CAM I - Dermatology

Current Blurb: ~Pearly papule, erythematous patch >6 mm, or non-healing ulcer, in sun exposed areas (face, trunk, lower legs). ~History of bleeding. ~Fair-skinned person w/hx of sun exposure (often intense, intermittent). Atlas: ~Clinically different types: nodular, ulcerating, pigmented, sclerosing, and SF ~Locally invasive, aggressive, and destructive but slow growing, and there's very limited (literally no) tendency to metastasize.

Neoplasms: BCC Caused by UVR; PTCH gene mutation in many cases. *Most common CA* 1) Surgical excision, Mohs micrographic surgery, electrodessication, and curettage. 2) Cryosurgery and imiquimod cream.

Current Blurb: ~Edematous, spreading, circumscribed, hot, erythematous area, +/- vesicles or bullae. ~Central face frequently involved. ~Pain, chills, fever, and systemic toxicity may be striking. ~SF form of cellulitis that occurs *classically on the cheek* ~pain, malaise, chills, and moderate fever. ~A bright red spot appears first, very often near a fissure at the angle of the nose. This spreads to form a tense, sharply demarcated, glistening, smooth, hot plaque. ~Margin characteristically makes noticeable advances in days or even hours. ~The lesion is somewhat edematous and may pit slightly with/the finger. ~Vesicles or bullae occasionally develop on the surface. ~The lesion doesn't usually become pustular or gangrenous and heals w/o scar formation. ~The disease may complicate any break in the skin that provides a portal of entry for the organism. Atlas: ~erysipelas is a variant of cellulitis involving cutaneous lymphatics ~painful macular rash w/*well-defined margins*; characterized by an abrupt onset and rapid progression ~rash is typically confined to the face, which becomes fiery red, but it may progress to the extremities; +/- flaccid bullae ~rash desquamates in 5-10 days Exam Master: ~This is a cellulitis with a characteristic bright red appearance, sharp demarcation of the normal skin, and a relatively abrupt presentation. ~Almost all cases of erysipelas with a classic presentation are due to beta-hemolytic Streptococcus, usually type A. ~These strains are classified as beta-hemolytic since they produce a zone of complete hemolysis around the bacterial colony when cultured on a blood agar plate. ~Subjecting the pt to an invasive aspiration of the skin margin is unnecessary and unlikely to yield an organism.

Bacterial: ERYSIPELAS GABHS Leukocytosis is almost invariably present; blood cultures may be positive. Current: 1) Place the pt at bed rest w/the head of the bed elevated. 2) IV Abx effective against GABHS and staphylococci are indicated for the first 48 hours in all but the mildest cases. ~7-day course is completed w/PCN VK, dicloxacillin, or a 1st-generation cephalosporin po qid. ~Alternatives in PCN-allergic pts are clindamycin po bid x 7-14 days or erythromycin qid po x 7-14 days (the latter only if the infection is known to be due to streptococci)

benign neoplasms of mature fat cells that pose no harm to the pt

LIPOMAS (DDx: EICs) adipose tumor Surgical excision may be appropriate for cosmetic reasons or if the lipoma is located where it's constantly irritated.

may be self-limiting, lasting from a few min to hrs most often, it's an allergic rxn to food or drugs IgE attaches itself to a receptor on the mast cell and causes a chemical release Exam Master Urticaria lasting <6 weeks is considered acute, and almost 60% of cases result from a proven or probable viral infection. A history will reveal recent nonspecific symptoms such as fever, sore throat, dysuria, or a sick contact. Urticarial lesions or wheals are characterized by the rapid appearance of a central swelling of variable size, usually surrounded by erythema and associated with itching or burning sensations. They typically resolve within 1 - 24 hours, though they may recur intermittently. They may be accompanied by angioedema (a sudden pronounced swelling of the lower dermis) and subcutis, that is at times painful and frequently involves the mucous membranes. This resolves slower than wheals, usually over 1 - 3 days, and 25% of people will experience urticaria with or without angioedema at some time in their life.

