Pharmacology Of Dermatological Agents - Panavelil

Front 1

Variables in determining pharmacological response:

Concentration Gradient

Back 1

-increasing the concentration gradient increases mass of drug transferred per unit time
*can lead to tolerance-tachyphylaxis

Front 2

Variables in determining pharmacological response:

Age

Back 2

-children have greater ratio of surface area to mass than adults
-given amounts result in greater systemic dose
-**esp careful w/ corticosteroids

Front 3

What are two depigmentation agents?

Back 3

-hydroquinone and monobenzone

Front 4

What do hydroquinone and monobenzone do?

Back 4

-both reduce hyperpigmentation
-hydro--> temporary lightening
-monobenzone--> permanent lightening (AE is that it can lead to hypopigmentation at other sites of the body)

Front 5

What is the MOA of hydroquinone and monobenzone?

Back 5

-inhibition of tyrosinase thus interfering with the biosynthesis of melanin

Front 6

What are two psoralens that are used for the repigmentation of depigmented macules of vitiligo?

Back 6

1. Trioxsalen (for vitiligo)

2. methoxsalen (for psoriasis)

-erythemogenic, melanogenic, cytotoxic

Front 7

What is the MOA for Trioxsalen and Methoxsalen?

Back 7

-psoralens must be photoactivated by UV light
-FORMATION OF DNA ADDUCTS THAT INHIBIT DNA REPLICATION
-inhibit cell proliferation and promotes differentiation of epi cells

Front 8

When should one use Methoxsalen?

Back 8

-severe disabling psoriasis, when pt is not responsive to other therapies, and only when dx is supported by biopsy

Front 9

What are a few AEs of Methoxsalen?

Back 9

-ocular damage, aging of skin, skin cancer possibilities

Front 10

What is another possible use of methoxsalen?

Back 10

palliative tx of cutaneous T-cell lymphoma

Front 11

What are some common acne preparations?

Back 11

-Retinoic acid, Adapalene, Isotretinoin, Benzoyl peroxide and Azelaic acid

-only oral or topical
-does NOT require UV activation

Front 12

Retinoic acid

Back 12

-all trans retinoic acid
-for tx of acne vulgaris
-oxidized form of Vit A
-influences cell prolif and differentiation, immune function, inflammation and sebum production

Front 13

What is the MOA of Retinoic Acid?*

Back 13

-binds to RARs and RXRs which then bind to retinoic acid response elements (RAREs) in the regulatory regions of direct targets, thereby activating gene transcription

Front 14

Why should pts taking retinoids avoid sun exposure?

Back 14

-b/c they can be tumorigenic upon UV radiation, and thus should avoid sun exposure

Front 15

Isotretinoin

Back 15

-first generation retinoic acid
-limited to SEVERE CYSTIC ACNE
-MOA: inhibits sebaceous gland size and function

Front 16

What are absolute contraindications for retinoids?

Back 16

-pregnant women and women with potential for child bearing (skeletal disorders)

Front 17

Etretinate

Back 17

-second generation retinoid for psoriasis
-aka Tegison
-aromatic retinoid for pustular psoriasis

Front 18

Benzoyl peroxide

Back 18

-tx for acne vulgaris
-penetrates S. corneum

Front 19

What is the MOA for Azelaic acid

Back 19

-antimicrobial effect and inhibitory effect on conversion of testosterone -> dihydrotestosterone

Front 20

What are 3 common drugs for psoriasis?

Back 20

-Acitertin
-Tazarotene
-Calcipotriene

Front 21

What is the cause of psoriasis?

Back 21

-due to increased epidermal cell proliferation
-characteristic scaly silvery patches

Front 22

Acitretin and some of its AEs

Back 22

-an etretinate metabolite treating pustular psoriasis
-AEs: elevation of cholesterol and triglycerides, teratogenic, contraindicated in pregos, no alcohol, no donating blood for 3 yrs

Front 23

Tazarotene (Tazorac)

Back 23

-acetylated retinoic acid (antiinflammatory and antiproliferative)

Front 24

Photochemotherapy and management of psoriasis

Back 24

-oral psoralen followed by UVA
-DNA adduct formation inhibits DNA replication
-inhibition of proliferation and differentiation of epithelial cells

Front 25

Calcipotreine

Back 25

-synthetic Vit D3 derivative
-inhibit prolif and diff of epi cells
-decreases local T-CMI
-AEs: itching, dryness, burning, irritation, erythema

Front 26

What are the two major properties of glucocorticoids?

Back 26

1. immunosuppressive
2. antiinflammatory

Front 27

MOA of glucocorticoids

Back 27

-varies:
1. inhib effects on arachidonic acid cascade
2. depression of prod of cytokines
3. effects on inflammatory cells

Front 28

Glucocorticoids and use in children

Back 28

-potent in children
-can cause systemic toxicity
-depression of hypothalamic-hypophyseal-adrenal axis
-growth retardation

Front 29

What can the insoluble preparation of triamcinolone, a glucocorticoid cause?

Back 29

-atrophy and hypopigmentation

Front 30

Trichogenic agents:

Minoxidil (Rogaine)

Back 30

-potent arterial vasodilator that can also reverse progressive miniaturization of terminal scalp hairs (androgenic alopecia)

-stoping leads to hair loss!

Front 31

MOA of Minoxidil (Rogaine)

Back 31

-either activate hair follicle directly or stimulate microcirculation surrounding follicle--> increasing cutaneous blood flow
***systemic therapy for hair growth stim, this topical use usually doesnt cause hypoT

Front 32

Trichogenic Agents:

Finasteride (Propecia)

Back 32

-testosterone analogue
-5 alpha-reductase inhibitor (blocks testosterone to andro 5 alpha-dihydrotestosterone)
-decreases scalp and serum [DHT]
-orally for andorgenic alopecia
-used in BPH (proscar)

Front 33

AEs and absolute contraindications of Finasteride

Back 33

-decreased libido, decrease ejaculation volume and dysfunction, erectile dysfunction
-ACs: children, females, pregos
*HYPOSPADIAS

Front 34

Finasteride and Hypospadiase

Back 34

-in male fetus if used/handled by pregos
-developmental anomaly characterized by defect on ventral surface of penis so urethral meatus is proximal to normal location