derm diseases

Card Set Information

Author:
alyspins
ID:
304682
Filename:
derm diseases
Updated:
2015-07-01 22:04:20
Tags:
Dermatology
Folders:

Description:
dz descriptions, symptoms and treatment
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user alyspins on FreezingBlue Flashcards. What would you like to do?


  1. Atopic Dermatitis
    • AKA eczema
    • "The itch that scratches"
    • Rash Itches->scratching->rash itches
    • Highly pruritic
  2. Atopic Dermatitis - Etiology
    • Genetic component
    • Family history of atopy (70%)
    • Food allergies may worsen AD in children
    • May b aggravated by topical irritation/affect skin barrier integrity
  3. Atopic dermatitis triggers
    • Irritants
    • Allergens
    • Perspiration
    • Heat
    • Tight clothing
    • Rough fibers
    • Emotional distress
  4. Atopic Dermatitis - Epidemiology
    • Most often onset in children
    • Many children "outgrow" as they get older
    • ~~May develop hand, eyelid, or postauricular dermatitis
  5. Atopic Dermatitis - Pathophysiology
    • T cells and Langerhans cells are hyperactive
    • Causes defect in cell-mediated immunity and overproduction of immunoglobulins by B cells
    • Barrier dysfunction
    • Ceramide deficiency
  6. Atopic Dermatitis ssx
    • 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
  7. Atopic Dermatitis Infantile Distribution
    • Cheeks, perioral, scalp
    • Extensor surfaces of the knees and elbows
  8. Atopic Dermatitis Childhood Distribution
    • Flexural areas
    • ~~Antecubital and popliteal fossae
    • ~~Neck
    • ~~Wrists, ankles
    • May become lichenified
  9. Atopic Dermatitis Adult Distribution
    • Flexural involvement
    • Hand dermatitis
    • Eyelid or lip dermatitis
    • Xerotic skin, ichthyosis vulgaris, keratosis pilaris
  10. Nummular Eczema
    • 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
  11. Atopic Dermatitis - Diagnostic Evaluation
    • Clinical diagnosis based on symptoms, exam, and family hx
    • No labs needed
    • Consider referral for allergy testing in children with severe or refractory AD
  12. Atopic Dermatitis - Treatment
    • Restore/protect skin barrier
    • Topical steroids BID x 10-21 days-not a cure
    • Topical immune modulators
    • If pruritus severe, consider antihistamines PRN
  13. Topical immune modulators-exzema
    • 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
  14. Atopic Dermatitis - Patient Education
    • Moisture, moisture, moisture
    • Limit baths to 5-10 minutes in lukewarm water
    • Avoid triggers
    • Symptoms will worsen with cool dry weather in the winter
  15. Atopic Dermatitis - Old School and New School Treatments
    • Bleach water baths
    • Wet pajamas
  16. Contact Dermatitis
    • Allergic or irritant reaction caused by skin contact with a substance
    • Rash will occur where the exposure occurs
  17. Allergic Contact Dermatitis - Etiology
    • 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
  18. Irritant Contact Dermatitis - Etiology
    • 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
  19. Contact Dermatitis presentation
    • Initial: occurs w/in 14-21 d (allergic)
    • subsequent rashes: occur more quickly after exposure
  20. Irritant contact dermatitis presentation
    • can present after one exposure to strong agents
    • more frequently after repeated use of mild irritants
  21. contact dermatitis ssx
    • 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
  22. Contact Dermatitis location-cause
    • Face - make up, sunscreen, shampoo
    • Eyelids - make up , nail polish
    • Feet - leather (dye)
    • Waist/umbilicus, finger, wrists, neck - nickel or metal
    • Sun-distribution - photodermatitis
  23. Rhus Dermatitis (contact)
    • Caused by delayed hypersensitivity reaction to plants
    • Poison ivy, oak, and sumac
    • Linear vesicles and erythema
  24. Contact Dermatitis - Diagnostic Evaluation
    • Clinical Diagnosis
    • If questionable, can biopsy (rarely needed)
    • Consider patch testing
  25. 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
  26. Contact Dermatitis - Treatment
    • 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
  27. Dyshidrosis
    • Also called pompholyx, dishydrotic eczema
    • Recurrent vesicular, eczematous dermatitis involving the hands and occasionally feet
    • Cause is unknown
  28. Dyshidrosis ssx
    • Usually occurs in atopic patient
    • Prodromal itching
    • Hyperhidrosis may worsen condition
    • Small vesicles (1-5 mm), monomorphic, filled with clear fluid="Tapioca like"
  29. Dyshidrosis later
    • As vesicles recede, develop scaling and peeling of skin
    • Pruritus improves
    • As healing occurs, may only have residual brown spots on an erythematous base
  30. Dyshidrosis - Diagnostic Evaluation
    • 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
  31. Dyshidrosis - Treatment
    • High potency steroid
    • Wet dressings or Burrow's solution
    • Oral antihistamines for pruritus
    • If result of ID reaction, treat fungal infection
  32. Lichen Simplex Chronicus
    • 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
  33. LSC - Clinical Presentation
    • 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
  34. LSC - Diagnostic Evaluation
    • 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
  35. LSC - Treatment
    • 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
  36. Dermatitis Herpetiformis
    • Vesicular disease seen in patients with gluten-sensitive enteropathy
    • Uncommon in children
    • Does not correlate with bowel symptoms
  37. Dermatitis Herpetiformis - Clinical Presentation
    • 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)
  38. DH - Diagnostic Evaluation
    • 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%
  39. DH - Treatment
    • STRICT GLUTEN AVOIDANCE
    • Steroid to reduce inflammation
    • Dapsone for recalcitrant cases
  40. Bullous Pemphigoid
    • Autoimmune disorder typically seen in older patients
    • Subepidermal blistering
  41. Bullous Pemphigoid - Etiology/Pathophysiology
    • Autoimmune - antibodies against hemidesmosomal proteins
    • Environmental trigger is often unknown
    • May be triggered by certain drugs
  42. Drugs trigger bullo0us pemphigoid
    • Furosemide
    • Captopril
    • Some NSAIDs
  43. Bullous Pemphigoid - Clinical Presentation
    • 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
  44. Bullous Pemphigoid - Diagnostic Evaluation
    • 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
  45. Bullous Pemphigoid - Treatment
    • 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
  46. Pemphigus Vulgaris
    • 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
  47. Pemphigus Vulgaris - Clinical Presentation
    • 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
  48. Nikolsky sign
    • Applying traction on intact skin causes formation of bulla
    • Applying pressure to intact bulla causes it to extend into surrounding tissue
  49. Pemphigus Vulgaris - Diagnostic Evaluation
    • Biopsy: One from edge of lesion, one from unaffected skin&DIF
    • Lab: May find antibodies in the blood
    • CORRELATES WITH DZ ACTIVITY
  50. Pemphigus Vulgaris - Treatment
    • Treat any active infection (frequent cause of death)
    • Prednisone, azathioprine (Imuran), cyclophosphamide
    • Monitor for comorbidities of steroid
    • Refer to derm (?tertiary care)
  51. Acne Vulgaris
    • 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
  52. Acne Vulgaris - Etiology/Pathophysiology
    • 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
  53. Acne Vulgaris - Aggravating Factors
    • Genetics
    • Diet (Dairy; Sugars?)
