Dermatology

Question 1

Process of drug absorption

Answer 1

1. Penetration of the stratum corneum
2. Permeation: diffusion through the viable epidermis to the dermis
3. Resorbtion: access to systemic circulation via the vascular system (in the dermis)

**Can pass through dermal/hypodermal layers to reach underlying tissue

Question 2

Penetration pathways

Answer 2

1. Transappendageal: through hair follicles, sweat ducts, sebaceous glands
2. Transepidermal route: intercellular versus transcellular

Intercellular: between corneocytes (lipids), most prominent route
Trancellular: through the corneocytes (lipids), hydrophilic drugs

Question 3

Gel

Answer 3

Better to be used by a dermatologist. Very drying, can be irritating.
Stronger than an ointment.

Question 4

Solution

Answer 4

Clear, two or more substances. Can be irritating.

Good for acute phase inflammation.

Question 5

Cream

Answer 5

Water in oil emulsion. Most common! Hydration/lubrication. More potent than lotions.

Question 6

Lotion

Answer 6

Good for hairy areas.

Question 7

Ointment

Answer 7

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.

Question 8

MOA topical corticosteroids

Answer 8

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

Question 9

Anti-inflammatory effects of topical corticosteroids

Answer 9

Inhibits arachidonic acid cascade, inhibits activation of pro-inflammatory genes, decreases release of pro-inflammatory cytokines from keratinocytes, stabilizes lysosome membranes from phagocytizing cells

Question 10

Immunosuppressive effects of topical corticosteroids

Answer 10

Lymphocyte and monocyte apoptosis, inhibits leukocyte migration to sites of inflammation, inhibits phagocytosis, interferes with the function of antigen-presenting cells

Question 11

Group 1

Answer 11

Super potent. Use <2-3 weeks, may see tachyphylaxis. Not for face, axillae, groin, or under breasts.

Psoriasis
Hand eczema

Question 12

Group 2-3

Answer 12

Super potent. Use <2-3 weeks, may see tachyphylaxis. Not for face, axillae, groin, or under breasts.

Atopic dermatitis, adults

Poison Ivy

Question 13

Groups 4-5

Answer 13

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

Question 14

Group 6-7

Answer 14

Low potency. Intermittent therapy. Re-evaluate if disease does not respond in 28 days. Avoid long-term continuous use.

Eyelid dermatitis
Diaper dermatitis

Question 15

General treatment guidelines with topical corticosteroids

Answer 15

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.

Question 16

Telangiectases

Answer 16

Spider veins, corticosteroid AE

Question 17

Atrophy

Answer 17

LEADING AE of corticosteroids

Question 18

Comedogenicity

Answer 18

Acne, AE of corticosteroids

Question 19

Topical drug metabolism

Answer 19

Metabolic activity in skin-surface microorganisms, appendages, stratum corneum, epidermis, dermis.
Transporter proteins found in keratinocytes.
Genetics involved.

Question 20

Glucocorticoid receptor

Answer 20

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.

Question 21

Acute phase of eczema

Answer 21

Papules, vesicles, bullae, intense erythema/pruritus.

Contact allergy, irritation, fungal infection

Question 22

Subacute phase of eczema

Answer 22

Erythema, scale, fissuring, dry, scalded. Mild to moderate pruritus. Pain, stinging, burning.

Contact allergy, irritation, fungal infection, atopic dermatitis.

Question 23

Chronic phase of eczema

Answer 23

Thickened skin, lichenified, excoriations, fissuring. Moderate to intense pruritis.

Atopic dermatitis, habitual scratching

Question 24

Atopic Dermatitis

Answer 24

Disorder of cutaneous immune/barrier function. Excessive macrophages, abnormal T-lymphocyte activation, imbalance of cytokines, IgE, eosinophilia, dysregulated desquamation

Question 25

Contact Dermatitis

Answer 25

Commonly involves the hands. Delayed hypersensitivity. Asymmetric lesions, sharply demarcated, itching. Acute or chronic.

Question 26

Pimecrolimus

Answer 26

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.

Question 27

Tacrolimus

Answer 27

Useful for moderate to severe AD. | Equivalent to moderate, more effective than low potency.

Question 28

TCI

Answer 28

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

Question 29

Psoriasis

Answer 29

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.

Question 30

Calcipotriene

Answer 30

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.

Question 31

Topical retinoid

Answer 31

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.

Question 32

Tazarotene

Answer 32

Category X topical retinoid

Question 33

Bacitracin

Answer 33

For gram positive. Prophylactic. Inhibits cell wall synthesis. Used alone or with neomycin, polymixin B Can cause allergic dermatitis

Question 34

Gramicidin

Answer 34

For gram positive. Prophylactic. Disrupts bacterial cell membrane. ONLY with other antimicrobial agents.

Question 35

Mupirocin

Answer 35

Gram positive aerobic bacteria, including MRSA. Inhibits protein synthesis. For impetigo, superficial skin infections, to eliminate nasal colonization of staph. Patients >2 mo.

Question 36

Retapamulin

Answer 36

Staph, strep. Inhibits protein synthesis. For impetigo, patients >9 mo. AE: irritation, headache, nausea, diarrhea.

Question 37

Aminoglycosides

Answer 37

Gram negative organisms

Question 38

Neomycin

Answer 38

Aminoglycoside For minor skin infections Causes CD

Question 39

Gentamicin

Answer 39

Aminoglycoside For minor skin infections Can cause high serum levels, can cause nephrotoxicity and ototoxicity

Question 40

Polymixin B

Answer 40

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