derm diseases

• AKA eczema
• "The itch that scratches"
• Rash Itches->scratching->rash itches
• Highly pruritic

• Genetic component
• Family history of atopy (70%)
• Food allergies may worsen AD in children
• May b aggravated by topical irritation/affect skin barrier integrity

• Irritants
• Allergens
• Perspiration
• Heat
• Tight clothing
• Rough fibers
• Emotional distress

• Most often onset in children
• Many children "outgrow" as they get older
• ~~May develop hand, eyelid, or postauricular dermatitis

• T cells and Langerhans cells are hyperactive
• Causes defect in cell-mediated immunity and overproduction of immunoglobulins by B cells
• Barrier dysfunction
• Ceramide deficiency

• Erythema and severe pruritus
• Red pruritic papules, patches, and scaling
• May have vesicular lesions with acute onset
• Chronic lesions become lichenified
• Look for signs of superinfection
• Also more prone to viral and fungal skin infections
• Hyper or hypopigmentation may result

• Cheeks, perioral, scalp
• Extensor surfaces of the knees and elbows

• Flexural areas
• ~~Antecubital and popliteal fossae
• ~~Neck
• ~~Wrists, ankles
• May become lichenified

• Flexural involvement
• Hand dermatitis
• Eyelid or lip dermatitis
• Xerotic skin, ichthyosis vulgaris, keratosis pilaris

• Round, coin-shaped eczematous lesions
• Most common in adults
• Sharply demarcated lesions on arms and legs
• Tends to recur when steroids with drawn
• One of the more difficult forms of eczema to treat
• DDx - fungal

• Clinical diagnosis based on symptoms, exam, and family hx
• No labs needed
• Consider referral for allergy testing in children with severe or refractory AD

• Restore/protect skin barrier
• Topical steroids BID x 10-21 days-not a cure
• Topical immune modulators
• If pruritus severe, consider antihistamines PRN

• Protopic (tacrolimus) or Elidel (pimecrolimus)
• Use twice daily for short term use, or intermittently for long-term use
• Used as steroid-sparing agents
• ?? Risk of CA

• Moisture, moisture, moisture
• Limit baths to 5-10 minutes in lukewarm water
• Avoid triggers
• Symptoms will worsen with cool dry weather in the winter

• Bleach water baths
• Wet pajamas

• Allergic or irritant reaction caused by skin contact with a substance
• Rash will occur where the exposure occurs

• Delayed (Type IV) hypersensitivity reaction
• Must be sensitized to a chemical before reactions occur
• Plants: Poison ivy, poison oak, poison sumac
• Metals: Nickel, chromate
• Rubber products
• Preservaties or addatives: Formaldehide, dyes, fragrances, quaternium-15, etc

• Repeated exposure to mild irritants
• Water, heat, soaps, friction
• About 80% of cases of contact derm are irritant contact derm
• Nonspecific response - does not require sensitization

• Initial: occurs w/in 14-21 d (allergic)
• subsequent rashes: occur more quickly after exposure

• can present after one exposure to strong agents
• more frequently after repeated use of mild irritants

• May have history of new exposure, but don't r/o if there is no "new" exposure
• Does the rash get better when away from work? Away from your hobby?
• May have photosensitization - sunlight + chemical = allergy ie Sunscreens
• Vesicles, edema, erythema, and extreme pruritus (allergic) or burning (irritant)
• As it becomes more chronic, becomes erythematous, scaling
• Occurs in area of contact initially, when chronic, may spread

• Face - make up, sunscreen, shampoo
• Eyelids - make up , nail polish
• Feet - leather (dye)
• Waist/umbilicus, finger, wrists, neck - nickel or metal
• Sun-distribution - photodermatitis

• Caused by delayed hypersensitivity reaction to plants
• Poison ivy, oak, and sumac
• Linear vesicles and erythema

• Clinical Diagnosis
• If questionable, can biopsy (rarely needed)
• Consider patch testing

• Tests for delayed hypersensitivity reactions
• Patches placed on patient's back
• Returns in 48 hours for first reading and removal of patches
• Returns again in another 48 hours for final read
• Standard panels or can customize panels

• Allergen/irritant avoidance is mainstay of treatment
• Topical corticosteroids can treat acute symptoms
• Simplify skin regimen to avoid further irritation
• For severe cases, tapering course of oral prednisone or Medrol may be needed
• Allx can develop @ any time
• treatments control sx but do not eliminate allergies

• Also called pompholyx, dishydrotic eczema
• Recurrent vesicular, eczematous dermatitis involving the hands and occasionally feet
• Cause is unknown

• Usually occurs in atopic patient
• Prodromal itching
• Hyperhidrosis may worsen condition
• Small vesicles (1-5 mm), monomorphic, filled with clear fluid="Tapioca like"

• As vesicles recede, develop scaling and peeling of skin
• Pruritus improves
• As healing occurs, may only have residual brown spots on an erythematous base

• Clinical Diagnosis
• Pictures may be helpful - patient may not see you until they are in the later stages
• IF ONLY INVOLVES 1 HAND-EXAMINE FEET
• ID reaction - vesicular rash on one hand as an immune response to distant fungal infection

• High potency steroid
• Wet dressings or Burrow's solution
• Oral antihistamines for pruritus
• If result of ID reaction, treat fungal infection

• Chronic plaques with enhanced skin markings that result from chronic inflammation
• Caused by continued rubbing and scratching
• More common in adults
• may be present in children with longstanding eczematous conditions

• Sharply demarcated, violaceous or red scaly plaques with lichenification
• On scalp, may present as sharply demarcated nodules
• Occurs most often in areas that can be easily reached
• ~~Lower legs, wrists, ankles
• ~~Posterior neck, scalp upper eyelids, behind the ear
• ~~Scrotum, vulva, and anal skin

• Clinical diagnosis
• DDx includes tinea - may need KOH stain to r/o
• Consider biopsy if lesion not straightforward
• Patch testing if caused by contact allergen or irritant

• Patient reassurance
• Try to break the itch/scratch cycle
• Topical steroids may help thin plaque and reduce itching but will be of little use if the patient continues to rub the area
• Manage stress
• Awareness of scratching
• Consider oral antihistamines for nighttime scratching

• Vesicular disease seen in patients with gluten-sensitive enteropathy
• Uncommon in children
• Does not correlate with bowel symptoms

• Clustered vesicles or excoriations
• on bilateral knees, elbows, sacrum, and base of the scalp-May only see excoriations
• HIGHLY pruritic, may be "burning" in nature
• May also have papules
• Generally, do NOT have bowel symptoms w/ their Celiac
• Less malabsorption than other pTs with Celiac
• Higher risk of lymphoma (as with other Celiac patients)

• Biopsy: Direct immunofluorescence (DIF) - look for antibodies deposited in the skin
• Refer to GI - c-scope and biopsy
• May order celiac labs - positive in 70%

• STRICT GLUTEN AVOIDANCE
• Steroid to reduce inflammation
• Dapsone for recalcitrant cases

• Autoimmune disorder typically seen in older patients
• Subepidermal blistering

• Autoimmune - antibodies against hemidesmosomal proteins
• Environmental trigger is often unknown
• May be triggered by certain drugs

• Furosemide
• Captopril
• Some NSAIDs

• Most commonly appears in flexural skin folds
• Starts with urticarial phase-Pruritic red papules coalesce and form plaques
• Within 1-3 weeks, plaques turn red, and bullae form
• "tense bullae on erythematous skin"
• Severe pruritus
• Bullae rupture within1 week, crust, then heal rapidly
• Negative nikolsky sign
• May also present with oral blisters (less commonly than in pemphigus vulgaris

• Biopsy
• ~~MARGIN OF BULLA
• ~~Include unaffected skin
• ~~Send for direct immunofluorescence (DIF) for immunologic stains
• May find circulating antibodies in the blood, DOESNTG CORRELATE TO DZ ACTIVITY

• REFER TO DERM
• About half of patients are in remission at 3 years
• Treat the itch
• Hydroxyzine
• High-potentcy steroids
• Minocycline, tetracycline, dapsone, low-dose methotrexate, prednisone