    • Hormones
    • Steroids
    • Hygiene (yes and no)
    • Chin straps, helmets
  54. Acne Vulgaris - Clinical Presentation
    • Noninflammatory lesions (Open and closed comedones)
    • Inflammatory lesions (Papules, pustules, cysts)
    • May cause scarring
    • ~~Hyperpigmentation
    • ~~Depressed scars
    • ~~Sinus tracts from cysts
  55. fx aggravate acne
    • 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
  56. Acne Vulgaris - Diagnostic Evaluation
    • Clinical diagnosis
    • Labs to r/o any associated conditions
  57. Acne Vulgaris - Treatment
    • 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
  58. Open the pores-acne
    • Benzoyl peroxide
    • Salicylic acid
    • Retinoids
  59. Reduce bacterial load &/or inflammation-acne tx
    • Topical erythromycin combinations
    • Oral doxycycline or minocycline
    • Topical metronidazole or topical dapsone
  60. Acne Vulgaris - Pearls for Treatment
    • 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
  61. Acne Vulgaris - Pt ed
    • 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
  62. Acne Vulgaris - Treating Scarring
    • Sunscreen
    • Erythematous macules tend to fade over months: Bleaching cream, YAG laser
  63. Pitting acne scars tx
    • Deeper resurfacing laser
    • Topical retinoids
    • Dermal fillers
  64. Acne Vulgaris - Prognosis
    • Potential for significant psychosocial effects
    • Acne is not just for teenagers!
    • No significant long-term mortality, but can be costly in the long run
  65. Rosacea
    • 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
  66. Rosacea - Etiology/Pathophysiology
    • Exact cause unknown
    • Demodex mite may contribute in some patients
  67. rosaceaTriggers (especially for flushing)
    • Hot food or drink
    • Red wine
    • Sunlight
    • Skin irritants
    • Embarrassment
    • Spicy food
  68. Rosacea - Clinical Presentation
    • 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
  69. Rhinophyma
    • Enlargement of the nose due to chronic inflammation and skin thickening
    • More common in men
    • Rosacea SYMPTOM
  70. Ocular rosacea
    • May occur with or without skin disease
    • Mild conjunctivitis
    • ~~Erythema, discomfort, FB sensation, tearing
    • ~~May cause blepharitis, chalazions, corneal vascularization over time
  71. Rosacea - Diagnostic Evaluation
    • Clinical Diagnosis
    • If NL folds are spared, consider biopsy to r/u lupus
  72. Rosacea - Treatment
    • Avoid triggers
    • Topical: Metronidazole; Sulfacetamide
    • Systemic therapy: Low-dose doxycycline (Oracea)
    • ~~May use full-dose tetracyclines for 2-4 weeks for exacerbation
  73. Ocular rosacea TX
    • Referral to ophthalmology
    • Oral antibiotics
  74. Treatment for erythema rosacea
    • Cover with green cosmetics
    • Laser or phototherapy
  75. Rhinophyma tx
    Surgery, CO2 laser
  76. Folliculitis
    • Inflammation of the hair follicle
    • Caused by infection (bacterial or fungal) or irritation
  77. Folliculitis - Etiology/Pathophysiology
    • Inflammation of the hair follicle
    • Infection with Staph
    • Fungal folliculitis spread from other dermatophyte infection
  78. Folliculitis - Clinical Presentation
    • 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)
  79. Hot tub folliculitis
    • Papules and pustules appear on torso after using a hot tub
    • Caused by Pseudomonas
  80. Folliculitis - Diagnostic Evaluation
    • Clinical diagnosis
    • KOH to rule out fungal
    • ~~Fungal folliculitis tends to be more destructive
    • May bacterial culture in recalcitrant cases
  81. Folliculitis - Treatment
    • 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
  82. Pseudofolliculitis Barbae "Razor bumps"
    • 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
  83. Cellulitis
    • Infection of the dermis and subcutaneous tissue
    • Associated with systemic symptoms
    • MC in immunocompromise, liver or renal disease, or use IV drugs or alcohol
  84. Cellulitis - Etiology/Pathophysiology
    • 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
  85. Cellulitis - Clinical Presentation
    • 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)
  86. Cellulitis - Diagnostic Evaluation
    • CBC - elevated WBC
    • ESR elevated
    • Culture: Group A Strep and S. aureus
    • If animal bite or scratch, consider Pasturella
  87. Cellulitis - Treatment
    • Rest, elevation, ice
    • Start empiric antibiotics (Staph and Strep)
    • ~~Augmentin, Cephalexin, Azithromycin
    • ~~Animal bite or scratch - Augmentin
    • Hospitalization may be required for severe infection
  88. Erysipelas
    • Acute, superficial cellulitis with prominent lymphatic involvement
    • Infection MORE SUPERFICIAL-DERMIS AND UPPER SUPCUTANEOUS TISSUE
  89. Erysipelas - Etiology/Pathophysiology
    • 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
  90. Erysipelas - Clinical Presentation
    • 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
  91. Erysipelas - Diagnostic Evaluation
    • Most cases due to Strep
    • Clinical diagnosis - difficult to culture
    • CBC - Elevated WBCs
    • ESR - Elevated
    • Consider blood cultures if high fever
  92. Erysipelas - Treatment
    • 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
  93. Impetigo
    • 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
  94. Impetigo - Etiology/Pathophysiology
    • 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
  95. Bullous impetigo
    • Thin-roofed bullae form
    • As bullae collapse, a HONEY-COLORED CRUST FORMS
    • Lesions may coalesce
    • Lesions in many stages of healing
    • mild adenopathy
  96. Non-Bullous Impetigo
    • Vesicles or pustules rupture and
    • scaling, tinea-like border forms
    • Honey colored or whitish crust forms
    • May have satellite lesions around the periphery
  97. Impetigo - Diagnostic Evaluation
    • Culture
    • S. aureus most common
    • Need sensitivity information
  98. Impetigo - Treatment
    • 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
  99. Candidiasis
    • 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
  100. Candidiasis - Risk Factors
    • Diabetes
    • Hormonal - pregnancy, OCP use
    • Systemic antibiotics or steroids
