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appearance of skin lesions (nothing to do with etiology or pathophysiology) through visual and tactile inspection and correct description.
Most important in diagnosing skin issues
1. Primary lesions: most characteristic lesion that is representative of skin disease
-macule, papule, plaque, nodule, cyst, patch, pustule, etc.
2. Secondary lesions: changes due to exogenous factors that can progress during the course of skin disease
-scale, crust, excoriations, erosion, ulcer, fissures, lichenification, induration, scar/atrophy Preferential areas of involvement and regions of the body affected by the skin disorder
Scalp: seborrheic dermatitis, psoriasis, tinea capitus
Face: Rosacea, contact dermatitis, pityriasis alba, lupus erythematosus
Trunk: tinea versicolor, psoriasis, pityriasis rosea, drug rash
Genital: syphilis, psoriasis, HSV
Groin: intertrigo, hidradenitis suppurativa, tinea cruis, candidiasis
Wrists/ankles: lichen planus
Arms: actinic purpura
Legs: stasis dermatitis, vasculitis, erythema nodosum
Hands/feet: tinea pedis, contact dermatitis Rash:
-How did it spread?
-How has is evolved?
-History of atopy?
Growth:
-How has it changed (size, shape, color)?
-Family Hx skin cancer?
Focal skin exam
Total body skin exam (increased risk for skin CA, new rash, 50+ moles, Hx dysplastic nevi)
Magnification, Dermoscopy (epiluminescence microscopy-patterns), Wood's lamp ("black" UV lamp-color differences), diascopy (red due to capillary or blood)
Start head to toe
(don't forget between toes, scalp, nails, etc) Variety of vehicles
MOA: anti-inflammatory, anti-proliferative, immunosuppressive, vasoconstrictive
ADRs:
-Atrophy: thinned epidermis and dermis, striae (common in abdomen, groin, thighs)
-Hypopigmentation of skin
-Acne, folliculitis, contact dermatitis
-Corticosteroid-induced rosacea-like dermatitis (CIRD) (perioral, perinasal, periocular, diffuse)
-Tachyphylaxis: "tolerance". Most likely related to compliance
-Systemic: (related to misuse and with occlusion) Cushing syndrome, HPA suppression
-Ocular: 36-40x penetration around the eyes can cause glaucoma, cataracts, poor wound healing, herpetic ulcers, and infection
Best practices: CORRECT
-potency, location, vehicle, quantity, duration Emollients
-Moisturizers decrease itching. Use immediately after bathing.
-Creams and lotions can sting more than ointments.
-Cannot overdo moisturizing.
Anti-histamines
-Don't stop the rash, but can help with itch/scratching
-High dose (cetirizine 10mg TID) for daytime
-Sedating at night (Benadryl, hydroxyzine)
Topical corticosteroids
-Help to control inflammation.
-Use lower strength steroids on the face, neck, axillae, groin
-Stronger steroids in other regions for short periods
-usually 2x daily
Steroid sparing agents
-Calcineurin inhibitors (Pimecrolimus = cream. Tacrolimus = ointment. Can sting)
-Crisaborole: ointment prevents flares, help itch. can sting
Abx if infection present (90% have staph at some point)
-Don't use too often as to cause resistance
-Bleach or vinegar baths decrease colonization and infection
Other preventative measures
-UV therapy (nbUVB, PUVA, Wolf beds, sunlight)
-Keep a diary of possible triggers/ allergy testing
-Avoid fragranced produces
-Wear gloves and avoid wet work
-Pets?
Systemic therapies
-Immunosuppressants (methotrexate, mycophenylate mofetil, azathioprine, cyclosporin) Typically involves areas of high sebum production and body folds (scalp, ears, eyebrows, nasolabial folds, chest, axillae, groin)
-Adult and infantile varieties
-Associated with overgrowth of yeast (Malassezia furfur)
Appearance:
-poorly marginated, yellowish-pink macules with "greasy" scales
Adult:
Presentation:
-Scalp (dandruff), eyebrow/glabellar region, perinasal, ear canals/behind ears.