ACUTE URTICARIA common causes: things that are ingested (drugs like PCN or other Abx, sulfa druges or other meds, shellfish peanuts, and food preservatives in processed and canned food) less common: things that the skin can contact (laundry detergents, shampoos, perfumes, cleaning solvents) or things the pt may breathe (fabric softeners) 1) Oral H1 antihistamines ~diphenhydramine (Benadryl) ~hydroxyzine (Vistaril) ~fexofenadine (Allegra) ~cetirizine (Zyrtec) 2) If it doesn't respond initially: H2 antihistamine (added to H1 regimen) ~famotidine (Pepcid) ~ranitidine (Zantac) If there's a concern that urticaria may progress to anaphylaxis, a Rx for an EpiPen s/b given to the pt along w/education regarding how to use it. Exam Master: ~Avoiding suspected and potential triggers (certain drugs and food) may prevent the occurrence of hives. ~Treatment consists of *reassurance and symptomatic care* (e.g., local and oral antihistamines). ~Generally, cool baths are recommended over warm/hot showers, which may be drying to the skin and increase the pruritis associated with urticaria. ~Using tight stockings or any type of tight clothing may be irritating to the skin and should also be avoided.

hyperpigmentation disorder commonly associated w/obesity, endocrine disorders (most notable insulin resistance), and paraneoplastic syndromes, or it may be drug induced develops insidiously ~initially: the skin darkens and appears to be dirty ~later: the skin is thick and velvety, w/accentuated skin lines

ACANTHOSIS NIGRICANS hereditary or acquired If the disorder is thought to be associated w/an underlying disorder, further investigation is needed. No tx except for that of addressing any underlying disorder.

Current Blurb: ~A chronic acneiform/facial disorder. ~A neurovascular component (erythema and telangiectasis and a tendency to flush easily). ~+/- An acneiform component (papules and pustules). ~A glandular component accompanied by hyperplasia of the soft tissue of the nose (rhinophyma). Atlas: ~common chronic inflammatory acneiform disorder of the facial pilosebaceous units ~coupled w/an increased reactivity of capillaries leading to flushing and telangiectasia ~may result in rubbery thickening of nose, cheeks, forehead, or chin due to sebaceous hyperplasia, edema, and fibrosis Zarbocks: ~Insidious onset of scattered, small papulopustules and sometimes nodules; comedones do NOT occur. Face appears red or flushed. ~Symmetric distribution on the face (cheeks, chin, forehead, glabella, nose). Sometimes, lesions appear on the neck, chest, back, or scalp. ~Later telangiectasia, hyperplasia, and lymphedema develop. ~Pts often complain of disfiguring appearance. When describing effects, the suffix "-phyma" ("enlarged") is used ~rhinophyma (nose) ~blepharophyma (eyelid) ~metophya (forehead) ~otophyma (ear) ~gnathophyma (mouth) mainly affects females 30-50 yoa Sanford: •Acne-like disorder of mid-life or older adults who suffer vascular dilations of the nose, cheeks, eyelids and forehead. •Erythematous Rosacea: In early stages, flushing reactions; involved skin persistently erythematous •Papulopustular Rosacea: In late stage disease, papular, pustular, cysts and nodules. In severe form leads to tissue hypertrophy and rhinophyma. Exam Master Rosacea needs to be differentiated from perioral dermatitis, seborrheic dermatitis, SLE, irritant or allergic contact dermatitis, and photodermatitis. The diagnosis of rosacea is most often a clinical one and there is no confirmatory laboratory test. 1) Perioral dermatitis is characterized by papules and papulovesicles appearing in groups, primarily in the perioral region, and are generally smaller than those occurring with rosacea. Telangiectasia occurs less commonly in perioral dermatitis than in rosacea, and moreover, no flushing or blushing is present. 2) Seborrheic dermatitis usually has more crusting, overlying dry scaling macules and papules. Seborrheic dermatitis characteristically presents as erythema and scaling around the nasolabial folds, eyebrows, scalp and postauricular folds. The lesions may also be present in the central chest, axillae, or groin. Flushing, presence of inflammatory papules, and pustules are not characteristic of seborrheic dermatitis. 3) DDx of facial erythema does include SLE, especially in young females. However, the malar rash in SLE has a butterfly distribution with absence of papules or pustules. An ANA test to rule out Lupus is not indicated, and is not helpful in differentiating rosacea from SLE, as a low antinuclear antibody titer may be present in rosacea, which can lead to the misdiagnosis. 4) Photosensitivity also presents as a facial erythematous rash. It also occurs secondary to sensitizing medications such as thiazides, FQ antibiotics, nalidixic acid, and doxycycline. However, photosensitivity presents as diffuse erythema with edema, like exaggerated sunburn. Again, there are no papules or pustules. In fact, the sine qua non of the diagnosis of rosacea is the small papules and the papulopustules.