    • Skin maceration
    • Conditions that affect cell-mediated immunity (viruses)
  101. Candidiasis - Clinical Presentation
    • 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
  102. Balanitis
    • Foreskin and glans
    • Red papules and pustules with pasty maceration under the foreskin
    • Pain and edema
    • Candidiasis sx
  103. Diaper dermatitis
    • Beefy red plaques in the inguinal and gluteal folds
    • Satellite lesions
    • candidiasis
  104. Candidal Intertrigo
    • Affects skin folds
    • Develop beefy red plaques within the skin folds
    • Advancing border - sharply defined
    • Satellite lesions
    • May have maceration of skin folds
  105. Candidiasis - Diagnostic Evaluation
    • KOH shows hyphae and pseudohyphae
    • Culture may be positive for X
    • Use judgment with culture X part of the normal skin flora
  106. Candidiasis - Treatment
    • 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?
  107. Tinea Versicolor
    • Due to overgrowth of Pityrosporum orbiculare
    • Normal skin flora
    • Increased in oily skin, heat and humidity
    • +/- contagious?
  108. Tinea Versicolor - Clinical Presentation
    • 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
  109. Tinea Versicolor Wood's light exam
    hypopigmented areas with a faint yellow-green fluorescence
  110. Tinea Versicolor - Predisposing Factors
    • DM, immunosuppression
    • Pregnancy, OCPs
    • Indoor tanning (Lower patient resistance)
  111. Tinea Versicolor
    • Clinical diagnosis
    • Can do KOH to confirm
    • ~~"spaghetti and meatballs pattern"
    • ~~Hyphae break into short, rod-shaped fragments
    • ~~Spores are round
  112. Tinea Versicolor - Treatment
    • 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
  113. Onychomycosis
    • Tinea infection of the nail plate
    • Usually asymptomatic
    • Increased risk with age
    • Infection does not clear without treatment
  114. Onychomycosis - Clinical Presentation
    • Thickening of the nail plate, most commonly at the distal end
    • Nail yellow, keratotic debris accumulates under the nail
    • Nail separates from nail bed
  115. Onychomycosis - Diagnostic Evaluation
    • 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
  116. Onychomycosis - 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
  117. Dermatophyte infections-types
    • Tinea Pedis-feet
    • Tinea Corporis-body
    • Tinea Cruris-jock strap
    • Tinea Capitis-head
  118. Dermatophyte Skin Infection
    • MCC Microsporum, Trichohphyton, Epidermophyton
    • Found in the keratinous layer of skin, hair, and nails
    • May spread through contact or fomite
  119. Dermatophyte Skin Infection - Clinical Presentation
    • Erythematous papule/plaque
    • As lesion enlarges, central clearing with an erythematous scaling papular or vesicular border
  120. Tinea Pedis
    • 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
  121. Plantar infection-tinea pedis
    • Scaling affects all of plantar surface
    • Fine scale with pink skin
    • Pruritus
    • May also involve the hands
  122. Vesicular-tinea pedis
    • May develop in patient with interdigital tinea pedis
    • cover plantar or dorsal foot
    • May trigger ID reaction
  123. Tinea Cruris
    • 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
  124. 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
  125. Tinea Capitis
    • 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
  126. Dermatophyte Skin Infection - Diagnostic Evaluation
    • Scrape active border
    • KOH stain - fungal hyphae
    • Culture
  127. Dermatophy infection culture
    • Needed for hair or nail infection
    • Swab active portion of the lesion
    • Takes 4-6 weeks for results
  128. Dermatophyte Skin Infection - Treatment
    • Topical antifungal (pedis&cruris)
    • Oral antifungals ( hair, nail, widespread)
    • Powders to prevent reinfection
    • Reduce RF
  129. Exanthem
    • 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
  130. Exanthems - Clinical Evaluation & treatment
    • 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
  131. Exanthems
    • Roseola
    • Fifth dz
    • kawasaki
  132. Roseola
    • 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
  133. Erythema Infectiosum (Fifth Disease)
    • "Slapped cheek syndrome"
    • Caused by parvovirus B19
    • outbreaks in the winter and spring
    • Most common ages 5-14
  134. Erythema infectiosum ssx
    • 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
  135. Kawasaki disease
    • Acute vasculitis
    • Most commonly affects infants and children (7 wks-12 years)
    • Conjunctivitis
    • Lips and oropharynx
  136. Conjunctivitis-kawasaki dz
    Conjunctival injection; Uveitis
  137. Kawasaki Disease-Lips and oropharynx
    • become red 3-5 days later
    • Lips dry, fissured, cracked
    • "Strawberry tongue" - hypertrophic tongue papillae
  138. Kawasaki Disease Skin findings
    • 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
  139. Kawasaki Disease-Long term complication
    • 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
  140. Kawasaki acute phase complications
    • half of patients develop myocarditis
    • Tachycardia, gallop rhythm
    • May lead to sudden death
  141. Kawasaki Subacute phase complications
    • 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
  142. Examthems-Diagnostic Criteria (need 5 of 6)
    • FUO > 5 days
    • Bilateral conjunctival injection
    • Changes in lips and oral cavity
    • Cervical lymphadenopathy
    • Polymorphous exanthema with vesicles and crust
    • Changes in peripheral extremities
  143. Kawasaki disease-Treatment
    • Aspirin
    • IVIG
    • If don't respond to IVIG, consider steroids
    • Monitor for long-term cardiac side effects
  144. Molluscum Contagiosum
    • 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
  145. Molluscum Contagiosum- Clinical Presentation
    • 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
  146. Molluscum Contagiosum - Diagnostic Evaluation
    • Usually a clinical diagnosis
    • If atypical, consider bx
    • Shows virus within the papule - "X body"
  147. Molluscum Contagiosum - Treatment
    • 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
  148. Herpes Simplex
