Dermatology

*A patient calls you to complain. He is an 18 year old with acne vulgaris. You prescribed tetracycline 500 mg. BID. He calls you three weeks later and says his skin is "no better." Your next action is to:* A. Counsel him that 6-8 weeks of treatment is often needed before significant improvement is achieved. B. Discontinue the tetracycline and initiate minocyline therapy C. Advise him that antibiotics are likely not an effective treatment for him and should be discontinued D. Add a second antimicrobial agent

A. Antibiotics - for moderate, severe inflammation - take 6-8 weeks or often longer

Which of the following is indicated for the treatment of acne rosacea? A. Metronidazole gel C. Erythromycin 2% solution B. Clindamycin lotion D. Azelaic acid 20%

A.

Mrs. S. asks you why you are prescribing a topical corticosteroid cream for her. Your best answer would be: A. "It is a good anti-inflammatory agent" B. "It is the cheapest remedy" C. "It is a sound anti-inflammatory agent as well as an effective vasoconstrictor" D. "I don't know what else to do!"

C.

One of the most common sites for atopic dermatitis in the adult is: A. dorsum of the hand C. Neck B. Face D. Flexor surfaces

D.

Which of the following is the best treatment for cellulitis? A. Cephalexin C. Metronidazole B. Amoxicillin D. Trimethoprim-sulfa

D. COVERS MRSA!

Superficial infections

Most common infecting organisms are *s. pyogenes and s. aureus* Patients with co-morbids, more serious infections Always think MRSA and cover for it

Rocky Mountain Spotted Fever

www.cdc.gov/ncidod/dvrd/rmsf/Q&A.htm

Malignant Melanoma

*ABCD's (actually ABCDEF) signs for malignant melanoma* A = asymmetric with non-matching sides B=border irregularity C=color is not uniform: brown, black, red, white, blue, purple D=diameter >6mm at greatest dimension (pencil eraser) E = enlarging or evolving (new); elevated F=feel - never could feel before, but now raised *>2 features = 100 sensitive, 98% specific; then BIOPSY to confirm; need expert follow-up to appropriately stage DD: Actinic keratoses Basal Cell Carcinoma Squamous Cell Carcinoma Malignant Melanoma Dysplastic Nevi: just an abnormal mole Venous Lake - common lesion Small, ectatic (dilated) vein with a damaged vessel wall due to chronic sun exposure Leading cause of death from skin disease Increasing more rapidly than any other CA Risk Factors: FAMM syndrome/family hx Sun exposure Blonde or red hair Marked freckling upper back 3 or more blistering sunburns before age 20 Three or more summers spent outside working as a teen Actinic keratoses Peaks at age 40 *having one or 2 factors increases risk 3.5 fold *can take several years to mature into dangerous lesion or happen quickly* Worry about new moles vs old! Lesions usually raised with irregular borders and range in color from brown to dark blue (variable pigmentation) Sub-types of melanoma on Most melanomas present as essentially flat (macular) freckles Incisional biopsy key. Will not cause melanoma to metastasize. Lesions are often pruritic, tender/painful

Kaposi Sarcoma

*AIDS defining complication* Painless Violaceous papules 0.5 - 2 cm in diameter On face, extremities, mouth Bluish to black Biopsy for DX, but very apparent May involve lungs, oral cavity, digestive tract

*Cellulitis*

*Acute cellulitis is a spreading skin and subcutaneous tissue infection of deeper dermis and subcutaneous fat* Begins when pathogens find a portal of entry through non-intact skin Initially see spreading erythema, induration, warmth, pain, fevers, chills, malaise; bullae, abscesses, erosions, necrosis Regional lymph nodes may be enlarged and tender (lymphadenitis) Involved area enlarges steadily *Lower extremity is most common site* Purulent or serous drainage at inoculation site. *NOT sharply demarcated margin* or elevation (as with erypsipelas) Edema may manifest as dimpling of overlying skin (peau d' orange) Skin may become necrotic-important to treat! *S. Pyogenes number 1 then S. aureus and H. Influenza* (usually GM + organisms - you will see GM - in immunocompromised clients) Think of co-morbids that can make situation worse (DM, PVD, immunosuppression) *Culture drainage to isolate pathogen (if after first treatment still not successful)* Diagnostics: If severe, CBC with diff, creatinine, bicarbonate, creatinine phosphokinase, blood cultures DD: Bursitis, osteomyelitis, erythema migrans, herpes zoster, contact dermatitis, urticaria, DVT Treatment: same as furnuncles, think MRSA (PCN, amoxicillin, amox-clav, dicloxacillin, cephalexin, clindamycin (C. diff) x5 days) Should see improvement in 3-4 days; follow-up in 48 hours Report worsening s/s Non-pharmacologic- postural drainage, compression, manage underlying disease Hospitalization? *Immunosuppressed patients (HIV, chemo, transplant) Refractory to oral antibiotics Hemodynamic alteration (T>38, HR >90, RR>24, WBC >12)* Extensive cellulitis Diabetes mellitus co-morbidity Diminished arterial pulse in cool, pale infected extremity Cutaneous necrosis Closed space infection of hand Periorbital (exophthalmos, restricted EOMs) Newer abx on market against MRSA worth looking at: Ceftaroline- cephalosporin, gram + and -, IV Dalbavancin- lipoglycopeptide, gram +, IV Tedizolid- oxazolidinone, PO and IV Oritavancin- lipoglycopeptide, IV

*Impetigo*

*Acute, contagious infection of skin caused by S. aureus (main cause) or S. pyogenes* Follows superficial trauma or secondary to scabies, herpes simplex, fungus or insect bites Nonbullous- Begins with pruritic, focal, superficial eruption of small 1-2 mm vesicles. Often on face, near nares, chin or lower extremities. Vesicles to pustules to crusted (*golden honey*) Bullous impetigo- more common in children; bulla contains clear, yellow fluid that turns cloudy, dark yellow. Rupture within 1-3 days, leave rim of scale around red, moist base, followed by brown-lacquered skin appearance Regional lymphadenopathy Disease usually self limiting, but persistence may lead to changes in pigmentation and scarring Treatment: *Mupirocin (Bactroban)* if few lesions present For multiple lesions: Dicloxacillin Cephalexin (Keflex) Cefadroxil If PCN allergy or MRSA: TMP-SMX, doxy, and clindamycin Daily soaking of lesions Improve hygiene with frequent skin cleansing If chronic - nasal culture - staph strep carrier? DD: Tinea Herpes Burns Contact dermatitis *Know difference between impetigo and bullous impetigo*

Molluscum Contagiosum

*Common in HIV patients* & children Caused by pox virus White 1-4 mm papules on neck, trunk, genitals, eyelids KOH prep to diagnose *Contagious through touching* Around eyes, nose, mouth, flesh toned, umbilicated center ("intertube" in center) Often flesh colored

Carbuncles

*Folliculitis deep in dermis* - drains through multiple openings and is usually systemic. *Several adjacent furuncles coalesce, inflammatory mass, pus drains from multiple follicles* *Most commonly caused by S. aureus* Common in diabetics S/s of systemic involvement - chills/fever Occurs in areas of dermal thickening - back of neck, lateral thigh Treat as you would furuncles (I&D)

*Key concepts: Secondary Lesions*

*Lesions altered by outside manipulation, treatment, natural course of disease* Know terms Any Size •Excoriation: Superficial linear abrasion of epidermis. Visible signs of itching caused by rubbing or scratching (contact dermatitis-nickel allergy) •Crust: •Lichenification: Epidermal thickening resulting in elevated plaque with accentuated skin markings. Usually results from repeated injury through rubbing or scratching (Callus; antecubital fossa chronic atopic dermatitis or eczema) •Scales: Dried fragments of sloughed epidermal cells, irregular in shape and size and white, tan, yellow, or silver in color, flake with ease (dandruff, dry skin, or psoriasis) >1cm •Erosion: A moist, demarcated, depresses area due to loss of partial or full-thickness epidermis. Basal layer of epidermis remains intact (ruptured chickenpox vesicle or open bulla) •Ulcer: Irregularly shaped, exudative, depressed lesion in which entire epidermis and all or part of dermis are lost. Results from trauma and tissue destruction (pressure ulcer, arterial ulcer, syphilitic chancre). •Fissure: Deep linear split through epidermis into dermis (tinea pedis or Athlete's foot)

Squamous Cell Carcinoma

*May metastasize* - 66% of all squamous cell cancers used to be keratosis that didn't get treated *Lesion may be new or arise from an actinic keratosis* Firm to hard *erythematous to brawny nodule* often with central hyperkeratotic scale ulceration Sun exposed areas *Biopsy/excision to confirm diagnosis!* Squamous cell - early lesions - "NO SUN" N=nodular O=opaque S=sun exposed areas U=ulcerating N=non-distinct borders