-Less common on central chest and axillae
-May be indistinguishable from scalp psoriasis
Flares: winter/dryness, HIV, Parkinson Dz
Treatment:
-Topical antifungal shampoos (ketoconazole, selenium)
-Other shampoos (tar, zinc pyrithione, salicylic acid)
-Topical steroids
-Pimecrolimus and tacrolimus
Infantile:
Presentation:
-1-2 weeks of age resolves around 8-12 months
-Lack of pruritus
-Can present as soft greasy scales that adhere to scalp "cradle cap"
-Inflamed plaques in inguinal region or axillae
Treatment:
-Frequent shampoo with antiseborrheics (sulfur and salicylic acid)
-Warm mineral oral/petrolatum to get crust off
-Small amounts of topical steroids if persistent and comb with 3-5% sulfur/salicylic acid Management:
-Not a problem with washing, do not over-exfoliate or overdry
-Diet is controversial (low glycemic index may be better. avoid skim milk)
-Adhere to treatment plan
Therapies:
Benzoyl Peroxide: (BPO)
-MOA: antibacterial, comedolytic, mild anti-inflammatory
-Decreases P.acnes resistance to topical abx
-Combo with abx is synergistic
-Should almost always be a part of acne regimen
-ADRs: skin irritation, fabric bleaching
Topical retinoids
-MOA: Vitamin A derivatives that normalize follicular keratinization, clear existing comedomes, prevent new comedomes
-Best used as preventative all over the face
-Different strengths and vehicles
-Fringe anti-aging benefits
-ADRs: Irritation, dryness, photosensitivity. DO NOT use in pregnancy
Topical Abx:
-MOA: reduce P. acnes, mild anti-inflammatory
-Common: erythromycin, clindamycin, dapsone/aczone
-Many combo products with BPO
-ADRs: skin irritation, dryness
Systemic Abx: (moderate to severe inflammatory acne)
-Common: tetracycline (minocycline and doxycycline), erythromycin, bactrim (severe acne), amoxicillin (pregnancy)
-6 to 8 weeks for improvement
-Tetracycline class is the gold standard
-ADRs: GI upset (take with food), Pseudotumor cerebri, photosensitivity, esophagitis (don't lie down for 30 ), serum sickness-like reaction, drug-induced lupus, autoimmune hepatitis
Hormonal therapy (estrogen-containing OCPs)
-MOA: block ovarian production, reduce serum androgens, reduce free testosterone by increasing SHBG, decrease sebum production
-Common: ethinyl estradiol/norgestimate or drospirenone
-ADRs: N/V, weight gain, abnormal menses, migraine, increased risk fo thromboembolism
Spironolactone
-MOA: anti-androgen and blocks effects on skin
-ADRs: menstrual irregularity, breast tenderness, lightheadedness, hyperkalemia, DO NOT use in pregnancy
Isotretinoin (oral)
-MOA: retinoic acid derivative that targets all 4 of pathogenic factors involved in acne
-When to use: severe nodulocystic acne or acne that failed other therapies
-Treatment: 5 to 6 months
-ADRs: MAJOR birth defects (Ipledge program), xerosis, dry everything, muscle/joint aches/pains, hypertriglyceridemia, elevated LFTs, depression/anxiety exacerbation, pseudotumor cerebri, IBS (questionable) Common chronic inflammatory disorder of the pilosebaceous unit that relapses and remits
Etiology (poorly understood):
-Cutaneous vascular changes
-Inappropriate activation of immune system
-US exposure and microbial exposure (demodex)
-Genetics
-More common in 30-50 years and light skin
-Erythema is usually localized to convex facial surfaces (nasolabial folds spared)
Absence of comedones helps distinguish from acne
Triggers:
-Sun exposure, emotional stress, hot/cold weather, alcohol, hot beverages, exercise, spicy foods
4 main subtypes
1. Erythematotelangiectatic rosacea (ET)
-Persistent erythema + telangiectasis on central face
-Flushing + burning/stinging of skin
-Most common
2. Papulopustular rosacea
-Acneiform papules and pustules
-Erythema and occasionally edema on central face (sparing of periocular areas)
-Absence of comedones!