    • 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
  149. Herpes Simplex - Primary Infection
    • Most often asymptomatic
    • Often transmitted through respiratory droplets or direct spread
    • If symptoms develop, occur after 3-7 days
  150. Herpes simplex-sx
    • Occur after 3-7days
    • Prodromal pain, tenderness, paresthesias
    • Lymphadenopathy, headaches
    • Pharyngitis and gingivostomatitis if oral disease
    • Vulvovaginitis, proctitis, anorectal pain if genital involvement
  151. HSV - Primary Infection sx
    • 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
  152. HSV - Recurrence
    • 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
  153. HSV - Common Locations
    • 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
  154. HSV - Diagnostic Evaluation
    • 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
  155. HSV - Treatment
    • 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
  156. Hsv Acute infection tx
    • 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
  157. Hsv Recurrent infection tx
    **Treat at first prodromal symptom**
  158. HSV Suppressive therapy
    • 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
  159. Varicella
    • Initial infection caused by varicella zoster virus (herpesvirus)
    • Highly contagious
  160. Varicella - Etiology/Pathophysiology
    • Human herpesvirus 3
    • Transmitted by droplets
    • Patients contagious for 2 days before onset of rash until lesions have crusted
  161. Varicella - Clinical Presentation
    • 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
  162. Varicella prodromal sx
    • Low grade fever
    • Malaise
    • Headache
    • Minimal in children
    • More pronounced in adults
  163. Varicella - Clinical Presentation
    • Risk of bacterial superinfection
    • Adults have more severe disease
    • Pneumonia may develop in adults
    • Immunocompromised may develop hepatitis
    • Infection conveys lifelong immunity
  164. Varicella - Diagnostic Evaluation
    • Clinical diagnosis
    • Can order Tzank smear if in question
    • Bacterial culture if concern for secondary infection
  165. Varicella - Treatment
    • 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
  166. Zoster
    • 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
  167. Zoster - Etiology/Pathophysiology
    • After varicella infection, virus migrates into the dorsal root
    • May be reactivated with immune system insult
  168. Zoster - Clinical Presentation
    • 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
  169. Zoster - rash
    • Vesicles may vary in size (are uniform size in herpes simplex)
    • Crust over several days to weeks
    • Post herpetic neuralgia
  170. Zoster-Ocular involvement
    • Hutchinson's sign
    • Half will develop ocular complications without antiviral treatment
    • Refer to ophthalmology
  171. Zoster - Diagnostic Evaluation
    • Culture available, but often false negative
    • ~~Unroof vesicle, culture base of lesion
    • Tzank smear - multinucleated giant cells
  172. Zoster - Treatment
    • Steroids for pain (does NOT decrease incidence of PHN)
    • Oral antivirals
    • Treatment for PHN (if develops)
    • ~~Gabapentin
    • ~~Amitriptyline
    • ~~Topical capsaicin
  173. Zoster - Vaccination
    • 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
  174. Condyloma Acuminatum
    • Genital warts
    • Infection caused by human papilloma virus
  175. Condyloma Acuminatum - Etiology/Pathophysiology
    • Spread by direct contact
    • Increased transmission in moist areas
    • Virus is present on normal skin that is contiguous to wart
  176. Condyloma Acuminatum - Clinical Presentation
    • 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
  177. Condyloma Acuminatum - Diagnostic Evaluation
    • Clinical diagnosis
    • Can biopsy
  178. Condyloma acuminatum - Treatment
    • Cryotherapy
    • Electrodessication and curettage
    • Podofilox (Condylox gel)-3 days on, 4 days off x 4 weeks
    • Imidquimod cream (Aldara)
  179. Condyloma Acuminatum - Patient Education
    • 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
  180. Verrucae
    • Verruca vulgaris - "warts"
    • Caused by HPV
  181. Verrucae - Etiology/Pathophysiology
    • Spread by contact
    • Inoculation occurs with simple trauma to the skin
    • Must reach basal epithelial cells in order to occur
  182. Verrucae - Clinical Presentation
    • 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
  183. Filiform warts
    • finger-like projections
    • more common on the face
  184. Flat warts-verrucae
    • Thin, less scaly
    • Still have disruption of normal skin lines
    • Found in patches with contiguous spread due to repeated trauma
  185. Plantar warts-verrucae
    • 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
  186. Verrucae - Diagnostic Evaluation
    • Typing is not clinically helpful
    • Biopsy if not healing AND sun exposed skin (r/o scc)
  187. Verrucae - Treatment
    • 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
  188. Verrucae - Clinical Pearls
    • Patient education about spread
    • ~~Shaving, picking, biting
    • No tx 100%
    • most rely on activating the body's own immune defense
  189. Seborrheic keratosis
    • Benign, persistent epidermal lesion
    • Variable clinical appearance
    • One of the most commonly encountered lesions
  190. Seborrheic Keratosis - Etiology
    • Increased incidence with age (rare before age 30)
    • Tendency toward multiple often inherited
  191. SK - Clinical Presentations
    • Varied-Most often asymptomatic
    • Pruritic, may be irritated by clothing
    • Often cosmetically unappealing
    • Usually multiple lesions
  192. Sk apperance
    • 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
  193. Leser-Trelat
    • Sudden, explosive onset of multiple SKs
    • Associated with internal malignancy
  194. SK - Diagnostic Tests
    None necessary unless lesion has suspicious characteristics
  195. SK - Treatment
    • No treatment needed
    • May remove/tx due to cosmetics or irritation/inflammation
    • ~~Salicylic acid
    • ~~Cryosurgery
    • ~~Shave excision
  196. Sk Prognosis
    • 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!