Burns

*Minor burns include primary and secondary covering <15% of total body surface (adults 10-50 years)* Types of burns (wet heat, flames, chemical, electricity, radiation) 1st degree (superficial)- only epidermis, no skin loss; red area 2nd degree (partial-thickness)- involves upper layers of epidermis; weeping and blistering, severely painful 3rd degree (full-thickness)- entire thickness of skin; absent sensation; white or charred Take good hx Exam - area/depth of burn consider abuse/neglect ***Referral to burn center *if respiratory injury; burns of hands, feet, genitals, or perianal area; full-thickness >2% of TBSA; minor burns >10% TBSA >50 years; burns >15% TBSA in patients 10-50 years* PE: ABCs, associated injuries; depth, extent and location of burn Diagnostics: Simple burn do not require; more serious CBC, glucose, electrolytes, BUN, creatinine, UA, CXR if inhalation injury DD: staphylococcal scalded skin syndrome, toxic epidermal necrolysis Treatment: 1st degree - cleanse with mild detergent and cool tap water/topical anesthetic 2nd degree - cleanse with mild detergent and cool tap water/leave blisters intact/bacitracin ointment Silvadene cream if larger area-contraindicated in sulfa allergy May need non-adherent second covering or leave open NSAIDs for pain- Ibuprofen, naproxen Tetanus Increase fluids Educate on s/s of infection Reevaluate in 24-48 hours then q week *If anything except a minor burn: REFER TO BURN CENTER/CLINIC* pg. 319 *Sunscreen at 6 months! If <6 months keep out of sun!*

*General Definitions related to skin : primary lesions*

*Result from a disease process* <1 cm Macule - flat discoloration, nonpalpable freckles Papule - solid elevation, wart or elevated nevus Vesicle - fluid filled (clear), blister, chickenpox, herpes simplex Pustule - vesicle like lesion with purulent content, impetigo >1cm Bulla - fluid filled, partial-thickness (2nd degree) burn Erosion - loss of epidermis, ruptured chickenpox vesicle Ulcer - loss of epidermis and dermis, pressure ulcer Patch - flat, non-palpable area of skin discoloration, larger than macule, vitiligo Plaque - raised lesion same or different color from surrounding skin, coalescence of papules, psoriasis vulgaris Any size Wheal - circumcised area of skin edema, mosquito bite or urticaria, serpentine pattern Purpura - flat red-purple discoloration caused by RBCs lodged in the skin, DOES NOT BLANCH WITH PRESSURE Cyst - raised encapsulated fluid filled lesion; intradermal cyst; type of fluid depends on location!; non-malignant and non-transformative *Dermatographism- phenomenon that occurs when the skin of a person with urticaria is lightly rubbed with a pointed object (fingernail) and histamine is released under the skin surface and the skin becomes raised and red where the object touched it

The NP suspects a diagnosis of shingles. She/he performs a ______ test to confirm diagnosis: a. Tzanck c. KOH b. Mineral oil prep test d. Patch test

A. Tzanck Smear

Alopecia

Abnormal hair loss Patho: Two types- scarring (cicatricial alopecia) and nonscarring (noncicatricial alopecia) Cycle of hair growth: anagen (growth), catagen (hair involutes), telogen (mature hair is shed) Anagen phase disturbances-androgenic alopecia, anagen effluvum (chemotherapy), alopecia areata Telogen phase disturbances- telogen effluvium due to fever, meds, endocrine abnormalities, childbirth, malnutrition Non-scarring -*Hair follicles are still present, no sign of inflamed tissue, scarring, or atrophy* -Characteristic of pattern hair loss (*androgenetic alopecia*), thyroid disease, lupus, drug induced hair loss, tinea capitus; *Alopecia areata* - immunologically mediated hair loss - 1-2 *coin shaped areas*, in beard area, recurrent; Autoimmune conditions Scarring Result of *intense inflammatory process of scalp* with skin atrophy and scarring Common in African American women Potential causes: lichen planus, chronic cutaneous discoid lupus, sarcoidosis Dermatologist referral Diagnostics: KOH preparation (tinea capitus), TSH (hypothyroidism), CBC (anemia), testosterone level, VDRL test (syphilis), scalp biopsy DD: atopic dermatitis, pregnancy, stress, scleroderma Management: Androgenic alopecia- finasteride (Propecia), minoxidil (Rogaine- *women can use!*), hair transplants Alopecia areata- resolve spontaneously or non-FDA approved therapy (UVB light, cyclosporine, topical corticosteroids, topical immunotherapy)

Screening for Skin Cancer

According to USPSTF, evidence is insufficient to recommend for or against routine screening for early detection of skin cancer by a total-body skin examination (TBSE) during a routine office visit ACS recommends skin cancer screening every 3 years for people 20-40 and annually if >40 BCC most common, but MM is most fatal 90% of all skin cancers are caused by the sun Patho: Ultraviolet radiation produces DNA damage, gene mutations, immunosuppression, oxidative stress, and inflammatory responses Clinical Presentation: Warning signs include 1) open sore that does not heal for 3 weeks 2) spot or sore that burns, itches, stings, crusts, or bleeds 3) any mole or spot that changes in size or texture, develops irregular borders, or appears pearly, translucent, or multicolored PE: Complete and thorough TBSE In darker skinned patients, abnormal lesions of nails, hands, or feet should be evaluated as these are common sites for melanomas! Diagnostics: Skin biopsy- shave or punch for nonmelanomatous skin cancers (NMSC), excisional biopsy for MM lesions DD: Seborrheic keratosis, actinic keratosis, BCC, SCC, or MM Management: BCC electrodessication and curettage or total excision If NMSC or MM recognized early, surgical cure is almost 100%!

Paronychial Infections

Acute or chronic inflammation of the tissues surrounding the nail, usually with underlying bacterial or fungal infection Patho: Infection from trauma, water or chemicals; follows nail margin or penetrates under nail If >6 weeks, chronic Antiretrovirals and chemotherapeutics may cause S/S: Localized to one finger, throbbing pain of nail fold, nail, and adjacent portions of finger May see onycholysis, discoloration, distortion, and ridging Diagnostics: KOH, Culture DD: herpetic whitlow, onychomychosis Management: ER REFERRAL IF PARONYCHIAL INFECTION OF TENDON SHEATH Acute- warm water/compresses 4x daily, topical antibiotic, neomycin if pseudomonal, oral abx (trimethoprim-sulfamethoxazole if MRSA), I&D Chronic- topical steroids (bethamethasone), if non-responsive then PO antifungal, corticosteroid, or I&D

Wound Management

Acute wounds-lacerations, abrasions, avulsions, crush injuries, puncture wounds, insect or mammalian bites, surgical wounds, burns, skin tears Chronic wounds-pressure ulcers, venous and arterial ulcers, diabetic foot ulcers, non-healing surgical or traumatic wounds Patho: Wound healing begins at time of injury and proceeds for several months through stages of inflammation, proliferation, and remodeling Anemia and pressure on site delay S/S: Healing wounds are pink to red, robust, and bumpy (granulation tissue), with pink healing edges Diagnostics: X-ray, MRI, CBC with diff, hemoglobin A1c, albumin, wound culture, biopsy DD: Venous and arterial ulcers, thermal wounds, Management: Documentation Normal saline 0.9% irrigating and cleansing product of choice Dakin solution <0.5% Silver sulfadiazine if infected for 14-21 days Debridement-surgical, mechanical, autolytic, biologic (larval) Dressings-algorithm Acute wounds- smooth edges can use adhesive, steri-strips, staples; abrasions, avulsions, crush injuries, bites, puncture wounds NOT CLOSED; Tetanus immunization if last dose >5 years ago; Skin tears- flap should NOT be removed unless necrotic Chronic wounds- remove pressure, leg elevation, compression, improve perfusion, blood glucose control, negative pressure wound therapy

Tinea Ungurium (Onychomycosis)

Any infection of nails caused by dermatophyte, yeast, or mold Most frequently occurs in toenails (great toe is first) Common 30% of all mycotic infections of skin nails Patho: Trichophyton rubrum/interdigitale; candida orgs are rarer, infection is located INSIDE the nail S/S: White discoloration, crumbly debris subungually, thickening of nails, pain Usually asymptomatic Diagnostics: KOH and culture DD: Psoriasis, leukonychia, eczema, subungal malignant melanoma (dark stripe) To treat or not to treat? Treatment difficult (greater risk for DM patients), most effectively treated systemically Ciclopirox nail lacquer (<50% cure rate) *Itraconazole or Terbinafine (oral lamisil)* - hepatotoxicity potential so monitor ALT/AST monthly after baseline 3 month course of meds Evaluate 3 mo after therapy Beau's lines-ridges Paronychia- infection along ridge of nail where meets skin Others: Fluconazole (Diflucan) 150mg weekly x4

Atopic Dermatitis (eczema)

Any type of eczema or red scaly rash associated with strong family hx of asthma and allergic rhinitis Pruritic inflammatory skin disorder characterized by exacerbations and remissions of dry, itchy red skin Associated with atopic diseases (*triad is allergic rhinitis, asthma, and eczema*) Diagnosis: presence of itching/scratching plus 3 or > of the following: 1) red/inflamed rash, 2) presence of excessive dryness/scaling, 3) location in skin folds of arms/legs DD: Seborrheic dermatitis, psoriasis, scabies, molluscum contagiosum, tinea, allergic dermatitis Treatment: avoid offending agents, minimize skin dryness, consistent use of lubricants. Acute disease (exacerbation) - antihistamines and/or topical and systemic corticosteroids to control flares. With acute flares, intermediate-potency topical corticosteroid usually needed. (once control achieved, switch to lowest potency) Tacrolimus - immunomodulator (inhibits mast cell activation) - non-steroidal or Elidel is similar atarax zyrtec-stop itching to prevent secondary bacterial infection!

