Dermatologic Pharmacology (Part 5) Flashcards
what is the initial choice for mild to moderate psoriasis?
emoliients + corticosteroids
how does topical vitamin D analogs help treat psoriasis?
the mechanism is unclear, but it reduces keratinocyte proliferation
what is a good initial choice for moderate- severe psoriasis?
UV light therapies
what are the clinical modalities of UV light therapies?
UVB radiation to point of erythema 3x per week +/- topical tar; photochemotehrapy (PUVA)
UVB radiation to treat psoriasis is thought to work via what?
immunomodulation
how does photochemotherapy (PUVA) work?
uses UVA radiation, which penetrates deeper into the skin without causing sunburn
what is the process of PUVA?
patients usually ingest the plant photosensitizer psoralen 2 hours before treatment; 3 times a week until remission
what are patients undergoing PUVA at increased risk of?
melanoma
what is the MOA of apremilast?
it inhibits phosphodiesterase 4 (PDE4) which is specific for cyclic adenosine monophosphate (cAMP)–> leads to an increased level of cAMP levels in cells
what are the effects of apremilast?
decreases nitric oxide synthase, TNF-alpha and IL-23; increases IL-10
what are the clinical applications of apremilast?
moderate to severe plaque psoriasis; active psoriatic arthritis
what are the pharmacokinetics of apremilast?
administered orally
what is the MOA of ustekinumab?
it is a human monoclonal antibody that targets proinflammatory cytokines IL-12 and IL-23
what are the effects of ustekinumab?
it blunts IL-12 and IL-23 so: there is a decrease in NK cell activation, a decrease in CD4 T cell differentiation and activation, a decrease in MCP-1, TNF-alpha, CXCL-10, IL-8 expression
what are the clinical applications of ustekinumab?
plaque psoriasis, psoriatic arthritis, crohn disease
what is the MOA of secukinumab?
it is a human monoclonal antibody that target proinflammatory cytokine IL-17A
what are the effects of secukinumab?
it blunts IL-17A effects thereby decreasing its ability to induce the production of many other proinflammatory signaling molecules
what are the clinical applications of secukinumab?
ankylosing spondylitis, plaque psoriasis, psoriatic arthritis
what is actinic keratosis?
cutaneous neoplasms that develop on sun-damaged skin, thought to be on a continuum with cutaneous squamous cell carcinoma
what are 6 treatment options for actinic keratosis?
liquid nitrogen cryotherapy; surgical therapy; pharmacotherapy; red light therapy; dermabrasion; and chemical peels
what are the 3 pharmacotherapy options for actinic keratosis we talked about?
topical 5-fluorouracil, Imiquimod, and ingenol mebutate
what is the MOA of imiquimod?
stimulates local cytokine induction leading to an inflammatory cell infiltration
what is the MOA of ingenol mebutate?
- chemoablation (cell necrosis) 2. neutrophil-mediated antibody dependent cellular cytotoxicity
what is the MOA of topical 5 flurouracil?
it inhibits thymidylate synthase, which is a critical enzyme in the synthesis of DNA; a lack of DNA synthesis in the fast-growing dysplastic cell prevents cell proliferation and causes cell death
what are the effects of topical 5 flurouracil?
causes inflammation and destruction of the lesions; after 4-6 weeks skin will have progressed from erythema through blistering, necrosis with erosion, and then re-epithelialization
for advanced basal cell carcinoma, what is the treatment option?
vismodegib
how do vismodegib work?
both are oral “hedgehog” signaling pathway inhibitors
what is the surgical treatment of melanoma?
surgical excision with 1-2 cm margins often combined with sentinel node biopsy
what is the conventional chemotherapy for melanoma?
dacarbazine
what is vemurafenib?
it is a MAP kinase pathway inhibitor leading to apoptosis
what are 2 treatment options for male pattern baldness?
minoxidil and finasteride
how does minoxidil work?
it vasodilates due to K+ channel opening; promotes hair growth by increasing the duration of anagen, shortening telogen, and enlarging miniaturized follicles
how does finasteride work?
it is an oral inhibitor of DHT production; increases hair count
what is the second line of treatment for female pattern baldness?
anti-androgens
what are the 3 different anti-androgens used for female pattern baldness?
spironolactone, finasteride, and flutamide
how does spironolactone work?
it is an androgen partial agonist
how does flutamide work?
it is an androgen antagonist
what is alopecia areata?
it is a chronic relapsing immune-mediated inflammatory disorder affecting hair follicles resulting in non-scarring hair loss
how does alopecia areata present?
ranges from small patches of alopecia on any hair-bearing area to the complete loss of scalp, eyebrow, eyelash, and body hair
what are two treatment options for alopecia areata?
intralesional or topical corticosteroids; topical immunotherapy
what is an example of a topical immunotherapy option?
DPCP (it causes contact dermatitis, which causes hair growth for an unknown reason)