  197. Actinic Keratosis
    • 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
  198. Actinic Keratosis - Etiology/Pathophysiology
    • 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
  199. Actinic Keratosis ssx
    • 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
  200. Actinic Keratosis ssx progression
    • Scale becomes thicker, more yellow
    • May form cutaneous horn as scale builds up
    • Advanced lesions impossible to distinguish from SCC
  201. Pigmented AK
    • pigmented lesion with fine scaling
    • May resemble solar lentigo or melanoma in situ
  202. Actinic chelitis
    • Involves lower lip
    • Focal crusting or scaling
    • Higher chance of progressing to SCC
  203. AK - Diagnostic Evaluation
    • Biopsy if suspicious of SCC
    • Most often clinical diagnosis
  204. AK - Treatment
    • Annual follow up
    • Sun protection/sun avoidance
    • Few lesions: Cryotherapy; Biopsy or shave if suspicious
  205. AK tx multiple lesions
    • 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"
  206. 5-fluorouracil (5-FU)
    • 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
  207. Squamous cell carcinoma
    • 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
  208. SCC - Etiology, Epidemiology
    • 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
  209. SCC ssx
    • 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
  210. Scc variants
    • Bowen's disease-full-thickness SCC in situ
    • Cutaneous horns
    • Keratoacanthoma-crater-like nodule w/ necrosis
  211. Keratoacanthoma
    • Large, nodular, crater-like nodule with central necrosis
    • Fast growing
    • Low-grade variant of invasive SCC
  212. SCC - Metastasis
    • More likely on mucous membranes or more advanced lesions
    • Mets first to regional lymph nodes
    • ~~Usually within 2-3 years of skin lesion
  213. SCC - Diagnostic evaluation
    • Biopsy suspicious lesions
    • Deep shave (include dermis)
    • Electrocautery and curettage to remove residual cells
    • Deeper lesions may require excision with clear margins
  214. SCC - Treatment
    • 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
  215. SCC - Prognosis
    • Excellent if adequately treated, not metastatic
    • Increased risk of metastasis in immunosuppressed patients, lesions on lip or ear, or arising from scar tissue
  216. Basal cell carcinoma
    • Primary skin malignancy arising from the basal layer of keratinocytes
    • Most common cutaneous malignancy
    • Untreated, will invade and destroy surrounding tissue
    • Rarely metastasize
  217. BCC - Etiology, Epidemiology
    • Sun exposure
    • More common later in life, lighter skin types
  218. BCC ssx
    • 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
  219. Pigmented BCC
    • May have pigmented area or be fully pigmented
    • Prognosis same as nonpigmented
  220. Superficial BCC
    • Thinnest, least aggressive
    • Appear in younger patients
    • May also appear on the trunk or extremities
    • Flat, may appear atrophic
    • Spreads peripherally
  221. BCC - Diagnostic Evaluation
    • Biopsy it!
    • Shave biopsy with curettage
  222. BCC - Treatment
    • 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
  223. Imiquimod/5-FU cream
    • Superficial bcc
    • Use daily x 6 weeks
    • Causes significant inflammation
  224. BCC - PT ed and Prognosis
    • Reassure patient
    • Sun avoidance/sun protection
    • Regular skin evaluation for further effects of sun damage
  225. Benign Nevi
    • 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
  226. Junctional Nevi
    • Nevus cells at the dermoepidermal junction
    • Flat or slightly raised
    • Skin markings are preserved
  227. Compound Nevi
    • 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
  228. Intradermal Nevi
    • 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
  229. Blue Nevi
    • 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
  230. Halo Nevi
    • 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
  231. suspicious?
    • Asymmetry
    • Border
    • Color
    • Diameter
    • Evolution
    • Does it bleed (without injury)
    • Ulceration
  232. Nevi - Treatment
    • 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
  233. Dysplastic Nevi
    • 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
  234. Dysplastic Nevus Syndrome
    • Familial syndrome of multiple atypical nevi
    • Associated with increased risk of melanoma
    • Relatively uncommon
    • nearly 100% lifetime risk of MM by age 70
  235. Dysplastic Nevi - Clinical Presentation
    • 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
  236. Dysplastic Nevi - Diagnostic Evaluation
    • 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%
  237. Dysplastic Nevi - Treatment
    • Excise suspicious nevi
    • Sun protection/avoidance
    • Skin exams every 6-12 months (including sun-protected areas)
    • Baseline eye exam
    • Self monitoring with skin exams
  238. Melanoma
    • 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
  239. Melanoma - Epidemiology
    • 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
  240. Melanoma - Risk Factors
    • 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)
  241. Melanoma ssx
    • 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
  242. Superficial Spreading MM
    • 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
  243. Nodular
    • 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
  244. Lentigo maligna
    • 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
  245. Acral lentiginous melanoma
    • 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
  246. MM - Diagnostic evaluation
    • BIOPSY!!-Full thickness, try to get clean margins
    • Palpate regional nodes for any adenopathy
    • Breslow level:
  247. 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
  248. MM - Treatment
    • 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
  249. MM - Prognosis
    • 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!