Tinea Pedis

Athlete's foot Cracks in feet/between toes good medium for s. pyogenes (secondary infection). KOH Prep dx. Responds well to clotrimazole cream 1% Treatment: Antifungal topical agents: most common clotrimazole 1% Lamisil (OTC) Spectazole Loprox Nizoral Oxistat Mentax Keep feet dry, wear white socks

Muprocin's spectrum of antimicrobial activity includes: A. Primarily gram-negative organisms B. Select Staphylococcus and Streptococcus species C. Pseudomonas species and anaerobic organisms D. Only organisms that don't produce beta-lactamase

B.

Lori, a new NP wants to order corticosteroid cream for Lexie, a 25 year old patient who has atopic dermatitis on both her hands. Lori knows that if she orders ____ gram/grams of the cream, it is an adequate amount for coverage: A. One gram C. Three grams B. Two grams D. Thirty grams

B. Two grams Two grams covers hands, head face or anogenitals 3g covers anterior or post trunk or an arm 4g covers a single lower extremity 30g - 60 g entire skin surface

Pityriasis Rosea (also spelled pitoriasis rosea)

Benign and common rash; most asymptomatic 10-35 years *Viral* in origin *Herald patch* (also called primary plaque or mother patch)- Christmas tree distribution Self limiting - 3- 4 months (some periodicals note rash disappears in 1-2 months)

You write a prescription for a topical agent and anticipate the greatest rate of absorption when it is applied to the: A. Palms of the hands C. Face B. Soles of the feet D. Abdomen

C. Face Face = greatest rate of absorption Axilla, genitals also (diaper area in babies)

Candidiasis

Candida albicans is a yeast found on mucous membranes, in GI tract, in vagina, and on skin Predisposing factors: obesity, antibiotics, malnutrition, immunosuppressed conditions, ELDERLY S/S: depends on location Mouth-"thrush," white or gray plaques adherent to buccal mucosa Skin-axillary, gluteal, interdigital, perianal, panniculus folds, shaved areas, genitals; pink or red moist patches bordered by think scale Nail-rounding and lifting of nail, thickened, discolored Diagnostics: KOH prep, skin culture or biopsy DD: depend on affected area; Oral- aphthous ulcers; Female genitals- BV, Trich; Male genitals- tinea, psoriasis; Intertriginous areas- miliaria, tinea cruris, scabies Management: Topical therapy, oral fluconazole if widespread Simple talc powder BID if active infection to prevent recurrence Aluminum sulfate (Domeboro) solution OTC to dry skin AVOID CORNSTARCH-encourages fungal growth Yogurt or probiotics help prevent vaginal or oral yeast infections Complications: Candidal esophagitis if severely immunocompromised like AIDS

*Dermatophyte Infections*

Caused by fungi that penetrate hair, nails and stratum corneum of skin Common dermatophytes are Trichophyton, Microsporum, and Epidermophyton Patho: Acquired through inhalation of endemic fungi in the environment, soil is natural reservoir Pruritis and stinging Transmission direct/indirect Tinea capitis-head Tinea faciei-face Tinea corporis-body Tinea cruris-jock itch Tinea pedis-feet Tinea manum-hands Tinea unguium-nail Diagnosis: KOH microscopy, fungal cultures, wood lamp for tinea capitus DD: Psoriasis, urticaria, pityriasis rosea Management: Acute, exudative lesions- aluminum sulfate (Domeboro) soaks, topical antifungals, keratolytic agents Topicals include: terbinafine, naftifine, butenafine, clotrimazole, econazole, ketoconazole (NOT ORAL), miconazole OTC *Products continued for 1 week after clearing to discourage recurrence* Systemic antifungals if widespread infection involving nails or scalp (griseofulvin treats tinea capitus)-REFER

Scabies

Caused by the infestation with Sarcoptes scabiei mite; close personal contact is needed for infestation (nursing homes, prisons, dar care centers) Patho: Female mite, oval, four pairs of legs burrows into stratum corneum and lays 2-3 eggs per day for 1-2 months Intense pruritus is hypersensitivity reaction S/S: LOOK FOR PLACES ON BODY THAT ARE WARM! Delayed reaction - 10 days to 2 weeks *Causes intractable pruritus which is worse at night* Thread-like linear lesions seen most often hands, wrists, soles, waist, penis, nipples, axillae, and gluteal cleft Macular/papular rash Diagnosis: Clinical findings Classic burrow, straight or S-shaped ridge 2-10 mm long *Scrape burrow end (black dot) with blade and put on slide with mineral oil.* DD: Insect bites, chickenpox, drug reactions Management DO NOT USE KWELL ANYMORE-NEUROLOGIC DAMAGE! 5% Permethrin (Elimite cream, 30 g per single application, 60 g tube) Apply neck down, leave on overnight (8-12 hours), shower Repeat in 1-2 weeks Treat pt and family Wash all linen, clothes and stuffed animals in hot water. May put stuffed animals in air-tight plastic bags for 2 weeks

Diabetic foot ulcers

Cellulitis without ulcer - think streptococci - groups A, B, C, D or s. aureus Infected ulcer (uncomplicated, macerated, chronic) Gangrenous foot Send to wound clinic and/or home care with wound care programs. Increased risk of amputation http://emedicine.medscape.com/article/460282-overview Causes: Arterial insufficiency - poor wound healing, decreased neutrophil delivery Hyperglycemia - impaired neutrophil function, poor wound healing Always culture to identify causative organisms after the clinical diagnosis of infection is made

Lichen Planus

Chronic inflammatory cutaneous and mucous membrane reaction pattern Unknown etiology Middle aged adults (30-70 years) Genetic? 6p's (pruritic, planar, polyangular, purple, papules, plaques) Wickham's striae Lesions (lace like) on tongue, lips, buccal mucosa Differential: drug eruption, psoriasis, aphthous stomatitis, leukoplakia, thrush Treatment: Triamcinolone cream (orabase for mouth)

*Acne Rosacea ("rosacea")*

Chronic inflammatory disorder of central portion of face; vascular dilation Erythema, papules, pustules, telangiectases and tissue hyperplasia (primary features - diagnosis made if patient exhibits one or more of the above) Unknown etiology Progressive No cure avoid the sun Fair skinned whites with light eyes; begins to develop at 20-30, *common ages 30-50 RARE in adolescents* Predominant theories: Inflammatory response Vascular disorder of cutaneous nature Bacteria - H Pylori Follicle - mites Genetics *Does not cause comedones* (good for differential dx with acne vulgaris) *Rhinophyma - bulbous nose enlargement* Caused by hyperplasia of sebaceous glands-inflammatory papules and pustules Prerosacea - sudden transient recurrence of reddening of the face (flushing, facial erythema) Can involve eyes - dry eye syndrome common problem (watery or irritated) Telangiectasia, edema Triggers: sun, dry skin, oily skin products, use ph neutral skin products Treatment: NO CURE, manage S/S and improve QOL Topical treatment - metronidazole 0.75% aqueous gel, lotion, or cream (metro gel) BID for 3-4 months or azalaic acid 15%; clindamycin or erythromycin can be used also. NO TOPICAL STEROIDS Systemic management with ocular symptoms, moderate papules or burning/stinging Tetracycline 500 mg BID (moderate - severe s/s) Doxycycline Erythromycin *reduce dose at 1-2 months if positive response. D/C drug at 3 mo and switch to topical therapy* Second line therapy - TMP/SMX (bactrim); Metronidazole and isotretinoin or Retin-A Complications: Ocular rosacea-refer to ophthalmologist

Ulcers with Secondary Infection

Chronic venous insufficiency PVD ulcers = toes Pressure sores = heels, coccyx Neuro disorder ulcers = bony prominences Culture wound