• Rare, potentially life-threatening autoimmune disease
• Intraepidermal blistering involving the skin and mucous membranes
• Occurs in older patients
• Highest incidence in people of Ashkenazi Jewish descent

• Initially develop oral lesions -weeks to months before skin symptoms
• Bullae 1-3 cm in size
• ~Minimally pruritic
• ~Tenderness or irritation of skin
• ~Rupture easily
• Most commonly involves torso, upper legs, can involve face and arms
• Nikolsky's sign
• dysphagia or sore throat d/2 blisters& erosions in pharynx/esophagus

• Applying traction on intact skin causes formation of bulla
• Applying pressure to intact bulla causes it to extend into surrounding tissue

• Biopsy: One from edge of lesion, one from unaffected skin&DIF
• Lab: May find antibodies in the blood
• CORRELATES WITH DZ ACTIVITY

• Treat any active infection (frequent cause of death)
• Prednisone, azathioprine (Imuran), cyclophosphamide
• Monitor for comorbidities of steroid
• Refer to derm (?tertiary care)

• Common polymorphous eruption seen on the face, chest, and back
• Most common during teenage years, but can persist into adulthood
• Hormone modulated
• Men have more severe disease but are less likely to seek treatment
• Women tend to have longer duration of disease

• Pores become plugged (comedones)
• Secretions become stagnant, bacteria from surface of skin invade
• Immune response causes erythema, edema (pustules, papules)
• Deeper glands may be affected, causing deep, painful cysts

• Genetics
• Diet (Dairy; Sugars?)
• Hormones
• Steroids
• Hygiene (yes and no)
• Chin straps, helmets

• Noninflammatory lesions (Open and closed comedones)
• Inflammatory lesions (Papules, pustules, cysts)
• May cause scarring
• ~~Hyperpigmentation
• ~~Depressed scars
• ~~Sinus tracts from cysts

• Women with hirsuitism and obesity - PCOS
• Young children - signs of secondary sex characteristics - precocious puberty
• Irregular menses in middle aged women - perimenopause
• Steroid use
• Bodybuilders/athletes - anabolic steroid use

• Clinical diagnosis
• Labs to r/o any associated conditions

• Open pores
• Reduce bacterial load &/or inflammation
• Severe disease-isotretinoin
• Cystic acne usually requires oral medication
• Tailor medications to account for skin dryness, give your patient a plan to prevent dryness

• Benzoyl peroxide
• Salicylic acid
• Retinoids

• Topical erythromycin combinations
• Oral doxycycline or minocycline
• Topical metronidazole or topical dapsone

• One med for opening pores, one med for bacteria, plus an oral antibiotic to have on hand for flares
• BUT fit the regimen to your patient
• Use combination products
• Lifestyle considerations; Consider the cost

• Let patient know the acne will get worse before it gets better
• Meds will take 6-8 weeks to have full effect
• No medi/combo is 100% effective

• Sunscreen
• Erythematous macules tend to fade over months: Bleaching cream, YAG laser

• Deeper resurfacing laser
• Topical retinoids
• Dermal fillers

• Potential for significant psychosocial effects
• Acne is not just for teenagers!
• No significant long-term mortality, but can be costly in the long run

• Common facial rash with redness, blushing, telangiectasias, papules and pustules
• NO comedones
• Tends to occur during adulthood
• ~~Most commonly appears as perioral dermatitis in children

• Exact cause unknown
• Demodex mite may contribute in some patients

• Hot food or drink
• Red wine
• Sunlight
• Skin irritants
• Embarrassment
• Spicy food

• More common on fair skin types, but can occur with any skin type
• Patients tend to have "sensitive skin"
• Papules and pustules on forehead, cheeks, nose
• INVOLVES NASOLABIAL FOLDS
• Erythema and telangiectasias
• Rarely lesions anywhere but the face

• Enlargement of the nose due to chronic inflammation and skin thickening
• More common in men
• Rosacea SYMPTOM

• May occur with or without skin disease
• Mild conjunctivitis
• ~~Erythema, discomfort, FB sensation, tearing
• ~~May cause blepharitis, chalazions, corneal vascularization over time

• Clinical Diagnosis
• If NL folds are spared, consider biopsy to r/u lupus

• Avoid triggers
• Topical: Metronidazole; Sulfacetamide
• Systemic therapy: Low-dose doxycycline (Oracea)
• ~~May use full-dose tetracyclines for 2-4 weeks for exacerbation

• Referral to ophthalmology
• Oral antibiotics

• Cover with green cosmetics
• Laser or phototherapy

Surgery, CO2 laser

• Inflammation of the hair follicle
• Caused by infection (bacterial or fungal) or irritation

• Inflammation of the hair follicle
• Infection with Staph
• Fungal folliculitis spread from other dermatophyte infection

• Abrupt onset of papules at the follicle
• Chest, scalp/face (areas that are shaved), legs, axillae, lower trunk
• May be painful or tender
• May have signs of dermatophyte infection elsewhere (fungal folliculitis)

• Papules and pustules appear on torso after using a hot tub
• Caused by Pseudomonas

• Clinical diagnosis
• KOH to rule out fungal
• ~~Fungal folliculitis tends to be more destructive
• May bacterial culture in recalcitrant cases

• Minimize heat, friction, occlusion
• Antibacterial soap, mupirocin ointment
• If extensive, consider dicloxacillin or cephalexin
• Oral antifungal therapy if fungal
• In recurrent cases, consider testing and treating for nasal S. aureus infection

• Papular and pustular eruption due to close shaving
• More common in African Americans and Hispanics
• Sharp point of hair caught under skin, forms papule and irritation
• Treat by d/c shaving

• Infection of the dermis and subcutaneous tissue
• Associated with systemic symptoms
• MC in immunocompromise, liver or renal disease, or use IV drugs or alcohol

• May occur as a result of wound, trauma, or break in the skin
• Break in skin may be relatively small and not apparent
• Deeper tissue layers are involved in the inflammatory reaction,
• ~~ causing erythema, edema, pain, warmth

• Initial symptom is localized pain
• Common sites are pinnae, lower legs, hands
• May have associated athlete's foot
• Develop red, swollen, painful plaque
• No distinct border
• May develop lymphangitis and adenitis (most commonly with S. pyogenes)

• CBC - elevated WBC
• ESR elevated
• Culture: Group A Strep and S. aureus
• If animal bite or scratch, consider Pasturella

• Rest, elevation, ice
• Start empiric antibiotics (Staph and Strep)
• ~~Augmentin, Cephalexin, Azithromycin
• ~~Animal bite or scratch - Augmentin
• Hospitalization may be required for severe infection

• Acute, superficial cellulitis with prominent lymphatic involvement
• Infection MORE SUPERFICIAL-DERMIS AND UPPER SUPCUTANEOUS TISSUE

• Infection most often results from break in tissue with entry of pathogens
• May not be able to identify the site of entry
• Staph and strep most common
• Those with immunosuppression, diabetes, poor circulation, or alcohol abuse more predisposed

• Prodrome of systemic symptoms
• Pain, burning, or tenderness
• Common areas - face, lower leg, arm
• Sudden onset of erythematous, tender, firm spot with sharply demarcated borders
• May have lymphatic streaking

• Most cases due to Strep
• Clinical diagnosis - difficult to culture
• CBC - Elevated WBCs
• ESR - Elevated
• Consider blood cultures if high fever

• PENICILLIN V ORALLY IS DRUG OF CHOICE-azythromycin
• Bed rest, elevation, ice
• Consider prophylactic antibiotics for recurrent disease
• Consider hospitalization if rapidly advancing
• Treat underlying skin injury/condition

• Highly contagious SUPERFICIAL SKIN INFECTION
• Caused by S. pyogenes or S. AUREUS (MOST COMMON)
• May develop on damaged skin or normal skin
• Infections more common in children or those who are in close contact with others

• Staphylococci from the skin and nose are introduced to broken skin
• May be due to underlying skin disease (i.e. eczema) or normal skin
• More common with poor hygiene or warm, moist climates