  250. Kaposi Sarcoma
    • 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
  251. Kaposi Sarcoma - Clinical Presentation
    • 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
  252. AIDS-related Kaposi
    • most often found on the face
    • May affect lymph nodes, GI tract, lungs
    • more likely to have systemic symptoms
  253. Kaposi Sarcoma - Diagnostic Evaluation
    • Biopsy to confirm
    • HIV test (if not known HIV), CD4 count
    • Oral evaluation - often oral lesions in patients with HIV
  254. Kaposi Sarcoma - Treatment
    • Excision of single lesion
    • Radiation if multiple lesions
    • Extensive lesions may also require chemotherapy
    • Consider d/c immunosuppressive therapy
    • AIDS-associated - Radiation therapy, cryotherapy
  255. Drug Eruptions
    • 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
  256. Morbiliform Drug Eruption rash
    • Maculopapular
    • Erythematous macules and papules become confluent
    • Symmetric, generalized
    • Usually spares the face
    • May involve mucous membranes, palms, soles
    • Pruritic
  257. Morbiliform Drug Eruption
    • Most common presentation
    • May be indistinguishable from viral rash
    • Starts 7-10 days after drug is started
    • Lasts 1-2 weeks before resolving
  258. Urticarial Drug Reaction
    • 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
  259. Fixed Drug Eruption
    • 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
  260. Fixed drug eruption dx
    • Provocation challenge confirms the diagnosis
    • May need to biopsy to r/o cutaneous T-cell lymphoma
  261. Photosensitive Drug Reactions
    • May be due to medicines administered internally or externally
    • Phototoxic reaction
    • Photoallergic rxn
  262. Phototoxic drug rxn
    • Dose dependent
    • Limited to area of sun exposure
    • Subsides when drug is stopped
    • Occurs within 24 hours of exposure
  263. Photoallergic drug reaction
    • Less common
    • No relation to dose
    • Does not begin until about 48 hours after exposure
    • May spread to non-sun exposed area
  264. Acneiform rash
    Steroids or hormones
  265. Lupus-like rash
    hydralazine, procainamide
  266. Photosensitivity
    thiazides, sulfonamides, tetracycline
  267. Amiodarone
    blue-grey in photodistribution
  268. Minocycline
    blue-grey on gingiva and teeth
  269. Antimalarial
    brown on the shins
  270. Oral contraceptives
    melasma on face
  271. Rifampin
    red man syndrome (high dose)
  272. Drug Reaction - Treatment
    • 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)
  273. Lichen Planus
    • Inflammatory papulosquamous disease
    • Etiology unknown
    • May affect hair, skin, or mucous membranes
    • 5 P's
  274. 5 ps lichen planus
    • Pruritic
    • Planar
    • Polygonal
    • Purple
    • Papules
  275. Lichen Planus - Clinical Presentation
    • 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
  276. Types of lichen planus presentation
    • Papular
    • Hypertrophic
    • Follicular
    • mucosal
  277. KOEBNERS Phenomenon
    New lesions appear in area of trauma
  278. Lichen Planus -papular
    • Most common
    • Papules on flexor surfaces of wrists, forearms, ankles, lumbar back
  279. Hypertrophic LP
    • Lesions become hypertrophic with coalescing papules
    • Most common on the shins
    • May form bullae
    • Residual brown hyperpigmentation
  280. Follicular LP (lichen planopilaris)
    • Papules occur at the hair follicle - scalp
    • Scarring causes hair loss
  281. Mucosal Lichen Planus
    • Non-erosive - lacy white reticulation
    • Erosive - beefy red desquamation
    • May involve penis or vagina
    • 3% go on to develop oral SCC
  282. LP - Diagnostic Evaluation
    • Biopsy
    • If scalp involved, obtain DIF to r/o cutaneous lupus
    • Screen for Hep C
  283. LP - Treatment
    • Antihistamines for pruritus
    • Class I or II steroids twice daily
    • Intralesional steroid for hypertrophic plaques
    • Dapsone, azathioprine, hydroxychloroquine for refractory cases
  284. Pityriasis Rosea
    • 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
  285. Pityriasis Rosea - Clinical Presentation
    • 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
  286. Herald patch
    • 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
  287. Pityriasis Rosea - Diagnostic Evaluation
    • 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
  288. Pityriasis Rosea - Treatment
    • Patient reassurance
    • Antihistamines, topicals (low-medium potency steroids) for pruritus
  289. Psoriasis
    • Common, chronic inflammatory papulosquamous disease predominated by T-cell dysfunction and autoimmune dysregulation
    • Genetic + environment
    • Affects 1-3% of the population worldwide
  290. Psoriasis - Pathophysiology
    • Abnormal maturation of keratocytes in the skin
    • Hyperkeratosis
    • Cell nuclei in the stratum corneum are retained
  291. Psoriasis - Triggers
    • Stress
    • Strep infection
    • HIV infection
    • Koebner phenomenon
    • Drugs (lithium, antimalarials, steroid withdrawal)
  292. Psoriasis forms
    • Plaque
    • Guttae
    • Pustular
    • inverse
  293. Plaque psoriasis
    • 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
  294. Guttae psoriasis
    • 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
  295. Pustular 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
  296. Inverse psoriasis
    • 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
  297. Psoriasis sx
    • Nail changes-Can occur with any form
    • ~Pitting
    • ~Onycholysis
    • ~Oil drop sign
  298. Psoriasis - Diagnostic Evaluation
    • 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
  299. Psoriasis - Treatment
    • Topical
    • Photo therapy
    • Systemic
  300. Topical-psoriasis tx
    • Tar preparations
    • Vitamin D analogues (Dovonex, Vectical)
    • Topical steroids (Group I-V)-Cyclical treatments
    • Retinoids (Tazorac)
  301. Phototherapy psoriasis
    • UVB 3-5 times/wk.
