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Skin Cancers

Basal Cell Carcinoma (BCC)

The most common human malignancy, it is a basal cell tumor of the epidermis found in about 1/3 of people. Sun and radiation exposure put patients at risk, along with a history of previous skin cancer and immunosuppression. It can be part of a genetic condition (Gorlin's Syndrome) or appear sporadically due to mutations in PTCH. It begins as a nodule that eventually can ulcerate and bleed (painless). On histology, basal cells appear as "palisading nuclei" and seem detached from the dermis because of artifact, indicative of BCC. It can be treated with imiquimod, surgery (Mohs), and radiation/chemotherapy.

Squamous Cell Carcinoma (SCC)

Although less common than BCC, SCC is more likely to metastasize. Risk factors include low Fitzpatrick skin type, sun exposure, genetics (xeroderma pigmentosum), radiation, and immunosuppression. Tumors are higher risk if they are large size, deeply invasive, poorly differentiated, or recurrent. SCC begins as a reddish plaque that can ulcerate and bleed (painful). Histology will show formation of keratin pearls and dermal invasion. It can be treated with imiquimod, surgery (Mohs), and radiation/chemotherapy.

Malignant Melanoma

Unlike BCC and SCC, which are tumors of the keratinocytes, melanoma is a tumor of melanocytes. Although rarer than the other types, it is much more likely to become malignant. Risk factors include family or personal history, light skin, increased number of dysplastic or congenital nevi, and immunosuppression. Pathogenesis is often linked to BRAF, p16, and p53 mutations. Melanomas present with the ABCDEs: Asymmetry, uneven Borders, multiple Colors, Diameter larger than 6mm, and Evolution of the lesion (not intelligent design). Melanomas should initially be excised with narrow margins, then more tissue can be removed as needed. The depth of invasion, known as the Breslow thickness, is used for prognostic value. A lymph node biopsy may also be indicated for staging. Metastatic melanoma can be extremely difficult to treat, though ipilimumab has shown some effect. Patients should follow up every year after excision for a full skin and lymph node exam.

Immunobullous Disorders

Pemphigus Foliaceus

Subcorneal scaling/crusting blisters caused by IgG against desmoglein-1. Lesions present on the face, chest, and back, but not found on mucous membranes. Histology shows separation of the corneum from the rest of the epidermis.

Pemphigus Vulgaris

Intraepidermal flaccid blisters caused by IgG against desmoglein-3. Appears on mucous membranes, face, axilla, and groin. It shows a positive Nikolsky sign (lateral shearing causes blistering). Immunofluorescence shows staining around each keratinocyte. Histology shows suprabasilar separation due to destruction of desmosomes but not hemidesmosomes, cells also acantholyse (rounding due to loss of connections). Treat with steroids and immunosuppressants, rituximab can also be used.

Bullous Pemphigoid

Subepidermal tense blisters cuased by IgG against hemidesmosomes. It tends to be found in older individuals. Immunofluorescence will show linear staining of IgG along the basement membrane. Histology will show separation of the epidermis from the basement membrane, along with eosinophilic infiltrate. Treat with steroids and immunosuppression.

Epidermolysis Bullosa Acquisita

Similar to bullous pemphigoid, caused by IgG. Hemorrhagic blisters form at areas of friction and eventually scar. Histology shows subepidermal blistering with neutrophils, monocytes, and eosinophils at the basement membrane.

Linear IgA Disease

Subepidermal blisters caused by IgA that is either idiopathic or drug-induced. Histology shows neutrophils and eosinophils at the basement membrane.

Dermatitis Herpetiformis

Subepidermal blisters caused by IgA antibodies against tissue transglutaminase, and is often connected to gluten intolerance (celiac disease). Patients present with pruritic, erythematous plaques with grouped vesicles. Immunofluorescence shows IgA staining along the basement membrane. Treat by abstaining from gluten.

Bullous SLE

Subepidermal blisters arising from SLE flares. Histology shows neutrophils infiltrating near the basement membrane. Immunofluorescence shows IgG at the basement membrane and positive ANA.

Stevens Johnson Syndrome (SJS)

A full-body blistering disease often caused by drug reactions and some infections. Toxic epidermal necrolysis (TEN) is a more severe subset of SJS.

Inflammatory Skin Disorders


A chronic inflammatory condition causing silvery plaques on an erythematous base. The disease occurs because naive CD4 cells activate Th1, Th22, and Th17 cells through production of IL-12 and IL-23, leading to production of IL-17, IL-22, and IFN-g, along with TNFa from macrophages. This causes thickening and proliferation of the skin, which shows on histology as acanthosis (thickened epidermis), hyperkeratosis (thickened stratum corneum), and parakeratosis (nuclei in the stratum corneum). Histology also shows lengthening of the dermal papilla, bringing blood vessels closer to the surface. Peeling of plaques results in spots of blood, known as Auspitz sign. Psoriatic plaques tend to appear on extensor surfaces, such as elbows and knees, though they also appear on buttocks and scalp. One subtype, guttate psoriasis, is preceded by Group A Strep infection and presents with plaques on the trunk. In addition to silvery plaques, patients present with nail pitting, plaque-formation in scars (Koebner phenomenon), and psoriatic arthritis. Treatment includes moisturizers, topical steroids, calcineurin inhibitors, UV therapy, and immunosuppression.

Atopic Dermatitis (Eczema)

A Type I hypersensitivity reaction to an allergen, causing edema and itching in the skin. The disease occurs because disruption of the skin barrier allows in allergenic proteins, which activate IgE production through IL-4 from Th2 cells, leading to allergic inflammation. Diagnosis requires 3 out of 4: chronic relapsing dermatitis, pruritis, age-appropriate morphology/distribution, and family history of atopic diseases. Almost all patients present with dermatitis by age 5. Patients tend to have other allergic conditions, such as asthma and rhinitis. Vasodilation from histamine release causes intraepidermal edema, presenting on histology as spongiosis. Treatments include moisturizers, topical steroids, calcineurin inhibitors, antibiotics, UV light exposure, and immunosuppression.

Contact Dermatitis

Contact with a hapten results in modification of proteins in the skin, activating a Type IV hypersensitivity response. Dendritic cells take up the haptenated proteins and present it to T-cells, resulting in a cell-mediated response. Eventually Tregs cause the reaction to calm, inhibitory cytokines (IL-10) are produced, and the haptenated protein is cleared.

Dermatology Medications


This medication works by activating TLR7 to stimulate cytokine production and dendritic cell recruitment. It is used against BCC and SCC.

Topical Steroids

Useful for any skin condition involving an overactive immune system, works to provide general immunosuppression while avoiding systemic toxicity. Overuse or chronic use can result in permanent thinning of the skin.


Vemurafanib is a tyrosine kinase inhibitor against BRAF, used for melanoma. Rituximab is an anti-CD20 antibody, used for pemphigus vulgaris. Ustekinumamb is an anti-IL-12, anti-IL-23 used against psoriasis. Infliximab is an anti-TNFa antibody, and etanercept is a soluble TNFa receptor. Both are used for psoriasis.

UV Radiation

Although UV is one of the major causes of skin cancer, it can be used for psoriasis treatment. It works by inducing immune cell apoptosis, reducing the autoimmune destruction. Therapy can be done either locally or full-body in a certain kind of UV booth.

Calcineurin Inhibitors

These can be used for atopic dermatitis and psoriasis. They work by inhibiting T-cell function to prevent activation of the immune response. Examples include cyclosporine, tacrolimus, and pimecrolimus.