Dermatology Test Interpretation
Diagnostic Test
Measures
Indications
Dermoscopy
Examination of skin lesions using a device made up of a magnifier, non-polarised light source, and a transplarent plate
Any skin lesion
ABCDE's of Dermatology
Process for inspecting pre-existing or new moles
Skin Biopsy
Shave Biopsy
Punch Biopsy
Excisional Biopsy
A B C D E
Asymmetry Borders Color Diameter Elevation / Evolve Find the newest lesion to sample
Timing
Timing is not important for basal cell carcinoma or dysplastic nevi
Histologic analysis of skin tissue
Skin lesion and a thin layer of surrounding skin are removed with a small blade
Multiple dermal layers are removed
Complete removal of lesion and surrounding skin
Site Selection
Most characteristic area of the lesion Go for advancing borders Avoid hyperkeratotic, hyperkeratotic, scarred, excoriated, or denuded areas
Basal cell carcinoma
Squamous cell carcinoma
Actinic keratosis
Verrucae
Moll Mollus uscu cum m cont contag agio iosu sum m
Dysp Dyspla last stic ic nevi nevi
Mali Malign gnan antt melan melanom oma a
Gran Granul ulom oma a annul annular are e
Erythema nodosum
Vasculitis
Dermal pathology
Depth of lesion is needed for staging
Melanoma
Thought to be in the deep dermis of subcutaneous fat
Result
Parameters
Melanoma
Asymmetric Irregular borders Various colors Larger than a pencil Elevated
Other
Procedure Clean biopsy site with alcohol Mark site (if needed) Anesthetize Shave lesion Perform wound care Send to pathology Procedure Clean biopsy site with alcohol Mark site (if needed) Anesthetize Punch lesion Remove specimen w/ tissue scissors Close with suture Perform wound care Elliptical excision usually with layered closure
Compiled by Drew Murphy, Duke Physician Assistant Class of 2015
Dermatology Diagnostic Test
Measures
Serology
Study of antibodies in plasma serum or other body fluids
Test Interpretation
Indications
Result
HSV I
HSV II
Lyme disease
Autoimmune diseases Lesion is cut.
Mohs Surgery
Other
Parameters
> 98% cure rate
Microscopically controlled surgery Tissue micrscopically analyzed. used to treat common types of Tissue repeatedly cut and analyzed until the tissue skin cancer is cleared of cancer cells.
Wood's Lamp
Black light
KOH Prep
Quick, inexpensive fungal test to differentiate dermatophytes and Candida albicans from other skin disorders
Diascopy
Test for blanchability by applying pressure with a glass slide and observing color changes
Vesicle Viral Culture
Determines presence of a viral infection
Tzanck Preparation Pustule Culture
TV lesion
Vitiligo
Erythrasma Tinea Capitus
Tinea cruris
Erythrasma
Vitiligo
Tinea versicolor
Dermatophytes
Candida albicans
Yeast
Tinea Versicolor
Blanching
Erythematous lesions
Non-Blanching
Vesicles Herpes zoster Herpes simplex
Alternative testing modality for viral infections
Bacterial culture of a pustule
Vesicular infections
Coral fluorescence No fluorescence Hypopigmentation visible Scale is collected by scraping the advancing border of the lesion with a Spaghetti and meatballs #15 blade or glass slide. Allow scale to fall onto second glass slide Inflammation Angiomas Purpura Ecchymosis Portwine stain Vasculitis Procedure Select a fresh lesion Use a #11 blade or swab to unroof the vesicle Roll swab over lesion to collect fluid and place in viral culture medium. Send to lab
Pemphigus
Viral Infection
Multinucleated giant cells
Procedure Blister is opened along side. Roof is folded back. Underside scraped. Material collected is smeared onto a microscope slide.
Procedure Select a fresh lesion. Use a #11 blade to gently nick the surface of the pustule Use a bacterial culture swab to collect content. Send for culture and sensitivity.
Compiled by Drew Murphy, Duke Physician Assistant Class of 2015
Dermatology Diagnostic Test
Scabies Preparation
Measures
Indications burrow or intact papule. Select a linear burrow or
Test to diagnosis scabies
Thin shave biopsy is performed Specimens placed on a microscope slide and covered with immersion oil. Look under low power Allergic contact dermatitis
Patch Testing
Test Interpretation Result
Determines sensitivities to specific allergens
Examples of Testable Allergens
Neomycin Black rubber Fragrance Propylene glycol Nickel Wool alcohols
Parameters
Other
Mite POSITIVE
Eggs Feces Patients avoids antihistamines or any steroid preparations for > 2 weeks before testing.
Compiled by Drew Murphy, Duke Physician Assistant Class of 2015
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms Flat (nonpalpable)
Macule
Primary lesion
Laboratory Test
Result
Treatment
Medications
Other Patch Large macule (> 1 cm)
≤ 1 cm Alteration in color Raised (palpable)
Papule
Primary lesion
Plaque Large papule (> 1 cm)
≤ 1 cm Variable color Bulla Large vesicle (> 1 cm)
Raised
Vesicle
Primary lesion
Filled with clear fluid
≤ 1 cm Raised (palpable)
Pustule
Primary lesion Varable size
Circumscribed Circumscribed collection of inflammatory cells and free fluid
Raised
Nodule
Primary lesion
Round and solid Deeper than papule
Wheal (Hive)
Primary lesion seen in type I hypersnesitivity reaction
≤ 1 cm Firm, edematous papule or plaque Unbound fluid
Flat-toppedelevations
Transient Very common in fungal skin infections.
Scale
Secondary lesion
Crust (Scab)
Secondary lesion
Collection of serum, blood, or pus
Focal loss of epidermis
Erosion
Secondary lesion Heals without scarring
Clinical Medicine Condition / Disease
Ulcer
Cause
Signs and Symptoms Focal loss of epidermis and dermis
Secondary lesion Heals with scaring
Fissure
Secondary lesion
Atrophy
Secondary lesion
Excoriation
Lesion from scratching
Comedo
Blackhead or whitehead
Milia
Small, superficial keratin cyst
Cyst
Closed sac that has a distinct membrane and devision compared to the nearby tissue
Burrow
Narrow, elebated tunnel due to a parasite
Linchenification
Thickening of the skin
Linear "crack"
Visible opening is often seen
Laboratory Test
Result
Treatment
Medications
Other
Clinical Medicine Condition / Disease
Cause
Telangectasia
Dilated superficial vessels
Signs and Symptoms
Laboratory Test
Result
Treatment
Other
Purpura Large petechaie (> 1 cm)
Nonblanchable
Petechiae
Medications
Blood deposit ≤ 1 cm Non-Bullous Impetigo
Impetigo
"Scabbing eruption" caused by group A β-hemolytic Streptococcus pyogenes or S. aureus
Bactroban
Small pustules or vesticles that erode and curst (honey-colored) (honey-colored)
Topical Antibiotics Altabax (MSSA only)
Usually inflammed Bullous Impetigo
Cephalosporins
Vesicles or bullae containing clear or turbid fluid Surrounding skin can be normal
Systemic Antibiotics Dicloxacillin Plaques with more defined borders
Can be confused with inflammatory dermatoses such as psoriasis, seborrheic dermatitis, or atopic dermatitis
No satellite lesions
Bacterial Intertrigo
The role of topical steroids is controversial.
Odor
Non-specific bacterial infection of opposed skin Etiologies
Group A and B Streptococci Non-dpihtheroid Non-dpihtheroid species of Corynebacterium
Topicalantibiotics
Neck-fold intertrigo in babies is due to Strep.
