Dermatology Flashcards
Process of drug absorption
- Penetration of the stratum corneum
- Permeation: diffusion through the viable epidermis to the dermis
- Resorbtion: access to systemic circulation via the vascular system (in the dermis)
**Can pass through dermal/hypodermal layers to reach underlying tissue
Penetration pathways
- Transappendageal: through hair follicles, sweat ducts, sebaceous glands
- Transepidermal route: intercellular versus transcellular
Intercellular: between corneocytes (lipids), most prominent route
Trancellular: through the corneocytes (lipids), hydrophilic drugs
Gel
Better to be used by a dermatologist. Very drying, can be irritating.
Stronger than an ointment.
Solution
Clear, two or more substances. Can be irritating.
Good for acute phase inflammation.
Cream
Water in oil emulsion. Most common! Hydration/lubrication. More potent than lotions.
Lotion
Good for hairy areas.
Ointment
Highly lipid. Occlusive, can be over-hydrating and cause maceration. Good for thickened skin but not hairy skin. Can be irritating.
Not for acute phase rashes, or intertriginous areas.
MOA topical corticosteroids
Mainly for immunosuppression and anti-inflammatory effects.
Vasoconstrictive: determines potency. Inhibits vasodilators (histamine, bradykinin, prostaglandins), inhibits mast cell degranulation.
Decreases capillary permeability: reduces histamine released by basophils and mast cells
Decreases epidermal cell mitosis: contributes to efficacy with psoriasis and conditions with rapid cell turnover
Anti-inflammatory effects of topical corticosteroids
Inhibits arachidonic acid cascade, inhibits activation of pro-inflammatory genes, decreases release of pro-inflammatory cytokines from keratinocytes, stabilizes lysosome membranes from phagocytizing cells
Immunosuppressive effects of topical corticosteroids
Lymphocyte and monocyte apoptosis, inhibits leukocyte migration to sites of inflammation, inhibits phagocytosis, interferes with the function of antigen-presenting cells
Group 1
Super potent. Use <2-3 weeks, may see tachyphylaxis. Not for face, axillae, groin, or under breasts.
Psoriasis
Hand eczema
Group 2-3
Super potent. Use <2-3 weeks, may see tachyphylaxis. Not for face, axillae, groin, or under breasts.
Atopic dermatitis, adults
Poison Ivy
Groups 4-5
Medium potency. Use <3 months, can see tachyphylaxis. Limit use 7-21 days in children. Limit use in intertriginous areas. Group 4 is a good starting place for therapy.
Atopic dermatitis children
Seborrheic dermatitis
Severe dermatitis of the face
Group 6-7
Low potency. Intermittent therapy. Re-evaluate if disease does not respond in 28 days. Avoid long-term continuous use.
Eyelid dermatitis
Diaper dermatitis
General treatment guidelines with topical corticosteroids
Group 4 is a good starting point. Treat for 3-10 days, once or twice daily, in 3-5 bursts. Decrease to once daily when you have control, add in bland moisturizer. Treat <2-3 weeks.
Tachyphylaxis: stop treatment for 7 days, resume.
Only low potency on face, genitalia, intertriginous areas.
Telangiectases
Spider veins, corticosteroid AE
Atrophy
LEADING AE of corticosteroids
Comedogenicity
Acne, AE of corticosteroids
Topical drug metabolism
Metabolic activity in skin-surface microorganisms, appendages, stratum corneum, epidermis, dermis.
Transporter proteins found in keratinocytes.
Genetics involved.
Glucocorticoid receptor
When glucocorticoid binds to its receptor, it relieves an inhibitory constraint (hsp90), when its released the receptor becomes active and initiates the transcription of target genes.
Acute phase of eczema
Papules, vesicles, bullae, intense erythema/pruritus.
Contact allergy, irritation, fungal infection
Subacute phase of eczema
Erythema, scale, fissuring, dry, scalded. Mild to moderate pruritus. Pain, stinging, burning.
Contact allergy, irritation, fungal infection, atopic dermatitis.
Chronic phase of eczema
Thickened skin, lichenified, excoriations, fissuring. Moderate to intense pruritis.
Atopic dermatitis, habitual scratching
Atopic Dermatitis
Disorder of cutaneous immune/barrier function. Excessive macrophages, abnormal T-lymphocyte activation, imbalance of cytokines, IgE, eosinophilia, dysregulated desquamation
Contact Dermatitis
Commonly involves the hands. Delayed hypersensitivity. Asymmetric lesions, sharply demarcated, itching. Acute or chronic.
Pimecrolimus
TCI, alternative for AD.
Useful for long-term maintenance of mild AD, beneficial for face/intertriginous areas.
Equivalent to low potency, less effective than moderates.
Tacrolimus
Useful for moderate to severe AD.
Equivalent to moderate, more effective than low potency.
TCI
Topical Calcineurin Inhibitor
MOA: inhibiting calcineurin (calcium-dependent phosphatase) needed for T cell activation. Block inflammatory cascade produced by pathologic T cells, prevent cytokine synthesis, T cell proliferation.
AVOID: <2 years, weakened immune system
Psoriasis
Chronic inflammatory condition characterized by epidermal hyperproliferation and vascular changes.
T-lymphocyte mediated, delayed hypersensitivity. T cell infiltration, cytokine/chemokine imbalance, chronic T-cell stimulation.
Unpredictable exacerbation/remissions.
Calcipotriene
Alternative for psoriasis.
Vitamin D analog: stimulates D3 receptor in keratinocytes to increase differentiation and inhibit proliferation.
For moderate psoriasis to relieve scaling. 6-8 weeks to max effect.
Combine with group 1 steroid, no tachyphylaxis, can use at intertriginous sites, long-term remission maintenance.
Topical retinoid
Alternative for psoriasis.
Tazarotene: used in combo with steroids, can be irritating which is controlled by the steroid.
Vitamin A analog: bind to skin retinoid receptors to normalize keratinization and reduce inflammation, weak inhibition of angiogenesis.
Tazarotene
Category X topical retinoid
Bacitracin
For gram positive. Prophylactic.
Inhibits cell wall synthesis.
Used alone or with neomycin, polymixin B
Can cause allergic dermatitis
Gramicidin
For gram positive. Prophylactic.
Disrupts bacterial cell membrane.
ONLY with other antimicrobial agents.
Mupirocin
Gram positive aerobic bacteria, including MRSA.
Inhibits protein synthesis.
For impetigo, superficial skin infections, to eliminate nasal colonization of staph.
Patients >2 mo.
Retapamulin
Staph, strep.
Inhibits protein synthesis.
For impetigo, patients >9 mo.
AE: irritation, headache, nausea, diarrhea.
Aminoglycosides
Gram negative organisms
Neomycin
Aminoglycoside
For minor skin infections
Causes CD
Gentamicin
Aminoglycoside
For minor skin infections
Can cause high serum levels, can cause nephrotoxicity and ototoxicity
Polymixin B
Gram negative, old.
Causes cell death.
ONLY with other antimicrobials for minor skin infections.
Don’t exceed 200 mg topically over denuded skin to prevent nephro/neurotoxicity