3. Phymatous rosacea
-Chronic inflammation and edema leading to thickening of skin
-Nose is most affected (usually men)
-Sebaceous hyperplasia with cobblestone appearance
4. Ocular rosacea
-Presents with conjunctivitis, blepharitis, and hyperemia (redness)
-Dry, itchy, and irritated eyes
-Can occur with or without cutaneous findings Chronic suppurative destructive disorder of the follicular epithelium in apocrine gland bearing skin (axillae, breasts, anogenital)
-Leads to occlusion of hair follicle, rupture, and severe inflammation and scarring
-"recurrent boils"
Predisposing factors: female, obesity, cigarette smoking, genetics
S/s:
-Look for double comedones on a single nodule/scar
-Very tender, inflamed papulonodules, abscesses and cysts
-May see scarring and sinus tracking under the skin that drain malodorous pus
Management: (difficult to treat)
-Encourage weight loss and smoking cessation
-Wear loose clothing and avoid excessive friction
-Psychological management (depression common)
Medications:
-Mild: topical BPO and topical Abx
-Acute flares: ILK and I&D
-Oral Abx: tetracyclines, dapsone
-Oral hormonal therapy: OCP, spironolactone, finasteride
-Systemic retinoids: Isotretinoin, acitretin
-Biological agents: Anti-TNR inhibitors
-Surgical techniques for end-stage management "ringworm" of any part of the body except hair, nails, palsm, soles, and groin
Cause: (any dermatophyte)
-T. rubrum or T. mentagrophytes
Risk factors:
-Perspiration
-AIDS if widespread tinea corporis
S/s:
-Hairy areas may show more inflammatory response (pustule-like)
-1 or more circular, sharply circumscribed, slightly erythematous, dry, scaly patches with central clearing
-Borders are raised, more inflamed, more scaly
-Pustules within the advancing border = very suggestive of tinea
Diagnosis:
-Biopsy (of the most active edges) with PAS (cultures aren't always positive)
Treatment:
-DO NOT use Lotrisone (antifungal + steroids and steroids make this worse)
-Topical Terbinafine
-Systemic Griseo, Terbinafine, Itraconazole, Fluconazole Cause:
-Trichophyton, microsporum, epidermophyton
-yeasts and non-dermatophytic molds
Risk factors: DM, PVD, immunosuprression, obesity, occlusive footwear, advancing age
Types
1. Distal subungual (most common- usually big toe)
-Distal nail bed and hyponychium (nail plate)
-Deep, insidious, non-inflammatory
-Yellowish discoloration that spreads. Thick and yellow
-Nails crumble
-T. rubrum
2. White superficial
-Invasion of nail plate on surface of the nail
-White chalky spots
-Nail is soft, dry and powdery
-T. mentag
3. Proximal subungual
-Nail plate starting from proximal nail fold
-AIDs
-T. rubrum and T. mentag
4. Candida onychomycosis:
-Involves all the nail plate
-Patients with chronic mucocutaneous candidiasis
-Candida albicans
Diagnosis:
-KOH (thin nail shavings) in a PAS stain
-Can culture if necessary but slow
Treatment;
-Terbinafine (lamisil) 6 weeks fingernails, 12 weeks toenails
-Itraconazole (sporanox)
-Fluconazole (Diflucan) If yeast is suspected
-Griseofulvin
-Topical treatments for 48 weeks Intertriginous (skin on skin) areas are most affected due to warmth, moisture, maceration which permits yeast to thrive.
-Yeast proliferates both budding and mycelial forms in the outer layers of the stratum corneum
-Does not attack hair and rarely involves the nails. Cannot break the stratum corneum
Cause: Candida albicans
Risk factors: DM, occlusion, hyperhidrosis, long-term steroids, broad-spectrum abx
Prevention:
-Keep intertriginous areas dry, clean and cool
-encourage weight loss
-loose clothing made of cotton
-powders an barrier creams are useful
Treatment:
-Topical antifungals for mild/moderate cutaneous, vulvovaginal, or oral infection
-Systemic if severe
-Can use oral agents for vulvovaginal disease in non-pregnant women (azoles are more effective than nystatin in vaginal area)
Pearls:
-Nystatin (only for candida)
-NO terbinafine (only for dermatophytes)
-Mucocutaneous candida you can use nystatin or azole lozenges (topical polyenes)
-IF systemic therapy is warranted, fluconazole or itraconazole Very common bacterial infection of the deep dermis that usually begins with loss of skin integrity/trauma.
