Core Dermatology States (Clin Med I)

Macule

Flat, nonpalpable lesion

Patch

Flat, nonpalpable lesion >1 cm

Papule

Palpable lesion

Plaque

Palpable patch

Nodule

Palpable lesion >1 cm

Pustule

Papule containing purulent material

Vesicle

Blister

Bulla

Blister >1 cm

Keloid

Fibrous hypertrophic tissue that forms at the site of injury

Acne keloidalis nuchae

Chronic inflammatory disorder of hair follicles on the posterior neck that causes papules/plaques, keloid formation, and eventual alopecia

Who is most commonly affected by acne keloidalis nuchae?

Black males

Risk factors associated with acne keloidalis nuchae

Close hair cutting practices and hair texture

AKN presentation

Pruritic/painful papules and pustules on the posterior neck → may progress to keloidal plaques, scarring, alopecia, and sinus tracts

AKN diagnosis

Usually clinical; histopathology may show perifollicular inflammation with lymphocytes/neutrophils and dermal fibrosis.

Main treatment goal for AKN

Reduce inflammation and control secondary infection

First-line/mainstay treatment for AKN

Topical corticosteroids + sustained topical retinoid therapy; BPO ± clindamycin

AKN with signs of infection

Oral antibiotic such as doxycycline

Additional AKN treatment

Intralesional Kenalog

Refractory AKN

Surgery, laser, or oral isotretinoin

Pseudofolliculitis barbae

"Razor bumps" caused by a cutaneous reaction to hairs penetrating the skin after shaving/hair removal

Classic pseudofolliculitis barbae presentation

Firm papules and pustules in the beard area after shaving

Who is at increased risk for pseudofolliculitis barbae?

Postpubertal males and people with curly hair

Potential complications of pseudofolliculitis barbae

Post-inflammatory hyperpigmentation, scarring, and infection

Extrafollicular pseudofolliculitis

Hair exits the follicle and then reenters the skin

Transfollicular pseudofolliculitis

Hair penetrates the dermis before exiting the follicle

Most important treatment for pseudofolliculitis barbae

Stop or modify hair removal

Shaving modifications for pseudofolliculitis barbae

Keep hair ≥0.5 mm, moisturize 5-10 min before shaving, consider electric razor/chemical depilatories, and gently exfoliate trapped hairs

Medications for pseudofolliculitis barbae

Low-potency topical steroids, BPO/clindamycin, retinoids, ILK, or oral tetracyclines

Pseudofolliculitis barbae differential diagnosis

Tinea barbae and bacterial folliculitis

Dermatosis papulosa nigra (DPN)

Benign variant of seborrheic keratosis causing multiple small pigmented papules

Typical DPN appearance

Multiple 1-5 mm pigmented papules, predominantly on the face and neck

DPN diagnosis

Clinical, but abnormal lesions may require biopsy to rule out malignancy.

DPN treatment

No treatment required; cosmetic treatment includes cautery or cryotherapy

General skin cancer pattern in skin of color

Skin cancer occurs at lower rates but may have worse outcomes because of later detection.

Basal cell carcinoma in skin of color

Often presents as a pearly pigmented papule, sometimes with central ulceration.

Common BCC location

Head and neck

BCC behavior

Rarely metastasizes but can become locally invasive

BCC treatment

Mohs surgery, excision, topical therapy, or radiation

Most common skin cancer in Black patients

Squamous cell carcinoma

Important SCC risk factors in skin of color

Immunosuppression, chronic inflammation, radiation, lupus, chronic ulcers/scarring, and HPV

Common SCC location in Black patients

Lower legs

SCC presentation

Nonhealing sore with crusting/easy bleeding OR pigmented warty growth

Melanoma

Deadliest form of skin cancer

Melanoma presentation in skin of color

Dark rapidly changing macule, changing nevus, or rapidly evolving nail band

Common melanoma locations in skin of color

Palms, soles, and nails; oral melanoma also occurs at higher rates

Concerning nail finding for melanoma

Rapidly evolving nail band/Hutchinson sign >3 mm

Melasma

Chronic hyperpigmentation disorder caused by hyperfunctional melanocytes in the dermis

Who commonly develops melasma?

Women of reproductive age, particularly those with darker Fitzpatrick skin types.

Melasma risk factors

Pregnancy, hormonal changes, genetics, sun exposure, and medications such as OCPs

Classic melasma presentation

Symmetric irregular light-brown/gray macules and patches on sun-exposed facial skin

Common melasma locations

Forehead, nose, cheeks, and upper lip

Melasma symptoms

Asymptomatic; chronic and recurrent

Melasma diagnosis

Usually clinical; Wood's lamp may be used, but dermal melasma will not illuminate.