Tinea Corporis

Classic lesions are ring like (annular) plaques that show a delicate scale at the advancing margin. Passed from dogs and cats to humans Differentials: atopic dermatitis, psoriasis, skin cancer, pediculosis, impetigo, pityriasis rosea, contact derm, etc. Many. Diagnosis: KOH test Topical imidazole antifungals (clotrimazole treatment of choice 2% cream BID for a week then QD for a week), cover lesion when children go to school Reserve systemic treatment for pts with great number of lesions or unresponsive to topical treatment. If it's on the head must use griseofulvin

Seborrheic Dermatitis

Common - 3-5% of population, chronic, across life-span Characterized by greasy, slightly erythematous scaling in areas with high concentration of sweat glands or sebaceous glands (scalp, face, postauricular, intertriginous areas) Onset early adulthood Remissions and exacerbations More common in AIDS pts; Parkinsons pts. Patho: Cause unknown...yeast? S/S: Cradle cap in infants-yellow or brown scaling lesions Adolescents and adults see dry, flaky scales on scalp-dandruff Face and auricular see greasy, erythematous, sharply marginated plaques Pruritis Daignostics: KOH wet prep, ANA, skin biopdy DD: Eczema, psoriasis, impetigo, tinea versicolor, OE, SLE Treatment NO CURE -"Top-down" disorder -Decrease skin hyperproliferation, decrease inflammation, decrease yeast -First-line therapy is topical antifungals or corticosteroids -Tars, hydrocortisone, ketoconazole (2% shampoo 3 days a week then go down to once a week once under control) and sometimes add fluorinated corticosteroid (Lidex), Selsun blue shampoo often effective -Facial - hydrocortisone cream; ketoconazole

Hyperhidrosis

Condition of excessive sweating marked by abnormal wetness, sweaty palms, excessive axillary sweating, gustatory-stimulated sweating, wet shoes, and offensive body odor Patho: Cooling perspiration is under hypothalamic control whereas emotional perspiration is under cerebral control Most common cause of generalized increased sweating is a decline in ovarian function, such as menopause Meds, ETOH abuse, Parkinson's disease S/S: Primary disease is excessive sweating unrelated to ambient heat or humidity of palms, soles, and axillae PE: H&P, miliaria rubra Diagnosis: TSH, T4, BG, FSH & LH DD: hyperthyroidism, TB, DM, pheochromocytoma Management: 20% aluminum chloride hexahydrate provides chemodenervation of eccrine sweat glands apply q2-3 days (6.25% if sensitive skin) Refer to derm if refractory

Surgical Office Procedures

Cryosurgery Application of cold, such as liquid nitrogen, to produce therapeutic tissue necrosis Freeze should spread laterally 2-3mm from edge of lesion Indicated in the treatment of skin tags, warts, and seborrheic keratosis/actinic keratosis, molluscum contagiosum AVOID topical antibiotics post-care due to contact dermatitis Contraindications are cold intolerance, cold urticaria, and cryoglobulinemia, Raynaud disease fingers, African American SE: bullae, scarring Electrocautery Delivery of direct current through heated metal wire to cause local tissue destruction or hemostasis Treat acrochorda (skin tags), AK, small angiomata, compound nevi, warts, seborrheic keratoses, VASCULAR LESIONS, nodular basal cell, invasive squamous cell NO contraindications, pacemaker and ICD okay! Good alternative for AA patients Curettage Scraping instrument, curet, to remove soft and superficial skin lesions Treats seborrheic keratoses, some warts, and molluscum, some skin CAs Biopsy Appropriate when nature of lesion or dermatitis is in question -Punch biopsy when knowledge of depth of lesion is required or when lesion is small and can be completely removed Referral for large lesions Suture removal 3-5 days face/neck; 7 days scalp, chest, abdomen, arms; 10-14 days legs and feet -Shave biopsy if full-thickness specimen not required nonmelanocytic lesions -Scissor excision on pedunculated lesions such as skin tags *If removal can't be accomplished with a punch biopsy, an elliptical excision of entire lesion with 1-3mm border is recommended*

What topical medication has the maximum absorption? A. Gels C. Creams B. Lotions D. Ointments

D. Ointments Then creams then gel/lotions last

Furuncles (purulent skin infections)

Deeper *infection of follicles* or cutaneous glands extends *deep into dermis* where abscess forms. *S. aureus (always worry about MRSA)* Pustular Boils/abscesses are large furuncles Painful or tender to palpation Appear as red with central pustule with erythematous margins Hairy areas/high friction areas - axilla, groin, forearm, waist DD: bursitis, inflamed epidermoid cyst, tophaceous gout Treatment - Oral doxycycline, sulfa or clindamycin (cover MRSA) -*If MSSA cephalexin or dicloxacillin* Warm, moist heat 4X/day 30 min to soften area and heal faster-may drain spontaneously Lesions over 1cm - I/D (pfenninger book) Usually systemic infection but can initially try: Mupirocin (Bactroban) ointment Bacitracin Gentamycin ointment If wide spread or high risk sulfa, doxycycline or clindamycin Control bacterial contamination of skin and hand washing Test for DM, immunosuppression, chronic disease in appropriate pts. Quickly ID patients at risk for bacteremia *If you I & D them, often no further treatment is needed even if MRSA!!!*

Skin Examination Technique

Diascopy: flat microscope slide or magnifying glass to blanch; blanching of blue to red lesion followed by refilling indicated blood in capillaries; absence of blanching indicated blood leaching outside of capillaries (petechiae) Gram stain: distinguish gram-positive and gram-negative Tzanck test: uncover multinucleated giant cells typical of herpes simplex or varicella-zoster virus; top of vesicle must be removed to obtain fresh fluid from base of lesion 10-30% potassium hydroxide (KOH) stain determines presence of hyphae and spores consistent with candidiasis or spaghetti and meatball appearance of tinea versicolor caused by skin fungus (dermatophyte) Malassezia furfurr/ovalis; obtain scrapings from top of lesion or advancing edge Culture for herpesvirus, Streptococcus, Staphylococcus, or Pseudomonas organisms requires removal of outer crust or cuticle of lesion to obtain fluid Scabies preparation requires superficial skin shaving from top of burrow examined under oil immersion, will be adult mites, eggs, or feces Patch tests - contact dermatitis *Realistically in primary care, we usually dx by appearance and refer if no improvement after 1-2 rounds of treatment*

Hidradenitis Suppurativa (Acne inversa)

Disease of apocrine glands Primary lesion is infundibular hyperkeratosis of sebaceous gland follicles with secondary infection of apocrine glands Characterized by recurrent abscesses , draining sinus tracts, and comedones Patho: Exact cause is unknown Theories of keratin plugging and primary failure of apocrine glands to drain Most common bacteria are S. aureus, Staph epidermis, Staph hominis S/S: Hallmarks are single or multiple areas of swelling, pain, and erythema accompanied by acute abscess formation May progress to chronic state of pain, sepsis, sinus tract and fistula formation, purulent discharge and keloids Unrelenting Found beneath breast, axillary, suprapubic, groin, and anogenital regions Predisposing factors: obesity, cellulitis of scalp, smoking, hirsutism, history of acne, use of lithium, and hyperandrogenism PE: Palpate lesions, Hurley stages used to classify disease (3 stages) Diagnostics: Clinical observation, C&S of lesions with discharge, skin biopsy stubborn cases DD: furuncle, carbuncle, lymphadenitis, bacterial folliculitis, inclusion cyst, cat-scratch disease, SCC, regional enteritis Management: Steroids, antibiotics (erythromycin, tetracycline, or minocycline), traditional surgery, CO2 laser surgery, monoclonal antibody therapy, isotretinoin; I&D Refer to derm if lesions recurrent after I&D or no response to oral therapy Many cases disappear after patients reach 35

Dyshidrosis

Disruption of skin on palms and soles Stress? Pruritis Vesicles on palms, sides of fingers and soles Vesicles to scaling to redness to lichenification DD: Contact dermatitis Tinea Atopic dermatitis Psoriasis Treatment: Topical corticosteroids and oral antibiotics (erythromycin) Cold, wet compresses LacHydrin

*Stasis Dermatitis*

Eczematous eruption, inflammation, or chronic dermatitis of lower extremities, result of CHRONIC VENOUS INSUFFICIENCY Recurrent swelling causes pruritus, excoriation, hyperpigmentation, papules, scaling, crust with predilection to medial ankle 30% cases lead to ulceration >50, female DVT, pregnancy, OCP, obesity, smoking, immobility Patho: Results from ambulatory venous hypertension, caused by abnormality of venous system resulting in reflux of blood S/S: *Hallmark sign is bronzing (hemosiderin staining)*, may be unilateral or bilateral, edema, varicose veins, cyanotic skin when in dependent position Diagnostics: Doppler ultrasound, D-dimer, wound culture DD: sickle cell anemia, cellulitis, tinea pedis Management: *Compression therapy is GOLD STANDARD*, elevate extremities above level of heart several times a day, topical emollients (petrolatum), mild soaps, midpotency topical corticosteroid; wound care, home exercise, good nutrition