Risk factors:
-Local trauma (bug bite, laceration, puncture, abrasion)
-Underlying skin lesion/infection (furuncle, ulcer, impetigo, tinea pedis)
-Immunosuppression, DM, vascular dz
-Inflammation (local dermatitis, radiation therapy)
-Edema and impaired lymphatic
Cause:
-Gram-positive organisms
-Group A step or Staphylococcus aureus
-IF animal bite- Pasteurella multocida
-IF human bite- Eikenella corrodens
Presentation:
-Spreading erythematous, non-fluctuant, tender, warm, plaque.
-Common in unilateral lower leg
-May have Fever and chills or lymphatic streaking
-Not usually scaly or with secondary changes
-May have leukocytosis
Key points:
-Cellulitis is rarely bilateral, and they usually have systemic symptoms
-Chronic course, "bound-down" appearance and dark pigmentation point to chronic disease or other etiology
-Stasis dermatitis is the most common mimic (but may have pigment changes, desquamation, non-pitting edema and is usually bilateral)
Treatment:
-recognize and treat early as it can lead to sepsis and death
-Use empiric abx then narrow after culture and sensitivity return "Cimex lectularius" (wingless, red-brown, insect)
-hides in cracks and crevices of beds, wooden furniture, floors, walls, etc.
-emerges at night to feed on humans
-infected saliva causes intense itching and welts
S/s:
-pruritic, urticarial-like papules on exposed areas (face, neck, arms, hands, trunk)
-Papules assume linear configuration of 3-4 bites (breakfast, lunch, dinner)
Treatment:
-Identify infected area and exterminate
-Bites will self resolve in 1-2 weeks
-Topical steroids/antihistamines for itch "Fifth's disease" caused by Parvovirus B19
-Transmits through respiratory droplets or from mother to fetus
-Incubation time until rash is usually 1-2 weeks
-Most infectious before the onset of the rash
-Tends to occur in outbreaks (school) in late winter/early spring
S/s:
-Prodrome: low-grade fever, malaise, HA, pruritus, coryza, myalgias, joint pain (more common in adult women)
-Exanthem: begins with bright red cheeks "slapped cheeks" and a facial rash that fades over 1-4 days. Symmetrick, erythematous reticular ("lacelike") eruptions appear on trunk and extremities
-Eruption usually lasts 5-9 days
Pregnancy:
-If infection occurs during pregnancy, this can cause hydrops fetalis, intrauterine growth retardation, and fetal death
Control measures:
-hand hygiene
-proper disposal of facial tissues
-avoid sharing eating utensils
Treatment:
-No vaccine
-symptomatic Majority of exanthems are non-specific and difficult to categorize
Prodrome:
-No indicative symptom complex
-Non-specific associated symptoms (fever, HA, myalgia, fatigue, respiratory, GI)
Exanthem:
-No unique lesion morphology or distribution
"generalized, nondescript, pink macules and papules"
Prognosis:
-Most resolve in 1 week without treatment
Causes:
-non-polio enteroviruses (summer months)
-Respiratory viruses (winter months) adenovirus, rhinovirus, parainfluenza, etc. "Rubeola"
-Spread by respiratory droplets
-Incubation period from 8-12 days
-Contagious 1-2 days before symptoms and 4 days after appearance of rash
-Immunocompromised pts can be contagious for duration
Risk factors:
-Un-vaccinated
-Family from places that don't vaccinate (Netherlands, Africa, Asia) with similar symptoms
S/s:
-Prodrome: fever, malaise, Cough, Conjunctivitis, Coryza
-Exanthem: erythematous macules and papules ("morbilliform") that begin on the face and spread cephalocaudally and centrifugally
-Enanthem: Koplik spots (bluish-white dots on mucosal surface) usually in prodromal
Diagnosis:
-Diagnose clinically
-Confirmed with serology (IgM and IgG with measles RNA) and reported to local health department
-Histology can show keratinocytic giant cells from skin lesions/respiratory secretions
Treatment:
-Rash improves within 3-4 days but lasts 6-7 days
-Uncomplicated infection lasts 10-12 days and is self-limiting
-Supportive care (antipyretics, fluids)
-Vitamin A may help
Complications: (immunocompromised, pregnant women, malnourished, extremes of ages)
