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Dermatology by Mind Map: Dermatology

1. Physiology

1.1. Penetration via...

1.1.1. Intact stratum corneum

1.1.2. Sweat ducts

1.1.3. Sebaceous follicle

1.2. Percutaneous absorption steps...

1.2.1. Conc. gradient

1.2.2. Release of drug from vehicle (logP)

1.2.3. Diffusion across skin

1.3. Pruritus

1.3.1. dry skin, atopic eczema, urticaria, infestations

1.3.2. Caused By... bites and parasites dermatitis herpetiformis atopic dermatitis exfoliative dermatitis jaundice leukemia hodgkins disease

1.3.3. Treated with... emollients for xerosis topical glucocorticoids PO sedating antihistamines ondansetron UVB radiation

1.4. Hyperkeratosis

1.4.1. thickening of stratum corneum calluses verrucae (warts)

1.4.2. treat with... keratolytic agents lactic acid salicylic acid glycolic acid urea sulfur destructive agents pdophyllum resin for warts

1.5. Androgenetic Alopecia

1.5.1. most common cause of hair loss in adults 40+

1.5.2. dihydrosterone binds androgen receptors in follicles, and this activates the genes responsible for miniaturized vellus follicles

1.5.3. Treat with... Minoxidil originally a HTN drug enhances follicle size Finasteride inhibits type II isozyme of 5 reductase (enzyme that converts testosterone to dihydrotestosterone

2. Acne

2.1. Inflammatory skin disorder -comedones -papules

2.2. Primarily inherited disorder

2.3. stick with any treatment regimen 6-8 weeks before changing

2.4. Pathophysiology

2.4.1. Contributing factors... trauma UV light humid or hot conditions emotions corticosteroids, OCs, some antiepileptics endocrine disorders luteal phase of menstruation

2.4.2. Mechanism... pilosebaceous units production of androgens - cause sebaceous gland to enlarge inflammatory acne caused by ruptured folicles papule: solid red or brown elevation pustule: papule filled with pus nodule: severe acne, firm, warm, tender cyst: inflamed, pus-filled nodule hormonal acne first line therapy... Alt therapy

2.4.3. Plugged sebaceous follicles open comedones = black heads (not dirt) closed comedone = white head

2.5. Characterization

2.5.1. mild comedones with or without pustules or papules treat with benzoyl peroxide salicylic acid topical retinoid topical abx

2.5.2. moderate comedones, several pustules or papules, with or without several nodules treat with topical retonoid + topical or PO abx

2.5.3. severe extensive pustules or papules and many nodules, extensive scarring, drainage, formation of sinus tract

2.5.4. very severe oral isotretinoin

2.6. Non-pharmacologic treatment

2.6.1. extraction

2.6.2. reduce triggers

2.6.3. hygeine wash face no more than 2x/d avoid antibacterial soaps use soapless cleanser

2.6.4. moisturizer oil fee non-comedogenic with sunscreen

2.7. Pharmacology

2.7.1. Antibiotics topical for superficial infections must be used in combination with other products Clindamycin Erythromhcin Tetracycline: use sunscreen systemic pt should never be on a PO abx as monotherapy. use for the shortest duration possible, and d/c after 3 months possible OC failure deeper infections acne vulgaris suppresses leukocyte chemotacxis

2.7.2. keratolytic: unclogs pores

2.7.3. comedolytic topical retiniods adapalene (Differin): less effective but less irritating tarazotene (Tazorac): most effective and irritating Tretinoin (Retin A): more effective than adapalene

2.7.4. PO retinoids isotretinoin (Amnesteen, Accutane, Clavarris): severe inflammatory acne only pregnancy category X iPledge program NO refills must fill rx in 7 days avoid alcohol

2.7.5. anti-inflammatory

2.7.6. hormonal: reduce androgens

3. Pharmacology

3.1. Preferrable Characteristics

3.1.1. <600 Da

3.1.2. Soluble in water and oil water soluble ions and polar mol do not penetrate unless they are very small

3.1.3. High logP

3.2. Glucocorticoids

3.2.1. Immunosuppressive and Anti-inflammatory

3.2.2. Initial high dose and then reduce

3.2.3. Application >2x/d does not improve response

3.3. Intralesional

3.3.1. Preparations (prolonged action) triamcinolone acetonide triamcinolone hexacetonide fluorocinolone causes perioral dermatitis and rosacea

3.3.2. Therapeutic Use SEREVE illness allergic contact dermatitis to plants life threatening vesiculobollous dermatoses

3.3.3. SE from long term use psychiatric problems cataracts myopathy osteoporosis avascular bone necrosis glucose intolerance (overt DM) HTN