• Thin-roofed bullae form
• As bullae collapse, a HONEY-COLORED CRUST FORMS
• Lesions may coalesce
• Lesions in many stages of healing
• mild adenopathy

• Vesicles or pustules rupture and
• scaling, tinea-like border forms
• Honey colored or whitish crust forms
• May have satellite lesions around the periphery

• Culture
• S. aureus most common
• Need sensitivity information

• Self-limited, but treat since it is highly contagious
• Limited disease (Bactroban)
• Widespread or bullous disease-Oral antibiotics
• ~~Dicloxacillin
• ~~Cephalexin
• Recurrent disease - consider culture of nose for carrier

• Overgrowth of Candida albicans on the skin and/or mucous membranes
• Decreased cellular immunity, damaged barrier function, and changes in normal skin flora may predispose

• Diabetes
• Hormonal - pregnancy, OCP use
• Systemic antibiotics or steroids
• Skin maceration
• Conditions that affect cell-mediated immunity (viruses)

• Prefers to grow in warm, moist areas
• Affects only the outer layer of the skin
• ~~KOH scraping may show hyphae and pseudophyphae
• Beefy red lesion
• Cigarette-paper-like scale along advancing border
• Satellite lesions
• balanitis

• Foreskin and glans
• Red papules and pustules with pasty maceration under the foreskin
• Pain and edema
• Candidiasis sx

• Beefy red plaques in the inguinal and gluteal folds
• Satellite lesions
• candidiasis

• Affects skin folds
• Develop beefy red plaques within the skin folds
• Advancing border - sharply defined
• Satellite lesions
• May have maceration of skin folds

• KOH shows hyphae and pseudohyphae
• Culture may be positive for X
• Use judgment with culture X part of the normal skin flora

• Topical antifungals
• Dry the skin
• Fluconazole oral 200 mg day one, 100 mg days 2-7
• recurrent or severe dz: consider underlying predisposing condition
• DM? immunosuppression?

• Due to overgrowth of Pityrosporum orbiculare
• Normal skin flora
• Increased in oily skin, heat and humidity
• +/- contagious?

• Common in teens, those with increased sebaceous activity
• More common in warmer climates, warmer weather
• Involves chest and back
• Different color on different skin tone (pink, hypopigmented)
• ~~uniform on pt; fine scale
• Woods light exam

hypopigmented areas with a faint yellow-green fluorescence

• DM, immunosuppression
• Pregnancy, OCPs
• Indoor tanning (Lower patient resistance)

• Clinical diagnosis
• Can do KOH to confirm
• ~~"spaghetti and meatballs pattern"
• ~~Hyphae break into short, rod-shaped fragments
• ~~Spores are round

• Selenium sulfide shampoo, zinc pyrithion soap
• Antifungal cream or shampoo
• severe dz - fluconazole 150 mg twice weekly for 2 weeks
• ~~Sweating helps fluconazole work
• Skin pigment is slow to come back
• Patient reassurance
• Consider periodic shampoo washes to prevent recurrence

• Tinea infection of the nail plate
• Usually asymptomatic
• Increased risk with age
• Infection does not clear without treatment

• Thickening of the nail plate, most commonly at the distal end
• Nail yellow, keratotic debris accumulates under the nail
• Nail separates from nail bed

• Culture of toenail reveals trichophyton spp.
• KOH of subungual debris shows hyphae
• Order CBC, LFTs before starting treatment (Lamisil) and after 6 weeks of treatment

• Topical treatments rarely effective
• Oral therapy - Lamisil po daily
• ~~6 weeks fingernails
• ~~12 weeks for toenails
• Doesn't change appearance of old nails,
• only prevents infection of new nails

• Tinea Pedis-feet
• Tinea Corporis-body
• Tinea Cruris-jock strap
• Tinea Capitis-head

• MCC Microsporum, Trichohphyton, Epidermophyton
• Found in the keratinous layer of skin, hair, and nails
• May spread through contact or fomite

• Erythematous papule/plaque
• As lesion enlarges, central clearing with an erythematous scaling papular or vesicular border

• Most common form
• Warm, moist conditions predispose (Gym; Communal showers/baths)
• commonly affects interdigital webs
• may cause scaly infection on plantar surface or vesicles
• Moist skin between toes-Interdigital maceration
• Extends on the plantar surface of the foot

• Scaling affects all of plantar surface
• Fine scale with pink skin
• Pruritus
• May also involve the hands

• May develop in patient with interdigital tinea pedis
• cover plantar or dorsal foot
• May trigger ID reaction

• Affects crural fold
• May result from infection transferred from the foot
• Occurs in males
• HALF-MOON SHAPED ERYTHEMATOUS PLAQUE
• WELL DEFINED SCALE ALONG BORDER
• May migrate to buttocks and gluteal cleft

• Tinea Corporis
• Round annular lesions (Ringworm)
• Flat scaly papules
• Spread into plaques w/ central clearing and peripheral erythema and scale
• Periphery may also have papules or vesicles
• May coalesce to form plaques
• Epidemics may occur in wrestlers
• Severe/widespread dz-eval 4 immunosuppression or RF for fungal dz

• Infection of the scalp, both the skin and hair follicle
• Acquired by close contact or sharing hair brushes
• Patchy white adherent scale on the scalp - mimics seborrheic dermatitis
• Inflammatory lesions may lead to alopecia
• Occipital adenopathy

• Scrape active border
• KOH stain - fungal hyphae
• Culture

• Needed for hair or nail infection
• Swab active portion of the lesion
• Takes 4-6 weeks for results

• Topical antifungal (pedis&cruris)
• Oral antifungals ( hair, nail, widespread)
• Powders to prevent reinfection
• Reduce RF

• Rash that occurs due to systemic disease
• Most commonly seen with viral infections
• Difficult to distinguish between viral cause
• A few viruses have characteristic rashes

• Get a good hx- consider time of year, outbreaks in the community, nonspecific symptoms that are associated
• Most common - erythematous maculopapular rash that is generalized, may coalesce into plaques
• Only symptomatic treatment needed

• Roseola
• Fifth dz
• kawasaki

• Young children (6 mos to 3 years)
• Caused by human herpesvirus 6 and 7
• Develop high fever
• As fever resolves, develop small, pink almond-shaped macules
• ~~ on the neck, trunk, proximal extremities, face
• Associated adenopathy
• Treat with symptomatic measures to control fever

• "Slapped cheek syndrome"
• Caused by parvovirus B19
• outbreaks in the winter and spring
• Most common ages 5-14

• Rarely have prodromal symptoms
• Erythematous patches on the face "slapped cheek" with circumoral pallor
• Two days later, develop lacy, reticulated rash on torso
• May wax and wane for 2-3 weeks

• Acute vasculitis
• Most commonly affects infants and children (7 wks-12 years)
• Conjunctivitis
• Lips and oropharynx

Conjunctival injection; Uveitis

• become red 3-5 days later
• Lips dry, fissured, cracked
• "Strawberry tongue" - hypertrophic tongue papillae

• 2-5 days after onset of rash
• -> erythema and edema of palms and feet
• ->followed by desquamation
• Rash begins with fever - polymorphous
• Generalized, diffuse deep red maculopapular lesions
• Diaper dermatitis and desquamation

• cardiac disease
• Abnormalities often resolve within a month, but sequelae may be long-lasting
• Cardiac involvement more common in males, patients < 1 yr or > 5 yr

• half of patients develop myocarditis
• Tachycardia, gallop rhythm
• May lead to sudden death

• 12-25 days after onset
• Coronary artery aneurysms and thrombi
• May cause stenosis as the inflammation resolves and scar forms
• Can lead to CHF, pericardial effusion, arrhythmia
• Death due to rupture of aneurysm or myocardial ischemia

• FUO > 5 days
• Bilateral conjunctival injection
• Changes in lips and oral cavity
• Cervical lymphadenopathy
• Polymorphous exanthema with vesicles and crust
• Changes in peripheral extremities