Poison Ivy/Oak

Eruption 6- 72 hours after exposure Take detailed hx to recognize irritants/allergens -Washing the skin with soap inactivates and removes the oleoresin (causative agent): 50% effective after 10 minutes; 10% after 30 minutes; ineffective after 60 minutes Treatment: med-high potency *corticosteroids* with emollients triamcinolone; *If 20% or > TBSA, severe rash, face, genitals, hands, or occupation then treat with systemic corticosteroid* Cool compresses, calamine lotion, oatmeal baths, PO antihistamines Face/hands/genitals or more acute reactions - Prednisone - larger than usual dose pack - 60 mg for 4 days; 50 mg. for 2 days, 40 mg for 2 days, 30 mg for 2 days, 20 mg for 2 days then 10 mg for 2 days

Dermatitis Medicamentosa (drug eruption)

Eruption of the skin or mucous membranes that can occur within 1 hour and up to 2 weeks after drug administration Maculopapular exanthema is most commonly induced Patho: Hypersensitivity manifestations of IgE or T-cell-mediated Nonimmunologic responses may be caused by cumulative accumulation of a drug, pharmacologic action of a drug, genetics, drug sensitization S/S: itching, burning, pain without rash; maculopapular or urticarial Diagnostics: CBC reveal eosinophilia, skin testing (PCN), serum tryptase DD: urticaria, purpura, bullous impetigo, scarlet fever, acne vulgaris Management: Identify offending agent and REMOVE; symptomatic treatment, hydration; cool compresses and tepid baths; oral antihistamines; oral corticosteroids if refractory

Actinic Keratosis

Focal areas of epidermal dysplasia *Can lead to squamous cell (1/100) that's why we treat this condition* Slightly rough pink or flesh colored lesion in sun-exposed area Sun induced Erythematous Scaly macules Ill defined border Diagnosis: Clinical, biopsy usually not required Treat with: Topical 5FU cream; cryotherapy (liquid nitrogen)

Herpes Simplex Virus- Cutaneous Herpes

HSV type I or II I= labialis (lip), oral II = genitalis *Either virus can cause infection at either site* Clinically, lesions are indistinguishable! Common in asymptomatic individuals-can still shed virus Blistering of skin = active infection Virus remains dormant in root nerve ganglia Lesions can recur at any time Transmission = direct contact with active lesions or with secretions containing the virus Acute herpetic gingivostomatitis - primary infection of oral cavity. Lesions heal in 1-2 weeks. Three distinct phases: primary, latent, and recurrent First occurrence usually most severe Prodrome of burning or tenderness multiple painful round vesicles then appear with tender lymphadenopathy, fever, dysuria, vaginal discharge, malaise, heal within 2-3 weeks Latent-dormant Recurrent-virus reactivation in dermatome but may not be exact same site; HSV-1 triggers are UV light, cold weather, hot food, lip biting, food allergy, fever; HSV-2 triggers are food allergy and menses If in doubt, what test do you perform? *Viral culture!* Quest has a HSV I & II antibody test, but expensive DD: Varicella, herpangina, aphthous stomatitis, impetigo, urethritis, atopic dermatitis Management: *Acyclovir* 400mg TID for 7-10 days Treat ALL patients Infection is lifelong, there is NO CURE Condom use! C-section if active herpes lesions at time of delivery Difference between canker sores and HSV? Canker sores have an unknown etiology but thought to be brought on by stress/immunosuppression, common in IBS/crohns etc. HSV II (genital herpes) covered in women's health Canker sores on inside, HSV on outside

Purpura

Hemorrhaging into the skin *Petechiae are lesions <3mm in diameter, indicate capillary bleeding* *Lesions 2mm-1cm are purpura* *Lesions >1cm are ecchymoses (meningococcal meningitis-blueberry muffin rash)* 2 groups: inflammatory (palpable) and non-inflammatory Patho: Characterized by extravasation of RBCs into dermis from small cutaneous vessels Palpable purpura- raised erythematous *lesions that DO NOT BLANCH, dilated capillaries (vascular) do blanch* S/S: ROS, inquiry into other bleeding sites PE: Skin, oral cavity, joints Diagnostics: CBC, ESR, CRP, PT, PTT, INR, BUN , creatinine, LFTs, immune studies, Hep B&C antibodies, HIV DD: Rocky mountain spotted fever, NSAIDs, trauma, DIC, ITP, stasis dermatitis, vit C deficiency Management: Referral to hematologist or rheumatologist if palpable purpura; if need skin biopsy refer to derm; moderate-potency topical steroid ointment for stasis dermatitis

Urticaria

Hives Caused by vascular reaction occurring in upper dermis Characterized by development of wheals on body surface Acute < 6 weeks, chronic > 6 weeks Acute common in young adults and children; food allergens, meds, contrast dye lasts 5-7 days Chronic cases idiopathic or autoimmune, middle-ages women; 15-25% physical urticaria (physical triggers like hot, cold, water) Part of continuum that include anaphylaxis Patho: Immediate hypersensitivity reaction after exposure to an allergen or antigen Mast cells release histamine that binds to H1 in response to exposure, capillaries dilate, vascular permeability; wheals develop (superficial itchy swellings), pruritus H2 binding increases gastric acid secretion Mast cells also activated by IgE 60% idiopathic S/S: Pruritus followed by hives; lesions last 2-3 hours and disappear; episodes can occur daily and can last up to 2 years if chronic Six I's: Infections, ingestants, injectants, insect stings, inhalants, internal disease (latex allergy) Angioedema if difficulty breathing PE: Edematous pink or red wheals surrounded by bright red flare, typically on torso; physical urticaria may show dermatographism Diagnostics: CBC, WBC diff, ESR, skin biopsy DD: anaphylaxis, insect bites, SLE, pityriasis rosea Management: Identify trigger and eliminate; H1 blockers (loratadine, fexofenadine); H2 blocker (ranitidine, famotidine) or TCA (doxepin, amitriptyline) if refractory; oral corticosteroids; epinephrine for emergency

*Psoriasis*

Idiopathic benign epidermal hyperproliferation Inflammatory papulosquamous eruption characterized by *well-circumscribed erythematous macular and papular lesions with loosely adherent silvery white scale* Genetic/environmental factors (stress, anxiety, illness precede flares) Lifelong disease Exacerbations and remissions Patho: Autoimmune; T cell activation results in hyperproliferation of keratinocytes (30x normal); strong *genetic associations* S/S: Lesions with erythematous base, silvery white plaques that are adherent *Auspitz sign- tiny pin-point bleeding points if scales removed* Common sites are elbows, knees, scalp, genitals, and intergluteal cleft Concomitant nail dystrophy- pitting, yellowing, separation of nail plate, and thickening of entire nail *Lichenification- thickening of skin* Koebner phenomenon- isomorphic response 4 types -Chronic plaque - most common Sharply demarcated oval plaques several cm in diameter with silvery white surface. -Guttae Psoriasis - 2nd most common Acute exanthem like eruptions (drop like) scaly papules Lesions on trunk and proximal extremities Usually triggered by infection (pharyngitis or URI) Screen for Streptococcus 2 other types rare - erythrodermic and pustular psoriasis (more serious) Nail involvement seen in 30% of patients Ice pick like marks on nail plate Onycholysis (separation of nail plate from bed) - white in color Subungual hyperkeratosis - scales between nail plate and bed High correlation between psoriasis and arthritis Diagnostics: Presentation, biopsy, nail cultures DD: Nummular eczema, flat warts, atopic dermatitis, pityriasis rosea Treatment - *avoid systemic corticosteroids*; chronic disease=chronic therapy and withdrawal from tapering may precipitate erythrodermic or pustular psoriasis Emollients (use alone if localized or with keratolytics such as LacHydrin OTC) *Topical corticosteroids* for rapid solution of mild-mod plaques (High-potency with *vit D* most effective!) Anthralin (Drithocreme) - antimitotic therapy Calcipotriene (Dovonex) Topical Vit D or Vit A Biologic agents in mod-severe Weight loss, omega-3 fatty acids Dermatologist referral - may use phototherapy (UVB) or corticosteroid injections NO CURE