3.3.4. Toxicity from chronic use atrophy striae telangiectasias: small dilated blood vessels in mucus membrane purpura acne

3.4. Retinoids

3.4.1. Classes 1st Generation Retinol Tretinoin Sotretinoin Alitretinoin 2nd Generation (aromatic) Acitretin 3rd Generation (arotinoids) Tazarotene Bexarotene Adapalene has retinoid like properties but does not fall into any class of retinoid derivative of naphotic acid similar efficacy to tretinoin less stable in sun less irritating Oral Retinoids Isotretinoin

3.4.2. MOA compounds of retinol that exhibit Vitamin A activity activates RARs and RXRs and affects gene expression gene products responsible for pharmacologic effect and SE

3.4.3. Therapeutic use inflammatory skin disorders skin malignancies treat premalignant skin cancer (isotretinoin) hyperproliferative disorders photoaging keratinization enhance penetration of topical meds

3.4.4. SE greater SE seen in 1st and 2nd generation xerosis epistaxis conjunctivitis hair loss

3.4.5. Toxicity can affect: vision, cell proliferation, bone growth, immunity, tumor suppression similar to vitamin A intoxication

3.4.6. Teratogenicity pregnancy category X fetal malformations

3.5. Beta Carotene

3.5.1. precursor of vitamin A

3.5.2. in green and yellow veggies

3.5.3. decreases production of free radicals

3.5.4. Clinical Uses... reduces photosensitivity in pts with erythropoetic protoporphyria deficiency of ferrochelatase leading to high levels of protoporphyria

3.6. Photochemotherapy

3.6.1. Chemistry Principles... UV C doesn't penetrate UV B 290-320 nm most erythrogenic and melanogenic sunburn / tanning skin cancer photoaging UV AI 320-340 nm and UV AII 340-400 nm 1000x less erythrogenic than UVB photoaging and photosensitivity diseases enhances UVB induced erythema increase risk for skin cancer visible light 400-800 nm

3.6.2. Phototherapy... Using UVB or High dose UV AI Monitor: phenothiazenes, thiazides, sulfonamides, NSAIDs, sulfonylureas, tetracyclines, benzos PUVA: psoralens and UVA chemotherapy vitiligo psoriasis cutaneous T cell lymphoma atopic dermatitis alopecia lichen planus urticaria pgmentosa promotes melanogenesis in normal skin PO administration 8-methylpsoralen followed by UVA

3.7. Sunscreen

3.7.1. For UVA avobenzene oxybenzone titanium dioxide zinc oxide

3.7.2. SPF: the time a person w/ sunscreen can be exposed to the sun before getting sunburn compared to a person w/o sunscreen

3.8. Capsaicin

3.8.1. neuralgia

3.8.2. diabetic neuropathy

3.8.3. arthritis pain

4. Atopic Dermatitis/Eczema

4.1. Overview

4.1.1. chronic relapsing disease that usually begins in infancy or childhood

4.1.2. Triad: atopic dermatitis + asthma + allergic rhinitis

4.1.3. Epidemiology mostly affects children common characteristics: low socioeconomic status, FH, urban area, smaller family

4.1.4. Pathophysiology genetic predisposition initial mechanism unknown Increased IgE S. Aureus colonization skin barrier dysfunction transepidermal water loss

4.2. Clinical Presentation

4.2.1. most cases before 5 years old

4.2.2. initial presentation is facial rash

4.2.3. spares diaper and nose region

4.2.4. rash can include... papules vesicles oozing vesicles

4.2.5. Signs and Symptoms xerosis lichenification (thickened leathery skin) bleeding secondary bacterial infections

4.3. Treatment

4.3.1. Non-pharmacological bathe in lukewarm water 5 min 1-2x/d bath > shower bathing 2x/d during flares enhances topical therapy and debrides mild liquid cleansers cetaphil Moisturizers DO NOT apply to a dressing avoid alcohol containing products Occlusives are most effective Minimize scratching Minimize triggers Avoid extreme temperatures keep home cool with low humidity Treat weeping lesions astigents

4.3.2. Pharmacology First Line Therapy... Topical corticosteroids Second Line... Topical calcineurin inhibitor PO corticosteroids short courses for severe intensify topical steroids and hydration to minimize rebound flares Phytotherapy alt for moderate to severe UV therapy UV + topical ointment psoralens + UVA Coal tar ointment, cream, gel, shampoo sheds dead cells for top layer to delay growth of new cells and decrease pruritus