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Dermatologyfor the Primary Care Provider

• Tirsa C Quartullo, DNP, FNP-C

• Arizona Dermatology & Cosmetic Surgery

Lecture Outline Skin Anatomy Topical Corticosteroids Eczema Contact Dermatitis Acne & Rosacea Papulosquamous Diseases

Seborrheic Dermatitis Pityriasis Rosea

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Lecture Outline Superficial Fungal

Infections Viral infections

Warts Herpes Zoster Molluscum

Contagiosum Benign Skin Tumors Actinic Keratosis

Non-melanoma skin cancers Basal cell CA Squamous cell CA

Malignant Melanoma

Difficult Dermatoses

Skin Anatomy Epidermis

Outermost part of the skin

Dermis Collagen, sweat

glands, nerve endings, oil glands

Subcutaneous Tissue

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Topical Costicosteroids Anti-inflammatory properties partly due to

vasocontriction Potency: Group I-VII Vehicle or Base Location Side effects/Long term use

Eczema The most common inflammatory skin disease Acute

Vesicles, blisters, intense redness and itch Subacute

Redness, scaling, fissuring, moderate itch, burning

Chronic Thickened skin (lichenified skin), excoriations,

fissuring

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Eczema

Eczema Adult presentation: Flexural, face and

neck with lichenification

Hand dermatitis most common form of adult eczema

Pediatric presentation:

Red skin, tiny vesicles, scaling, exudation, with wet crusts and cracks

Commonly seen on the antecubital and popliteal fossae

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Eczema Genetic aspects: familial correlation Skin barrier disruption:

Reduced ceramide (lipid) levels Increased trans-epidermal water loss

Microbial agents: Staph Areus, Strep, candida

Autoallergens: Elevated IgE levels

Foods: Children flare with eggs, milk, peanuts,

soybeans, fish, and wheat

Eczema Treatment Intramuscular steroids Topical steroids Intra-lesional steroid injections Anti-histamines Antibiotics Lubricants Systemic drugs (First Biologic: Dupixent) Lifestyle modifications

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Contact Dermatitis Irritant CD

Non-immunological (physical or chemical alteration)

Organic solvents, soaps

Onset slow, progressive

Allergic CD Genetically

predisposed Delayed

hypersensitivity reaction

Due to metals, formalin

Onset is rapid 12-24 hours (once sensitized)

Contact Dermatitis Treatment Remove offending agent Topical corticosteroids Patch test useful in ACD Use ointments over creams

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Acne Vulgaris Common chronic inflammatory condition

of the pilosebaceous unit Pathogenesis:

1. Increase sebum production2. Follicular hyperkeratinization3. Proliferation of Propionibacterium Acnes (

P. acnes)4. Inflammation

Acne Vulgaris Exacerbating factors:

Touching, rubbing, and over-cleansing the face Occlusion or rubbing from sports equipment Medications:

Progesterone only BCP, oral steroids, topical steroids, lithium

Diet: Excessive dairy, Gluten?, Westernized diets (high

glycemic diet)

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Acne vulgaris

Acne Vulgaris Treatment Oral Antibiotics

Doxy 100mg BID, minocycline 100mg BID Topical Therapy

Clinda/BPO (Benzaclin, Onexton) BID Retinoids (Retin-a, Tazorac) QHS Retinoid/BPO (Epiduo) QHS Dapsone (Aczone) BID

Oral Isotretinoin Amnesteen, Claravis (teratogenic!)

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Isotretinoin

Rosacea/Acne Rosacea Rosacea/Acne Rosacea

A common chronic inflammatory acneiformdisorder, of the facial pilosebaceous unit

Coupled with reactivity of capillaries leading to flushing and telangectasia

May result in rubbery, thickening, of nose cheeks, forehead, or chin due to sebaceous hyperplasia, edema, and fibrosis

Skin types 1-3; F>M (rhinophyma worse in males-”Clinton nose”)

Triggers should be identified

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Rosacea/Acne Rosacea

Rosacea/Acne Rosacea Treatment

Rosacea skin in sensitive skin! Identify triggers and avoid them Topical:

Topical metronidazole gel or cream BID Topical Soolantra (targets demodex mites)

