Common Skin Disorders

A. Eczema
• Contact Dermatitis
• Atopic Dermatitis
• Lichen Simplex Chronicus
• Dyshidrotic Eczema
• Nummular Eczema
B. Psoriasis
C. Drug Reactions
D. Acne Vulgaris
E. Melasma
F. Vitiligo
G. Skin Cancers
BCC
SCC
Melanoma

Allergic Contact Dermatitis

 Immunologic rxn
 Due to reexposure to substance by a sensitized person
 Delayed cell-mediated hypersensitivity
 Intense pruritus
 Confined to site but spreading to periphery, may become generalized
 Independent of amount
Irritant Contact Dermatitis
 Defense of skin is unable to maintain normal skin integrity
 Predisposing factors: atopy, cold temp, occlusion, mechanical irritation
 Usually due to chronic cumulative exposure
 Occupational hazards: hairdressing, cleaning, medical, dental, food
preparation, construction
Phyto CD
 Management:
 Avoid cause
 Barrier clothing, creams, gloves
Patch test
Treatment
 Remove causative agent
 Topical Steroids
 Antihistamines

Atopic Dermatitis
 Relapsing
 Begins in infancy
 Dry skin & pruritus
 Elevated IgE
  + family hx of atopy
 35% develop asthma later in life
 Decrease barrier function
 Reduced cerumide levels
 Inc transepidermal water loss
Exacerbating factors:
 Inhalants fr dust mites & pollens
 Food: eggs, milk, peanuts, soy, fish, wheat
 Infection: S. aureus
 Season
 Wool clothes, fur in carpets
 Emotional stress
Prurigo Nodularis
 From repetitive scratching and rubbing
 Chronic lesions
 Pruritus
 Areas on the feet at night are rubbed with the heels and toes
 Unconscious habit
Treatment :
 Intralesional triamcinolone

Dyshidrotic Eczema
 Tapioca-like vesicles on hands and feet
 Glucocorticoids: topical or oral
 PUVA

Nummular eczema
 Coin-shaped plaques composed of grouped papules and vesicles
 Lower legs
 Males
 Winter months
 Rule out psoriasis, MF, impetigo
 Topical steroids
 Emollients

Seborrheic dermatitis
 Redness & scaling
 Active sebaceous glands: face, scalp, presternal area, body folds
 Cradle cap in infants
 Malasezzia furfur
 Face: forehead, nasolabial folds, retroauricular meatus
 Ketoconazole shampoo
 Other antifungal shampoos
 Low potent steroid: hydrocortisone, desonide, fluocinolone
 Topical antifungals
 Scalp
  “Sebopsoriasis”
 “Seboriasis”

Psoriasis
 Polygenic trait: 8% chance if 1 parent has it
 Triggers:
Trauma
Drugs: B-blockers, systemic steroids, lithium, antimalarials
Alcohol
 Well-defined erythematous plaque with silvery-white scale
 Scales are loose and when removed produce blood droplets (Auspitz’ sign)
 Scalp: thick, adherent scales
 Koebner Phenomenon: physical trauma
 Elbows
 Knees
 Sacral-gluteal area
 Scalp
 Guttate: Palms & soles
 Streptococcal infection
 May resolve or become chronic type
 Inverse:
 Moist intertriginous area
 Ddx: candidiasis

Drug Reactions
 Maculo-papular drug reaction
 Looks like measles
 Delayed hypersensitivity
 Time: < 14 days, >9 days
 Generalized distribution
 Ddx: viral
 Drug reactions are asx except for pruritus
 Other drug reactions: fixed, hyperpigmented, pustular, hypersensitivity
syndrome, SJS, urticaria
Urticaria
 Erythematous
 Edematous
 Plaques
 Wheals
 Acute: <30 d
 Chronic: >30 d, idiopathic in 80%
 Immunologic: IgE mediated
1. Atopic background
2. Food- milk, eggs, wheat, shellfish, nuts
3. Therapeutic drugs
  Physical:
1. Dermographism
2. Cold
3. Solar
4. Pressure
5. Cholinergic- exercise
6. Aquagenic
7. Rx: antihistamines, oral steroids, prevention