P. aeurginosa
Erythrasma
Chronic superficial skin infection by C. minutissimum
Commonly seen in intertriginous intertriginous skin
Benzoyl peroxide Topical Antibiotics
Appears bright red with Wood's lamp
Systemic Antibiotics Dermal ulceration
Ecthyma
Impetigo that extends into dermis
Yellowish-graycrust Crust is thicker and harder than seen in impetigo
Very common in child but adults can also be infected Pre-Disposing Factors Trauma Underlying Underlying dermatoses Poor hygiene Previous antibiotic therapy Warm temperatures and high humidity Ecthyma Impetigo that extends into dermis
Mupirocin ± Imidazoles Doxycycline Macrolides
Clinical Medicine Condition / Disease
Cause
Abscess
Localized, walled-off collection of pus
Signs and Symptoms
Carbuncle
Result
Treatment
Medications
Systemic antibiotic Warm compresses Antibacterial soaps
Deep-seated erythematous nodule
Carbuncle
Large area of coalescing abscesses or furuncles
Trauma Diabetes Obesity Minor Immunologic Deficits
Pre-Disposing Factors Chronic carriage of S. aureus Poor hygiene Bactericidal defects Chemotactic defects
Prevention
MonthlyBetadine or Hibiclens showers Control of any predisposing conditions
Culture and sensitivity
CA-MRSA Skin Infection
Abscess, furuncle, or carbuncle
Most common clinical manifestion of MRSA
Risk Factors S ki ki n t ra ra um um a C os os me me ttii c b od od y s ha ha vi vi ng ng Sharing equipment not washed between uses Acute, diffuse Warmth inflammation Tenderness Lack of systemic symptoms (common) Pre-Disposing Factors Trauma Surgery Mucosal infection Immunologicdeficiency Underlyingdermatoses Cellulitis Extends into subcutaneous tissue
Soft Tissue Infections
Infection of the skin and the soft tissue below it
Other
Incision and drainage
Abscess
Furuncle
Furuncle
Laboratory Test
Incision and drainage (large abscesses) Surveillence (small abscesses) Antibiotics (adjunctive therapy)
Penicillinaseresistant synthetic penicillins
Systemic Antibiotics Cephalosporins
Indistinctborders
Etiologies
Macrolides (if PCN allergic)
Group A Strep S. aureus Others (in special clinical settings) Erysipelas
Rest
Superficial cellulitis
Lower extremities and face most commonly affected
Raised borders with clear demarcation Etiologies Group A Strep S. aureus (rare)
Supportive Treatment
Elevation
Warm compresses
At-Risk Populations Sulfamethoxazole Native Americans / Trimethoprim African Americans Homeless Clindamycin Populations Populations in close quarters Competitive atheltes Linezolid
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Result
Treatment
Medications
Begins with soft-tissue Progression into infection multi-organfailure Pain out of proportion to physical findings Etiologies
Necrotizing Soft-Tissue Infection
Infection of the skin and soft tissue that leads to necrosis
Fournier's Gangrene
Type of necrotizing infection or gangrene usualy affecting the perineum
Infectious Folliculitis
EMERGENCY 10 ♂ : 1 ♀
Fulminant NSTI of the perineum and genitalia Complicates GU or anorectal surgery Etiologies E. coli Proteus Single, scatteed papules or pustules
Klebsiella Bacteroides No tenderness No pruritis Pre-Disposing Factors Shaving Friction / occlusion of hair-coveredareas Immunosuppression Topical corticosteroids Sites of Prediliction
Face Neck Trunk
Scalp L eg s Buttocks
PRSPs Oral Antibiotics (7 - 10 days)
First gen. cephalosporins Macrolides (if PCN allergic)
Correct any predispoing condition
Keloidal Folliculitis
Chronic folliculitis found at the nape of the neck
Can evolve into a pyoderma Bacterial Agents S. aureus Gram (-) bacteria Pseudomonas Special Types of IF Pseudofolliculitis barbae Keloidal folliculititis "Hot tub" folliculitis
Encourage antibacterial soaps
Shaving cessation
Barber's itch
Pseudomonas Folliculitis
Common Infection Sites Perineum Extremities Trunk
Clostridium Bacteroides Peptostreptococcus Enterobacter Proteus Pseudomonas Risk Factors Impairedcellular PAD immunity IVDU Smoking Alcoholism Hypertension CAD Chr on oni c s te te ro roi d us e L ym ym ph phe de de ma ma V ar ar ic el el la la l es es io ions Ge ni ni ta tal t ra ra um uma
Infection of the upper portion of the hair follicle
Pseudofolliculitis Barbae
Other
Common in shaved areas of the face
Small curly hairs become ingrown resulting in foreign-body reaction to the hair.
Antibiotictherapy
Papules that coalesce into nodular masses Develops over slowly over months or years
Antibiotic therapy (cyclic administration common)
Occurs on the trunk after bathing in tubs
"Hot tub" folliculitis
Resolves spontaneously in 1 - 2 weeks Incubation period of 1 - 5 days
Far less common than S. aureus folliculitis Very alarming to patients
Clinical Medicine Condition / Disease
Acute Lymphangitis
Cause
Infection of the subcutaneous lymphatic channels
Signs and Symptoms
Vibro Cellulitis
Result
Treatment
Medications
Other
Erythematous Erythematous linear streaks extending from wound / skin break Antibiotic coverage for Strep and Staph
Etiologies Group A Strep
S. aureus P. multocida Mycobacteria Sporothrix
Subacute Etiologies (rare)
Cellulitis due a Gram negative bacteria found in marine animals that inhabit warm water
Laboratory Test
Starts as macular area that develops into bullous lesions Occupation with fish and seafood Common In…
Brackish water exposure Immunocompromised ↑ Serum iron levels
Mycobacterial Skin Infection
Infrequent cause of skin infection
Cutaneous Anthrax
Very rare infection of the skin
Anti-TB drugs are not helpful Suspect M. marinum in patients with frequent aquatic exposure
Single nodule that ulcerates or crusts
Resolve spontaneously spontaneously
Joined by satellite lesions
Excision may hasten resolution Papulovesicular Papulovesicular lesion ↓ Necrosis ↓ Eschar-covered Eschar-covered ulcer
7 - 10 day course of ciprofloxacin or doxycycline
Predisposing Factors
Dermatophytic Infections
Skin infection by a unique group of fungi that infect keratinized epithelium
Atopy
Occulsion
Steroid use
↑ Humidity
KOH Wet Mount
Diagnostic
Dry skin
Dermatophytic infection of the feet
Tinea Pedis "Athlete's foot"
Erythema Predisposing Factors ↑ Sweating Scaling Vesicles Occulsion (by shoes) Contaminated public Maceration floors Involvement of toe nails Interdigital Type Scaling Maceration (between 4th and 5th toes) Moccasin Type Erythema Scale and papules on heels, soles, and lateral foot borders Inflammatory / Bullous Type Fluid-filled vesicles that erupt into erosions
Imidazoles
Topical Antifungals (2 - 4 weeks)
Allylamines For severe or refractory cases Imidazole
Oral Antifungals (2 - 6 weeks)
Allylamines Monitor liver function if therapy to exceed 4 weeks
Treat any secondary infection Open infection to air
Usually acquired via contact with infected animals, animal products, feed, or soil contaminated with spores of the bacillus Etiologies Microsporum Trichophyton Epidermophyton Routes of Transmission Person-to-person Animal-to-human Environmental Ulcerative Type Interdigital infection spreads to plantar and lateral surfaces of foot
Clinical Medicine Condition / Disease
Tinea Cruris
Cause
Signs and Symptoms
Subacute infection of neck, trunk, and/or extremities
Treatment
Result
Erythematous,scaling, andwell-demarcated plaques
Subacute or chronic infection of the groin / medial thighs "Jock itch"
Tinea Corporis
Laboratory Test
Topical antifungals
Dull red, tan, or brown Plaques with sharp borders Smaller pustules or vesicles within borders Enlargeperipherally Central clearing
Topical antifungals
Asymptomatic
Dermatophtyic infection of the scalp
Systemic Antifungals (6 - 12 weeks)
Imidazoles
Terbinafine
Black Dot
Antibiotics for any secondary infections Kerion
Tinea Incognito
Any type of tinea in which the appearance of the lesion has been altered by inappropriate treatment (usually a topical steroid)
Topical ketoconazole or selenium sulfide (reduces transmissibility) transmissibility)
L es es s de ma mar ca ca te te d
F la lat te te r bo rd rde rs rs
Lack scaling
Larger lesions
Tinea (Pityriasis) Versicolor
Infection involving sites where maceration and occulsion create a warm, moist environment
Chronic skin infection by the opportunistic pathogen Malasezzia furfur
Most common in African-American children between 6 - 10 years old. Ectothrix Infection is outside hair shaft Endothrix Infection is inside hair shaft "Black Dot" Broken-off hairs resemble dots "Gray Patch" Arthrosporse Arthrosporse give gray appearance appearance and circular areas of alopecia Kerion Infection accompanied by swollen, painful nodule
More pustular in appearance
Nystatin
Intertriginous Candidiasis
Other Risk Factors Obesity Tight clothing
Griseofulvin
Tinea Capitus
Medications
Imidazoles
Glucocorticoids Glucocorticoids (usedsparingly)
Asymptomatic Multiple welldemarcated macules Hyper- or hypopigmenting Fine scaling Common Sites Upper trunk Groin Sites of Oil / Grease Applications
Axillae Thighs Neck Face Scalp
Selenium sulfide Yeast
Microscopic Study
Topical Antifungals
Works only in limited disease Imidazoles
Pseudohyphae Ketoconazole
"Spaghetti and meatballs"
Oral Antifungals
Fluconazole Itraconazole
Predisposing Factors Obesity Diabetes Hyperhydrosis Steroid use Infection in the small body folds is more common in cooks, bartenders, health-care workers, or others that keep their hands frequently in water.
