Disorders of Hyperpigmentation Flashcards

1
Q

What groups are more likely to get melasma?

A

Young to middle-aged women of Asian, Hispanic, African or Middle Eastern descent (Fitz III and above often)

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2
Q

Though the exact pathophysiology of melasma is largely unknown, what is an important/primary trigger?

A

UV radiation and visible light may activate hyper-functional melanocytes to produce more melanin

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3
Q

What factors may worsen melasma?

A

Sun exposure, estrogen (pregnancy, OCP’s and HRT), genetic influences, thyroid dysfunction, and medications like phenytoin and other phototoxic medications

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4
Q

What is the clinical presentation of melasma and what are the 3 clinical patterns?

A

Symmetric light to dark brown/gray irregular patches on the face

3 types: 1. Centrofacial, 2. Malar, 3. Mandibular

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5
Q

What are the 4 types of melasma (not clinical subtypes)?

A

Epidermal, dermal, mixed, and indeterminate

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6
Q

How can the Wood’s lamp help differentiation epidermal from other types of melasma?

A

The epidermal type is accentuated by the Wood’s lamp whereas the dermal type is not accentuated (or ones that are primarily dermal)

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7
Q

Treatments for melasma?

A

Everybody should be encouraged to use broad-spectrum sun protection/avoidance. Hydroquinone, tretinoin, steroids, and resurfacing can be offered as well. Some are starting to use systemic tx like tranexamic acid. Patients must be asked about hx of clotting disorders/DVT/stroke etc as this can increase the propensity to clot.

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8
Q

What is the histology of lichen planus pigmentosus?

A

Sparse band of lymphs with mild perivascular infiltrate in upper dermis. Also see dermal melanophages and basal cell degeneration (note this is one of the few lichenoid disorders with vacuolar interface inflammation

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9
Q

What skin types are most commonly affected by lichen planus pigmentosus?

A

Skin types III-V

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10
Q

What is the clinical appearance of lichen planus pigmentosus?

A

Irregular oval, brown to gray-brown macules and patches in sun exposed or intertriginous areas

Usually symmetric, may be reticulated or follicluar in pattern too

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11
Q

What is linear and whorled nevoid hypermelanosis?

A

Heterogenous, sporadic mosaic skin condition in which a clone of skin cells leads to increased pigment production

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12
Q

What is the clinical appearance of whorled nevoid hypermelanosis?

A

Hyperpigmented macular Blaschkoid whorls and streaks typically occuring before 1 year of age

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13
Q

What are some associated findings with whorled nevoid hypermelanosis?

A

Neurologic, MSK, or cardiac findings can be seen

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14
Q

Tx of whorled nevoid hypermelanosis?

A

No tx, persists indefinitely

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15
Q

Who is affected by prurigo pigmentosa?

A

Occurs in young adults F>M; Japanese especially

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16
Q

What is the clinical appearance of prurigo pigmentosa?

A

Pruritic erythematous papules and papulovesicles on back/neck/chest, which develop rapidly and involute in < 1 week leaving residual reticulated macular hyperpigmentation

17
Q

What is the treatment for prurigo pigmentosa?

A

Minocycline/doxycycline, dapsone

18
Q

What are the genetics of familial progressive hyperpigmentation?

A

AD; mutation of KIT ligand gene (KITLG)

19
Q

What is the clinical appearance of familial progressive hyperpigmentation?

A

Begins in infancy and hyperpigmentation increases in surface area with age

Diffuse hyperpigmented patches involving the soles, palms, lips, and conjunctiva

20
Q

What endocrinopathies can affect hyperpigmentation?

A

Addison’s, Cushing’s, acromegaly, and hyperthyroidism can ll affect ACTH and MSH levels leading to general increase in pigmentation

21
Q

What are pigmentatry demarcation lines (Futcher’s lines, Voight lines, Ito’s lines)?

A

Lines of demarcation between dorsal and ventral skin surfaces, dorsal skin tends to be more hyperpigmented

*More apparent in darker-skinned individuals