a. Describing A Lesion:

1. Primary lesion:

Dermatology 1

2. Secondary lesion:Dermatology 2

3. Shape, configuration, distribution, additional components:Dermatology 3



b. Papulosquamous Disorders

1. Psoriasis:

  • Profile: two peaks: 22 + 55 yo. Polygenic trait (genetic predisposition + environmental
  • Triggers:
    • Trauma (sunburn, linear scratch): Koebner phenomenon
    • Acute strep throat: Guttate psoriasis
    • Drugs: systemic steroid, lithium, antimalarial, B blockers, interferons, alcohol
    • Stress
  • Clinical appearance: sharply demarcated plaque, erythematous, silvery-white scales
  • Distribution:
    • Extensor surfaces of elbows and knees, palms\soles, scalp, nails
    • Nails psoriasis (20%): pitting, onychlysis, oil spots (yellow-brown), subungual hyperkeratosis
    • Psoriatic arthritis (10-25%): destructive, interphalangeal -> sausage digits
  • Treatment:
    • General: explain the chronicity to the pt, avoid triggers
    • Topical: steroids, vit D\A, tacrolimus
    • Phototherapy: UVB
    • Systemic: vit A (oral Acitretin), immunosuppressants (Methotrexate, Cyclosporine), biologic agents


2. Pitryiasis rosea:

  • Profile: young ages: 10-43 yo. Mostly in spring and fall seasons
  • Causes: possibly HHV-7 or HHV-6
  • Clinical appearance: oval, less sharp demarcation, erythematous papules\plaques, Collarette scales
  • Distribution: Herald patch\mother lesion, Christmas tree distribution
  • Treatment:
    • Spontaneous resolution in 6-12 wks
    • If pruritic -> oral antihistamines or topical steroids


3. Lichen planus:

  • Profile: 30-60 yo. F>M
  • Clinical appearance: well-demarcated purple papules\plaques, polygonal, white fine scales (Wickham striae), pruritic + significant pigmentation when resolves
  • Causes: T-cell mediated response
    • Drugs: ACEI, B blockers, furosemide, thiazides, antimalarial
    • Metals: mercury (dental fillings)
    • Infections: hep C
    • Koebner phenomenon
  • Distribution: flexor aspect of the writs, lumbar, genital, shins, oral mucosa (reticulated Wickham striae)
  • Treatment:
    • General: explain chronicity (takes yrs to resolve), stop offending drug\metal, consider hep C serology
    • Phototherapy: UV light
    • Topical: steroids, tacrolimus
    • Systemic: steroids, vit A (oral Acitretin), immunosuppressants (Cyclosporine)


c. Itchy Skin Rashes: 

1. Atopic dermatitis (eczema):

  • Genetic + environmental, associated w\ other atopic ds: asthma, allergic rhinitis, food allergies
  • Starts in infancy acutely (cheeks, scalp, extensors) -> chronic in older children\adults (flexors)
  • Triggers: irritants\allergens, sweating, soaps\fabrics, stress, bacterial infec (improved by sun exposure)
  • Major diagnostic features (3\4):
    • Pruritus
    • Typical morphology\distribution of skin lesions
    • Chronic\chronic-relapsing
    • Personal\family Hx
  • Minor diagnostic features:

Dermatology 14

Dermatology 13

  • Other minor features: xerosis, elevated serum IgE, keratoconus, recurrent conjunctivits, ant subcapsular cataracts, chelitis, intolerence to wool and lipid solvents
  • Complications:

Dermatology 15

  • Treatment:
    • General: proactive approach, avoid triggers, daily moisturizing
    • Topical: steroids (1st line), tacrolimus\pimicrolimus
    • Phototherapy: UVA\UVB
    • Systemic: steroids, cyclosporine\methotrexate, mofetil, biologic agents
    • Adjuctives: antihistamines, antimicrobials (if impetiginized)


2. Contact dermatitis:

  1. Irritant (80%): local toxic reactions to an irritant (soaps, solvents, acids\alkalis) can affect any person
  2. Allergic (20%): delayed type 4 hypersensitivity to an agent previously sensitized to
  • Clinical picture: well-defined eczematous plaque w\ scales\vesicles corresponding to the area of contact
  • Diagnosis: patch test
  • Management: id cause, avoid it, topical steroids
Dermatology 16
Contact dermatitis


3. Seborrheic dermatitis: 

  • Profile: infantile and adult forms (4th-6th decades), M>F
  • Causes: related to high sebum production + Malassezia furfur (yeast)
  • If severe and persisting -> think of HIV
  • Clinical appearance: sharply demarcated pink-yellow patches\plaques w\ greasy scales (cradle cap)
  • Management:
    • Topical antifungal, mild topical steroids
    • Bathe w\ mild soap to remove scales + moisturize
Dermatology 17
Cradle cap