Clinical Medicine Condition / Disease
Subcutaneous Fungal Infections
Cause
Rare and slow progressing subcutaneous infection by saprophytes found in soil
Signs and Symptoms
Treatment
Result
Sporothrix Exophila Fonsecaea madurella Pseudallescheria Rash preceded by Self-limiting prodrome Oral lesions (possible) Common Childhood Viral Exanthems
Generalized skin eruption secondary to systemic viral infection
Hand-Foot-Mouth Disease
Systemic Coxsackie viral infection
Oral lesions (erosions)
Perioral infection by HSV-1 or HSV-2
Group vesicles on erythematous base
"Cold sore" or "fever blister"
Preceded by prodrome of sensory complaints
Rubeola Rubella (measles) (German measles) Varicella Roseola (chicken pox) (sixth disease) Erythema infectiosum (fifth disease)
Outbreaks every 3 years
Vesciualr exanthem limited to the distal extremtriteis
Penciclovir(topical)
Valacyclovir
Fever
Rare but severe disseminated HSV infection that generally occurs at sits of skin damage
VaricellaZoster Virus Infection
Primary infection (varicella) permanent infection and latency until reactivation that results in zoster (shingles)
Molluscum Contagiosum
Viral skin infection caused by pox virus
Wart
Keratinocyte and mecusous membrane infection by HPV
Other
Scarlatinform Type Generalized erythema Worse in body creases Morbiliform Type Maculopapular Vesicular Type Vesicles → papules → pustules → erosions
Acyclovir
Eczema Herpeticum
Medications
Usually acquired by Outdoor occupations trauma Persistent lesions that are poorly responsive to antibiotics Etiologies
Viral Exanthem
Herpes Labialis
Laboratory Test
Complications Systemic symptoms Conjunctival/corneal autoinoculation Bell's palsy Erythemamultiforme Eczema herpeticum Severe, diffuse infection (in immunocompromised) HSV-1 > HSV-2
Malaise
Eruptions may take 1 week to compeletely evolve
Distinct flesh-colord or pearly white papules with umbilicated centers
Possible secondary infection by S. aureus Necrosis (possible) Single dermatome distribution
↑ Dose acyclovir, valacyclovir, famciclovir, or foscarnet (acyclovir-resistant (acyclovir-resistant strains) Prednisone Prednisone (if ≥ 50 years old) Analgesics Gabapentin Pregabalin Post-Herpetic Tricyclics Neuralgia Capsaicin Lidocaine
Spontaneous Spontaneous resolution
Post-herpetic neuralgia (PHN) is the most worrisome complication. complication. Oral steroids may help prevent. Thoracic > trigeminal > lumbosacral lumbosacral > cervical Zosatvax is a live vaccine for the prevention of shingles.
Very common in children and sexually active adults Transmission is through skin-to-skin contact
Oncogenic potential Cutaneous Warts Common Filiform Flat
Clinical Medicine Condition / Disease
Cause
Contact Dermatitis
Eczematous dermatitis caused by exposure to environmental agents
Irritant Contact Dermatitis Acute Irritant Contact Dermatitis Chronic Irritant Contact Dermatitis
Most common occupational skin disease
Acute damage to keratinocytes
Disruption of normal skin barriers
Signs and Symptoms Papules
Laboratory Test
Treatment
Result
Medications
Environmental Environmental agents are characterized as irratants or allergens.
Vesicles Pruritus
Burning Stinging Pruritus Recurs within days of return to work
Pain Discomfort Clears within 2 - 3 break from work
Other
Slight improvement over weekend is unlikely with allergens Patch Test
Diagnostic
Identify and remove the offending agent
Chronic lip licking
Erythema Bizarre configuration configuration ↓ Vesciulation Lesions do not spread ↓ beyond area of contact Crusting Sharp borders Dryness Erythema ↓ Hyperkeratosis
Chapping Scaling ↓ Crusting
Fissuring
Hands (most common)
Wet dressings with Burrow's solution Patch Testing
NEGATIVE
Potent topical steroids Oral steroids (in severe cases) Seen particularly in frequent handwashers
Potent topical steroids + lubrication
Barrier creams
Occupations
ICD Chrome Ulcers
Ulcers caused by the corrosive necrotizing effects of chromates
Tanning Electroplating Chrome production Intense pruritus
Allergic Contact Dermatitis
Acute
Sensitized T-lymphocytes respond to a recognized antigen to produce inflammation
Subacute
Dry skin
Mechanical
Atopic Dermatitis
Macules Papules Vesicles Bullae Erythematous plaques with scale Firm papules with scale
Chronic
Disruption of the epidermal barrier Acute
Immunologic T cells and Langerhans cells trigger Secondary Infection with S. aureus IgE-mediatedinflammatory response Chronic
Test only known substances Concentrations predetermined
Phytodermatitis
Lichenified plaques Scaling Fissured lesions Excoriation Co-existing atopic manifestations Ill-defined papules Plaques and patches Erythematic (± edematous) underlying skin ± Linear excoriations Pustules Crusting and oozing Lichenification Fissuring
Scalp, plams, and soles are relatively resistant. Mucous membrane involvement is uncommon. See PowerPoints for specific antigen reactions
Wet dressings Potent topical steroids
Avoid testing with Systemic steroids acute dermatitis (if widespread involvement) Patch Test Test site should be Oral antihistamines free of dermatitis Phototherapy or cyclosporine Patches applied (in more severe cases) for 48 hours Read 72 - 120 Allergen avoidance hours later Moisturizers (emollients only) Tacrolimus Topical steroids Topical immune modulators Pimecrolimus Oral antihistamines Phototherapy Manage secondary infection with systemic therapy
Cyclosporine
Sites of Predilection Flexual surfaces Face Wrist Dorsal feet Infantile, child, adult, hand, and follicularvariants Exacerbating Factors Specific autoallergens Winter season Wool clothing Emotional stress
Clinical Medicine Condition / Disease
Cause
Lichen Simplex Chronicus
Atopic dermatitis associated disorder due to repetitive scratching and rubbing
Dyshidrotic Eczema Nummular Eczema
Signs and Symptoms
Treatment
Result
Deep, tapioca-like tapioca-like vesicles
↑ potency topical steroids
Coin-shaped papuless and vesicles grouped in a plaque Underlying skin may be erythematous
Oral steroids (severe cases) More common in winter months More commonly found on extremities
Moisturizers
Intensely pruritic
Chronic plaque Acute guttate Palmoplantar Inverse Erythroderma Pustular Trigger Factors
Topical steroids Anthralin Steroids Tars
Psoriais Vulgaris
Psoriasis
Other
Bullae Fissuring
Shortened keratinocyte cell cycle with increased CD8 cells causues epidermal hyperproliferation
Medications
Localized area of lichenification
Vesicular eruption on hands and feet
Also known as discoid dermatitis
Laboratory Test
Injury / trauma ↓ Humidity Overtreatment with Emotional stress steroids Lithium β blockers CCBs Exacerbating Drugs ACE inhibitors Antimalarials NSAIDs Systemic steroids Months to years Plaque distribution Palms / soles / scalp may somewhat symmetrical be the only sites affected
Topical Therapy
Retinoids Taclonex UVB
Chronic Plaque Psoriasis
Chronic type of psoriasis
Guttate Psoriasis
Psoriasis usually seen in children and young adults
Small papules of short duration (weeks to months)
Streptococcal Streptococcal URI within 1 - 2 weeks of presentation
Inverse Psoriasis
Psoriasis that affects intertriginous areas
Marcerated scales
Erythematous plaques with shiny appearance
Cyclosporine
Peak incidence in 20s. Associations Cardiovascular disease Depression Lymphoma
Adalimumab
Narrowband UVB PUVA Retinoids
Systemic Therapy
Tazarotene
Vitamin D analogs
Streptococcal infection Drugs
Phototherapy
Dovonex
Methotrexate Immunemodulating therapy
Alefacept Etanercept Infliximab Ustekinamab
Nail involvement (10 - 25%)
Can co-exist with chronic plaque psoriasis
Relatively rare form Spontaneous Spontaneous resolution
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Treatment
Result
Medications
Other
Guttate Lesions Salmon-pink papules Loose scales Scales not readily visible
Psoriasis Vulgaris
Most common form of psoriasis
(+) Auspitz sign Chronic Stable Lesions Well-demarcated erythematous plaques with silvery white scale
Variable pruritus
Erythrodermic Psoriasis
Extremely dangerous form of exfoliative dermatitis in adults
Plaques coalesce to form variable patterns More common in scalp and anogential areas EMERGENCY Serious Underlying Illnesses Hypo- / hyperthermia Protein loss Dehydration Renal / cardiac failure
Diffuse erythema Skin thickening Scale Pustules (instead of papules) Surrounding skin
Pustular Psoriasis
Uncommon form of psoriasis consisting of widespread pustules on an erythematous background
± Erythema
Palmoplantar
Chronic pustules limited to palms and soles
Generalized Acute (Von Zumbusch)
Rare Pustules develop in waves over entire body "Lakes" of pus Systematic symptoms Can precede or follow psoriasis vulgaris
Erythema
Scaling
Seen in areas with ↑ sebaceous gland activity
Seborrheic Dermatitis
Common, chronic, and inflammatory dermatitis
Infants (Cradle Cap) Greasy adherent scale on vertex Accumlations Accumlations of scales andinflammation
2⁰ Infection may occur Adults Erythematous / grayish plaques with greasy or white scale May appear as severe dandruff Blepharitis Variable pruritus
M. furfur may be a possible causative factor.
In infants…
Scale removal
Triamcinolone
Treat infection Reduceinflammation
Frequent washing of all involved areas
Acetonide
Topical steroids
Change shampoo Betamethasone Valerate Maintenance Maintenance therapy
Genetic and environmental factors influence onset and course.