-Otitis media, pneumonia, laryngotracheobronchitis (croup), encephalitis
-Pneumonia is the most common fatal complication of measles in children and most common complication overall Any drug is capable of cutaneous reaction
Risk factors:
-Polypharmacy, extremes of age, women, viral infection, genetics, systemic diseases
Types:
-Immunologic: IgE dependent. delayed-type/cell mediated
-Non-immunologic: Overdose, cumulative toxicity, metabolism alteration, underly skin exacerbation
-Idiosyncratic: unknown
Cause: antimicrobials, NSAIDs, anticonvulsants, analgesics
Diagnosis:
-History of rash + drug history
-Physical exam
-Lab studies/skin biopsy
S/s:
-Do not have scales usually
-Exanthematous: hypersensitivity
-Urticarial: serum sickness, anaphylaxis
-Vesiculobullous: SJS/TEN
-Pustula: acute generalized exanthematous pustulosis Chronic, inflammatory disease that is immune-mediated.
Affects skin, nails, and joints
-Bimodal pattern of incidence (childhood and adulthood)
Cause: (exact cause is unknown)
-Polygenic disease (combo of various genes and environmental triggers)
-Triggers: infection (strep), medications (prednisone, lithium, beta-blockers), tobacco, comorbidities (pregnancy, obesity), trauma
Types of psoriasis:
-Plaque
-Inverse
-Guttate
-Erythrodermic (90% of body is covered)
-Pustular
-Palmoplantar
S/s:
-Scale is loose and easily removed
-"Auspitz sign"=removal of scale reveals pinpoint bleeding
-"Koebner phenomenon"=lesions induced by trauma inflammatory condition of skin, mucous membranes, hair follicles, and nails where T-lymphs attack basal keratinocytes
Triggers: trauma, stress, viruses, contact allergens, meds (CCBs, NSAIDs, thiazides, BBs)
S/s: (5 P's)
-Papule
-Purple
-Planar (flat)
-Polygonal
-Pruritic
-Usually seen on wrists and flexural areas
-Usually bilateral and symmetric but can be widespread
-"Koebner phenomenon"= hallmark (lesions in areas of trauma)
-"Wickham's striae"
Diagnosis:
-Biopsy will confirm
-Consider offending medications
-Can be associated with Hep. C
-Mucosal LP increases risk for SCC
Treatment:
Topical:
-1st line: topical steroids
-Topical Calcineurin inhibitors (Pimecromlius or tacrolimus)
-Intranasal steroids
-IF oral, topical steroid gels, topical retinoids, cyclosporin rinse, viscous lidocaine...concomitant candidiasis common
Systemic agents:
-Corticosteroids for severe disease
-Retinoids
-Metronidazole or cyclosporin
-Methotrexate
-Hydroxychloroquine
-Antihistamines for itch
Others:
-Narrowband UVB or PUVA Mucocutaneous reaction characterized by skin tenderness and erythema that progresses to epidermal necrosis and detachment
- <10% is SJS
- >30% is TEN (life threatening)
Causes:
-Allopurinol
-Antibiotics (bactrim)
-Anti-convulsants (Lamictal)
-NSAIDs
-Rarely infections (Erythema multiforme only to SJS never to TEN) and immunizations
S/s:
-Prodrome: 1-3 days of URI symptoms that precede rash
-Lesions typically appear on trunk then spread to palms/soles, proximal extremities, and face
-Lesions appear like macular erythema and evolve into ill-defined, dusky (purple) patches with crinkled skin then to bullae and to erosions
-Sheet like loss of epidermis
-90% have mucosal lesions (in eyes can lead to blindness)
-Systemic symptoms: malaise, HA, N/V/D, cough, myalgia, chest pain, arthralgia, fever
- TRIAD: Mucous membrane erosions, target lesions, epidermal necrosis (targets are atypical with only 2 colors)
Treatment:
-Early diagnosis and discontinue causing agent
-Admission to ICU/burn unit
-Replacement of fluids (IV)
-Wound care
-Pain control
-Diagnose and treat comorbid infections
-Ophthalmology consult
-High dose steroids, IVIG, cyclosporin and plasmapheresis
Risk of mortality increases with:
-Increased age, hyperglycemia, tachycardia, elevated BUN, decreased HCO3, visceral involvement, malignancy, greater BSA involvement Up to 50% of hairs enter telogen (resting) phase
-Usually post-illness, injury, infection, surgery, crash diet, stress, giving birth, thyroid dz, IDA, drugs, etc.