• Aspirin
• IVIG
• If don't respond to IVIG, consider steroids
• Monitor for long-term cardiac side effects

• Localized viral infection of the skin spread by skin-to-skin contact
• Caused by a pox virus
• More common during childhood, teenage years
• More likely to occur or be more widespread in atopic patients

• Small (1-2 mm) flesh colored papules that are dome shaped
• Evolve to become UMBILICATED, slightly larger (2-5 mm)
• May also become more pink
• Generally last 6-9 months without treatment, then resolve on own
• May occur as an STD in older population

• Usually a clinical diagnosis
• If atypical, consider bx
• Shows virus within the papule - "X body"

• Limit skin-to-skin contact, sharing towels, etc.
• Cover lesions, avoid picking
• If treatment is required (or desired)
• ~~Curettage
• ~~Cryosurgery
• ~~Cimetidine given as an adjunct to enhance immune response

• Viral skin infection caused by HSV I and HSV 2
• Type I - above the belt
• Type 2 - below the belt
• Not as true now
• After primary infection, the virus becomes latent in nerve ganglion, may develop recurrent disease at the same site

• Most often asymptomatic
• Often transmitted through respiratory droplets or direct spread
• If symptoms develop, occur after 3-7 days

• Occur after 3-7days
• Prodromal pain, tenderness, paresthesias
• Lymphadenopathy, headaches
• Pharyngitis and gingivostomatitis if oral disease
• Vulvovaginitis, proctitis, anorectal pain if genital involvement

• Grouped vesicles on an erythematous base
• More numerous in primary outbreak
• May occur on the skin or mucous membranes
• As vesicles rupture, crust forms
• Can last 2-6 weeks
• As rash resolves, virus migrates to nerve roots near area of infection, migrate to dorsal root ganglion and become latent

• May be precipitated by trauma, UV, illness, immunosuppression
• Prodromal symptoms
• Occur 2-24 hours before onset of rash
• Pain, paresthesia, burning sensation in the area affected
• Lesions develop - grouped vesicles on an erythematous base
• Vesicles umbilicate then rupture and crust
• Lasts about a week
• Systemic symptoms and lymphadenopathy rare

• Lips most common
• Herpetic whitlow (finger)
• Genital areas
• May occur anywhere on skin, but recurrences will happen in same area
• Does not protect the patient from developing HSV in other areas

• May make diagnosis clinically
• Culture vesicle
• ~~Unroof vesicle and obtain culture from base
• ~~Tzank smear - multinucleated giant cells
• ~~Rapid tests may be available
• ~~Can perform serology to determine HSV 1 or 2
• Culture may be negative

• Prevent spread
• Will resolve without treatment - choice to treat can be individualized in healthy people
• In patients with recalcitrant or very active/widespread disease, consider source of immunocompromise
• Remind patient they are contagious, even with treatment
• May shed virus even when asymptomatic

• Valacyclovir (Valtrex) 1 g BID x 10 days
• Famciclovir (Famvir) 250 mg TID x 7-10 days
• Acyclovir 200 mg 5 x/day x 7-10 days

**Treat at first prodromal symptom**

• Consider based on number of recurrences/year (usually ~6)
• Lower dose antivirals taken daily to prevent outbreak
• If patient develops outbreak, switch to typical dose for outbreak, then back to lower doses

• Initial infection caused by varicella zoster virus (herpesvirus)
• Highly contagious

• Human herpesvirus 3
• Transmitted by droplets
• Patients contagious for 2 days before onset of rash until lesions have crusted

• Prodromal symptoms - low-grade fever, malaise, headache
• Vesicular rash on trunk, spreads to face and extremities
• Highly pruritic
• Initially presents as small papule, becomes vesicle,
• then becomes umbilicated and cloudy.
• Ruptures and forms a crust-"Dew drop on a rose petal"
• Patients will have lesions in all stages of healing
• May have vesicles in mucous membranes - rupture to form aphthous ulcers

• Low grade fever
• Malaise
• Headache
• Minimal in children
• More pronounced in adults

• Risk of bacterial superinfection
• Adults have more severe disease
• Pneumonia may develop in adults
• Immunocompromised may develop hepatitis
• Infection conveys lifelong immunity

• Clinical diagnosis
• Can order Tzank smear if in question
• Bacterial culture if concern for secondary infection

• Symptomatic treatment for itching
• For severe disease, immunocompromised, consider oral medications
• Acyclovir at the first sign of symptoms
• Pregnant women who have been exposed should consider post-exposure prophylaxis due to risk of complications in the mother
• Less common now that vaccine is available

• Reactivation of varicella zoster virus causes vesicular rash in a dermatomal distribution
• Generally involves one or adjacent dermatomes
• In immunocompetent individuals, generally does not cross the midline

• After varicella infection, virus migrates into the dorsal root
• May be reactivated with immune system insult

• Usually occurs in older individuals or those with decreased immunity or increased stress
• Prodromal pain and paresthesia (May occur up to 5 days before onset of eruption)
• Clusters of vesicles on an erythematous base along a dermatome or two adjacent dermatomes
• Other patterns associated with immuncompromise
• Most commonly affects thoracic region

• Vesicles may vary in size (are uniform size in herpes simplex)
• Crust over several days to weeks
• Post herpetic neuralgia

• Hutchinson's sign
• Half will develop ocular complications without antiviral treatment
• Refer to ophthalmology

• Culture available, but often false negative
• ~~Unroof vesicle, culture base of lesion
• Tzank smear - multinucleated giant cells

• Steroids for pain (does NOT decrease incidence of PHN)
• Oral antivirals
• Treatment for PHN (if develops)
• ~~Gabapentin
• ~~Amitriptyline
• ~~Topical capsaicin

• Zostavax indicated for individuals > 60 years old
• ~~Reduces risk of Zoster by 51%
• ~~Reduces risk of PHN by 67%
• Live vaccine-Avoid in immunocompromised individuals
• Expensive, insurance coverage variable
• Difficult for people outside of guideline age to receive

• Genital warts
• Infection caused by human papilloma virus

• Spread by direct contact
• Increased transmission in moist areas
• Virus is present on normal skin that is contiguous to wart

• May differ in appearance from one person to another
• Pale pink, white, or brown papules with rough surface
• May be just barely raised
• May have papillae or filiform look
• Small lesions may look smooth or velvety
• Coalesce in rectal or perineal to form cauliflower-like mass
• May extend into internal mucosa

• Clinical diagnosis
• Can biopsy

• Cryotherapy
• Electrodessication and curettage
• Podofilox (Condylox gel)-3 days on, 4 days off x 4 weeks
• Imidquimod cream (Aldara)

• Use of condoms reduces spread by 95%
• Have partners checked
• Warts caused by HPV 6, 11
• Cervical cancer caused by HPV 16, 18
• Recommend pap smear
• Warts in children under 3 may be transmitted perinatally. In older children, consider sexual abuse

• Verruca vulgaris - "warts"
• Caused by HPV

• Spread by contact
• Inoculation occurs with simple trauma to the skin
• Must reach basal epithelial cells in order to occur

• Flesh-colored papules raise up
• May be black, brown
• Have rough surface and disturbance of normal skin lines
• Black dots - thrombosed capillaries
• May be solitary or numerous

• finger-like projections
• more common on the face

• Thin, less scaly
• Still have disruption of normal skin lines
• Found in patches with contiguous spread due to repeated trauma

• More common at points of pressure
• Depressed or flat, loss of normal skin markings
• Tender
• "Kissing lesions" on adjacent toes
• Much more refractory to treatment

• Typing is not clinically helpful
• Biopsy if not healing AND sun exposed skin (r/o scc)

• May resolve on own (2/3 regress w/in 2 yrs in kids)
• Less likely to resolve in immunocompromised
• No one "treatment of choice"
• Salicylic acid topically;+/- tape occlusion
• ~~Treatment for 8-12 weeks
• Cryotherapy
• Imiquimod (Aldara)
• Electrocautery and curettage
• Laser treatment

• Patient education about spread
• ~~Shaving, picking, biting
• No tx 100%
• most rely on activating the body's own immune defense

• Benign, persistent epidermal lesion
• Variable clinical appearance
• One of the most commonly encountered lesions

• Increased incidence with age (rare before age 30)
• Tendency toward multiple often inherited

• Varied-Most often asymptomatic
• Pruritic, may be irritated by clothing
• Often cosmetically unappealing
• Usually multiple lesions

• anywhere but palms, soles, or lips-Common on arms, back, face
• 0.2-2.0 cm in diameter
• black, brown, skin colored
• Flat or raised with a smooth, warty, or oily texture
• Sharply demarcated with a "stuck on" appearance

• Sudden, explosive onset of multiple SKs
• Associated with internal malignancy

None necessary unless lesion has suspicious characteristics

• No treatment needed
• May remove/tx due to cosmetics or irritation/inflammation
• ~~Salicylic acid
• ~~Cryosurgery
• ~~Shave excision

• Benign process with no malignant transformation
• HOWEVER - have been cases of melanoma, basal cell, or squamous cell arising within an SK
• If lesion has changed or have clinical suspicion - biopsy it!