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms Abrupt onset
Scaling flat plaque on trunk or proximal extremities Papules and smaller scaling plaques (7 - 14 days after onset)
Pityriasis Rosea
Common, benign, and self-limiting dermatoses
"Christmas tree" arrangement
10 - 35 years old (75%)
40 - 50 years old
Lichen Planus
Acanthosis Nigricans Hailey-Hailey Disease Dermatitis Herpetiformis
Pemphigus
Familial Benign Pemphigus
Other
Topical steroids
Acyclovir
Oral prednisone ± UVB phototherapy phototherapy (in severe cases)
Topical Intralesional Systemic
Cyclosporine
Pruritis
4 P's of Lichen Planus
Pruritic Polygonal Purple Papule
Methotrexate PUVA Antihistamines Associations Obesity Endocrine abnormalities Certain drugs Malignancy (onset is rapid)
Typically on the neck and other body folds
"Velvety" appearance Vesicles ↓ Erosions
Topical / oral antibiotics
Occur in body folds
Topical steroids
Papules and vesicles near the elbow
Serous-filled vesicles and bullae On scalp, axillae, face, groin, and trunk
Aggressive systemic steroid treatment
Immunosuppressive Immunosuppressive therapies
(+) Nikolsky sign Initial lesions start on oral mucosa
Triggers Drugs Chemical exposure Bacterial infection Post-bone marrow transplants
Retinoids
Wickham's striae on papules
Chronic blistering skin condition
Autoimmune bullous disease that leads to acantholysis
Medications
Appears as salmon pink in whites and hyperigmented in African-Americans.
Oral antihistamines
Steroids
1 - 10 mm flat-topped papule with an irregular angulated border
Hyperpigmentation of the skin Rare genetic disorder characterized by chronic oozing lesions that fissure and crack
Treatment
Result
Collarete scale
Pruritus worse at night Asymptomatic and with heat (if present) Recent history of acute infection with fatigue, headache, sore throat, lymphadenitis, and fever (20%)
Inflammatory dermatitis of skin and/or mucous membranes
Laboratory Test
Skin lesions typically develop months later
Correct any electrolyte discrepancies discrepancies
Lesions frequently become colonized with S. aureus ± Candida
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Result
Treatment
Medications
Other
Generalized erythematous papules
Bullous Pemphigoid
Most common autoimmune bullous disease
Urticarial lesions Systemic steroids ± azothioprine azothioprine Bullae 60 - 80 years old
Follicular plugging and dilatation
Affects face, neck, upper trunk, and arms
± Inflammation and pustules
Acne Vulgaris
Comedonal Acne Acne Conglobata
Common inflammatory disease of the hair follicles and sebum-producing glands of the skin
Acne with a high number of comedones
Possible cyst formation
May lead to scarring or keloid formation
Blackheads
Whiteheads
Cysts Fissures Abscess formation Deep scaring High inflammation
Severe, chronic, and cystic acne B eg eg in in s i n p ub ub er er ty ty
W or or se se ns ns wi wi th th ti ti me me
Flouri Flourish shes es on on trun trunk k
Not as seve severe re on on face face
Behavioral Modiciation No picking No mechanical exofoliation Mild, gentle cleansing twice a day Oil-free, non-comedogenic products Topical Comedolytics
Retinoids (Vitamin A)
↑ Cell turnover Prevent new comedones Chemically exfoliate
Azelaic acid Glycolic acid preparations Salicyclic acid preparation Benzoyl peroxide For specific details Clindamycin Topical on acne Erythromycin Antibacterials Sulfur-containing medications, see preparations PowerPoint slides. PowerPoint slides. Metronidazole Dapsone (inflammatory acne) Oral antibiotics Severe, nodularcystic acne Isotretinoin Inflammatory, recalcitrant acne Teratogenic Oral Hormone Therapy contraceptives Spironolactone Comedo extraction Photodynamic therapy Laser therapy Chemical peels
Most common in adolescents Flaring Elements Sweating Chocolate Cell phones Hands on face Cosmetics Complications Scarring Keloids Psychological Psychological impact Pyogenic granulomas
Clinical Medicine Condition / Disease
Hidradenitis Suppurativa
Cause
Sinus tract formation possibly caused by obstruction and infection of an apocrine duct
Signs and Symptoms
Fistulas Scarring
Rosacea
Occurs in the axillae, inguinal folds, perianal, and scalp (rare)
Perioral Dermatitis
Wart
Unknown inflammatory etiology
Pustules Flushing Occurs on cheeck and nose
Pain
Tenderness
Mobility limitations
Cosmesis
Malignantdegeneration
Obscure skin lines
Necrotic capillaries
Occur in sites of skin trauma
Thrombosedcapillaries
Common wart Dermatoglyhic loss 5 - 20 years old
Periungual Warts
Difficult-to-treat wart near the nail matrix
Prefers hands or places of trauma
Around the nail bed
Flat-toppedsurface Pink to brown
Verruca Plana
Flat Wart
Topical Treatments
Metronidazole Sulfacetamide / sulfur Azelaic acid Brimonidine
Oracea Laser therapy
Metronidazole Erythromycin Clindamycin Spontaneous resolution (if immune-competent) immune-competent) Cryotherapy Duct tape occlusion Laser therapy or cautery Excision Chemical destruction Immunodulation Topical Therapy
Verrucous surface
Verruca Vuglaris
Mostly ♀ 30 - 50 years old; peak 40 - 50 Triggers Hot / spicy food or drink Sun Alcohol Exercise
Avoidance Avoidance of triggers
Avoidance Avoidance of triggers
No comedones
Small, rough growth due to human papilloma virus
Other
Incision and drainage (simple cases) Excision by surgery (complex cases)
Papules
No comedones Telangiectasia Rhinophyma Grouped 1 - 2 mm erythematous papules Symmetrical around border of mouth
Medications
Oral prednisone (14 days)
Lingering erythema
Chronic condition characterized by facial erythema and sometimes pimples
Treatment
Result
Oral / topical antibiotics Intralesional triamcinolone triamcinolone
Deep undermining cysts
Double comedone
"Acne Inversa"
Laboratory Test
Multiple Prefers the face, dorsal hands, wrists, neck, and legs Flat warts frequently Koebner's Phenomenon occur in a linear formation
Cantharadrin Podophyllin Retinoids Salicylic Acid 5-FU Imiquimod Cimetidine Sinecatechins
Triggers Cinnamon products Tartar control toothpastes Whitening ag agents Heavy facial moisturizers Topical steroids HPVs can cause both benign and malignant lesions. Regression of warts is dependent dependent on cell-mediatedimmunity. Warts occur more often in immunosuppressed individuals.
5% prevalence in children
Clinical Medicine Condition / Disease
Cause
Laboratory
Signs and Symptoms
Test
Result
Treatment
Medications
Other
Verrucous surface
Verruca Plantaris
Thrombosedcapillaries
Plantar wart
Multiple and coalescent ("mosaic warts") "Kissing lesions" on adjacent toes are common Most common STD High risk lesions are often hyperpigmented Caused by HPV 6, 11, 16, and 18
Lobulated surface
Condyloma Acuminata
Cauliflower-like
Genital wart Gray or pink Can occur on cervix, vulvovaginal skin, anus, penis, and perianal skin
"Exclamation point" hairs
Alopecia Areata
Hair is lost from some or all areas of the body
Patchy, nonscarring alopecia
May involve entire scap or body
Topical / intralesional corticosteroids
Scalp Biopsy
↑ Lymphocytes around hair bulb
Androgenetic Alopecia
Increased 5-α reducatase causes testosterone conversion to DHT resulting in hair miniaturization on scalp but increased hair on other body areas
♂
♀
Starts with recession of frontal hairline ↓ Shaft length and thickness Castrationprevents alopecia
Later onset Less progressive Advance loss or male pattern is associated with hirsutism
No treatment (regrowth < 1 year)
Systemic steroids (severe cases)
Inheritedcondition Minoxidill(Rogaine)
Finasteride (Propecia)
Hair transplantation transplantation
Wigs, hairpieces, or "comb over"
Anagen Effluvium
Hair loss due to chemotherapy or radiation therapy
Telogen Effluvium
Diffuse hair shedding as more follicles are shifted from anagen to telogen phase
Rapidly dividing hair follicles
Hair regrows after offending agent is removed
High metabolism in hair follicles Can occur 3 months after events Occurs After "System Shock"
Beau's lines in the nails
Stressful event Childbirth Ma ss ss iv ive blo od od l os oss High fever
Surgery Thyroid disease Cr as as h di et et in ing Car accident
Worse prognosis with acute onset of hair loss, extensive hair loss, or hair loss beginning over the ears. Associated Diseases Diseases Thyroid disease Stress Vitiligo Autoimune disease Diabetes Atopic dermatitis Nail pitting
Surveillence (hair loss is temporary)
Clinical Medicine Condition / Disease
Trichotillomania
Traction Alopecia
Cause
Pleasure / relief from pulling hair out
Signs and Symptoms Irregular pattern of alopecia Broken and variable length hair in affected areas Usually occurs with psychosocial psychosocial stress
Pigment casts
Scalp Biopsy
Muercke's Lines
Nonspecific nail manifestation that associated with decreased protein synthesis
Stretching of epithelium
Other 7x more common in children and 2.5x more common in ♀
Treat underlying psychiatric disorders
Pharmacotherapy
↑ Incidence in African Americans
Get a new hairstyle
Discoloration
Alternating white and pink lines Blanchable Located in the nail bed Usually Staph
Inflammation of the nail folds
Affects proximal nail fold Usually Candida
Chronic
Affects lateral nail folds
Common in diabetics, waitstaff,bartenders, and food handlers
Blue Nails
Referral to child psychiatry
Medications
Can lead to scarring alopecia if ignored
Acute
Half and Half Nails
Achordion
Treatment
Nail Pitting
Nail changes seen in patients with psoriasis
Beau's Lines
Result
Most common in frontotemporal frontotemporal scalp
Constant pulling or traction on hair follicles from wearing tight braids and cornrows leads to hair loss
Nail Manifestations of Psoriasis
Paronychia
Laboratory Test
Nail growth arrest caused by severe illness, high fever, or pregnancy Nail changes seen in chronic renal disease "Lindsey's Nails"
Nail color change due to Wilson's disease, argyria, and ochronosis
Horizontal grooves in nail plate
White proximal nail
Red-brown distal nail
May be caused by cirrhosis or nephrotic syndrome
Clinical Medicine Condition / Disease
Cause
Pseudomonas Nail Infection
Infection of the nail by Pseudomonas
Digital Mucous Cyst
Benign ganglion cysts of the digits Myxoid Cyst
Longitudinal Melanonychia
Nail discoloration due to melanoma
Squamous Cell Carcinoma of the Nail
Neoplasm around the nail bed
Signs and Symptoms
Treatment
Medications
Other
Translucent papule at proximal nail fold Clear, viscous, jelly-like substance at DIP joint space Longitudinal Longitudinal ridge or indentation in the nail plate distal to growth Common and normal in African Americans. May be a sign of melanoma in caucasians.