Oral: Doxy/Mino 100mg BID, then maintenance dose

(50mg qd/bid) Isotretinoin – resistant

Cosmetic Photofacial/IPL

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Seborrheic Dermatitis Inflammatory condition that affects the

sebum rich areas of the body: face, scalp, chest and upper back

May be R/T an immune response to Pityrosporum yeast

Onset: Infants due maternal androgens and adults in 4th/5th decade of life

Presents as dry, itchy, fine, greasy scales Better in summer months, worse in winter

Seb Derm

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Seb Derm Treatment No cure, relapses are common Topicals for scalp:

Rx: Ketoconazole 2% shampoo TIW, OTC T-Sal, Tree Tea oil/shampoo

Rx: Dermasmoothe oil qhs Topicals for face:

Rx: Ketoconazole 2% cream BID Rx: low potency steroid: Desonide,

hydrocortisone 2.5% Rx: Sulfa based washes

Pityriasis Rosea Acute exanthematous eruption with an initial

plaque lesion or “herald patch” usually on the trunk

1-2 weeks later, a generalized secondary eruption develops in a “Christmas tree” distribution

Oval, slightly raised plaque or patch, salmon-red, with fine collarette scale at periphery

Spring and Fall season HHV-6 or HHV-7 reactivation Spontaneously clears in 6-8 weeks

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Pityriasis Rosea

Superficial Fungal Infections

Tinea Versicolor Etiology: Malassezia furfur Chronic, well-demarcated scaling patches

with hyper/hypo-pigmented lesions, most commonly found on the trunk.

Predisposing factors: Sweating, warm seasons, oily skin, summertime, aerobic exercise

Treatment: Selenium Sulfide lotion/shampoo 2.5%; ketoconazle cream/shampoo 2%; oral Fluconazole 400mg x1 dose

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Tinea Versicolor

Tinea Corporis Scaling, sharply marginated plaques with

peripheral enlargement and central clearing that produce annular configuartions

Transmission: Fomites (less so by direct skin contact), pets, and soil (least common)

Predisposing factors: Atopic patients, topical corticosteroids, immuno-compromised

Different locations: T. Cruris, T. Pedis, T. Capitis, T. Barbae

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Tinea Corporis Sampling:

KOH preparation will reveal multiple, septated, tubelike structures (hyphae) and spore formation- “spaghetti and meatballs”

Treatment: Topical: Ketoconazole 2% QD x 2 weeks (

except T. Pedis= 6 weeks) Oral: Terbinafine 250mg QD x 2 weeks

Tinea

Tinea Corporis Tinea Cruris

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Tinea Corporis Ddx: Granuloma Annulare

Benign Inflammatory dermatosis

Dermal papules and annular plaques seen in feet, ankles, lower limbs, and wrists

Women>Men Etiology: unknown

Hypothesized to be associated with: TB, insect bites, trauma, sun exposure, viral infections, and chronic stress

Tx: potent topical steroids, ILK, narrowband UVB, plaquenil or Dapsone(generalized GA)

GA

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Viral infections: Warts Caused by HPV (certain strains) Discrete, benign, epithelial hyperplasia

surface hyperkeratosis Transmission: Skin on skin contact Occurs at site of trauma: hands, fingers,

feet and knees Treatment: LN2, cantharidin,

electrodessication, topical imiquimod TIW, Tazorac qhs

Viral infections: MolluscumContagiosum

Due to the Pox virus Self-limiting epidermal viral infection, skin

colored papules often umbilicated More common in children and sexually

active adults Treatment: LN2, electrodessication,

cantharidin, Imiquimod TIW

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Molluscum Contagiosum

Viral Infections: Herpes Zoster Acute dermatomal infection associated with

reactivation of VZV Commonly known as “shingles” 3 clinical stages:

1.)Prodrome: Unilateral pain, tenderness, paresthesia

2.)Active infection: papulesvessiclespustlescrust

3.)Post herpetic neuralgia (PHN): 40% risk in patients >60 y/o, highest incident after ophthalmic zoster

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Herpes Zoster

Herpes Zoster Treatment:

Vaccination against VZV reduces incidence by 50%

Oral: Famciclovir 500mg q8h x 7days Valaciclovir 1gm q8h x 7 days, or Acyclovir 800mg 5/day x 7 days

Bed rest, pain management PHN treatment: Gabapentin 300-600mg TID,

Doxepin 300mg qhs

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Benign Neoplasms Seborrheic

Keratosis: Most common

benign epithelial tumor

Genetic inclination Appear >30 y/o Warty surface with

a “stuck on appearance”

Benign Neoplasms Dermatofibroma:

Common, button like dermal nodule, usually found in extremities

Usually due to a late reaction to arthropod bite

+”dimple sign”

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Benign Neoplasms Junctional Nevus:

Macule or slightly raised mole

Uniform tan, brown Round/oval or

smooth with regular borders

Benign Neoplasms Compound Nevus:

Papules or small nodules, dark brown or black

Dome-shaped , smooth or cobblestone like surface with sharply defined borders

<1cm in size

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Benign Neoplasms Dermal Nevus:

Sharply defined papule or nodule

Skin colored, tan or flecks of brown, often with telangectasia

Round, dome shaped, smooth

May be hairy

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Actinic Keratoses Neoplastic condition in which pre-

cancerous epithelial lesions are found on sun-exposed areas of the body

Increased in fair skinned patients “Rough” localized papules with ill-defined

borders that patient feels, but cannot see Asymptomatic If left untreated, can evolve into

squamous cell carcinoma

Actinic Keratosis

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AK treatment Cryotherapy PDT Field therapy:

Imiquimod cream (Aldara 5% BIW x 16 weeks; Zyclara 3.75% QHS x 2 weeks)

5-Flouroracil cream (Efudex 5% BID x 2-4weeks, Fluoroplex 1% BID x 2-6 weeks)

(Pre) Topical 5-fluorouracil

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Post 1st treatment of 5-FU

Post 2nd treatment of 5-FU

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2 Weeks post 5-FU discontinuation

Basal Cell Carcinoma Most common skin cancer in humans 80% of NMSC’s Locally invasive, aggressive, destructive,

but slow growing- no chance of metastasis

Skin Types 1&2 with prolonged sun exposure mostly at risk

Heavy sun exposure during youth Age: >40; M>F

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BCC Nodular BCC

Papule or nodule, “pearly” with telangectasia Ulcerating BCC

Ulcerated center with a rolled border Sclerosing BCC

Small whitish/flesh colored patch with peppery pigmentation

Superficial BCC Thin pink or red plaque with scaling

Pigmented BCC Brown, black or blue pigment

BCC

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sBCC

sBCCPost-Erivedge

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BCC Treatment Surgical excision Mohs Micrographic surgery ED&C Cryosurgery Topical Imiquimod (Aldara, Zyclara) Brachytherapy Erivedge

Squamous Cell Carcinoma Usually arises in epidermal precancerous

lesions ( AK’s) Sun induced lesions have a low rate of

distant metastasis Skin Types 1&2; >55 age; M>F

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SCC Differentiated SCC

Indurated papule, plaque or nodule with thick keratotic scale, may have a crust in the center. Horny material can be expressed

Undifferentiated SCC Fleshy, granulating, papules/nodules, friable,

and vulnerable SCC in-situ

Pink or red sharply defined scaly plaques. Often caused by sun exposure or HPV

SCC

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SCC Treatment Surgical excision Mohs Micrographic surgery ED&C Cryosurgery Topical 5-Flourouracil (Efudex, Fluoroplex) Brachytherapy

Mohs Micrographic Surgery Single most effective treatment for BCCs

and SCCs Cure rates: 98-99% Mohs 4 steps:

Surgical removal of tissue Mapping the piece of tissue, freezing,

cutting and staining the tissue Interpretation of microscope slides Reconstruction of the surgical defect

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Mohs- pre surgery

Mohs defect

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Mohs- closure

Mohs – 6 months post op

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ABC’s of Melanoma A: Asymmetry

Irregular in shape B: Border

Irregular, ill-defined borders C: Color

Presence of >1 color ( brown, black, tan) D: Diameter

>6mm E: Evolution

Recent change

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Dysplastic Melanocytic Nevus Precursor of Malignant Melanoma (MM) Acquired pigmented lesions with atypical

melanocytes Clinically: larger, variegated in color,

asymmetrical, with irregular borders Fair skinned individuals M=F

Dysplastic nevus

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Malignant Melanoma The most malignant tumor of the skin Arises from the malignant transformation of

melanocytes at the dermal-epidermal junction or from DN

In 2016: about 76,380 new melanomas will be diagnosed (about 46,870 in men and 29,510 in women)

In 2016: about 10,130 people are expected to die of melanoma (about 6,750 men and 3,380 women).