Lyme Disease

Infection caused by *Borrelia Bugdorferi* Ticks (infant) transmit disease to humans Incubation period 3-31 days Highest incidence in Northeast and North Central states April through October <50% of victims remember tick bite First stage - EM (erythema Migrans) - starts as red macule or papule and enlarges. Central clearing. Lesion > 5 cm to be considered EM Fever, malaise, HA, stiff neck, arthralgias may occur with rash. -If bitten in an endemic area and on for more then 48-72 hours or unsure, treat with one dose of 200mg of doxycycline. Adults and children over the age of 9. Second stage - early disseminated disease; characteristic rash 3-5 weeks after tick bite, annular, erythematous lesions Palsies of cranial nerves, meningitis, HA, fatigue, arthralgia Third stage - late disease (months or years after bite) Arthritis affects large joints esp. in knees CNS symptoms - encephalopathology and neuropathy DD: RA Lupus Meningitis Bells palsy Diagnosis: With EM or arthritis or noticeable lesion or hx of characteristic rash AND Hx of previous tick bite ELISA test if criteria not met but suspect Send tick out-costly Western blot Treatment: First line: Doxycycline (only if 9 years or >, discolored teeth!) 100 mg po BID X21 days*;OR Amoxicillin (children <9 years) 500 mg TID X21 days; Cefuroxime axetil 500 mg BID X21 days (2nd line includes erythromycin 250-500 mg 4X/day X21 d or azithromycin 500 mg daily X7 d) www.cdc.gov/ncidod/dvbid/lyme/qa.htm

Erysipelas

Infection of upper dermis Distinctive, superficial cellulitis including lymphatics *Sharply demarcated borders* Red, warm tender, indurated Lymphatic involvement is common Progressive rapid spread of infection through superficial layers of skin and lymphatics (infection of dermis and upper subcutaneous tissue) *Lower legs, face, ears are common sites* Usually prior injury or disease with impaired venous drainage (chronic venous insufficiency or lymphedema) *Number one cause - S. Pyogenes* (group A strep); Group C or G strep (S. aureus cause very rare) Facial involvement may follow a strep infection of the upper respiratory tract such as strep throat Rapidly spreading Marked erythema - unilateral Warmth Local pain Elevated sharp margin between involved/uninvolved skin Firm edema *"orange peel" appearance* Purulent drainage from site Regional lymphs tender/enlarged - "streaking" *Chills and fever common* Treat expeditiously If on face - chance for intracranial spread Management: Culture asap Blood cultures if systemic s/s-inpatient Same as for furnuncles: sulfa, doxy or clindamycin unless MRSA then use doxycycline or bactrim or vancomycin May need IV abx and hospitalization for severe cases Soak lesions daily to remove crusts (phisohex and warm H20) Glomerulonephritis - s/s - hematuria, acute HTN, edema, CHF Meningitis Follow-up 24-48 hours after therapy initiated

Pediculosis (lice)

Intense pruritis Scalp/back of neck usually Permethrin shampoo Lindane shampoo-NEUROTOXIC Treat family Treat as you would scabies

*Contact Dermatitis*

Irritant Contact Dermatitis Caused by direct cytotoxic action of agent on cells of epidermis and dermis Irritants most commonly chemical (soap, detergent, cosmetics, acids, alkalis) May have to reach threshold prior to development S/S: well-demarcated area of erythema, scaling, or crusting at site of exposure; hands MOST COMMON area followed by wrists and forearms Cumulative ICD will see hyperkeratosis (thickening), lichenification, scaling, and fissuring Irritant - scalded, erythematous . Moist appearance; peeling skin leaving lacy border. *Eruption limited to area of contact*-differentiate from atopic dermatitis DD: atopic dermatitis, nummular dermatitis Management: AVOIDANCE of offending agent, use petroleum, domeboro solution, hand-washing with warm water kept to a minimum (alcohol based cleanser less irritant), hand protection, emollients Allergic Contact Dermatitis Type IV delayed hypersensitivity reaction; requires prior sensitization for s/s to be induced (sensitized T cells in 10-15 days), once sensitized appears in 8-48 hrs persisting for days-weeks Eruption limited to area of contact Causes: chemicals, metals (NICKEL), latex, and plants (most common cause poison ivy or oak) S/S: pruritus, inflammation, vesicles DD: impetigo, herpetic infections, dermatophyte infections Management: AVOIDANCE of offending agent, topical application of medium-high potency corticosteroids (ointment), PO steroid if periorbital or genital with 2-3 week taper Complications: Uncontrolled scratching may lead to lichen simplex chronicus Refer if questionable diagnosis or treatment refractory

Brown Recluse Spider Bite

Known as "violin spider" Produces necrotic lesion Blister with concentric white/red circles Bulls eye appearance No pain at first then usually develops within about one hour Sometimes nausea, fever, chills Monitor for anaphylaxis Monitor first 72 hours Tetanus toxoid Found central Midwest south to the Gulf of Mexico Needs treatment, can cause significant tissue loss/limb loss-debridement; ice to limit venom spread; AVOIDANCE

Atypical Moles (dysplastic nevi)

Larger than 6 mm Irregular or ill-defined Variegated in color *FAMM - familial atypical mole and melanoma syndrome - high risk of melanoma* Family hx of melanoma in at least one first or 2nd degree relative *Worry more about new mole popping up than "mole has always been there"*

Folliculitis

Minor inflammation of individual hair follicles due to bacteria (s. aureus), chemical irritation or injury Painful yellow pustules Hair in center of pustule, *extends only as deep as epidermis* Could be secondary to topical steroids Cleanse with mild soap - hexachlorophene 5% benzoyl peroxide gel erythromycin solution 2% Clindamycin solution Consider oral antibiotics depending on severity

Bites

Morbidity and mortality associated with mammalian bites mostly related to tissue injury or polymicrobial infection *Aerobic bacteria- Pasturella, Strep, Staph* Anaerobic- bacteroides, actinomyces Viral disease- rabies (infects CNS, death) Eikenella corrodens- closed fist injuries (CFIs) Risk factors for infection: location on hand or foot, puncture wounds, advanced liver disease, >50 years, alcoholism, PVD Dog and cat - soft tissue infection Puncture wounds irrigate with sterile saline Augmentin Dog vaccinated for rabies? Public health dept wonderful resource Wild animals - greater risk of rabies-procedure to report! Human bites polymicrobial; *S. aureus most common, MRSA increasing* Rarely HSV 1&2, hepatitis B&C, M. tuberculosis, HIV Human - cellulitis can result Augmentin Clindamycin (PCN allergy) Tetanus shot-if no Td booster within past 5 years, or whose status is unknown Diagnostics: Systemic infection-blood cultures and CBC, cultures of infected wounds; hepatitis, HIV if human bite; X-ray if bone or joint involvement or foreign body Management: Irrigate wound with sterile saline solution, cautious debridement, wound packing, prophylactic therapy with amoxicillin-clavulanic acid or cefoxitin, if PCN allergy clindamycin plus doxycycline Rabies vaccine for animal handlers, vets, country with high risk Infection is most serious complication (cellulitis, lymphangitis, tenosynovitis, septic arthritis, osteomyelitis) Hospitalization if: systemic manifestations of infection, severe cellulitis, underlying illness, refractory to outpatient therapy, involvement of joint nerve bone tendon, significant hand bites, extensive wounds, head injuries

Basal Cell Carcinoma

More common than squamous cell *Rarely metastasizes* Head/neck sites are common *New lesion* or lesion that gets red, peels, bleed, then begins again. *Pearly*, painless, ulcerated Sun exposed areas - 80% on nose and upper lip *Telangiectasia* *Papular/nodular lesions with rounded borders* *Biopsy/excision to confirm diagnosis!* Basal Cell Carcinoma - "PUT ON S"unscreen P=pearly papule U=ulcerating T=telengectasia O=on the face, scalp, pinnae N=nodule S=slow growing

Bullous Pemphigoid

Most common of the autoimmune blistering diseases Affects primarily elderly population >70 Patho: Circulating IgG autoantibodies against structural proteins of dermal-epidermal junction leading to tissue damage and blister formation S/S: Nonbullous prodromal phase- severe pruritis; erythematous, eczematous papules and/or urticarial lesions lasting several weeks to months Bullous phase may appear suddenly with intense pruritus and widespread blister formation, symmetrically on abdomen and flexor aspects of extremities, may persist for several days, rupturing, collapsing, crusts; oral lesions in 20% Triggers: trauma to the skin, drugs, EBV, CMV, hepatitis PE: Nikolsky sign negative Diagnostics: Gold standard is direct immunofluorescence microscopy of skin biopsy specimen , ELISAs, western blotting DD: Allergic dermatitis, scabies, pityriasis lichenoides Management: Topical steroids, systemic PO corticosteroids (prednisone); Referral to dermatologist