Dark brown or black pigmentation at the proximal nail fold (Hutchnson's (Hutchnson's sign)
May mimic a wart located around the nail folds
Biopsy
Oral ulcers Photosensitivity Acute Cutaneous LE Malar or butterfly rash Papules / papular urticaria
Scaly plaques Discoid lesions Bullae Palmar erythema Subacute Cutaneous LE Annular / papular lesions
> 85% of SLE patients have skin manifecstions
Result
Green discoloration
Alopecia
Systemic Lupus Erythematosus
Laboratory Test
Start as small erythematous papules with scale Resembles erythema multiforme (less common) Seen on shoulders, forearms, neck, and trunk Chronic Cutaneous LE
Associated with anti-Ro and anti-La antibodies
Discoid lesions Start as well-defined scaling plaques that extend into hair follicles Expa nd nd s lo low ly ly Dyspigmentation Dyspigmentation ± atrophy
H ea eal wi th th s ca ca rr rr in ing Seen on face, neck, and scalp
Confirm diagnosis
Sun exposure may trigger acute lesions. Non-Specific Lesions / Rashes Lupus profundus Vasculitic lesions (purpura) (purpura) Livedo reticularis Urticaria
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Result
Treatment
Medications
Other
Gottron's Papules Slightly raised pink, dusky red, or violaceous papuls over the dorsal sides of MCP/PIP ± DIP joints Gottron's Sign Macular rash in the same areas as Gottron's papules
Dermatomyositis
Connective-tissue disease related to polymyositis that is characterized by inflammation of muscles and skin
No papules Shawl Sign Macular rash over posterior shoulders and neck Poikiloderma Mottled red or brown discolorationthat develops from old DM lesions Calcifications Periungualerythema Telangiectasias Cuticle overgrowth Sclerodactyly (95%)
Systemic Scleroderma
Chronic autoimmune disease that primarily affects the skin
Sclerosis of face, scalp, and trunk Pigmentation abnormalities
Linear erythema over extensor surfaces of joints Raynaud's phenomenon (79%) Periungual and mat-like telangiectasia Calcinosis cutis
Palpable purpura
Vasculitis
Inflammation of blood vessels Primarily on lower extremities
Well-defined raised petechaie and macules ± central area of hemorrhage Can become ulcerative or necrotic
Flaring Factors Infections Drugs Connective tissue disease
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Result
Skin infection manifestations Diabetic Dermopathy Atrophic, Atrophic, small (< 1 cm), brown lesions on lower extremities Asymptomatic Last 18 - 24 months Diabetic Bullae Appear spontaneously on hands or feet Sterile (no scarring) Hemorrhagic Non-scarring Non-scarring (triggered by sun exposure) Necrobiosis Lipodica Diabeticorum
Treatment
Medications
Other
Acanthosisnigricans
Diabetes Mellitus
Endocrine disorder that leads to multiple skin manifestions
Topical / intralesional steroids (NLD)
Flesh-colored or reddishbrown plaques that evolve into waxy plaques May become ulcerative or necrotic Diabetic Ulcers
Ulcer prevention
Result from neuropathic or ischemic causes Often surrounded by callus formation Secondary to loss of protective sensation
Granuloma Annulare
Generalized granuloma annulare has been associated with systemic disease.
Papules and plaques in annular distribution
Uncommon benign skin disorder
Self-limiting Localized Generalized Perforating
Variants
Xanthelasma
Yellow plaques occuring near medial canthus of eyelid
Non-painful skin lesion of the eyelid
Urticaria
Edematous papule or plaque Transient Very pruritic
Acute
Chronic
Occurs once Individual Individual lesions resolve < 24 hours Lasts days to 6 weeks Recurrent or constant > 6 week duration Undetermined trigger
50% of cases are associated with ↑ lipid levels.
Surgical excision
Upper lid > lower lid Soft lesions Wheal
Localized swelling of the skin and mucous membranes with immunologic and nonimmunologic etiologies
Reduction of serum lipids
CBC LFT Thyroid Tests Renal Function Tests
Evaluation
ESR / CRP Hepatitis Serologies ANA Biopsy
In cases of vasculitis
H-1 and H-2 blockers (synergistic effect) Doxepin Glucocorticoids Epinephrine (Epi-Pen) Allergist or rheumatologist referral Avoid systemic corticosteroids Chronic Identify causative factors Management Constant antihistamines
Up to 20% of the population will have an acute episode.
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms Pitting edema
Venous Insufficiency
Multiple skin manifestations secondary to decreased or absent return of venous blood and increased capillary pressure
Atrophie blanche
Laboratory Test
Treatment
Result
Varicose vein Compression
Hyperpigmentation (mottled blue or purple)
Skin fibrosis Venous ulcers (lipodermatosclerosis) Stasis Dermatitis
Stasis Dermatitis
Erythematous papules Scale Erosion Excoriation Occurs on lower legs and ankles
Medications
Other
≈ ⅓ of patients with venous insufficiency insufficiency will develop ulcers.
Oral antibiotics
Topical steroids
Asymptomatic Most common Macules / Papules
Sarcoidosis
Chronic multisystem granulomatous disease
Brown, yellow, or purple Occur on face and extremities Annular or serpiginous Possibly scaly Occurs on buttock, trunk, and extremities
Plaques
Lupus Pernio
Infiltratingviolaceous plaque Occurs on nose, cheeks, ears, and lips Macule ↓ Papule with vesicle or bulla in center
Analgesics
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis are considered separate clinical entities.