• Keratotic, precancerous lesions
• Precursor to squamous cell carcinoma
• Most commonly seen in areas of sun exposure
• More common in those with high lifetime exposure, fair skin types, elderly

• Sun exposure damages keratinocytes-> dna error
• More sun-> localized immunosuppression -> more damaged DNA
• Over time, may lead malignant transformation
• (10% ->SCC if untreated)
• Increased risk in transplant patients

• Patients > 40 y/o with fair skin types
• "scab" or "dry skin" that won't heal or keeps recurring
• Most commonly seen on face, scalp (if bald), neck, dorsum of the hands
• Initial: poorly demarcated erythema
• Later: more defined, develops a thin, adherent white or yellow scale
• ~~May be easier to detect by palpation

• Scale becomes thicker, more yellow
• May form cutaneous horn as scale builds up
• Advanced lesions impossible to distinguish from SCC

• pigmented lesion with fine scaling
• May resemble solar lentigo or melanoma in situ

• Involves lower lip
• Focal crusting or scaling
• Higher chance of progressing to SCC

• Biopsy if suspicious of SCC
• Most often clinical diagnosis

• Annual follow up
• Sun protection/sun avoidance
• Few lesions: Cryotherapy; Biopsy or shave if suspicious

• Visible lesions are only a small portion of cells with atypia
• Likely that these patients will develop further lesions
• Patients with multiple AKs have 20% risk of developing SCC
• "treat the field"

• Treat field AK
• Causes immune response to atypical cells
• "hidden" become red, inflamed, ooze
• Course of treatment - 3 weeks, then skin clears
• Also available - Imiquimod cream

• Primary cutaneous malignancy arising from keratinocytes of the skin and mucous membranes
• Most often seen in elderly, fair skin types, those with high cumulative sun exposure
• May arise from AKs or de novo

• Sun exposure
• Lifetime risk - 5-15%
• 100,000 new cases each year in the US, 2,500 deaths yearly due to metastasis
• Increased risk in transplant patients and those who are immunosuppressed

• Most commonly-face, head, neck, hands
• Surrounding skin is sun damaged
• Initial: appear like hypertrophic AK
• Pink or red, dome-shaped nodule with adherent yellow-white scale
• Progression: increases in size and develops necrotic, crusted center

• Bowen's disease-full-thickness SCC in situ
• Cutaneous horns
• Keratoacanthoma-crater-like nodule w/ necrosis

• Large, nodular, crater-like nodule with central necrosis
• Fast growing
• Low-grade variant of invasive SCC

• More likely on mucous membranes or more advanced lesions
• Mets first to regional lymph nodes
• ~~Usually within 2-3 years of skin lesion

• Biopsy suspicious lesions
• Deep shave (include dermis)
• Electrocautery and curettage to remove residual cells
• Deeper lesions may require excision with clear margins

• Excisional biopsy (shave or excision with clear margins) is diagnostic as well as therapeutic
• Increased surveillance for other malignant or premalignant skin lesions
• Monitoring of the scar site for recurrence
• May require MOHS surgery
• Palpate regional lymph nodes, lip if affected

• Excellent if adequately treated, not metastatic
• Increased risk of metastasis in immunosuppressed patients, lesions on lip or ear, or arising from scar tissue

• Primary skin malignancy arising from the basal layer of keratinocytes
• Most common cutaneous malignancy
• Untreated, will invade and destroy surrounding tissue
• Rarely metastasize

• Sun exposure
• More common later in life, lighter skin types

• Most commonly appear in sun-exposed areas - face, scalp, ears, neck
• Pink, violaceous, or pearly white nodules
• May appear translucent
• Overlying telangiectasias
• Rolled borders and central ulceration as lesion progresses
• Bleed, become crusted, or ulcerate
• May notice "mushy" texture during curettage

• May have pigmented area or be fully pigmented
• Prognosis same as nonpigmented

• Thinnest, least aggressive
• Appear in younger patients
• May also appear on the trunk or extremities
• Flat, may appear atrophic
• Spreads peripherally

• Biopsy it!
• Shave biopsy with curettage

• Excision of lesion can be diagnostic and therapeutic
• Cryotherapy - if superficial
• Shave biopsy with electrodessication and curettage
• Excision
• MOHS surgery
• Rarely radiation - based on location, patient's ability to tolerate surgery
• Imiquimod cream (Aldara), 5-FU (Carac, Efudex) -superficial

• Superficial bcc
• Use daily x 6 weeks
• Causes significant inflammation

• Reassure patient
• Sun avoidance/sun protection
• Regular skin evaluation for further effects of sun damage

• Benign skin tumors composed of melanocyte-derived nevus cells
• Appear at birth or within first two years - congenital
• Acquired nevi occur throughout life, peak during adolescence
• Sun exposure can stimulate growth
• May change appearance over years-decades

• Nevus cells at the dermoepidermal junction
• Flat or slightly raised
• Skin markings are preserved

• Nevus cells at the dermoepidermal junction and within the dermis
• Raised pigmented papules
• Surface is smooth or slightly warty
• Center is more heavily pigmented than the periphery
• Increase in thickness during childhood and adolescence

• Nevus cells within the dermis, may extend to subcutaneous tissue
• Papules that are flesh colored to slightly pigmented to dark brown
• May have coarse hair growing from them
• Develop after adolescence

• Blueish macules or papules due to deeply pigmented melanocytes in the deep dermis
• Most commonly seen on the head, neck, buttocks
• Present early in childhood, enlarge and persist for 10-15 years

• Preexisting nevus develops an annular ring of hypopigmentation
• Over several months, the nevus disappears
• Caused by lymphocytic infiltration - host response against nevus cells
• May be seen in patients with vitiligo or melanoma - require full skin exam

• Asymmetry
• Border
• Color
• Diameter
• Evolution
• Does it bleed (without injury)
• Ulceration

• Most require no treatment
• If suspicious - biopsy it
• ~~~Punch or excision; May consider deep shave
• Get clear margins
• Patient reassurance
• Multiple or RF 4MM=more routine skin surveillance

• Nevi with potential for malignant transformation
• Cellular architecture is disordered but cells have mild or no atypia
• May be isolated or have multiple dysplastic nevi
• Isolated dysplastic nevus is fairly common (5-20%)
• Continue to appear through adulthood

• Familial syndrome of multiple atypical nevi
• Associated with increased risk of melanoma
• Relatively uncommon
• nearly 100% lifetime risk of MM by age 70

• One or multiple irregular nevi (ABCDE's)
• Patients with dysplastic nevus syndrome have multiple nevus morphologies
• Tend to be larger (6-15 mm)
• May be maculopapular
• Often have nevi in sunprotected areas

• Only way to diagnose - Biopsy it!
• Excision
• Regular skin exams
• Lifetime risk of MM in general population - 1.3%
• Lifetime risk of MM in pt with atypical nevi (without family hx of MM) - 6%

• Excise suspicious nevi
• Sun protection/avoidance
• Skin exams every 6-12 months (including sun-protected areas)
• Baseline eye exam
• Self monitoring with skin exams