Angioedema
 Subcutaneous edema
 Eyelids, lips, tongue
 Laryngeal
 Ears

Acne Vulgaris
• follicular hyperkeratinization
• increased sebum production
• colonization with P acnes
• inflammation
• Skin lesions
• Comedones: open or closed
• Pustules
• Cysts
• May clear spontaneously in early 20s
• PCOS
• Hereditary
• Treatment
• Topical antibiotics
• Clindamycin, erythromycin
• Topical retinoids
• Tretinoin, retinoic acid, adapalene
• Benzoyl Peroxide
• AHA
• Treatment takes 2 to 5 months
• Oral antibiotics
• Minocycline or doxycycline 50 to 100mg BID
• Lymecycline
• OCP
• Oral isotretinoin

Melasma
• Brown hyperpigmentation that occurs in the exposed areas from exposure to
sunlight
• Females
• Associated with pregnancy, OCP, medications
 • Sunblock
• Topical bleaching agents:
• Hydroquinone
• Vitamin C
• Azelaic acid
• Glycolic acid
• Tretinoin
Vitiligo
• 10 to 30 years old in 50% of cases
• Transmission is polygenic
• THREE theories re mechanism of destruction of melanocytes
1. Autoimmune theory
2. Neurogenic theory
3. Selfdestruct hypothesis
Chalk or pale white macules
With sharp margins
Diagnosis is clinical
Associated with thyroid diseases
Chronic course

• Repigmentation
– Return to normal melanin pigmentation
– Topical glucocorticoids
– Topical PUVA
– Systemic PUVA
– Narrowband UVB
– Tacrolimus, pimecrolimus
• Minigrafting: for stable and segmental types
• Depigmentation
– Monobenzylether of HQ 20%
• Permanent and irreversible
• Sunscreens
• Cosmetic cover up

BCC
• Most common type of skin cancer
• Locally invasive, nonmetastatic
• Older than 40 y.o.
• Males>females
• Nose and face are common sites
• Risk factors:
• UV exposure
• Light hair and eye color
• Northern European ancestry
• Inability to tan
• Types:
• Nodular
• Most common type
• Sun exposed area of head and neck
• Larger lesions: “rodent ulcer” has central necrosis

• Sclerosing/morpheaform
• Ivory white appearance
• Resemble a scar
• Absence of trauma or surgical history

• Superficial
• Trunk
• Erythematous patch that resembles eczema
• Isolated eczema that does NOT respond to treatment

• Pigmented
• Exhibits increased melanization
• Hyperpigmented, translucent papule
• Ddx: melanoma
•
• Ulcerating
• Fibroepithelioma of Pinkus

• Punch biopsy
• Large nuclei with little cytoplasm
• Nuclei may appear atypical
• Mitotic figures are absent
• Mohs micrographic surgery:
• Superior analysis of tumor margins with maximal conservation of
tissue
• Treatment of choice for morpheaform, poorly delineated,
incompletely removed
• For recurrent BCC
• For high risk sites (nasofacial junction, retroauricular areas)
• Standard excision
• 4mm margins
• Curettage and dessication: if lesion is less than 1cm
• Cryosurgery: two freeze thaw cycles
• Imiquimod- biologic response modifier
• Elicits IFN and IL 12
• 10-16 weeks of treatment
• BID for 6 weeks
• S/E: erythema, edema, pain, vesicles, ulceration and scabbing
• 5 FU
• Photodynamic therapy
• Radiation therapy
 SCC
• Usually arises from AK and Bowen’s disease
AKTINIC KERATOSIS
• Solar keratosis
• Single or multiple
• Dry, rough, adherent scales
• On sun-exposed areas