Acneiform Lesions: (ACNE) ROSACEA •Etiology is unknown. Role of mites and/or helicobacter and/or other microorganisms is uncertain. •Skin mite: Demadex folliculorum thought to play a role •Helicobacter pylori may be involved. disease of the pilosebaceous units associated w/increased activity of capillaries (leads to flushing and telangiectasis) outbreaks are episodic and typically occur in response to heat, alcohol, sun, or hot, spicy foods; coffee and tea stimulate outbreaks b/c of the heat not caffeine Clinical dx, no confirmatory tests. Z: 1) Reduce triggers (alcohol, hot beverages) 2) Topical metronidazole (most effective), sodium sulfacetamide, or erythromycin often is sufficient. 3) If topical tx fails: ~systemic abx (tetracycline, minocycline, or doxy) are tried until remission and then continued at lower doses for maintenance 4) Very severe cases: ~may need oral isotretinoin under the care of a dermatologic specialist Atlas: ~Prevention~ 1) marked reduction or elimination of alcohol may be helpful in some pts ~Topical~ Metronidazole gel or cream once or twice daily Topical abx (i.e. - erythromycin gel) less effective 1) Systemic: Oral abx are more effective than topical tx ~Minocycline or doxycycline one or twice daily (very effective) ~tetracycline ~oral etronidazole bid 2) severe diseases not responding to Abx and topical tx: Oral Isotretinoin 3) massive demodex infestation: Ivermectin 4) Rhinophyma and Telangiectasia ~surgery or laser surgery ~beta-blocker carvedilol bid can reduce Sanford: Goal is control, not cure. 1) General treatment measures: •Avoid potential triggers of flushing: e.g, spicy food, alcohol, others •Skin care: use moisturizing creame, gentle skin cleansing, avoid topical irritants •Use sun screen 2) Primary Regimen ~Fascial erythema rosacea~ •Brimonidine gel (Mirvaso). Apply bid to affected area •Soolantra cream 1% (Topical ivermectin). Apply once daily ~Papulopustular rosacea~ •Topical Azelaic acid 20% cream, apply 2x/day or •Metronidazole 1% gel (30 gm tube), apply once daily •Only for refractory severe cases, consider po isotretinoin (all expensive) •For advanced rhinophyma, no known effective drug regimen. Consider surgical and laser ablation options 3) Alternative Regimen •Doxycycline once daily po. Does not benefit the telangiectasia, flushing or rhinophyma. May take months or years to work. •Topical benzoyl peroxide, clindamycin, erythromycin and 5% permethrin (for Demodex mites) have been used. •Topical retinoids used: e.g., Tretinoin-generic: 0.025 to 0.1% cream have been used. Pt Education: •Avoid activities that provoke flushing, e.g., alcohol, spicy food, sunlight. Exam Master: ~The initial therapeutic step is avoidance of exacerbating factors for rosacea; in this case alcohol consumption. Common exacerbating/ triggering factors include hot or cold temperatures, alcohol, beverages, spicy food, wind, exercise and emotional stress. ~The treatment for mild rosacea includes topical treatments with metronidazole gel, clindamycin lotion, or a sulfacetamide/sulfur lotion. ~Oral antibiotics are indicated if papular or pustular component is more extensive, or if mild edematous changes are seen. ~Patients with rosacea should use a noncomedogenic sunscreen, as added protection. ~Rosacea, which is severely inflammatory, refractory, or persistent, may be treated with isotretinoin therapy. ~Surgical therapy is indicated when telangiectasia and rhinophyma do not respond to medical therapy, in which case pulse dye laser therapy may be used.