• Primary skin malignancy affecting the melanocytes
• Curable with early detection and treatment
• Often fatal if caught late (15% 5 year survival rate)
• Only 2% of skin cancer cases but causes 75% of deaths due to skin cancer

• Most common form of cancer in age 25-29, second most common form of cancer for adolescents
• More common, increasing more in females
• Approximately 120,000 new cases yearly
• 8600 deaths yearly (one every 61 minutes)
• Rate of MM increasing more quickly than any other cancer

• Fair skin (Types I and II)
• Atypical nevi in both sun exposed and sun protected areas
• Personal history of MM
• Family history of atypical nevi or MM
• History of blistering sunburn
• Congenital nevi (risk increases with size)

• Increase in size, shape, or color of existing lesion (30%)
• May occur as a new lesion (70%)
• Usually asymptomatic early-May itch
• As progresses, develops tenderness, bleeding, and ulceration
• Appearance varies
• Darker skin tones are not 100% protective
• Check palms, soles, mucous membranes, nails
• Focal area of color change within a preexisting lesion
• Look for the ABDCEs

• Most common (70-80%)
• Most mm arise from preexisting lesions are X
• Lesions spread laterally over the skin before becoming nodular
• Most common on trunk and extremities
• Flat, asymmetric, color variation, >6 mm

• 10-15%
• More common on extremities
• Brown-black raised papules that appear and grow rapidly
• May have focal hemorrhage
• Tend to extend vertically in the skin

• 5-10% of cases
• Melanoma in situ
• Develop over years/decades on sun exposed skin
• Flat, irregular, variation in pigment
• May look "washed out" in areas or be skin colored

• Occurs in all skin types (including IV-VI)
• Most common melanoma in Asians and African Americans
• Occurs on hands or feet (including nails)
• May have similar lesions around the mouth, anus, or genitalia

• BIOPSY!!-Full thickness, try to get clean margins
• Palpate regional nodes for any adenopathy
• Breslow level:

• For MM dx
• Measure of vertical thickness of the melanoma
• Most important prognostic factor
• Ulceration of the lesion may cause an underestimated Breslow level

• Remove it! - complete lesion into subcutaneous fat
• Melanoma in situ - reexcision with 0.5 cm margins
• Lentigo maligna - may have microscopic extension - consider MOHS
• Consider sential node biopsy in patients with Breslow level > 1.0 mm
• More advanced disease may require chemotherapy
• Lots of experimental trials of chemotherapy ongoing
• Patients need regular skin exams (every 3-6 months), biopsy of other suspicious moles
• Baseline chest x-ray, palpation of lymph nodes and liver
• First degree relatives should have regular skin screening

• Better prognosis with lower Breslow depth
• 95% 5-year survival with Breslow < 1.0 mm without ulceration
• 7-19% 5-year survival with distant metastasis
• Prevention and early detection is key!

• Malignancy of lymphocytic endothelial cells
• Associated with a gamma herpesvirus
• Before advent of immunosuppressive medications, uncommonly seen
• ~~Sporadic in men of Eastern European or Mediterranean descent
• ~~Eastern and southern Africa - endemic cases of childhood soft tissue tumors
• With immunosuppression, patients of Mediterranean and eastern European descent more likely to develop than other patients
• Much more wide spread as an HIV-related malignancy
• Most common AIDS-associated malignancy

• Polymorphic, can vary with clinical variant
• Start as purple patches that may thicken and darken into brown verrucous patches
• Classic and immunosuppressive starts at the feet/ankles, spreads proximally
• May affect lymph nodes, gi tract and lungs

• most often found on the face
• May affect lymph nodes, GI tract, lungs
• more likely to have systemic symptoms

• Biopsy to confirm
• HIV test (if not known HIV), CD4 count
• Oral evaluation - often oral lesions in patients with HIV

• Excision of single lesion
• Radiation if multiple lesions
• Extensive lesions may also require chemotherapy
• Consider d/c immunosuppressive therapy
• AIDS-associated - Radiation therapy, cryotherapy

• Reaction to drugs taken internally
• Multiple morphologies
• May occur w/new med or one taken for months-years
• Once sensitized, usually react within minutes up to 24-48 hours
• May be due to hypersensitivity reaction (Types I-IV) or nonimmunologic cause

• Maculopapular
• Erythematous macules and papules become confluent
• Symmetric, generalized
• Usually spares the face
• May involve mucous membranes, palms, soles
• Pruritic

• Most common presentation
• May be indistinguishable from viral rash
• Starts 7-10 days after drug is started
• Lasts 1-2 weeks before resolving

• Most common causes ASA, NSAIDs, PCN, blood products
• Includes anaphylactic reactions, serum sickness
• May have immediate reaction (anaphylaxis) or occur hours to days later
• Certain medications trigger histamine release:Not true hypersensitivity
• ~~Codeine, morphine

• Sharply demarcated, dusky red plaques
• Present shortly after drug is started, reappear in the same place each time the drug is taken
• Prodromal itching or burning
• May occur anywhere on the skin, but the glans penis is the most common location

• Provocation challenge confirms the diagnosis
• May need to biopsy to r/o cutaneous T-cell lymphoma

• May be due to medicines administered internally or externally
• Phototoxic reaction
• Photoallergic rxn

• Dose dependent
• Limited to area of sun exposure
• Subsides when drug is stopped
• Occurs within 24 hours of exposure

• Less common
• No relation to dose
• Does not begin until about 48 hours after exposure
• May spread to non-sun exposed area

Steroids or hormones

hydralazine, procainamide

thiazides, sulfonamides, tetracycline

blue-grey in photodistribution

blue-grey on gingiva and teeth

brown on the shins

melasma on face

red man syndrome (high dose)

• A good history is key!!
• D/C offending medication
• Antihistamines for pruritus
• Hospitalization and epinephrine for severe reaction
• Avoid other medicines in the class as well as other medicines that may cross react (i.e. sulfa and HCTZ)

• Inflammatory papulosquamous disease
• Etiology unknown
• May affect hair, skin, or mucous membranes
• 5 P's

• Pruritic
• Planar
• Polygonal
• Purple
• Papules

• Small, flat topped papule with an irregular, angulated border
• May initially present as pinkish papules-"Purple Polygonal Papule"
• Surface of papule has white, reticulated pattern=Wickham's striae
• + Koebner's phenomenon

• Papular
• Hypertrophic
• Follicular
• mucosal

New lesions appear in area of trauma

• Most common
• Papules on flexor surfaces of wrists, forearms, ankles, lumbar back

• Lesions become hypertrophic with coalescing papules
• Most common on the shins
• May form bullae
• Residual brown hyperpigmentation

• Papules occur at the hair follicle - scalp
• Scarring causes hair loss

• Non-erosive - lacy white reticulation
• Erosive - beefy red desquamation
• May involve penis or vagina
• 3% go on to develop oral SCC

• Biopsy
• If scalp involved, obtain DIF to r/o cutaneous lupus
• Screen for Hep C

• Antihistamines for pruritus
• Class I or II steroids twice daily
• Intralesional steroid for hypertrophic plaques
• Dapsone, azathioprine, hydroxychloroquine for refractory cases

• Common, self-limited rash lesions resolve over 4-12 weeks
• May be asymptomatic or cause mild pruritus
• Most patients are ages 10-35
• May be preceded by viral infection
• More common in Spring and Fall
• May have local outbreaks in close quarters

• HERALD PATCH
• 1-2 weeks later, multiple smaller lesions erupt
• Usually also have COLLARETTE OF SCALE
• CHRISTMAS TREE DISTRIBUTION
• Torso, upper arms, upper legs
• Rarely involves face

• Salmon-colored plaque occurs on chest or torso
• Thin collarette of scale along border
• Generally 1-2 cm in size
• ASSOC W/ PITYRIASIS ROSEA
• May mimic tinea

• Clinical Diagnosis
• If lesions on palms and soles MUST test for syphilis
• ~~~Consider in other cases based on history and presentation
• Herald patch may mimic tinea - KOH to r/o