Acne Vulgaris

Most common skin disease in U.S. This disease can cause severe psychological trauma Disorder of pilosebaceous follicles Gather med hx (may be aggravating acne like lithium or dilantin) Topical - wide variety Creams = greasy Gels = drying Lithium and dilantin stimulate formation of acne Steroids stress Types: Comedonal - primary lesions (blackheads) Inflammatory - secondary lesions Papular-pustular (pictured) Cystic/nodulocystic Patho: Acne begins when adrenals begin secreting and stimulating sebum production (adolescence) 4 key processes: -Inflammation (inflammatory mediators released into skin) -Altered keratinization and desquamation of cells lining follicles of sebaceous glands -Sebaceous glands produce and sebum proliferates -Sebum plugs pores (due to Propionibacterium acnes metabolization which causes increased glycerol and free fatty acids) Comedones or blackheads (open comedone) AAD Acne Classification system Mild-few to several papules/pustules; no nodules or scarring Moderate-several to many papules/pustules; few to several nodules, few scars Severe-numerous papules/pustules and many nodules and scars Diagnosis: PE, labs if adrenal or gonadal dysfunction is possible cause DD: Milia, rosacea, nevus comedonicus, flat warts, molluscum contagiosum Management: Mild cleansers are helpful to remove sebum from the surface of the skin Topical therapy is considered first-line, reduces inflammation, inhibits growth of P.acnes, regulates keratinocyte desquamation to prevent comedone formation Adapalene (Differin)/tretinoin (Retin A)/tazarotene (Tazorac): for comedones Mechanism: comedolytic (unlike benzoyl) and prevents new lesions from forming Applied to clean skin once daily before bed Available in multiple formations: creams, gel, solution Side effects: irritation, dryness, photosensitivity Antibiotics for mild papules, pustules- decrease P. acnes proliferation and inhibit production of inflammatory mediators Erythromycin gel Clindamycin gel Available in solutions, gels, ointment and pads Not recommended in monotherapy! Duac or benzaclin: *clindamycin & benzoyl peroxide* Often insurance will not cover combos even though VERY effective Benzoyl peroxide - for all forms of papulopusular acne Mechanism: antibacterial, drying agents Side effects: irritation, bleaching of clothing Need to use noncomedogenic moisturizer! Systemic *Antibiotics - for moderate, severe inflammation - take 6-8 weeks or often longer* *Tetracyclines*- doxycycline, minocycline Side effects: GI, *phototoxicity*, candidiasis, pigmentation, pseudotumor, cerebriataxia Erythromycin - GI side effects; safe in pregnancy Once improvement is seen, abx discontinue and start retinoids! Antiandrogen medications to suppress sebaceous glands Oral contraceptives: for older teens, women refractory to conventional therapy, for patients with significant sebum production, comedones Almost all forms of OCP's now are low dose estrogen and will be helpful for acne. Accutane/Isotretinion: for severe, nodulocystic acne unresponsive to conventional therapy Mechanism: decrease sebum production, antibacterial Available in 10, 20 ,40 mg, treat for 4-6 months 60% achieve long-term remission Always tell patients they need sunscreen - photosensitizing drug Side effects - dose related; dryness, conjunctivitis, arthralgias, hair thinning, decreased night vision *Laboratory abnormalities - liver functions, lipid elevations* (*also do pregnancy test before you start*) *Absolute contraindications: pregnancy!! Should be on reliable contraceptives prior to Accutane and monitor blood work and only by derm* Complications: Scarring, hyperpigmentation, and keloids

Miliaria

Occlusion of ducts of eccrine glands Separate from hair follicles Active people who perspire heavily Differential dx: Folliculitis Similar concept in neonatal acne

Emollients/ointments

Oil in H2O Eucerin/Nivea/Petroleum jelly If added Alpha hydroxy A, could irritate skin *Ointments - maximum absorption* (creams next best, gel/lotions last) *Transport via passive diffusion so increasing concentration gradient increase absorption* Thicker applications DO NOT increase skin penetration or effectiveness of the medication Not useful in hairy areas Best for dry, lichenified lesions Creams Usually applied 1-2 times a day. Often continue until resolution unless otherwise specific instructions (every other day for 2 weeks after resolution) Non-hairy areas such as palms and soles Solutions Best for open or closed dressings, infected dermatoses, or hairy areas Gels Liquefies on contact with skin Excellent for HAIRY areas Rate of absorption Face = greatest rate of absorption (LOWER potency steroids for SHORTER amounts of time) Axilla, scalp, genitals also (diaper area in babies) predisposed to increased absorption (any place skin meets skin like antecubital) Educate patients!

Black Widow Spider

Over 45,000 species of spiders Only Brown Recluse and Black Widow are worrisome Female Black Widow most venomous of all spiders Found temperate climates all over the world Most common in South & West US Humans are not usual prey, other insects are Found in basements, gardens, woodpiles & garages *Painful bite* vs. unpainful of brown recluse & cramping progresses to large muscle groups & the abdomen. Can mimic peritonitis (*abdomen pain*) Treatment: basic supportive care BLS/hospitalization

Corns and Calluses

Painful reaction to pressure or friction on the underlying dermis covering the digital and plantar surfaces of the FEET Two kinds of corns: soft (heloma molle) and more common hard (heloma durum) Calluses are less bothersome, reaction to friction on bony prominences and may be response to body weight distribution, not well circumscribed and lack central hyperkeratotic painful core found in corns Patho: Soft corns- hyperkeratotic development in response to excessive pressure or friction; EXTREME PAIN due to inflammation exciting pressure on the nerve receptors in the dermis Other causes of corns/calluses: short shoes, shoes with stiff soles, arthritic changes, fractures, foot deformity S/S: Corns-problems when symptoms interfere with ADLs; soft corns white, macerated appearance as a result of absorbed perspiration, secondary infection can develop PE: Dorsolateral aspect of 5th toe and dorsal surface of distal interphalangeal joints of 2nd, 3rd, and 4th toes most commonly affected by pressure Seed corns small, localized lesions anywhere on plantar surface Hard corns over bony prominences Soft corns between the toes (4th web space) Haglund deformity on back of calcaneus Diagnosis: Inspection and examination Hard corns vs warts- slow onset, location over bony prominences, painful response to direct pressure, lack of punctate bleeding, furrowed skin lines on magnification Sometimes X-ray to see structure of foot DD: plantar warts Management: Paring skin with No. 15 scalpel blade and applying 40% salicylic acid plaster (contraindicated if peripheral neuropathy) Soft corn infections-BID warm soaks and application of topical antibiotic (mupirocin- gram +); if cellulitis (dicloxacillin, cephalexin, or erythromycin), lab's wool, proper shoes! Calluses- pumice stone after softening foot in warm water In general 1)pain relief 2)correct the cause of increased mechanical stress 3) appropriate footwear 4) surgery if conservative approaches fail-REFER to podiatrist or ortho

Topical antifungals

Polyenes (Nystatin) for candida Imidazoles (clotrimazole, sulfonazole, ketoconazole, mycelex, Lotrimin AF) for candida and dermatophytes Allyamines (Lamisil) for dermatophytes

Herpes Zoster (Shingles)

Reactivation of the varicella-zoster virus following a primary varicella-zoster infection Varicella-zoster virus lies dormant in dorsal root or cranial nerve ganglia 1-2 day prodrome of pain or dysesthesia prior to lesions erupting *Herpes zoster itself is not transmissible, but may transmit primary varicella infection* Transmission possible, but unlikely Risk factors: Increasing age (2/3 of cases in >50 years of age) Altered cell-mediated immunity Chronic comorbid conditions (RA, IBD) HIV seropositive S/S: *Pain, dysesthesia, or pruritus* before lesions erupt Headache Malaise Eruption initially erythematous and maculopapular, becomes clusters of clear vesicles within several hours Disseminated in immunocompromised Affects *DERMATOMES* (rash that crosses midline? NOT ZOSTER!) Thoracic dermatome 50% Cervical dermatome 20% Trigeminal dermatome 15% (immediately refer or consult with physician) Lumbosacral dermatome 10% (Barker, 2003) 20% develop protracted pain syndrome called *postherpetic neuralgia (PHN)* Assessment: Acute pain Clustered red rash Characteristic fluid filled vesicles Unilateral acute pain Prodromal symptoms - fever, chills, GI disturbances, weakness (*flulike*) Lesions clustered over torso, back, buttocks, face ears, scalp Rapid onset *More common in immunosuppressed and elderly* Diagnosis: Assessment/*visualization* Tzanck Smear, DFA test, PCR analysis Differentials: Dermatitis Herpes Simplex virus Poison ivy, oak, sumac Cellulitis Eczema or psoriasis impetigo Management: Resolves 2-4 weeks Goal: decrease severity and duration Decrease potential for PHN (post herpetic neuralgia) *Antiviral therapy within 48-72 hours of onset* Antiviral/systemic therapy: Valacyclovir (Valtrex)-daily, better compliance Famciclovir (Famvir) BID Acyclovir (Zovirax) q4hrs Oral corticosteroids (3 week taper) to reduce duration and severity of pain Topical therapy = damp dressings to promote drying of lesions; topical ointment petrolatum or antibiotic (avoid bacitracin and neomycin due to allergic dermatitis) Pain management: NSAIDs; amitryptiline or narcs, *Neurontin*/lyrica *Key to get zostavax vaccine over age 60 or if immunocompromised, regardless of chickenpox history* Postherpetic Neuralgia (PHN) Pain after the cutaneous lesions have resolved Topical: Zostrix, Zostrix HP [OTC] reduces substance P in peripheral sensory nerves EMLA Tricyclic antidepressants (nortriptyline, amitriptyline) Gabapentin (Neurontin), lyrica Intractable pain: may need to refer to pain management