4. Urticaria (hives): 

  • Transient (<24hrs) pruritic pink plaque w\ pale centers
  • Deep form -> angioedema: painful, less demarcated, no color change
  • Causes:
    • Acute (<6wks): URTI, drugs, food
    • Chronic (>6wks): ordinary, physical, vascular
  • Treatment:
    • 1st line -> antihistamines: should be taken daily for 2-4 wks (even if no visible lesions)
    • If no response, add 2nd\3rd line: steroids, cyclosporine\methotrexate, ….


d. Common Skin Infections

1. Tinea pedis:

  • Athlete’s foot”: MC fungal infection in developed countries
  • Types:
  1. Interdigital: most common, + maceration
  2. Moccasin: chronic hyperkeratotic type -> lateral borders of feet ± onychomycosis
    • May present as “one hand, two feet syndrome”: the hands show unilateral fine scaling in the creases
  3. Vesiculobullous: grouped vesicle on the arch\instep, itchy\painful
  • Diagnosis: KOH (showing hyphae)
  • Treatment:
    • Hygiene: dry the area, ….
    • Topical antifungal: 1st line -> Imidazoles, 2nd line -> Allylamines (terbinafine, naftifine, butenafine)

Dermatology 21


2. Tinea corporis:

  • Ringworm” -> itchy annular lesion w\ central clearing, affecting the trunk and limbs
    • A variant of tinea corporis -> tinea cruris “jock itch”
  • Do fungal culture, why? Caused by different fungal species + guides tx
  • Treatment:
    • Topical antifungals: 1st line -> Imidazoles, 2nd line -> Allylamines (terbinafine, naftifine, butenafine)
    • Oral antifungal: if poor response to topical, animal source is suspected, large surface area

Dermatology 22


3. Onychomyocosis:

  • Chronic fungal infection of the nailbed -> thickened nail, subungual debris, separation of the nail
  • Most common type: distal subungual onychomycosis
  • Cause: Trichophyton rubrum (dermatophyte)
  • Diagnosis: fungal culture of subungual debris (confirmation is required before starting oral tx)
  • Treatment:
    • 1st line -> oral Terbinafine, 2nd line -> oral Flucanazole
      • Risks of terbinafine: hepatotoxicity, drug interactions, reversible taste disturbance, skin reactions

4. Tinea versicolor:

  • Cause: colonization of Malassezia (yeast), summer months
  • Well-demarcated, asymmetric, hypo\hyper-pigmented patches -> trunk\arms
  • Diagnostic feature? When tubbed w\ finger or scalpel -> you can see scales!
  • Diagnosis: KOH
  • Treatment:
    • 1st line: Topicals: antifungal shampoo or Imidazole creams
    • 2nd line: oral Fluconazole
    • Maintenance therapy; if recurrence -> use topicals 1-2 times\wk
Dermatology 23
Tinea versicolor

5. Intertrigo:

  • Inflammation of large skin folds: inframammary, gluteal, inguinal folds
  • 10% are complicated by candida colonization (yeast)
  • Clinical presentation: burning (more than itchy) satellite macule\papules\pustules around the erythema in the fold
  • Diagnosis: KOH (may reveal pseudohyphae), but culture is more sensitive
  • Treatment:
    • Topical antifungal: 1st line -> Imidazole, 2nd line -> Nystatin
    • Low-strength topical steroids for the burning and itching
Dermatology 24


6. Pediculosis (lice):

  • Spread by close physical contact and fomites
  • Clinical presentation: nits in the retroaurical and occipital scalp, scalp pruritus, post cervical lymphadenopathy, dermatitis on post neck
  • Treatment: OTC permethrin 1% or pyrethrin
Dermatology 25
Pediculosis (lice)


7. Scabies:

  • Spread via direct contact or fomites, more common in women and children
  • Clinical presentation: papules -> wrists, finger webs, axillae, breasts, scrotum
  • Hallmark? Itching at night + burrows
  • Crusted (Norwegian) scabies: hyperkeratotic scabies -> immunosuppressed \ neurologically impaired pts
  • Treatment:
    • 1st line -> Permethrin (for > 2 mo and not pregnant)
      • Post-scabietic pruritus\dermatitis: the body’s response to the dead mites (not a treatment failure)



Download the PDF version: here


  • Master the boards
  • Dr. Aljasser, Dr. Alkhodair, and Dr. Almohideb’s lectures

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