Mild
Symmetric
Erythema Multiforme
Steven-Johnson Syndrome / Toxic Epidermal Necrolysis
Cutaneous immunologic response to varied antigens
Pain ± pruritic Occurs on hands, forearms, feet, face, and possibly mucous membranes No bullae Mild Lesions on upper extremities and face Severe EM ≥ 1 mucous membranes involved Major Epidermaldetachement < 10% of total body surface area
Topical steroids
Major
Discontinue any offending drugs / factors
EMERGENCY Monitor fluid / electrolytes
Widespread bullae
Occurs on trunk, face, and mucous membrane Systemic steroids
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Treatment
Result
Cutaneous reaction to antigenic stimuli
Infective Endocarditis
Infection of endocardium
Meningococcemia
Gram (-) blood infection that can cause disseminated intravascular coagulation
Lyme Disease Skin Manifestations
Infectious disease caused by bites from Borrelia tick
Arthropod Bite
Papular Urticaria
Other Triggers Infections Drugs Systemic disease
Erythematous nodules
Erythema Nodosum
Medications
Limited to extensor surfaces of lower extremities Very painful
Associated systemic symptoms
Osler nodes
Janeway lesions
Subungual hemorrhages Petchiae Purpura Necrosis Eryt Erythe hema ma mig migra rans ns
Lymp Lympho hocy cyto toma ma cut cutis is
Acrodermatitis chronica
Atrophicans
Dermatologic reaction
Pruritis
Allergic reaction
Inflammatoryreaction
Lesions
Transient erythema Papular urticaria Bullae ↓ Erosions Hemorrhagic ulcers Necrotic
Bite from a bug or spider
Most Common Biters Fleas Mosquitoes Bedbugs
2 - 8 mm erythematous, papulovesicular papulovesicular lesions
Hallmark lesion of arthropod bite
Arranged in clusters Children > adults
Seen in exposed areas Possible secondary infections
Systemic symptoms
Black Widow Spider
Potent neurotoxin whose site of action is neuromuscular junction
Muscle cramping
Brown Recluse Spider
Analgesics Antibiotics (if needed) Dark, dry places Dermal necrosis
Antivenom RICE Update tetanus immunization
Systemic symptoms Dark, quiet places
Extremely toxic venom
Update tetanus immunization
Hypertension Tachycardia
Toxic effect caused by a protein that stimulates platelet aggregation and infiltration of site by neutrophils
RICE
Found in clothing and shoes
Analgesics Antibiotics (if needed)
Found in the southeast US
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms Tunnels
Scabies
Result
Treatment 5% Permethrin cream
Excoriated papules and pustules
Highly contagious mites that are spread by direct or sexual contact
Laboratory Test
1% Lindane lotion
Hypersensitivity
Sites of Predilection
Medications
Other At Risk Populations Young, sexually active adults Bed-ridden patients Care-givers of bed-ridden patients
Oral ivermectin Finger webs Flexor aspects of wrist Elbows Axillae Penis External genitalia Feet Ankles
Treat family members (even if asymptomatic) Wash bedding / clothing in hot water Sedatingantihistamines (at bedtime)
Severe crusting
Norwegian Scabies
Limited number of papules and burrows
Crusted scabies Variable pruritus Usually underlying immunodeficiency
Can infest head, neck, and genital and perianal (homosexual ♂)
Dermatitis Immediate bath in hot soapy water Papules / hives
Chiggers
Known as bedbugs or jiggers
Severe pruritis
Sites of Predilection
Prevention Avoid brush Proper clothing Repellant (DEET)
Antihistamines Ankles Back of knees Groin Axillae
Topical steroids
Rosacea (possibly)
Demodex Mite
Ticks
Mite found in hair follicles and sebaceous glands
Arthropods that are frequently vectors of human disease
Sites of Predilection
Nose Cheeks Forehead Neck Chest
Papules
Local edema
Local erythema
Induration (after a few days)
Nodular (after a few days)
Pruritus ± tenderness
Granulomatous Granulomatous reaction (rare)
Oral antihistamines ± medium to high potency topical corticosteroids Intralesional steroids (if severely symptomatic) Excision (if severely symptomatic) Permethrin and DEET
Attracted by the smell of sweat, body heat, and color white Advise patients that local raections may persist for 3 - 4 weeks
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Treatment
Result
Medications
Erythema Migrans
Erythema Chronicum Migrans Erythema migrans lasting longer than 4 weeks
Bull's eye lesion
Lyme Disease
Infectious disease caused by bites from Borrelia tick
Other
4 day - 3 week onset Occurs ≈ 50% of cases Vesicles Malar rash Variants Urticaria Nodules Lymphocytoma Cutis Single 1 - 5 cm bluish nodule See Ticks treatment section
Develops in response to antigenicstimulation Site of bite Earlobe Areola Neck Acrodermatitis Chronica Atrophicans Atrophicans Bluish erythema + edema Can lead to atrophy of all layers of skin if untreated Small erythematous Hemorrhagic puncta papules Linear excoriations Bluish-brown or gray Maculae Ceruleae macules at the site of the bite Secondaryinfection Vesicles possible Body Lice Sites
Pediculosis
Infestation of lice
Removal of nits Permethrin
Wash all bedding, clothing, hats, and combs
Head Lice
Infe Infect ct clot clothi hing ng Lay Lay egg eggss on on sea seam m fib fiber erss Not seen on skin except Reemerging in US in when feeding homeless ± Pruritus Head Lice Scalp pruritus Excoriations Cervical adenopathy Major problem in school Rare in Africanchildren Americans Transmission through Diagnosis made by direct contact or observing nits in scalp formites Public Lice Small erythematous 1 - 2 mm lice are often papules visible
Blight upon humanity
Pruritic wheals and papules
Possiblyvesicular, eczematous, or granulomatous granulomatous lesions
Malathion
Pediculicides Sklice
Ivermectin
Pubic Lice
Lindane lotion
Sklice
5% permethrin Manual removal Eyelashes
Inguin Inguinal al aden adenopa opathy thy Can infest infest eyelas eyelashes hes Moderate pruritus (worse at night)
Flies and Mosquitoes Bite
Pediculicides are not ovicidal, and patients need to be re-treated in 1 week.
Prevention
Petroleum jelly TID for 5 days Prophylactic antihistamine Insecticide
Lindane
Allergic response to irritating salivary secretions
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Treatment
Result
Flat bugs that feed at night
Other Spread by travelers in clothing and baggage
Papularurticaria
Bedbugs
Medications
May be vesicular / eczematous lesions Linear arrangement Erythematousmacules
Fleas
Blood-sucking insects
Oral prednisone (for severe) Excoriations Grouped lesions
Bee Sting
Fire Ants
Destroy fleas at home
Urticarial-likepapules
Erythema Pain Diffuse urticaria Anaphylaxis Angioedema Shock
Potentially fatal insect sting
Worst creatures in existence
Secondary infections are common
Lesion ↓ Vesicle ↓ Itchy pustule ↓ Crusting
Age > 30 Appear "stuck-on" but can come off
Oral histamine Immediate pa pain
Acrochordon
White, pink, tan, light and dark brown, or black
Multiple keratin cysts imbedded within surface of lesion Sign of Leser-Trelat
Single or multiple
Sudden eruption of many seborrheic keratosies
Skin tag
≈ 4% of US population is sensitized.
Ice
Can be seen anywhere on the body Smooth, velvety, verrucous, or hyperkeratotic
Very common, benign, epidermal growths
Stinger removal RICE Antihistamines Antihistamines (questionable) (questionable) Oral steroids (if severe) Epi-Pen Medic-Alert bracelets Local cleansing
Flare reaction
Seborrheic Keratosis
Antibiotics for secondary infections
Maybe a cutaneous sign of internal malignancy
Oral steroids Update tetanus (if needed)
Cryotherapy
Shave removal
Light electrocautery
Curettage
Most common in ♀ and obese
Fleshy filiform or pedunculated papules
Surveillence(asymptomatic)
Flesh-colored, pink, or brown
Cryotherapy
Occur in the axilla, neck, groin, eyelids, antecubital and popliteal fossa, inframammary folds, beltline, and other friction areas
Scissors-snip removal Electrodessication
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms
Laboratory Test
Result
Treatment
Most common in legs but can occur on trunk and arms
Dermatofibroma
Very common, benign, firm dermal papule
Lipoma
Subcutaneous, benign fatty tumors
Flesh-colored,brown, Slightly to very raised or pink, red, or tan slightly depressed Pruritus Tenderness Dimple sign Button sign Arise spontaneously or secondary to insect bites or trauma when shaving legs
Excision (if symptomatic)
Medications
Other Dimple Sign Pinching surrounding skin between 2 fingers cause the lesion to dimple Button Sign Pinching surrounding skin between 2 fingers cause the lesion to raise
Single or multiple
Pa lp lpa bl bl e Epidermoid Cyst Epidermal Inclusion Cyst
Epidermal Cyst
Ove rl rl yi yi ng ng s ki ki n i s mo bi bil e Filled with keratin
Sebaceous Cyst
Cheesy consistency when ruptured or manually expressed
Infundibular Cyst Pilar Cyst Wen
Excision (if needed)
Variable size
Nasty odor Firm and mobile Possible visible opening
Asymptomatic
Treatment is not indicated unless symptomatic or on the face
Incision and drainage
Be suspicious of new moles appearing or moles that are growing, changing shape, or changing colors in adults.