• Patient reassurance
• Antihistamines, topicals (low-medium potency steroids) for pruritus

• Common, chronic inflammatory papulosquamous disease predominated by T-cell dysfunction and autoimmune dysregulation
• Genetic + environment
• Affects 1-3% of the population worldwide

• Abnormal maturation of keratocytes in the skin
• Hyperkeratosis
• Cell nuclei in the stratum corneum are retained

• Stress
• Strep infection
• HIV infection
• Koebner phenomenon
• Drugs (lithium, antimalarials, steroid withdrawal)

• Plaque
• Guttae
• Pustular
• inverse

• Most common form
• Red, sharply demarcated scaling papules
• May coalesce to form round to oval plaques
• Adherent silvery scale that bleeds when removed (Auspitz sign)
• Most common on extensor extremities, scalp, and sacrum

• Sudden appearance of multiple small psoriasiform papules on the torso
• Widespread
• May occur after Group A strep infection or viral infection
• Usually occurs in adults
• May be initial presentation of psoriasis

• Pustules form on palms and soles
• Painful, may be debilitating
• As reach surface, pustules become brown and scaly
• Also usually have associated nail changes

• Less common
• Typical erythematous plaques occur in flexural and intertriginous areas
• ~~Groin, axilla, inframammary folds
• May become macerated
• Diabetic patients or those on chronic steroids may develop secondary candida infection

• Nail changes-Can occur with any form
• ~Pitting
• ~Onycholysis
• ~Oil drop sign

• Clinical diagnosis
• Biopsy if unsure
• KOH to r/o fungal
• Consider ASO titer with flares of guttae psoriasis
• HIV test if significant, recalcitrant disease
• r/o strep-avoid rheum fever

• Topical
• Photo therapy
• Systemic

• Tar preparations
• Vitamin D analogues (Dovonex, Vectical)
• Topical steroids (Group I-V)-Cyclical treatments
• Retinoids (Tazorac)

• UVB 3-5 times/wk.
• Narrow band has fewer side effects but limited availability
• PUVA

• Consider in patients with > 10% BSA or based on patient discomfort/disability
• Managed by dermatology
• Methotrexate
• Cyclosporin
• Acetretin (Soriataine)
• Biologics (Enbrel, Humira, Remicade &Stelara)

• Both the disease itself as well as treatment may carry long-term effects
• Increased risk CAD
• AE from steroids or chronic immunosuppression
• AE from phototherapy
• Monitor lipids, HTN
• Regular skin cancer screenings
• Other f/u as warranted by their medications
• Desquamation and Hypersensitivity Syndromes

• Recurrent, inflammatory condition with "target" lesions
• Fairly common
• Commonly associated with HSV, Mycoplasma and URIs
• Less commonly seen with medications, internal malignancy
• Idiopathic in half of cases

Theorized to be immune system response against keratinocytes that present viral or drug antigens

• Multiforme = multiple morphologies
• ~~Target lesions, macules, papules, urticarial, vesicles
• ~~NEED TO HAVE TARGET LESIONS TO DX CLINICALLY
• Pruritus and burning
• Sudden onset
• Palms, soles, hands, feet, distal arms and legs

• Crops of lesions appear
• Oral bullae or erosions
• Urticarial lesions last >24 hours
• + Koebner phenomenon
• +/- signs of accompanying infection

• May diagnose clinically if target lesions are present
• Biopsy

• Self limited - usually resolves within a month
• If associated with reactivations of HSV, may need suppressive therapy
• Systemic steroids if widespread
• Topical steroids if limited

• Severe, blistering mucocutaneous syndrome
• Involves at least two mucous membranes
• Most common in children and young adults

• Similar to erythema multiforme
• Immune response directed against keratinocytes that are expressing foreign antigens

• Associated with Mycoplasma
• Medications

• Phenytoin, phenobarbital, carbamazepine
• Sulfa drugs, PCNs
• Usually started within 1 month of onset

• Acute onset of erythematous papules, vesicles, purpura, and target lesions
• Skin is tender and burning
• Erosions and bullae develop on mucosa
• Central distribution on face and trunk

• Lesions erupt over 10-14 days, improve over 3-4 weeks
• Fever and constitutional symptoms
• With increased skin break down, develop dehydration and are at risk for sepsis

• Biopsy: Necrosis of the full thickness of the epidermis, dermis remains intact
• Watch for S&Sx of infection: Wound culture &CBCs
• Often require hospitalization for fluid maintenance and monitoring for infection

• Find the causative agent
• Maintain fluid and nutritional requirements
• Wound care
• Ophthalmology consult if eye involvement
• Burn care
• +/- systemic steroids
• Narcotics for pain
• IVIG

• With good supportive care, mortality is < 1%
• Recurrence rare unless exposed to causative drug again

• Life-threatening disease with blistering and sloughing of the skin and mucous membranes
• Most often caused by medication: Within 1-3 weeks before onset
• ~~~~~Sulfa, antimalarials, anticonvulsants, NSAIDs, allopurinol
• Other causes triggered by recent immunization or infection

• Cause - unknown
• Skin sloughing theorized to be due to increased apoptosis

• Begins as diffuse "sunburn" and tenderness
• Scattered target lesions and bullae form
• Bullae coalesce to cause widespread sloughing
• Painful erosions on mucous membranes
• +Nikolsky sign
• May have non-skin findings similar to SJS

Bx to r/o staph scalded skin syndrome

• Control pain
• Find the cause
• Burn care
• Maintain fluid and nutrition
• IVIG
• Steroids? Use with prophylactic antibiotics
• May require other immunosuppressant therapy

• Mortality rate 30-50%
• d/2 complications-infection etc

• Thick, velvety plaques
• neck, groin and axillae
• patients w/ abnormal glucose metabolism or malignancy (rare)

• Not fully understood
• Related to insulin resistance

• Gradual onset of thickened, hyperpigmented skin
• Brown or tan thickened, velvety
• Most commonly seen on the back of neck and axillae
• May also be seen in the inguinal creases
• May have multiple skin tags associated

• Look for other signs of insulin resistance
• ~~Obesity
• ~~PCOS characteristics in women

• High suspicion if doesn't fit "typical" picture
• Rarely sign of internal malignancy
• (90% in the abdomen)
• ~~Middle aged patient
• ~~Abrupt onset
• ~~Not obese

• Clinical Diagnosis
• Evaluate for insulin resistance

• Retinoids, dermabrasion
• Treat underlying condition
• ~~Treat insulin resistance/excess
• ~~Weight loss
• ~~Screen/treat for malignancy

• Common skin condition with smooth, discolored plaques
• Most common in children and teenagers, but can occur at any age
• Asymptomatic - mildly tender if bumped
• May mimic tinea

• Delayed hypersensitivity reaction to component of the dermis
• Mediated by TNF-a
• Trigger unknown
• Local disease may be associated with thyroid disorder
• Widespread disease may be associated with DM, hyperlipidemia, lymphoma, solid tumors

• Begins as erythematous papule
• Expands to annular, erythematous plaque
• Raised, papular border
• Center is flatter, lighter colored

• May occur anywhere on the body
• More likely to occur on skin around joints
• Localized, occasionally widespread (more common in adults)
• Clears on its own over months-years

• KOH to r/o fungal infection if needed
• Clinical diagnosis, but may bx to confirm

• Self limited
• Steroid (high potentcy)
• Intralesional steroid
• Disemminated disease
• ~~Isotretinoin, methotrexate, dapsone, hydroxychloroquine

• Inflammatory skin condition affecting areas with apocrine sweat glands
• Recurrent nodules and abscesses that have sinus tracts

• Exact cause unknown
• Characterized by follicular occlusion
• Apocrine gland ducts are occluded causing inflammation
• Follicle ruptures, forms abscess
• Sinus tracts form between abscesses

• Genetics
• Female > male
• Obesity, PCOS
• Pro-inflammatory cytokines
• Cigarette smoking
• Secondary bacterial infection