S/s:
-loss of 30-50% of all hair
-Shedding lasts about 2-4 months
-Diffuse, uniform shedding (especially after showering/brushing hair)
-follicular ostia are intact and no scalp inflammation or scaling is present
Diagnosis:
-positive hair pull test with >10 telogen hairs pulled
Treatment: (self-limited)
-Reassurance
-Ensure healthy diet to promote hair growth
-IF drugs suspected, stop agent
-IF serum ferritin <40 ng/mL = iron supplement
-Biotin supplement
-Cosmetic (powder, extensions)
-Topical minoxidil Brittle: rough and dull (females 50+ and hypothyroid)
Onychoschizia: lamellar splitting of free edge of nail
Onychorrhexis: longitudinal grooves of nail plate lead to a distal split
Beau's lines: transverse grooves in nail from trauma, dermatitis paronychia, meds, viral infections, pemphigus, kawasaki
Longitudinal nail grooves: focal compression of nail matrix (tumor or trauma) makes a single longitudinal groove
Pitting: focal areas of abnormal keratinization of the nail matrix that make foci of parakeratotic cells. Psoriasis, alopecia areata, dermatitis
Trachyonychia: roughness, excessive longitudinal ridging, pitting, thickening of cuticle and distal brittleness. Normal in kids (idiopathic). Psoriasis, lichen planus, alopecia areata, atopic dermatitis. Usually arise in 40's and continue to arise throughout life
-Benign neoplasms fo epidermis with no melanocytes
-Cannot become skin cancer
-Strong genetic component
types:
1. stucco keratosis: whitish on lower ankles and dorsal feet
2. Dermatosis papulosa nigra: cheeks, temples. Darker skin types
S/s:
-sharply marginated, pigmented lesion
-Can be on any body surface besides palms/soles
-usually papular but may appear macular
-variable color (black, tan, flesh, pink, blue)
-Texture can be velvety to verrucous
-"stuck-on" like wax (barnacles)
-greasy or warty
-Pseudohorn cysts can be seen clinically or on dermoscopy
Diagnosis:
-try picking off/scratching lesion. It may crumble, flake, or lift off revealing superficial waxy character
-When in doubt, biopsy or refer
Treatment: (cosmetic)
-curettage, cryotherapy, electrodesiccation, shave removal Metastasis is rare (.028 to .1 %)
Risk factors:
-Fair skin/pigment disorders
-UV radiation exposure
-Organ transplant recipient (5-10x risk)
Types:
1. nodular (most common)
-pearly, pink papule with rolled border and telangiectasies
-usually on nose
-central erosion or crusting that progresses to ulceration "rodent ulcer"
2. superficial
-erythematous, scaly, eroded macule or patch
-pearly thread-like ridge at periphery
-common on trunk, extremities. Uncommon on face
3. morpheaform (+ pigmented BCC)
-scar-like appearance. Waxy, whitish, sclerotic plaques resistant to radiation and electrodesiccation
Diagnosis:
-Shave biopsy
Treatment:
-Mohs micrographic surgery: gold standard for BCC on head/neck and high risk areas
-excision, radiation, cryosurgery, curettage, electrosurgery
-PDT, 5FU, Imiquimod
-Vismodgeib (oral for metastatic BCC) Permanently dilated small blood vessels
-venules, capillaries, and arterioles
-form as arterioles (spider body ) become more prominent near the surface of the skin and radiate (spider legs)
Cause:
-Primary: idiopathic (more common in young adults and children)
-Secondary: Cirrhosis, sun damage, pregnancy, topical steroids, OCP, rosacea, scleroderma/SLE
S/s:
-commonly seen on face, neck, and upper trunk
Treatment:
-cosmetic only: pulse dye laser Velvety, brown, epidermal thickening (hyperkeratosis) of the skin and darkening (hyperpigmentation) that occurs in body folds
Classifications:
1. Hereditary Benign: no associations
2. Benign: associated with endocrine disorders but not CA
3. Pseudo: associated with obesity and can lead to insulin resistance
4. Drug-induced: nicotinic acid, stilbestrol, steroids, OCP, GH
5. Malignant: paraneoplastic with adenocarcinoma of GI to GU. Less common with lymphoma. More extensive lesions on mucosa, palms and soles
S/s:
-first appears as darkening and skin looks "dirty"
-Skin then thickens and can look velvety with accentuated skin line and appear mammillated (lots of bumps)
-Located usually on axillae, back, sides of neck, groin, knuckles, etc.
Evaluation:
-rule out DM
-rule out carcinoma (imaging/endoscopy)
Treatment:
-symptomatic
-nutritional counseling
-keratolytics (cosmetic) Natural sunburn:
-acute or delayed inflammatory response of normal skin after UVR exposure
-erythema, vesicles, bullae, edema, and tenderness
-pruritus is common
-Very severe sunburns can make a patient toxic
Photoxic (drug/chemical induced):
-Causes: antimicrobials (doxy), NSAIDs, Antipsychotics, cardiac drugs, diuretics, hypoglycemia meds
Phytophotodermatitis (PPD)
-Plant + light = dermatitis
-limes, celery, meadow grass
-Usually in spring/summer
-Phototoxic reaction is caused by photoactive psoralens in plants
S/s: lesions are often in artificial patterns
-Residual hyperpigmentation will resolve on their own or with topical steroids
Polymorphous light eruptions (most common photodermatosis) (chronic and recurrent)
-delayed hypersensitivity reaction to an auto-antigen induced by UVR (usually UVA)
-Occurs within hours of exposure and can last for 7-10 days
S/s: popular and papulovesicular lesions that are pink tor ed and spare habitually sun-exposed sites (face). Most frequent on forearms, and chest)
-Evaluate with skin biopsy and immunofluorescence and phototesting
-Mange with PUVA, sunblock, beta carotene, oral prednisone Raised wheals caused by the release of histamine and other vasoactive substances from mast cell
-allergic and non-allergic triggers
s/s:
-Wheals are superficial and well defined. Individual lesions last less than 24 hours
-Angioedema larger area that involves deeper layers (dermis and subcutaneous tissues and is ill-defined. Usually involves face or part of an extremity. More pain than itch, lasts longer than wheals)
-Can have wheals and angioedema together or individually
-sharply demarcated, erythematous, edematous papules and plaques often with a place center or halo
-Variety of sizes and shapes
-Common on trunk
-Pruritus is cardinal symptoms
Acute: <6 weeks (most cases) (children)
-large wheals and angioedema
-Usually IgE dependent (immediate)
-Caused by infection, food, drug, viral, or idiopathic
Chronic: > 6 weeks (adults)
-rarely IgE dependent
-most are idiopathic, may be autoimmune
Physical urticarias: cold, solar, cholinergic, aquagenic, pressure angioedema (24 hour delayed), vibratory angioedema, exercise-induced
Treatment:
-Allergy testing for acute type
-1st line: H1 blockers (cetirizine, loratadine/diphenhydramine, hydroxyzine)
-H2 blockers: Pepcid
-Singulair
-Prednisone
-Omalizumab (Xolair) 