Current Blurb: ~Occurs at puberty, though onset may be delayed into the 3rd or 4th decade. ~Open and closed comedones are hallmark. ~The most common of all skin conditions. ~Severity varies: purely comedonal to papular or pustular inflammatory acne to cysts or nodules. ~Face and upper trunk may be affected. ~Scarring may be a sequela of the disease or picking and manipulating by the patient. Inflammatory follicular, papular, and pustular eruption involving the pilosebaceous apparatus. Lesions can be open comedones or closed, non-inflammatory comedones: ~Open comedones = blackheads (melanin depositions on a keratin plug) ~Closed comedones = whiteheads (flesh-colored 1 mm papules) ~Open or closed comedones can become erythematous papules, pustules, nodules, or cysts, ranging in size from 1-5mm. Sinus tracts occur w/nodular acne. Inflammatory lesions can lead to hyperpigmentation and scarring. ~Affects all age groups, from neonates to adults. ~Most prevalent in teens and more severe in males. ~When a resistant case of acne is encountered in a woman, hyperandrogenism may be suspected. This may or may not be accompanied by hirsutism, irregular menses, or other signs of virilism. PCOS is the most common identifiable cause. Sanford: •Progressive condition. •3 stages of comedonal acne: early w/o inflammation, mild inflammatory, and severe. 1) Early: "blackheads" or "whiteheads", no inflammation. 2) Mild: Small papules or pustules present. 3) Severe: Comedones, papules and pustules. Less common: deep nodules (cysts). Exam Master: Acne is classified into 4 categories: Grade I: noninflammatory acne with comedones Grade II: moderate acne with inflammation, comedones, papules, and occasional pustules Grade III: severe localized inflammatory acne Grade IV: severe, generalized inflammatory acne with pustules, nodules, and cysts Treatment of mild to moderate acne consists of the topical preparations benzoyl peroxide and retinoic acid in varying strengths. Topical antibiotics may be helpful as adjuncts in decreasing the growth of P. acnes. They are most effective if used in conjunction with the other topical preparations. Patients who do not tolerate or who have not responded to topical medications are prescribed oral antibiotics, generally tetracycline. These patients typically have moderate to severe acne with papules, pustules, nodules, and cysts. Patients with severe nodulocystic acne with or without scarring are given isotretinoin for up to 4 months. This medication is teratogenic and is absolutely contraindicated in pregnancy. Individual painful nodulocystic lesions may be treated with intralesional injection of steroids, such as triamcinolone.