Tinea Cruris

Ringworm of groin Semicircular scaly plaques on superior medial thighs extending into inguinal folds and onto perineum Treat with topical antifungal: clotrimazole cream 1-2%

Herpetic Whitlow

Self-limited viral infection of area between fascial planes of distal finger, usually surrounding nail Most often seen in patients with gingivostomatitis caused by HSV, genital herpes, and health care workers Patho: Infecting pathogen is HSV 1 or 2 Virus is dormant in nerve ganglia S/S: Herpetiform vesicles or blisters erupt on distal phalanx after prodromal period of flulike symptoms and throbbing, tingling, numbness, or pruritus May persist for 8-12 days Enlargement of axillary lymph nodes Diagnostics: H&P, Tzanck smear, HSV culture, serum antibody titers DD: Paronychia, warts Management: Cool compresses, analgesics, oral antivirals (check creatinine clearance) ER REFERRAL IF PARONYCHIAL INFECTION OF TENDON SHEATH

Pruritus

Sensation that leads to a desire to scratch Patho: Characterized by activation of a network of distinct free nerve endings situated at dermoepidermal junction by local mediators such as histamine and numerous other peptides and proteases Impulse carried by unmyelinated C fibers to CNS Prostaglandins in skin lower threshold for itching S/S: H&P, evaluate for organomegaly and adenopathy; pruritus of scalp and face is MOST common manifestation of psychogenic pruritus Diagnostics: CBC with diff, serum glucose, LFTs, BUN, creatinine, TSH, UA, CXR, skin biopsy DD: If no diagnostic skin lesions and undiagnosed after 2 weeks then pruritus of undetermined origin and may be systemic or psychiatric or secondary to meds Management: Avoid irritants, stop causative meds, cooling of skin, tepid baths, hydrochloride + TCA cream, naltrexone cream, UVB light, capsaicin, acupuncture, electrical nerve stimulation, mechanical vibratory stimulation NOT TOPICAL ANTIHISTAMINES OR ANESTHETICS (sensitizers) Systemic therapy: Second-generation antihistamines, oral TCAs, naltrexone, oral activated charcoal, questran, gabapentin, danazol, aspirin, psychotherapy

Pigmentation Changes (Vitiligo)

Skin disorder characterized by lifelong or rapid disappearance of pigment-producing melanocytes in epidermis and hair follicle Lack of melanin leads to progressive, symmetrically patterned, milky-white macules that merge Two forms-A, nondermatomal, more common; B, dermatomal- rapid spread May be genetic Risk factors: fam hx of thyroid disease, pernicious anemia, SLE, IBD, vitiligo Onset between 10 and 30 years Patho: Cause is unknown Type A associated with *autoimmune disorders DM I, thyroid disease, and pernicious anemia* also RA S/S: Progressive and invasive hypopigmentation of skin found on sun-exposed areas and extensor surfaces of upper body Most people have NO other clinical findings PE: Type A- depigmentation on extensor surfaces appears first in symmetric fashion Type B- border not sharply demarcated, tricolored, uneven appearance, band-type distribution on one side of body Diagnostics: Clinical presentation, wood light, KOH, biopsy; TSH, CBC, fasting BG DD: Albinism, tinea versicolor, psoriasis Management: Sunscreen (SPF 15-30), cosmetic cover-up REFER TO DERM once coexistent autoimmune disorders have been excluded

Seborrheic Keratosis

Stuck on appearance Warty lesions on back, chest Can mimic malignant melanoma Harmless but unattractive Can send to derm for removal Warrants being investigated by derm Tends to be familial

Intertrigo

Superficial inflammatory skin disorder with persistent skin-to-skin contact, friction, moisture, warmth, and inadequate ventilation Characterized by varying degrees of erythema, peripheral scaling, and macerated erythematous plaques Common intertriginous ares: inframammary and abdominal folds, inner thighs, axillary, interdigital, perineal areas If not treated secondary infection common with Candida, S. aureus, Pseudomonas aeruginosa Patho: Altered barrier function allowing yeast/bacteria/fungi growth in skin folds, causing maceration, leading to erosion and skin breakdown S/S: Mildly erythematous, moist, glistening plaques, patches, papules, and/or pustules Well defined borders Itching, burning, stinging initially Diagnostics: Clinical appearance, KOH wet mount, gram stain, culture, wood lamp Differential: Seborrheic dermatitis Psoriasis Candida Management: Keep areas cool and dry/weight reduction Reduce friction, often caused by bras/constriction Antifungals Antibiotics if infection If >2 weeks no resolution refer to derm

Tinea Versicolor

Superficial, chronic yeast infection of skin that is asymptomatic Common in teens and young adults Causative org is Malassezia furfur, found on normal skin, but host's resistance changes (periods of high heat or humidity) Commonly affects trunk, neck, and upper extremities Appears as round, oval, scaly, hypopigmented (white or light pink), hyperpigmented (tan or brown), or salmon colored macules that form into a large patch over upper trunk and shoulders. Pruritis may be present DX - KOH "spaghetti and meatballs" Wood light-fluoresce white to yellow DD: vitiligo, seborrheic dermatitis Daily ketoconazole shampoo or Nizoral AD for 5 days Oral Itraconazole 200 mg every day for one week Topical shampoos containing selenium sulfide or pyrithione zinc

General Pharmacotherapy with skin

Topical Corticosteroids *Major effects are reduction of inflammatory response, vasoconstriction, and decreased collagen synthesis* Occlusive dressings=increased drug penetration Topical corticosteroids - 4 typicals Low potency - (hydrocortisone) - 0.5-2.5% Mid potency - (triamcinolone) - 0.1% High potency - fluocinonide Super potency: clobetasol (propionate) Low potency =face (thinnest skin on body) and other thin skin areas In primary care use low-mild, if higher potency derm should handle! General guidelines One gram of corticosteroid covers a 10X10 cm area Two grams covers hands, head face or anogenitals 3g covers anterior or post trunk or an arm 4g covers a single lower extremity- *For BLE for BID for 10 days prescribe 120g* pg 243 30g - 60 g entire skin surface Educate! BID every day for a week then every day for a week then once a day every other day then maybe once a week for eczema for example!

Compresses/Baths

Used to dry/debride areas of acute dermatitis Burow's aluminum acetate 1:20 Domebro aluminum sulfate Calcium acetate Aveeno colloidal oatmeal

Warts

Viral infection of skin Verruca vulgaris formal nomenclature Caused by HPV infection Mucosal and non-mucosal surfaces; Warts common on hands Transmission via direct skin contact HPV Type 16 most common high-risk genotype for cervical cancer, type 18 accounts for 70% of all cervical cancers HPV vaccine prevents cancer related strains (age 9 to 26) Patho: Virus comes into contact with skin that is broken or traumatized; remains within epidermis; spontaneous remission within 2 years may occur; incubation period of 1-8 months S/S: Papules <1mm -Verruca vulgaris or common wart is skin-colored, hyperkeratotic papule on backs on hands, periungual areas, and on knees -Filiform wart has fine, fingerlike projections, on face, tender -Verruca plana, flat wart on face and extremities, 1-2 mm papules, skin-colored to brown -Verruca plantaris, plantar wart, skin-colored papule or plaque on weight bearing surface of foot and digits, often confused with corns -Condylomata acuminata or anogenital warts are sexually transmitted, small skin-colored papules to large cauliflower-like growths; begin as flat papules then spread Diagnostics: Clinically, debridement Pap tests DD: seborrheic keratosis, callus, lichen planus, molluscum contagiosum Management: Most warts are benign and asymptomatic, will regress spontaneously over time NO CURE Topical txs need to extend at least 2mm outside visible confines Treatment: salicylic acid on common, flat, periungual, and plantar Liquid nitrogen cryotherapy every 2-4 weeks for months (genital, flat, filiform) Genital warts - podofilox 0.5% tx 3x week for 8-12 weeks. Imiquimod topical (immune modulator-stimulates body's immune system to develop antibodies against HPV!)

Dry Skin

Xerosis is skin that lacks moisture or water Affects elders >60 years, teens, obese, those in low humidity environments Patho: Stratum corneum layer is composed of lipids, water, proteins, and salts; either more oil in water or water in oil emulsion; androgens stimulate layer whereas estrogen, progesterone, and corticosteroids inhibit S/S: rough, cracks, fissures, Eczema craquele-uneven diamond pattern with erythema at edges DD: eczema, ichthyosis vulgaris, scabies Management: Lubricants, water-in-oil emulsions 2-3x daily, steroid creams for a week max if needed

Key concepts: Distribution of lesions

•Annular-ring-shaped •Scattered •Confluent or coalescent •Clustered •Linear •Reticular-net-like •Dermatomal