• Multiple, deep-seated cysts in the axillae and groin
• Often have sinus tracts and two openings
• Cysts tend to have chronic, low-level inflammation
• occasionally develop 2ndry infection and cause increase in pain, swelling, and discharge
• axillae, inframammary folds, neck, groin, perianal folds

Clinical diagnosis

• Earlier treatment is better
• d/c smoking
• Weight reduction
• Hair removal
• Topical antiseptic soaps

• Clindamycin/benzoyl peroxide topical
• Tetracyclines for prolonged courses
• Spironolactone
• Isotretinoin 6-12 months
• TNF inhibitors for severe disease
• I&D inflamed abcesses for pain reduction
• Surgical debulking

• Common, benign tumors consisting of adipose cells
• Located within the subcutaneous tissue

• Cause unknown
• Genetic predisposition, especially in patients with multiple lipomas
• Blunt trauma may trigger solitary lipoma, but most often cause is unknown

• Very slow growth of soft, palpable nodule beneath the skin
• Smooth, not fixed to underlying tissue
• Most common on the neck, trunk, and arms
• Usually asymptomatic but may have tenderness with palpation

• Clinical Diagnosis
• May be removed for cosmetic reasons (general surgery?)
• If quickly enlarging or painful, consider biopsy to r/o liposarcoma

• Surgical excision
• Squeeze technique
• Liposuction

• Epidermal cysts
• Pilar cysts

cystic structure filled with soft, cheese-like keratinous contents

• small cysts on the scalp
• filled w/ firm, white content
• arise from the hair root sheath

• May result from plugging of sebaceous glands with oil backing up
• Body "walls off" debris, which is retained

• well-circumscribed cystic lesion
• May have tract open to the skin
• Firm, not fixed to underlying tissue
• When inflamed, may become more fluctuant and tender, red
• May spontaneously open and drain

• Well, circumscribed, firm nodules on the scalp
• Usually multiple
• Not attached to underlying tissue
• Usually do not spontaneously open and drain unless secondarily infected

• Not usually necessary
• Bacterial culture if infected

• No treatment if small (<5 mm)
• Try to avoid treatment when inflamed
• I&D, treat with antibiotics
• Return for excision of sac when quiet
• Excision of cyst best chance to avoid recurrence, but this may still occur

• Hyperpigmentation of the face
• Typically occurs in women during pregnancy and on OCPs
• More common in darker skin types

• Hyperpigmented macules - sharply demarcated with an irregular border
• May be brown, tan, blue-gray

• Clinical Diagnosis
• Biopsy suspicious area

• If due to pregnancy, may resolve after pregnancy
• May recur with subsequent pregnancies
• Hydroquinone
• Laser

• Chronic sinus tract in the sacrococcygeal region
• filled with nests of hair
• May become infected and inflamed

• Congenital - pits or dimples at the base of the spine
• Higher risk if prone to follicular plugging
• With friction, follicles are injured and hair protrudes into surrounding skin
• Skin and perineal bacteria invade and cause infection
• S. aureus or Bacteroides

• M>F
• Obesity
• Genetics
• Poor hygiene
• Prolonged sitting or friction on the buttocks
• Repeated injury to the area
• Coexisting hidradenitis suppurativa

• May be asymptomatic - pit or dimple at the base of the spine
• Develop tenderness in the area after prolonged sitting
• Pain, redness, swelling of the skin
• Small holes that drain fluid (clear, cloudy, or pus-like)
• Fever, malaise, or nausea
• May have visible tracts with recurrent disease

Clinical Diagnosis

• Keep area clean, free of hair
• I&D
• Excision of tract
• Marsupialization of cyst

• Bed sores, decubitus ulcers
• Area of reddened skin
• progresses to skin breakdown that results in sores and ulcers

• Due to lack of blood flow and mechanical stress to the skin over a bony area
• Occurs when area has been under pressure for a prolonged period
• If blood supply cut off for 2-3 hours, skin is deprived of oxygen and begins to die
• Exposure to irritants increases risk

• Immobility
• Peripheral neuropathy
• Elderly

• Skin is red or pink but unbroken
• May look like a mild sunburn
• Tender, itchy or painful

• Skin is red, swollen, and painful
• Blisters present (intact or broken)
• Upper layers of skin begin to die

• Skin is broken, wound extends down to deeper layers of skin
• Crater-like ulcers present
• Wound is prone to infection

• Sore extends into deeper tissue
• Necrosis and eschar in deep, opened wound

Clinical diagnosis

• Prevent, treat early
• Treatment by wound care
• Topical vac therapy
• Hyperbaric oxygen
• Hydrotherapy
• Debridement
• Treat infection

• Wheals resulting from edema of the dermal tissue
• Angioedema results from edema of deeper structures

• (< 6 weeks)
• Post viral
• Allergic reaction (IgE mediated)

• (> 6 weeks)
• Allergic (chronic exposure)
• Autoimmune (lupus, vasculitis, thyroid)
• Idiopathic (~50%)

• Pruritic wheals, often confluent
• Angioedema is swelling of deeper cutaneous tissue
• Hands, feet, lips, eyelids, genitalia
• Lesions evolve over hours
• Pruritus and/or burning
• May be exacerbated by heat, cold stress, pressure

• Individual lesions last >24 hours
• Burning sensation
• Residual bruising
• (especially with chronic urticaria)

• Individuals with chronic urticaria may have specific triggers
• Cold induced urticaria, heat induced urticaria
• Dermatographism

• No labs needed
• Review medication history, exposures
• Any signs/sx of viral infection?

• CBC, CMP, Complements
• IgE, ANA, TSH, thyroglobulin antibody, thyroid peroxidase antibody
• Sed rate
• Consider evaluation with allergist for allergy testing

• Avoid heat, pressure
• NSAIDS may enhance rxn
• d/c any potentially triggering meds
• Treat underlying causes of chronic urticaria
• Antihistamines
• Steroids
• Epinephrine

• Long-acting antihistamine (Zyrtec, Claritin) - can use once or twice daily
• Benadryl as needed for breakthrough symptoms
• May add H2 blocker

• Consider oral steroid for severe outbreak
• Topical steroids DO NOT help

May be needed for angioedema if airway is compromised

Acquired condition where impaired or absent melanocyte function leads to hypopigmentation of the skin

• Exact mechanism unknown - autoimmune
• May be associated with thyroid disorder, pernicious anemia, Addison's disease
• Usually starts between age 10-30
• Melanocyte function is impaired or absent

• Asymptomatic
• Small white macule expands in size
• May affect any part of the body
• May cause depigmentation of the hair if hairy area is affected
• Affected skin is depigmented and sharply demarcated
• Use Wood's lamp to evaluate

• Most commonly affected
• Extensor bony surfaces
• Periorificial areas

• May biopsy if in question
• CBC, TSH to screen for underlying disorder

• Very difficult to treat
• Only 15-20% have full resolution
• 20% show no improvement
• Earlier treatment has better results
• Topical steroids - watch for AE
• PUVA or UVB therapy
• Cosmetics to cover affected areas

Inflammatory panniculitis with erythematous, deep nodules on the shins

• Panniculitis - inflammation of the subcutaneous fat
• Most common ages 20-30, Women >> Men
• Some cases preceeded by infection or illness
• Appears to be hypersensitivity reaction

• Pharyngitis
• Mycoplasma infection
• Sarcoidosis
• Tuberculosis
• Pregnancy or OCPs
• Meds - sulfa, ASA, NSAIDs
• Inflammatory bowel disease

• Erythematous nodules appear on shins (6-12)
• Painful nodules erupt over 10 days
• Become smaller and darker purple as they age
• Aching and swelling of the legs may last 3-6 weeks
• May have systemic symptoms when first starts
• Arthralgias, rarely conjunctivitis

• Clinical diagnosis
• Biopsy may be helpful (have to get subcutaneous fat)
• Check for other risk factors
• Throat culture
• CBC, CRP, ESR
• ASO titer
• Consider screening for TB

• Treat underlying infection
• Rest if pain or swelling is severe
• Compression, ice
• NSAIDs