Dermatologic Agents Flashcards

1
Q

skin penetration of an agent is affected by what factors?

A

Decreased molecular size, increased lipid content, increased drug concentration, skin integrity, skin thickness, surface area of application

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2
Q

Polymyxin B- Neosporin/ Neomycin

A

Topical anti microbial used for prophylaxis of infection after injury
MOA: bactericidal, interacts with phospholipids and disrupts the cell membrane (bacitracin interacts with cell wall peptidoglycans)
Char: ointment, can be mixed with corticosteroids
SE: some local irritation, anaphylaxis rare, ototoxic (AVOID using optic applications there is possible perforated TM)

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3
Q

Mupirocin/ Bactroban

A

Topical antibiotic
Indic: impetigo, highly active against staph, strep, MRSA (not effective against fungal/viral infx)
MOA: inhibits bacterial protein synthesis
Char: ointment, BID/ TID dosing
Apply to nares in MRSA Tx to avoid carriage status
SE: local irritation with burning, itching, local pain/ rash

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4
Q

Ketoconazole/ Nizarol

A

Topical antifungal
Indic: Tinea pedis, tinea cruris, tinea corporis, seborrheic dermatitis, superficial yeast infx
MOA: inhibits sterol synthesis
SE: local irritation
Char: topical ointment, PO available for systemic infx

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5
Q

In order to have a systemic effect, topical drug agents need to penetrate what layer of the skin?

A

Stratum corneum

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6
Q
How are glucocorticoids rated for relative strength? 
What class of glucocorticoids are considered to be the strongest?
A

Class 1-7; 1 is most potent, 7 is least potent

Halogenated corticosteroids are considered to be the most potent

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7
Q

Glucocorticoid side effects

A

Striae, skin atrophy, telangectasia, purpura, acneiform lesions, perioral dermatitis, overgrowth of skin fungus/bacteria, hypopigmentation, rosacea, suppressed HPA axis, inc risk hyperglycemia, osteoporosis, osteonecrosis
Atrophy of fat, muscle at injection site in IM applications

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8
Q

What are factors that can affect systemic corticosteroid absorption?

A
Increased absorption at inflamed skin
Amount applied
Size of area to be treated
Frequency of application
Length of tx 
Drug potency
Barrier use
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9
Q

Hydrocortisone/ Cortef

A

Class: glucocorticoid/ corticosteroid
Indic: atopic dermatitis, contact/ allergic dermatitis, psoriasis, eczema, pemphigus, SLE, granulomatous dz, sarcoidosis
MOA: anti-inflammatory, affects gene transcription
Char: cream, ointment, PO/IV/IM; minimize use on face/ thin skin

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10
Q

What kinds of processes do retinoids affect?

A

Cellular proliferation, differentiation, immune function, inflammation, sebum production

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11
Q

What are some indications for retinoids?

A

Cystic/papular acne, basal cell ca, squamous cell ca, actinic keratosis, psoriasis, cutaneous aging

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12
Q

What are some etiologies for acne?

A
Follicular hyperkeratosis
Bacteria (probionoibacterium acnes)
Increased inflammation
Increased sebum production
Androgens
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13
Q

What is the general initial treatment for acne? What is a secondary treatment option if acne is refractory to initial tx?

A

Initial tx: TOPICAL salycylic acid, benzoyl peroxide, erythromycin, clindamycin, metronidazole, retinoids (tretinoin)

Secondary Tx: ORAL tetracycline, retinoids (accutane)

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14
Q

Tretinoin/ Retin A

A

Class: vitamin A derivative
Indic: acne, photodamaged skin
MOA: dec hyperkeratinization, inc epidermal thickness, inc dermal collagen production
Char: topical 0.01-0.1% qd in hs
May take months to see effects
SE: erythema, peeling, burning, stinging, photosensitivity

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15
Q

Isoretinoin/ Accutane

A

Class: vitamin A derivative
Indic: acne, acne rosacea, hydradenitis supperativa
MOA: dec hyperkeratinization, dec # sebaceous glands, doc sebum production, dec p.acnes bacterium
Char: PO; acne recurs 40% of the time within 6 months of discontinuation
SE: teratogenic, esp in the first 3 months! Also depression, suicidal ideation, psychosis, suicide, HA, myalgias, arthralgias, hyperlipidemia, fatty liver disease, hepatitis, pancreatitis
CI IN PREGNANCY recommended that female pt of childbearing age use two forms of contraceptive

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16
Q

What is occurring to cause psoriasis pathology?

A

Autoimmune disease, causing immune cells to migrate from the dermis to the epidermis. This stimulated keratinocyte proliferation.

17
Q

What is the conventional progression of drug tx in psoriasis?

A

Topical corticosteroids
Topical vitamin D (calciprotiene)
Phototherapy
Systemic tx: oral steroids, methotrexate, TNF inhibitors (infliximab/ remicade)

18
Q

PUVA

A

Psoralin plus UVA ( historical use dates back to 1500 BCE!)
Photochemotherapy
MOA: may inhibit DNA synthesis, stimulates melanocytes, anti-inflammatory effect, may also suppress immune system
Indic: psoriasis, vitiligo, alopecia areata, urticaria pigmentosa, T-cell lymphomas
SE: nausea, painful erythema, blistering, increased risk of skin cancer, increased aging, increased risk actinic keratosis