Malignant Melanoma- Types Melanoma in situ:

confined to the epidermis

Lesions are macules, multi-colored

no stage + radial growth,

no vertical growth

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Malignant Melanoma- Types Lentigo Maligna

Melanoma: Older persons Sun exposed areas Switches from

radial growth to vertical growth

Multi-colored with a “geographic shape”

MM Classification:

Breslow: thickness Clarks: Level 1( involves only epidermis)through

Level 5 (invades subcutaneous tissue) TNM Stage 1-5 (thickness of Tumor, lymph Node

involvement, & distant Metastasis) Treatment:

Surgical resection Sentinel lymph node biopsy Chemo/Biological therapy Clinical trials

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Prevention is key! Seek the shade, especially between 10 AM

and 4 PM Do not burn Avoid tanning and UV tanning beds Cover up with clothing, including a broad-

brimmed hat and UV-blocking sunglasses Use a broad spectrum (UVA/UVB) sunscreen

with an SPF of 15 or higher every day. For extended outdoor activity, use a water-resistant, broad spectrum (UVA/UVB) sunscreen with an SPF of 30 or higher.

Prevention is key! Apply 1 ounce (2 tablespoons) of sunscreen

to your entire body 30 minutes before going outside. Reapply every two hours or immediately after swimming or excessive sweating

Keep newborns out of the sun. Sunscreens should be used on babies over the age of six months

Examine your skin head-to-toe every month. See your physician every year for a

professional skin exam

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Difficult Dermatoses Bullous Pemphigoid Leukocytoclastic Vasculitis Erythema Multiforme

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Bullous Pemphigoid

Chronic autoimmune subepidermal blistering disease most frequently seen in the elderly

IgG autoantibodies bind to antigens that comprise the hemidesmosome adhesion complex in the basement membrane of the skin

This triggers complement activation and release of inflammatory mediators

The result is the formation of local or generalized, tense bullae.

Bullous Pemphigoid

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Bullous Pemphigoid Pruritus is prominent and may actually

precede the appearance of skin lesions BP should always be highly considered

when tense bullae are present in patients aged older than 60

BP rarely has mucosal lesions Tx: Prednisone, Dapsone, topical steroids,

methotrexate, doxycycline

Leukocytoclastic Vasculitis Heterogeneous group of disorders that

are uniformly characterized by purpuric or erythematous papules, vesicles, urticarial lesions, or petechiae

LCV is an inflammatory process of small blood vessels due to a complex interplay of immune complex deposition and autoantibody production

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LCV

LCV

Inciting factors: Medications (especially antibiotics, NSAIDs, and

diuretics), pathogens (hepatitis viruses, HIV, streptococci), malignancy, inflammatory bowel disease, or collagen vascular diseases (check labs to R/O systemic disease)

Up to 50% of cases, however, have no identifiable cause and are considered idiopathic

Treatment: Prednisone, Methotrexate, Dapsone

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Erythema Multiforme Self-limited hypersensitivity reaction of the skin

and mucous membrane Characterized by acute onset of target

lesions (mostly acral region) Primary trigger: HSV (90% cases) in adults Primary trigger: Penicillin, Group A strep, and

EBV in children Cutaneous lesions appear within 24-72 hours

and spontaneously resolve in 2 weeks

Erythema Multiforme

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Erythema MultiformeTreatment

Treat any identifiable underlying condition Symptomatic relief: NSAIDs, antihistamine,

cool compresses Mid potency steroids For early lesions or or recurrent episodes:

antiviral therapy (Valtrex 500mg-1gm qd)

QUESTIONS/COMMENTS?