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36 Cards in this Set

  • Front
  • Back

What is the rate limiting step of topical drugs?

partition coefficient = absorption through the stratum corneum

(higher = faster absorption, better)

(palm/sole thickness > body > scrotum > face)

(absorption is faster w/ thinner skin, hydration, ointment, heat, & coverage)

What causes acne?

1. Hyperkeratinization--> Inc loose cells, clogs follicles, caused by Incr Androgens

2. Increased Sebum production, caused by Incr Androgens--> substrate for bacteria enzymes, clogs follicles

3. Propionibacterium acnes, use lipase to form FFA (free fatty acids) from sebum

4. Inflammation, response to FFA irritation

Hyperkeratinization, inc sebum & P. acnes form microcomedos (acne precursor), then mechanical insult causes comedo to close & inflammation leads to........

inflammation causes comedo to progress to papules, pustules, nodules, cysts (acne) w/ potential to scar

Mild acne, localized to face is not likely to scar & should be tx w a ____________

While ___________ is preferred for severe acne on back, chest, arms, that is more likely to scar

topical medication for mild

oral medication for severe, may use topical additionally

_________ is used for mild acne or in combos w/ erythromycin or clindomycin for more severe acne


+Keratolytic- solubilizes intracellular connections btwn keratinocytes, reducing hyperkeratinization

+Comedolytic- prevents closure, reduces comedones

+Bactericidal- kills P. acnes via radical formation

Benzoyl Peroxide

*lipophillic, good penetration

What are the SEs of Benzoyl peroxide?

Irritation, dryness, peeling & erythema

Bleaching of hair/ clothes

Contact dermatitis (rare)

__________ is used for mild acne or psoriasis


+keratolytic (solubilizes intracellular cement, reduces hyperkeratinization)

What are the SE's?

Salicylic Acid


salicylism (rare, life threatening)

________ is used for mild/ moderate acne & acne rosacea, hyperpigmentation



Antimicrobial- Inhibitor of thioredoxin reductase & tyrosinase, inhibits DNA synthesis

Antiinflammatory- scavenger of free radicals

Azelaic Acid (azelex)

What are the SEs of Azelaic Acid?

irritation, itching

hypopigmentation (tyrosinase inhibition interferes w/ melanocyte)

First line acne therapy-


Retinoids (Vit A analogs)


retinoic acid (RA) binds endogenous Retinoic acid (RARs) & retinoic X (RXRs) nuclear receptors-->

RA-RAR complex forms transcription factor-->

regulate gene transcription & translation-->

altered cellular function of translated proteins-->

Regulate epithelial cell proliferation (hyperkeratinization)

Bone growth

Immune function

Reproductive function

1st & 2nd generation retinoids have more flexible structures, allowing them to _________

What does this cause?

allows binding to several retinoid receptors

*causes worse SE's than 3rd generation retinoids (arotinoids)

________, is a topical 1st gen topical retinoid, trans-retinoic acid, used for acne & as an anti-wrinkle cream

MOA: (binds RAR)

+Keratolysis- by incr mitosis (cell turnover)--> decr cell adhesion--> exfoliation & desquamation

+Anti-comedolytic- prevents formation of new microcomedones

Tretinoin (Retin A)

What are the SEs of Tretinoin?

Irritation, erythema, peeling dryness

Initial appearance of worsening acne (top layer sloughed & reveals comedones below)

De-activated by UV light & Benzoyl peroxide

(use at night & DONT use w/ Benzoyl peroxide)

*Antiwrinkle effects (vasodilation & inc collagen)

_________ is a 3rd gen topical retinoid, used for acne

MOA: same as Tretinon (binds RAR)



How does this drug differ from Tretinon?

Adapalene (Differin)

* NOT degraded by UV or benzoyl peroxide

*similar SE's, but less severe

_______ is a 3rd gen topical, UV-stable retinoid, used for acne & psoriasis

MOA: Pro-drug, converted to tazarotenic acid (by esterase, when rubbed on skin)--> binds RAR-->

+Keratolysis- normalizes keratinocyte growth


What are the SEs?

Tazarotene (tazorac, avage)


Similar SEs to Tretinoin (use every other day to reduce skin irritation)

Teratogen category X

_______ is a 3rd gen, ORAL, cis-retinoic acid, MOST EFFECTIVE acne tx

*short term use--> permanent effects

MOA: (binds RAR)

+keratolysis- normalizes follicular epithelium

+Decreases Sebum production



(targets all 4 causes of acne!)

Isoretinoin (generic for accutane)

Despite being the most effective tx, Isoretinoin may not be used d/t neg SEs. What are they?

(Accutane no longer on market d/t these)

Dry, peeling, itchy skin

Dry eyes


Alopecia (reversible)

Inflammatory Bowel disease

Joint pain

Lipid profile changes

Depression/ Suicidal ideations (DO NOT used in pts predisposed to depression!)

Teratogen category X

Pts taking Isotretinoin must agree to do the following before starting;

Use 2 forms of birth control (severe teratogenesis)

Take pregnancy test

Not donate blood (for at least 1 month following discontinuation)

Not take Vitamin A supplements (toxicity)

________ is a macrolide Abx, used in BOTH Topical & Oral acne tx, alone or in combo w/ benzoyl peroxide



binds 50s ribosomal subunit-->

inhibits translocation-->

inhibits translation of mRNA to protein

What are the SEs?


SE: (w/ oral use*)

(CYT P450) Liver enzyme inhibitor--> Incr concentration of theophylline, caffeine, coumadin, digoxin, warfarin, corticosteroid (toxicity)

_______ abx, used in BOTH topical & oral acne tx, alone or in combo w/ Benzoyl peroxide



binds 50s-->

inhibits protein synthesis

What SEs does it cause?


