Derm lecture for PCP · 2018. 4. 2. · Herpes Zoster Herpes Zoster Treatment: Vaccination against...
Transcript of Derm lecture for PCP · 2018. 4. 2. · Herpes Zoster Herpes Zoster Treatment: Vaccination against...
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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?