinoin?

A

Increased UV sensitivity

23
Q

What is significant about the activation of methoxsalen?

A

activated by UVA exposure and is a topical pigmenting agent

24
Q

What is the MOA of methosalen?

A

conjugation and cross linking of DNA resulting in cell death

25
Q

Once activated, how does the MOA of methosalen continue to work?

A

delayed erythema followed over several weeks by increased epidermal melanization and stratum corneum thickening

26
Q

What diseases are indicated for methoxsalen tx?

A

vitiligo; psoriasis relief; cutaneous T cell lymphoma; alopecia areata; dermatoses; eczema; lichen planus

27
Q

What is the source of stem cell for hair regrowth? affected by CTX?

A

bulge => no affect from CTX

28
Q

What does apoptotic death involve?

A

decreased Bcl-2 and increased Bax and p53

29
Q

Alopecia severity is dependent on what?

A

drug, dose, intensity and route dependent

30
Q

What are the concerns for scalp cooling?

A

viability of scalp micro-metastases experiencing sub-lethal drug exposure

31
Q

What patients have persistent high drug levels after cooling process is terminated?

A

patients w/ renal or hepatic disease

32
Q

What are frequent severe causes of alopecia from CTX agents?

A

Doxorubin; daunorubicin; paclitaxel; docetaxel; cyclophosphamide; ifosfamide; etoposide