Goal of melasma treatment

Inhibit melanogenesis + increase cell turnover

Melasma treatment

Photoprotection, hydroquinone, steroid/tretinoin/hydroquinone combinations, azelaic acid, or chemical peels

Hydroquinone

Inhibits melanin formation

Post-inflammatory hyperpigmentation (PIH)

Hyperpigmentation occurring after inflammation due to excess melanation

Common causes of PIH

Acne, eczema, burns, and trauma

Who tends to have more significant PIH?

Patients with darker Fitzpatrick skin types

PIH treatment

Photoprotection + hydroquinone

Post-inflammatory hypopigmentation

Loss/decrease of pigmentation following inflammation

Causes associated with post-inflammatory hypopigmentation

Pityriasis alba, tinea versicolor, laser/cryotherapy, vitiligo, and discoid lupus

Post-inflammatory hypopigmentation treatment

Treat the underlying cause

Prurigo nodularis

Chronic inflammatory skin condition characterized by symmetric, intensely pruritic, firm nodules

Typical patient with prurigo nodularis

Older adult with severe itching and multiple firm nodules

Prurigo nodularis presentation

Erythematous dome-shaped nodules, commonly on upper extensor surfaces, with severe pruritus

Prurigo nodularis diagnosis

Biopsy is not required but is commonly performed

When should systemic workup be considered in prurigo nodularis?

When pruritus is out of proportion to the skin findings

Prurigo nodularis workup when indicated

CBC, LFTs, BUN/creatinine, HIV, urinalysis, TSH, and chest X-ray

Conditions associated with prurigo nodularis

Atopic dermatitis, renal failure, diabetes, cardiovascular disease, hepatitis C, and psychiatric disorders

Main goals of prurigo nodularis treatment

Break the itch-scratch cycle, reduce pruritus, decrease lesion burden, and treat underlying disease

Few/localized prurigo nodularis lesions

Intralesional Kenalog or super-potent topical corticosteroids such as clobetasol/betamethasone

Diffuse prurigo nodularis

Dupilumab or narrow-band UVB phototherapy

Pemphigus

Life-threatening group of autoimmune blistering disorders caused by acantholysis

Acantholysis

Loss of adhesion between keratinocytes → blister formation

Mechanism of pemphigus

Circulating IgG autoantibodies attack cellular adhesion molecules

How is pemphigus diagnosed?

Biopsy with and without direct immunofluorescence (DIF) + serology

Four major pemphigus types in this lecture

Pemphigus vulgaris, pemphigus foliaceus, IgA pemphigus, and paraneoplastic pemphigus

Pemphigus vulgaris presentation

Middle-aged patient with mucosal and skin erosions

Pemphigus foliaceus presentation

Fragile blisters WITHOUT mucosal involvement

IgA pemphigus presentation

Vesicles and crusting plaques with herpetiform morphology

Paraneoplastic pemphigus presentation

Severe stomatitis with variable cutaneous findings and restrictive bronchitis

Pemphigus treatment

Emergent referral; oral glucocorticoids + IV rituximab

Why is pemphigus important to recognize?

It is life-threatening and may require burn-unit-level care.

Pemphigoid

Autoimmune blistering disease occurring primarily in older adults

Pemphigoid blister location

Subepithelial

Bullous pemphigoid prodrome

Weeks to months of urticarial or eczematous patches

Classic bullous pemphigoid presentation

Tense, fluid-filled bullae, typically 1-3 cm.

Common bullous pemphigoid distribution

Trunk, extremities, and axillary/inguinal folds

Bullous pemphigoid course

Can flare for years or spontaneously resolve and may be drug induced.

Mucous membrane pemphigoid

Chronic relapsing/remitting mucosal blistering and erosions ± skin involvement

Most common site of mucous membrane pemphigoid

Oral cavity

Pemphigoid diagnosis

Lesional biopsy for H&E + perilesional biopsy for DIF + serology

Pemphigoid DIF

IgG and/or C3

Pemphigoid serology

BP180/230

Localized pemphigoid treatment

High-potency topical corticosteroids

Initial systemic pemphigoid treatment

Prednisone or doxycycline

Refractory pemphigoid treatment options

Dupilumab, MMF, IVIG, or dapsone

Pemphigoid with ocular or oral involvement

Refer

Pemphigus pathology

Loss of keratinocyte adhesion (acantholysis) → fragile blistering/erosions; can involve mucosa; life-threatening