• Dermpath: large bright staining keratinocytes with pleomorphism in the

basal layer
• Treatment
– Prevention: sunscreen
– Crysurgery
– 5FU BID for 2-4 weeks
– Imiquimod BID for 16 weeks
– Retinoids
– TCA peels
– Laser

BOWEN’S DISEASE
• Carcinoma in situ
• Caused by UVB or HPV infection
• Solitary or multiple macules, papules or plaques, with scaling or
hyperkeratosis
• UVR: in areas with photoaging
• HPV: genital area
• Dermpath: loss of epidermal architecture, keratinocyte polymorphism,
increased mitotic rate, multinuclear cells
• Basement membrane intact
• Treatment: 5 FU, imiquimod, cryosurgery, PDT, surgical excision

SCC
• Older than 55 y.o
• Males > females
• Less common than BCC
• Carries a risk of metastasis
• Associated with increased UV exposure, persons with white skin and poor
tanning capacity
FACTORS:
• Precursor lesion
• UV exopsure
• Ionizing radiation
• Carcinogens- pitch tar, crude paraffin oil, fuel oil, lubricating oil,
nitrosoureas, arsenic
• Immnosuppression
 • Scars
• Burns, chronic heat exposure
• HPV
• Genodermatoses
• Sun exposed areas: head, neck, hands
• Legs (women)
• Arises in solitary fashion
• Flesh or erythematous keratotic papule or plaque
• May be pigmented
• May be a smooth nodule
• May be a thick cutaneous horn
• Genital SCC
• Vulva: anterior labia majora
• Pruritus or bleeding
• Cervix
• Oncogenic HPV 16, 18, 31, 33, 35, 39, 40, 51-60
• Scrotum
• Penis
• Uncircumcised males
• Diagnosis is always made by skin biopsy
• Hallmark is extension of atypical keratinocytes beyond the basement
membrane and into the dermis
• TX:
• Nonexcisional ablative techniques for in situ cases
• EDC
• Cryotherapy
• Carbon dioxide laser
• Intralesional chemotherapy
• PDT
•
• Conventional surgical excision – treatment of choice
• 4mm margins
• Mohs micrographic surgery
• Infiltrative, poorly defined
• Lip, ear, nail bed, nasal tip, eyelid, genitalia
• Involvement of nerve, bone and muscle
• History of radiation at site
• Immunosuppressed patient
• Recurrent or large scc
• SCC from scars
•
Melanoma
• Solar radiation: major cause
• Men: upper back, upper extremities
• Women: upper back and lower legs
• Asians and blacks: soles, mucous membranes, palms, nail beds
 • Risk factors:
• Pigmentary characteristics:
• Blue eyes
• Blond, red hair
• Light complexion
• Response to sun exposure:
• freckling, tendency
• Inability to tan
• Tendency to sunburn
• immunosuppression
• Upper socioeconomic status
• Family history of melanoma
• Nevi
• Melanocytic nevi
• Dysplastic nevi
• Changing mole
• Congenital nevus
• History of prior melanoma

• Superficial spreading 70%

• Most common type
• Arises within preexisting nevus
• Earliest change is darkening within a nevus
• Borders with notching and scalloping
•
• Nodular melanoma 15%
• Acral lentiginous 10%
• Common in darker complexions
• Palms, soles, beneath the nail plate
• Tan, brown to black flat lesions with variegations in color
• More aggressive with poorer prognosis
•
• Lentigo maligna melanoma 5%
Metastases
• Regional LN
• Nonvisceral sites: most common
– Skin, subcutaneous tissue, distant LN
– Lung, brain, GIT
• Pattern of coloration
• Histopath: fully evolved cytologic atypia
– Cellular enlargement, nuclear enlargement,
– Variations in nuclear size and shape
– Pagetoid spread
Treatment
• Surgical excision
• Sentinel LN biopsy
• Adjuvant therapy with regional metastases
– IFN alpha
• Therapy for distant mets
– Radiation, chemotherapy, biologics