Can appear, grow, darken, lighten, and disappear during lifespan
Junctional Nevus
Benign lesions composed of organized clusters of melanocyte-derived nevus cells
Flat or slightly raised Tan or brown Round or oval Most on palms, soles, genitals, and mucosa, but they can occur anywhere. Compound Nevus Slightly to markedly raised Tan, brown, or black
Nevus
Center may be more elevated and pigmented Common on face, scalp, trunk, and extremities
Found at both the DEJ and in the dermis Intradermal Nevus
Raised and soft papules Flesh-colored, tan, or brown
Mole
Course hairs may grow Common on the face, scalp, and neck, but can be seen on trunk and extremities
Exicision (if symptomatic or concerned about malignancy)
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms Blue Nevus Cells located within the deeper dermis Tyndall effect Macu Macule less or papu papule less Blue Blue,, gray gray,, or blac black k Common on head, neck, buttock, and dorsal hands / feet Halo Nevus Surrounded by a rim of depigmentation Autoimmune phenomena preceding its disappearance Area usually repigments
Nevus Continued…
Mole
Spitz Nevus Dome-shaped smooth papules Pink, tan, or brown History of rapid growth Common on face, scalp, neck, and legs Nevus Spilus Sharply-defined tan to brown patch with multiple hyperpigmented macules ± papules Can occur anywhere Becker's Nevus Brown patch, a patch of hair, or both Vary in size May enlarge Not a true nevus because it lacks nevus No malignant potential cells Congenital Melanocytic Nevus
Ephilides
Verrucous surface Dark brown and raised Greatly vary in size Present at birth of during infancy Recommend excision after puberty
↑ Risk of malignant melanoma in lesions > 20 cm
Appear in childhood Fade in winter
1 - 2 mm Well-defined Red, tan, or browncolored macules Darken with sun exposure
Freckles
Laboratory Test
Result
Treatment
Medications
Other
Clinical Medicine Condition / Disease
Lentigo
Cause
Age Spots
Multiple lesions are referred to as lentigines
Liver Spots
Do not darken in sun and Appear in childhood Part of several fade is absence of hereditarysyndromes sunlight Solar Lentigines Occur on sun-exposed ↑ Size and number with caucasians ↑ age 1 - 3 mm elevated papules
Fordyce Spots
Laboratory Test
Treatment
Result
Medications
Other
Juvenile Lentigines
Wisdom Spots
Sebaceous Hyperplasia
Signs and Symptoms
Common and benign enlargement of the subaceous glands on the face
Flesh-colored or yellow May have central umbilication Could be solitary but common occur in multiples on the forehead, nose, cheeks, and eyelids
Ectopically-located sebaceous glands on the buccal mucosa and vermillion of lips
Cherry Angioma
Extremely common, benign proliferation of dilated superficial capillaries
Venous Lake
Dilated blood-filled vascular channel
Small, pinpoint macules ± papules No treatment Orange or yellow Single or multiple 0.5 - 5 mm Smooth and domeshaped, flat, or polypoid papules
Eruptive onset of hundreds of these may be seen with the sign of LeserTrelat.
Cherry red to purple May occur anywhere but more common on the trunk 2 - 10 mm papule on sunexposed skin Single or multiple Soft and usually compressible Common on the lower lip and ears, but almost always on the face
Spider Angioma
Common, benign, dilatation of superficial bleed vessels
Composed of an arteriole (body) perpendicular to the skin Multiple radiating capillaries parallel to skin surface
Diascopy Common on face and hands, but also occurs on trunk and arms
Blanching
Electrocautery or laser (risk of scarring)
In both children and adults Those appearing during pregnancy and in childhood tend to disappear spontaeously.
Clinical Medicine Condition / Disease
Cause
Signs and Symptoms S lo w g ro rowi ng ng L oc oca l y de st st ru ruct iv ive Most common on the Usually > 40 years old face, scalp, ears, and ♂ > ♀ Nodular BCC Most common variant Dome-shaped papule with overlying random telangectasias Center becomes flattens Borders become raised or ulcerates or rolled Frequently bleed and develop crust ± scale Superficial BCC
Laboratory Test
Treatment
Result
Excision
Nodular BCC
Most common skin cancer
Erythematous and scaly plaques ± rolled border
MMS (for recurrent or high risk) ED&C Superficial BCC Excision ED&C Excision
Pigment BCC
MMS (for recurrent or high risk)
More common on the trunk and extremities Pigmented BCC Morpheaform BCC May resemble melanoma
Actinic Keratosis
Scaly, hyperkeratotic, or rough-textured papules Flesh-colored,yellow, brown, pink, or red Most commonly seen on May present as sun-exposed skin of faircutaneous horns skinned patients Usually occur on face, scalp, neck, ears, dorsal hands, and forearms
Squamous Cell Carcinoma
MMS
Vismodegib
Locally-advanced disease not amenable to surgery or radiation Gorlin syndrome
Cutaneous horns should always be biopsied. 5-FU (Efudex) and imiquimod (Aldara) Cryotherapy
ED&C
Excision MMS
Flesh-colored,pink, yellow, or red
Chemotherapy Chemotherapy (if metastatic) May be ulcerated or eroded
Face, scalp, neck, and hands of older patients
Bowens Disease SCC in situ Slow-growing, slightly raised, red plaque with scale
Actinic Cheilitis Actinic keratosis on the lower lip Palpate lesions for induration and if present, the lesion should be biopsied to rule out SCC.
Photodynamic therapy
ED&C
Indurated papules, plaques, or nodules with scale
Potentially invasive, primary cutaneous malignancy of keratinocytes in the skin or muscous membranes
Vismodegib
Metastatic BCC
Morpheaform BCC Least common varient White to yellow patch with poorly-defined borders Tumor may extend beyond borders of clinical lesion
Common, persistent, keratotic growth with malignant potential caused by cumulative sun exposure
Other Risk Factors Cumulative sun exposure White-skinned White-skinned patients with poor tanning Albinos Sunburns prior to age 14 Arsenic ingestion Prior XRT
ED&C
Least aggressive variant
Basal Cell Carcinoma
Medications
5-FU Bowens Disease (dependent on location, patient, and size of lesion)
Cryotherapy ED&C Excision MMS
Risk Factors Ultraviolet radiation (causative) Radiation Chemicals (arsenic and hydrocarbons) Tobacco Chronic infection Chronicinflammation Burns HPV infection Accounts for approximately 20% of all skin cancers Palpate regional LNs for mets, especially for lesions on the ear, scalp, lips, and temples Erythroplasia of Queyrat SCC in situ of the penis
Clinical Medicine Condition / Disease
Cause
Keratochanthoma
Cannot be clinically distinguished from an invasive SCC
Signs and Symptoms
Dysplastic nevus
Atypical Nevus Clarks Melanocytic Nevus
A B C D E
Treatment
Result
Medications
Biopsy
> 50 years old Solitary lesions appear sporadically and are common May start in childhood but more common in adults Asymmetry Border irregularity Color Diameter Evolving
Diagnostic
Excision
Observation Excision
Mild Atypia
Biopsy
Grade atypia
Moderate Atypia
Excision
Severe Atypia
Treated as if it is melanoma
Multiple lesions are thought to be of autosomal dominant inheritance and are uncommon.
Mole mapping (multiple atypical nevi) Deramatology referral Breslow Level Depth of lesion (in mm) from the top of the clinical lesion to the bottom of of the lesion in the tissue specimen Most important prognostic indicator Clark Level Level of anatomic invasion Important in areas of thinner skin May appear anywhere in the body and exam should include LN palpation for mets
Flat, raised, nodular, or ulcerated Early detection
Punch Biopsy Variable color
Malignant Melanoma
Metastatic Melanoma
Malignancy of melanocytes
Any new mole presenting in adulthood or any mole changing in size, shape, or color Risk Factors PMH or FMH Blue eyes
Fair skin Blond or red hair Many moles UV exposure from both History of blistering sun and tanning beds sunburns Most common metastatic site is the skin, but any organ can be involved. C NS mets are most common cause of death Lentigo Maligna
Deadly form of skin cancer
Other Most commonly occurs on sun exposed skin of caucasians
Rapidly growing Solitary, firm, and red nodule with a central keratotic plug or cutaneous horn ♂ > ♀
Laboratory Test
Melanoma in situ Usually seen in older caucasians Commonly seend on face, neck, and arms Superficial Spreading MM Most common type of MM Asymmetric and flat > 6 mm Variable color Most common in Usually seen on the caucasians trunk and extremities Spread laterally but may develop deeper Nodular MM Very rapid growth Most common on the extremities 10 - 15% of all MM Grow vertically
Diagnostic
Incisional Biopsy
Excision
IL-2
Ipilimumab
BRAF inhibitors
IL-2
Ipilimumab
Vemurafenib
MEK inhibitor
Dabrafenib
Treatments only halt or delay progression of the disease and are rarely curative.