    • Narrow band has fewer side effects but limited availability
    • PUVA
  302. Systemic psoriasis therapy
    • Consider in patients with > 10% BSA or based on patient discomfort/disability
    • Managed by dermatology
    • Methotrexate
    • Cyclosporin
    • Acetretin (Soriataine)
    • Biologics (Enbrel, Humira, Remicade &Stelara)
  303. Psoriasis complications
    • 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
  304. Erythema Multiforme
    • 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
  305. Erythema Multiforme - Pathophysiology
    Theorized to be immune system response against keratinocytes that present viral or drug antigens
  306. Erythema Multiforme - Clinical Presentation
    • 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
  307. Erythema Multiforme progression
    • Crops of lesions appear
    • Oral bullae or erosions
    • Urticarial lesions last >24 hours
    • + Koebner phenomenon
    • +/- signs of accompanying infection
  308. Erythema Multiforme - Diagnostic Evaluation
    • May diagnose clinically if target lesions are present
    • Biopsy
  309. EM - Treatment
    • 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
  310. Stevens-Johnson Syndrome
    • Severe, blistering mucocutaneous syndrome
    • Involves at least two mucous membranes
    • Most common in children and young adults
  311. Stevens-Johnson Syndrome - Pathophysiology
    • Similar to erythema multiforme
    • Immune response directed against keratinocytes that are expressing foreign antigens
  312. SJS - Etiology
    • Associated with Mycoplasma
    • Medications
  313. Sjs medications
    • Phenytoin, phenobarbital, carbamazepine
    • Sulfa drugs, PCNs
    • Usually started within 1 month of onset
  314. SJS - Clinical Manifestations
    • 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
  315. Sjs progression
    • 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
  316. SJS - Diagnostic Evaluation
    • 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
  317. SJS - Treatment
    • Find the causative agent
    • Maintain fluid and nutritional requirements
    • Wound care
    • Ophthalmology consult if eye involvement
    • Burn care
    • +/- systemic steroids
    • Narcotics for pain
    • IVIG
  318. SJS - Prognosis
    • With good supportive care, mortality is < 1%
    • Recurrence rare unless exposed to causative drug again
  319. Toxic Epidermal Necrolysis
    • 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
  320. TEN - Pathophysiology
    • Cause - unknown
    • Skin sloughing theorized to be due to increased apoptosis
  321. TEN - Clinical Manifestations
    • 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
  322. TEN - Diagnostic Evaluation
    Bx to r/o staph scalded skin syndrome
  323. TEN - Treatment
    • Control pain
    • Find the cause
    • Burn care
    • Maintain fluid and nutrition
    • IVIG
    • Steroids? Use with prophylactic antibiotics
    • May require other immunosuppressant therapy
  324. TEN - Prognosis
    • Mortality rate 30-50%
    • d/2 complications-infection etc
  325. Acanthosis Nigricans
    • Thick, velvety plaques
    • neck, groin and axillae
    • patients w/ abnormal glucose metabolism or malignancy (rare)
  326. Acanthosis Nigricans - Etiology/Pathophysiology
    • Not fully understood
    • Related to insulin resistance
  327. Acanthosis Nigricans - Clinical Presentation
    • 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
  328. Acanthosis Nigricans - pt
    • Look for other signs of insulin resistance
    • ~~Obesity
    • ~~PCOS characteristics in women
  329. Acanthosis nigicans-malignancy
    • High suspicion if doesn't fit "typical" picture
    • Rarely sign of internal malignancy
    • (90% in the abdomen)
    • ~~Middle aged patient
    • ~~Abrupt onset
    • ~~Not obese
  330. Acanthosis Nigricans - Diagnostic Evaluation
    • Clinical Diagnosis
    • Evaluate for insulin resistance
  331. Acanthosis Nigricans - Treatment
    • Retinoids, dermabrasion
    • Treat underlying condition
    • ~~Treat insulin resistance/excess
    • ~~Weight loss
    • ~~Screen/treat for malignancy
  332. Granuloma Annulare
    • 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
  333. Granuloma Annulare - Etiology/Pathophysiology
    • 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
  334. Granuloma Annulare - rash
    • Begins as erythematous papule
    • Expands to annular, erythematous plaque
    • Raised, papular border
    • Center is flatter, lighter colored
  335. Granuloma Annulare - distribution
    • 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
  336. Granuloma Annulare - Diagnostic Evaluation
    • KOH to r/o fungal infection if needed
    • Clinical diagnosis, but may bx to confirm
  337. Granuloma Annulare - Treatment
    • Self limited
    • Steroid (high potentcy)
    • Intralesional steroid
    • Disemminated disease
    • ~~Isotretinoin, methotrexate, dapsone, hydroxychloroquine
  338. Hidradenitis Suppurativa
    • Inflammatory skin condition affecting areas with apocrine sweat glands
    • Recurrent nodules and abscesses that have sinus tracts
  339. Hidradenitis Suppurativa - Etiology/pathophysiology
    • Exact cause unknown
    • Characterized by follicular occlusion
    • Apocrine gland ducts are occluded causing inflammation
    • Follicle ruptures, forms abscess
    • Sinus tracts form between abscesses
  340. Hidradenitis Suppurativa - Aggravating factors
    • Genetics
    • Female > male
    • Obesity, PCOS
    • Pro-inflammatory cytokines
    • Cigarette smoking
    • Secondary bacterial infection
  341. Hidradenitis Suppurativa - Clinical Presentation
    • 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
  342. Hidradenitis Suppurativa - Diagnostic Evaluation
    Clinical diagnosis
  343. Hidradenitis Suppurativa - Treatment
    • Earlier treatment is better
    • d/c smoking
    • Weight reduction
    • Hair removal
    • Topical antiseptic soaps
  344. Hidradenitis Suppurativa - meds
    • 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
  345. Lipomas
    • Common, benign tumors consisting of adipose cells
    • Located within the subcutaneous tissue
  346. Lipomas - Etiology/Pathophysiology
    • Cause unknown
    • Genetic predisposition, especially in patients with multiple lipomas
    • Blunt trauma may trigger solitary lipoma, but most often cause is unknown
  347. Lipomas - Clinical Presentation
    • 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
  348. Lipomas - Diagnostic Evaluation
    • Clinical Diagnosis
    • May be removed for cosmetic reasons (general surgery?)