SE: (w/ oral use)

pseudomembrane Colitis

______ abx, used in BOTH topical & oral acne tx



binds 30s-->

inhibits translation of mRNA into protein

What SEs does it cause?


SE: (oral)

alters normal intestinal flora


Binds Ca2+ (tooth & bone effects)--> absorption/ efficacy is decreased w/ Antacid use-->* Avoid dairy, antacids iron**

_______tetracyline class abx, use in oral acne tx only



same as tetracycline (binds 30s)

How does this differ from tetracycline?


Oral use only & Increased incidence of SE's

_____ tetracycline class Abx, use in oral acne tx only, expensive**



same as tetracycline


less incidence of SEs than tetracycline

Ototoxicity* (vestibular effects)


________ is the only hormone therapy approved for acne tx in FEMALE pts


Inc SHBG-->

Decreased free Androgen (testosterone)-->

+Keratolytic (decr hyperkeratinization)

+Decreased Sebum

What are the SEs?


(ethinyl estradiol & noregestimate)


Inc risk of CVD (MI, stroke, etc) in smokers >35

Inc risk of clotting (dose related)

Inc risk of breast cancer

*takes a few months to see effects & acne relapse w/ discontinuation

What cause Plaque formation in psoriasis?

APC presents Ag to T cell in LN-->

clonal expansion-->

activated TH1 cell travels to dermis-->

encounters new APC-->

reactivation & further clonal expansion-->

cytokine release-->

keratinocyte inflammatory damage-->

plaque formation

Psoriasis is a disorder of hyperkeratinization (inc cell sloughing/turnover).

Somewhat genetic, onset usually after some "trigger"--> disruption in arachidonic acid metabolism (inc rate)

How does this present clinically?

thick plaques w/ silver scale

red skin (capillary dilation)

inflammation (lymphocytes in dermis & neutrophils in epidermis)

________ & _________ target the superficial epidermis & are used topically on reduce scales

Emolients (lotions)- minimize dryness, pruritis, soften scales


Keratolytics (Salicylic acid)- smooth skin & remove scale, decrease hyperkeratosis

__________ are used topically in severe psoriasis (start w/ more potent rx, followed by less potent rx)

MOA: immunosuppression

antimitotic effects on the epidermis-->

suppress proinflammatory genes (IL-1, IL-2, IL-6)-->

decrease inflammatory cell production & migration to dermis



SE: (may have systemic SE at high dose*)

Steroid rosacea

contact dermatitis

skin atrophy


*NEVER use on face, only on small body areas

________ oral rx, used for psoriasis

MOA: immunosuppression

binds cyclophylin-->

inhibits calcineuron-->

prevents dephosphorylation of NFAT-->

decr IL-2 production-->

decr T cell activation

What are the SEs?

Cyclosporine (sandimmune)


renal dysfxn (nephrotoxicity)



___________ is a biologic used in the tx of moderate to severe chronic plaque psoriasis

MOA: immunosuppression

dimeric fusion protein binds to CD2 on T cells-->

interferes w/ T cell interaction w/ APC-->

reduces active T cells


Alefacept (amevive)


CD2 binding on T cell-->

Increased CD4+ apoptosis

*requires weekly CD4+ monitoring

*don't use in pts w/ infections

_______ is a biologic used to tx psoriasis

MOA: immunosuppresion

humanized monoclonal anti-TNF-alpha Ab-->

binds TNF-alpha-->

cell-toxic effects

What are the SEs?

What is required before starting?

Adalimumab (Humira)


allergic rxns

reactivation of latent Tb*

incr susceptibility to infection

lupus-like syndrome

Require Tb screen before starting, don't use w/ infeciton

___________ is a retinoid that can be used to tx moderate to severe psoriaisis (not commonly used for acne)

MOA: keratolytic

prodrug converted to etritinate


What other retinoid can also be used to tx psoriasis?

Acitretin (soriatane)


similar to isoretinoin (dry skin, dry mucous membranes, hair thinning)

severe teratogenesis (worse than isoretinoin, caution in preg for 3 yr after discontinuing)

wait 1 month to donate blood after stopping

*Tazarotene also used to tx psoriaisis

________ are topicals used to tx psoriasis, dermatitis, lichen simplex chronicus (alt to corticosteroids)

MOA: Keratolytic

phenolic compounds--> antipruritic

cytostatic epidermal thinning


Tar compounds


transient epidermal hyperplasia (followed by epidermal thinning)

Difficult application--> staining, stinky

Irritant folliculitis


_________ topical ointment used for moderate plaque type psoriaisis

MOA: Vit D3 derivative-->

inhibit keratinocyte differentiation & proliferation (keratolytic)-->

Decrease TH1 stimulating cytokines (IL-2)


Calcipotriene (Dovonex)


Avoid mucous membrane (eyes) & open skin (prevent systemic effects)

Irritation, drying, erythema

_______ is used in moderate to severe psoriaisis

MOA: anti-inflammatory

inhibits dihydrofolate reductase (DHFR)-->

blocks DNA synthesis (esp of rapidly dividing cells = immune cells)-->

Decrease IL-1-->

death of active T cells




hepatic fibrosis (d/t high dose req)

CI w/ sulfamethoxazole, probenecid, salicylates

__________ is used in combination w/ UV A light therapy (PUVA therapy) to tx psoriasis

*applied prior to light exposure


photoaddition to pyrimidine in DNA-->

creates reactive oxygen-->

anti-proliferative, immunosuppressive, & anti-inflammatory


Methoxalen/ Psoralens


Nausea, cataracts (if oral, can be used in bathwater or lotion topically)


(UVB is more likely than UVA to cause cancer)