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 Toronto Notes 2019 Common Skin Lesions
Management
• neworchangingpigmentedlesionsshouldbeevaluatedforatypicalfeatureswhichcouldindicatea melanoma
• excisionalbiopsyshouldbeconsideredifthelesiondemonstratesrapidchange,asymmetry,varied colours, irregular borders and persistent pruritus or bleeding
Dermatology D9
OTHER ACQUIRED PIGMENTED LESIONS
Table 6. Comparison of Other Acquired Pigmented Lesions
  Atypical Nevus
(Dysplastic Nevus)
Ephelides
(Freckles)
Solar Lentigo
(Liver Spot)
Becker’s Nevus
Melasma
Clinical Presentation
Variegated macule/ papule with irregular distinct melanocytes in the basal layer
Risk factors: family history
Small (<5 mm) well- demarcated light brown macules
Sites: sun-exposed skin
Well-demarcated brown/black macules Sites: sun-exposed skin
Hairy, light brown macule/patch with a papular verrucous surface
Sites: trunk and shoulders, onset in teen yr
Symmetrical hyperpigmentation on sun-exposed areas of face (forehead, upper lip, cheeks, chin)
Pathophysiology
Hyperplasia and proliferation of melanocytes extending beyond dermal compartment of the nevus
Often with region of adjacent nests
Increased melanin within basal layer keratinocytes secondary to sun exposure
Benign melanocytic proliferation in dermal- epidermal junction due to chronic sun exposure
Pigmented hamartoma with increased melanin in basal cells
Increase in number and activity of melanocytes Associated with estrogen and progesterone
Epidemiology
>5 atypical nevi increase risk for melanoma
Numerous dysplastic nevi may be part of familial atypical mole and melanoma syndrome
Skin phototypes I-II most commonly
Most common in Caucasians >40 yr
Skin phototypes I-III most commonly
M>F
Often becomes noticeable at puberty
F>M
Common in pregnancy and women taking OCP or HRT
Risk factors: sun exposure, dark skin tone
Can occur with mild endocrine disturbances, antiepileptic medications and other photosensitizing drugs
Differential Diagnosis
Melanoma
Junctional nevi Juvenile lentigines
Lentigo maligna, seborrheic keratosis, pigmented actinic keratosis
Hairy congenital melanocytic nevus
Post-inflammatory hyperpigmentation
Clinical Course and Management
Follow with baseline photographs for changes
Excisional biopsy if lesion changing or highly atypical
Multiply and darken with sun exposure, fade in winter
No treatment required
Sunscreen and sun avoidance may prevent the appearance of new freckles
Laser therapy, shave excisions, cryotherapy
Hair growth follows onset of pigmentation
Cosmetic management (usually too large to remove)
Often fades over several mo after stopping hormone treatment or delivering baby
Treatment: hydroquinone, azelaic acid, retinoic acid, topical steroid, combination creams, destructive modalities (chemical peels, laser treatment), camouflage make-up, sunscreen, sun avoidance
   Vascular Lesions
Table 7. Vascular Tumours Compared to Vascular Malformations
 Vascular Tumours
Endothelial hyperplasia Usually postnatal 1:3-5
Phases
Proliferating Involuting Involuted
Vascular Malformations
 Definition Presence at Birth M:F
Natural History
HEMANGIOMAS
Congenital malformation with normal endothelial turnover 100% at birth (not always obvious)
1:1
Proportionate growth (can expand)
 Clinical Presentation
• redorbluesubcutaneousmassthatissoft/compressible,blancheswithpressure;feelslikea“bagof worms” when palpated
Pathophysiology
• benignvasculartumour
• includes:cavernoushemangioma,capillary/infantilehemangioma,spiderhemangioma
A spider angioma will blanch when the tip of a paperclip is applied to the centre of the lesion
  



















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