    • If quickly enlarging or painful, consider biopsy to r/o liposarcoma
  349. Lipomas - Treatment
    • Surgical excision
    • Squeeze technique
    • Liposuction
  350. Epithelial Inclusion Cysts
    • Epidermal cysts
    • Pilar cysts
  351. Epidermal cysts
    cystic structure filled with soft, cheese-like keratinous contents
  352. Pilar cysts
    • small cysts on the scalp
    • filled w/ firm, white content
    • arise from the hair root sheath
  353. Epithelial Inclusion Cysts - Etiology/Pathophysiology
    • May result from plugging of sebaceous glands with oil backing up
    • Body "walls off" debris, which is retained
  354. Epidermal cysts ssx
    • 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
  355. Pilar cysts ssx
    • Well, circumscribed, firm nodules on the scalp
    • Usually multiple
    • Not attached to underlying tissue
    • Usually do not spontaneously open and drain unless secondarily infected
  356. Epithelial Inclusion Cysts - Diagnostic Evaluation
    • Not usually necessary
    • Bacterial culture if infected
  357. Epithelial Inclusion Cysts - Treatment
    • 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
  358. Melasma
    • Hyperpigmentation of the face
    • Typically occurs in women during pregnancy and on OCPs
    • More common in darker skin types
  359. Melasma - Clinical Presentation
    • Hyperpigmented macules - sharply demarcated with an irregular border
    • May be brown, tan, blue-gray
  360. Melasma - Diagnostic Evaluation
    • Clinical Diagnosis
    • Biopsy suspicious area
  361. Melasma - Treatment
    • If due to pregnancy, may resolve after pregnancy
    • May recur with subsequent pregnancies
    • Hydroquinone
    • Laser
  362. Pilonidal Disease
    • Chronic sinus tract in the sacrococcygeal region
    • filled with nests of hair
    • May become infected and inflamed
  363. Pilonidal Disease - Etiology/Pathophysiology
    • 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
  364. Pilonidal disease - Risk Factors
    • M>F
    • Obesity
    • Genetics
    • Poor hygiene
    • Prolonged sitting or friction on the buttocks
    • Repeated injury to the area
    • Coexisting hidradenitis suppurativa
  365. Pilonidal disease - Clinical Presentation
    • 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
  366. Pilonidal Disease - Diagnostic Evaluation
    Clinical Diagnosis
  367. Pilonidal Disease - Treatment
    • Keep area clean, free of hair
    • I&D
    • Excision of tract
    • Marsupialization of cyst
  368. Pressure Ulcers
    • Bed sores, decubitus ulcers
    • Area of reddened skin
    • progresses to skin breakdown that results in sores and ulcers
  369. Pressure Ulcers - Etiology/Pathophysiology
    • 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
  370. Pressure Ulcers - Risk Factors
    • Immobility
    • Peripheral neuropathy
    • Elderly
  371. Ulcers Stage 1
    • Skin is red or pink but unbroken
    • May look like a mild sunburn
    • Tender, itchy or painful
  372. Ulcers Stage 2
    • Skin is red, swollen, and painful
    • Blisters present (intact or broken)
    • Upper layers of skin begin to die
  373. Ulcers Stage 3
    • Skin is broken, wound extends down to deeper layers of skin
    • Crater-like ulcers present
    • Wound is prone to infection
  374. Ulcers Stage 4
    • Sore extends into deeper tissue
    • Necrosis and eschar in deep, opened wound
  375. Pressure Ulcers - Diagnostic Evaluation
    Clinical diagnosis
  376. Pressure Ulcers - Treatment
    • Prevent, treat early
    • Treatment by wound care
    • Topical vac therapy
    • Hyperbaric oxygen
    • Hydrotherapy
    • Debridement
    • Treat infection
  377. Urticaria
    • Wheals resulting from edema of the dermal tissue
    • Angioedema results from edema of deeper structures
  378. Acute urticarial path/etiology
    • (< 6 weeks)
    • Post viral
    • Allergic reaction (IgE mediated)
  379. Chronic urticarial path/etiology
    • (> 6 weeks)
    • Allergic (chronic exposure)
    • Autoimmune (lupus, vasculitis, thyroid)
    • Idiopathic (~50%)
  380. Urticaria - Clinical Presentation
    • 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
  381. Urticaria - Concerning characteristics
    • Individual lesions last >24 hours
    • Burning sensation
    • Residual bruising
    • (especially with chronic urticaria)
  382. Chronic urticaria
    • Individuals with chronic urticaria may have specific triggers
    • Cold induced urticaria, heat induced urticaria
    • Dermatographism
  383. Acute Urticaria dx
    • No labs needed
    • Review medication history, exposures
    • Any signs/sx of viral infection?
  384. Chronic urticarial dx
    • CBC, CMP, Complements
    • IgE, ANA, TSH, thyroglobulin antibody, thyroid peroxidase antibody
    • Sed rate
    • Consider evaluation with allergist for allergy testing
  385. Urticaria - Treatment
    • Avoid heat, pressure
    • NSAIDS may enhance rxn
    • d/c any potentially triggering meds
    • Treat underlying causes of chronic urticaria
    • Antihistamines
    • Steroids
    • Epinephrine
  386. Antihistamines-urticaria
    • Long-acting antihistamine (Zyrtec, Claritin) - can use once or twice daily
    • Benadryl as needed for breakthrough symptoms
    • May add H2 blocker
  387. Steroids-urticaria
    • Consider oral steroid for severe outbreak
    • Topical steroids DO NOT help
  388. Epinephrine-urticaria
    May be needed for angioedema if airway is compromised
  389. Vitiligo
    Acquired condition where impaired or absent melanocyte function leads to hypopigmentation of the skin
  390. Vitiligo - Etiology/Pathophysiology
    • 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
  391. Vitiligo - Clinical Presentation
    • 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
  392. Vitiligo distribution
    • Most commonly affected
    • Extensor bony surfaces
    • Periorificial areas
  393. Vitiligo - Diagnostic Evaluation
    • May biopsy if in question
    • CBC, TSH to screen for underlying disorder
  394. Vitiligo - Treatment
    • 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
  395. Erythema Nodosum
    Inflammatory panniculitis with erythematous, deep nodules on the shins
  396. Erythema Nodosum - Etiology/Pathophysiology
    • 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
  397. Erythema Nodosum - Risk Factors
    • Pharyngitis
    • Mycoplasma infection
    • Sarcoidosis
    • Tuberculosis
    • Pregnancy or OCPs
    • Meds - sulfa, ASA, NSAIDs
    • Inflammatory bowel disease
  398. Erythema Nodosum - Clinical Presentation
    • 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
  399. Erythema Nodosum - Diagnostic Evaluation
    • 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
  400. Erythema Nodosum - Treatment
    • Treat underlying infection
    • Rest if pain or swelling is severe
    • Compression, ice
    • NSAIDs

What would you like to do?

Home > Flashcards > Print Preview