Trametinib
Lentigo maligna represent 5 - 10% of all melanoma. 70 - 80% of all melanoma is superficial spreading MM
Clinical Medicine Condition / Disease
Cause
Acral Lentiginous Metastatic Melanoma
Most common type of metastatic melanom in Asian-Americans and African-Americans
Amelanotic Metastatic Melanoma
Nonpigmented melanoma of any subtype
Signs and Symptoms
Laboratory Test
Result
Treatment
Medications
Other Least common type of MM in caucasians. ≈ 7% of all MM
Primarily occurs on the hands, feet, and nails
♂ > ♀
Pink to red colored papules
↓ Enlarged plaques and nodules
Scares the crap out of all dermatologists
≈ 2% of all MM
Pharmacology Drug
Generic Examples / Brand Name
Mechanism of Action
Indications
Inhibit macrophage accumulation in inflamed areas
Topical Steroids
↓ Capillary permeability and edema formation
Potency Formulation Factors for Absorption
Medium Potency High Potency Very High Potency
Contraindications
Adverse Effects
Bacterial infection Viral infection Fungal infection
Skin drying / cracking / thinning Skin atrophy Purpura
D: "Fingertip unit" Onset: 1 - 2 days
Tolerance / tachyphylaxis Adrenal suppression
Use with dressings
Monitoring / Other Discontinuation of Therapy Depends upon dose, duration, and disease Risk of rebound flare when discontinued
Frequency of application
Histamine antagonist
Low Potency
Pharmacokinetics A: After bathing when sk in i s moist
% of total dose absorbed through skin Face
Genitals
Armpits
Skin folds
Children
Chronic use
Occlusive dressings
Large body areas
HC butyrate
Trunk
Arms
HC valerate
Legs
Face (limited)
clocortolone
C hr hr on on ic ic e cz cz em em a
R ad ad ia ia ti ti on on d er er ma ma ti ti ti ti s
hydrocortisone
halcinonide triamcinolone augmented betamethasone dipropionate
Severe psoriasis
Skin conditions where steriod will not be discontinued abruptly
Cream
Face Intertriginous areas
Use with caution in occlusive dressings
Occlusive dressings Face Groin Armpit Skin folds
Do not use more than 2 weeks. Be aware of symptoms of adrenal suppression
Eczema
clobetasol
halobetasol
Generally choose nonfluorinated products
Mo st st s ki ki n a rre ea s
M os os ttll y a bs bso rb rbe d
Drying effect
Opaque
Dry, scaly lesions
Skin that needs protection
D: Should not exceed 50 grams/week
Hairy areas
Ointment
Therapeutic advantage of ointment + cosmetic advantage of cream
Gel
Can have cooling effect
Lotion Occulsive Dressings
Fingertip Unit
Amount of steroid squeezed out of tube that covers from the tip to the first crease of the finger
Weeping lesions in areas subject to chafing
Evaporates quickly
Penetrates easily
Drying effect (if contains alcohol)
↑ Skin penetration by ↑ moisture content of stratum corneum
Beneficial in resistant cases
Hand Foot Face and Neck Arm Leg Front or Back Trunk
1 fingertip unit 2 fingertip unit 2.5 fingertip unit 3 fingertip unit 6 fingertip unit 7 fingertip unit
High potency steroids
Increases adverse effects of steroid
Do not use for > 12 hours / day
1 fingertip unit = 500 mg of cream or ointment
Pharmacology Drug
Generic Examples / Brand Name
Mechanism of Action
Indications
Pharmacokinetics
Free-radical oxidation
Benzoyl Peroxide Clearasil
Stridex
Desquamation of the horny layer
Salicyclic Acid Sulfur / Resorcinol
Irr itation Peeling Redness Contact dermatitis Bleach hair / towels / carpeting
Acne
Nongential warts
Diabetes (use caution) Poor circulation Infants Pregnancy (category C)
Increases horny cell adhesion
Noticeable color and odor
Benzoyl peroxide use
Acne
Photosensitivity Changes in skin pigment
Stinging / burning Pruruitis Photosensitivity
Acne
Blistering Dermatitis Eczema Pregnancy
Modulates differentiation differentiation and proliferation of epithelial tissue
Acne
Anti-inflammatory
50S ribsome subunit inhibitors
A: Foam or gel D: Daily (Clindagel and foam) or BID P. acnes
Acne
D: Daily or BID
Erythromycin
50S ribosome subunit inhibitor
Edema Blistering Peeling / dry skin
D: Q evening
Modulates cell differentation, keratinization, keratinization, and inflammatory processes
Clindagel
Peeling / dry skin Stinging / burning Erythema Pruruitis
Stimulates mitosis and turnover in epithelial
Clindamycin
Gels are the most effective formulation
Dark brown scale (reversible)
D: Q evening Effect: 2 - 3 weeks with optimal > 6 weeks
Tretinoin
Tazarotene
Apply th thin la lay er Avoid eyes, mouth, lips, and nose
Stinging / burning Confusion Headache Dizziness Peeling Ophthalmic irritation
D: Daily Acne
Reduces the adhesiveness of follicular epithelial cells
Adapalene
Monitoring / Other Directions for Use Wash sk in
↑ Sun sensitivity D: Daily
Keratolytic Clearasil
Adverse Effects Stinging / burning Dryness
Acne
Mild keratolytic with drying and desqamative actions
Removes excess keratin
Contraindications
D: Daily Effect: 4 - 6 weeks
P. acnes
P ee ee lili ng ng / d ry ry sk sk in in
S ec ec on ond- lili ne ne re ret in ino id id
Stinging / burning Irritation Pruritis Pain Discoloration Edema Photosensitivity Contact dermatitis Fissuring Peeling / dry skin Stinging / burning Irritation Pruritis Oiliness Folliculitis Photosensitivity Nausea / vomiting / diarrhea P ee ee lili ng ng / d ry ry s ki ki n Burning Erythema Pruritis Oiliness Eye irritation
R es es is is ta ta nc nc e i s i nc nc re re as as in in g. g.
Pharmacology Drug
Generic Examples / Brand Name
Sodium Sulfacetamide
Mechanism of Action
Inhibits bacterial dihydrofolic acid synthesis Azelex Cream
Azelaic Acid Finacea Gel
Microbial cellular protein synthesis inhibitor
Indications
Stinging / burning Pruritus Erythema Peeling / dry skin Contact dermatitis
Acne
Oxygen radical scavenger
Minocycline
30S and (possibly) 50S ribosomal subunit inhibitor
Doxycycline
30S and (possibly) 50S ribosomal subunit inhibitor
Acne
Dapsone
Inhibits bacterial dihydrofolic acid synthesis
Acne
norethinodrone
Decrease circulating androgen
norgestimate
Decreases sebum production
Acne
Adverse Effects
Monitoring / Other
Irritation Hypersensitivity
D: BID Effect: 4 weeks
Inhibits bacterial protein synthesis
Hypersensitivity Photosensitivity Rash Nausea / vomiting / diarrhea Tooth discoloration ↑ Intracranial pressure (rare)
A: Oral on empty stomach D: Q6 hours for 1 - 2 weeks
Patients with dark complexions should be monitored for early signs of hypopigmentation.
Monitor LFTs and CBC for longterm treatment
A: Oral D: BID
Dizziness / vertigo Hypersensitivity SLE Bulging fontanelle Pseudotumor cerebri (rare)
Monitor LFTs, renal function, and CBC for long-term treatment Do not take calcium, iron, magnesium, or aluminum antacids or supplements ≤ 4 hours.
A: Oral
Photosensitivity GI disturbance ↑ BUN Bulging fontanelle
Monitor LFTs, renal function, and CBC for long-term treatment Do not take calcium, iron, magnesium, or aluminum antacids or supplements ≤ 4 hours
A: Topical (safer) or oral D: BID for 12 weeks
Peeling / dry skin Erythema Oiliness
Acne
Acne
D: BID
Isotretinoin
Inhibits sebaceous gland function and keratinization
Acne
Mupirocin
Bacterial isoleucyl t-RNA synthetase inhibitor
Bacterial infection
Interfere with cellular permability
Fungal infection
Allylamines
Contraindications
Acne
Tetracycline
Oral Contraceptives
Pharmacokinetics D: BID
butenafi ne naftifine terbenafine tolnaftate
Pregancy (category X)
Severe birth defects Peeling / dry skin and mucous membranes
Lip inflammation Hypertriglyceridemia Myalgia Anemia Conjunctiviitis Various skin conditions A: Topical or nasal D: TID
Burning / pruritis Headache Rhinitis Nasal congestion
Under restricted distribution Monitor for depression or aggressive behavior, LFTs, lipids, CBC, and hearing changes.
High level resistance has been reported in S. aureus and coagulase (-) staphylococci Shor t time to cur e
Pharmacology Drug
Azoles
Generic Examples / Brand Name clotrimazole econazole ketoconazole miconazole oxiconazole sulconazole
Mechanism of Action
Indications
Pharmacokinetics
Contraindications
Adverse Effects
Monitoring / Other Requires skin turnover for complete effect
Fungistatic
Dermatophyte infection
Yeast skin infection
sertaconazole
Ciclopirox
Loprox
Polyvalent cation chelator
Dermatophyte infection
Penlac
Inhibits metal-dependent fungal enzymes
Yeast skin infection
Alters membrane permability
Fungal infections
Nystatin Acyclovir
Zovirax
Antiviral
HSV-1 infection
Seizures
Discolors light-colored hair
Immunosuppression
A: Cream or oral D: 5x a day for 4 days (cream) or 5 days (oral) E: Renal
Headache Nausea / diarrhea Malaise Mild pain / burning / stinging Neutropenia
D: 2 g Q12 hours for 1 day or 1 g TID for 7 days (shingles) E: Renal D: 500 mg Q8 hours for 7 days E: Renal
See Acyclovir See Acyclovir
↑ LFTs
Valacyclovir
Valtrex
Antiviral
Famcyclovir
Famvir
Antiviral
Docosanol 10% Cream
Abreva
Interferes with viral entry into target cell
Shingles Vaccine
Zostavax
Prevention of shingles in patients > 60 years old
HSV-1 infection
Shingles
HSV-1 infection Shingles
D: 5x a day
Breastfeeding
See Acyclovir See Acyclovir
Penciclovir Active metabolite of famcyclovir Decreases healing time
HSV-1 infection
Shingles
May be used in patients with previous shingles episodes
Avoid antivirals for 1 day before and 14 days after vaccination.