Acneiform Lesions: ACNE VULGARIS Plugged follicles, retained sebum, bacterial overgrowth, and release of fatty acids. Angdrogens stimulate sebum production. 1) Early: •Excessive sebum production and gland obstruction. •No Propionibacterium acnes 2) Mild: •Proliferation of P. acnes •Abnormal desquamation of follicular cells 3) Severe: P. acnes Testosterone, FSH, LH, or DHT 5 levels can be measured if an endocrine disorder is suggested (majority of cases aren't endocrine based). Z: 1) Mild acne ~keep the affected areas clean ~apply topical preparations (retinoids, azelaic acid, salicylic acid) 2) If inflammatory lesions are present: ~topical benzoyl peroxide, tretinoin, erythromycin, clindamycin, or sodium sulfacetamide can be used 3) More serious or cystic acne: oral abx in conjunction w/topical praparations ~Tetracyclines were the drug of choice early on and are still effective. Erythromycin, doxycycline, minocycline, Bactrim, and clinda are also frequently used. ~The bacterium that's involved in acne is becoming resistant to some meds. It's best to tx as conservatively as possible and only for as long as needed. ~Recurrence after cessation of tx is common. 4) Accutane (oral isotretinoin) ~Can be prescribed only be a dermatologic provider approved by Roche (see p.255 for reasoning) ~Have to perform *pregnancy test* before prescribing, due to tetrogenicity. Sanford: Goal of tx is prevention, reduction in # of new comedones and creation of an environment unfavorable to P. acnes. 1) Primary Regimen ~Early~ •Topical salicylic acid and benzoyl peroxide OTC •Once daily HS: Topical Tretinoin-generic (cream 0.025% or 0.05%) or (gel 0.01% or 0.025%): $73 gel and $53 cream •Clindamycin generic 1% gel; $39 •Clindamycin/benzoyl peroxide generic 1%/5% gel: apply bid: $107 •Erythromycin generic 2% gel; $13 •Dapsone 5% gel; $173 •Azelaic acid 20% cream; $200 ~Mild~ •(Topical Erythromycin 3% + benzoyl peroxide 5%); $89 •Doxycycline bid; $4 •TMP/SMX bid; $4 •Veltin (0.025% tretinoin/1.2% Clindamycin phosphate gel). $160 ~Severe~ •(Topical Erythro 3% + benzoyl peroxide 5% bid) ± (Doxycycline or Minocycline bid) •Expensive extended release once-daily Minocycline (Solodyn); $705 •Oral retinoid (Absorica, Amnesteem, Claravis, Myorisan, or Sotret) x 15-20 weeks. Expensive $551-1416. 2) Alternative Regimen ~Early~ •Once-q24h: Topical Adapalene 0.1% gel or Azelaic acid 20% cream once daily ($158 for 45 gm), or Tazarotene 0.1% cream apply once daily (Pregnancy Category X). ~Mild~ •Can substitute Clindamycin 1% gel for Erythromycin ~Severe~ •Oral antibiotics: Tetracycline, Erythromycin, TMP-SMX, or Clindamycin •Systemic Isotretinoin is reserved for pts w/severe widespread nodular cystic lesions that fail oral Abx therapy; if used, need a 4-5 month course. Retinoids have potentially severe side effects: Pregnancy Category X and require practitioner registration. ~Other~ •Oral contraceptives. May help in women; estrogen decreases androgens and thereby suppresses sebum secretion. •Spironolactone: used off label to due to anti-androgen effect.

Zarbock's p.301-303

BURNS

Current Blurb: ~Edematous, expanding, erythematous, warm plaque with or without vesicles or bullae. ~Lower leg is frequently involved. ~Pain, chills, and fever are commonly present. ~Septicemia may develop. Atlas: ~acute, spreading infection of dermal and SQ tissues ~characterized by red, hot, tender area of skin ~portal of entry of infection is usually apparent ~erysipelas is a variant of cellulitis involving cutaneous lymphatics, and is usually caused by beta-hemolytic streptococci ~fever and chills can develop before cellulitis is clinically apparent (higher fever >38.5C and chills usually associated w/GAS infection) ~local pain and tenderness ~necrotizing infections associated w/more local pain and systemic sx ~red, hot, edematous, shiny plaque originating at the portal of entry ~enlarges w/proximal extension; borders usually sharply defined, irregular, and slightly elevated ~vesicles, bullae, erosions, abscesses, hemorrhage, and necrosis may form in plaque ~lymph nodes can be enlarged and tender (regionally) ~lower leg is most common site; if arm is involved, think IV drug user Zarbocks: need to check this w/Sanford b/c cellulitis and erysipelas are different acute, spreading inflammation of the dermis and SQ tissue swollen, red, hot, and tender +/- lymphadenopathy, fever, chills, malaise manifests w/local swelling, erythema, and pain skin is pinkish and indurated Sanford: •Treatment of uncomplicated cellulitis, erysipelas in extremities, non-diabetic; acute bacterial skin and skin structure infection (ABSSSI) •Acute onset of rapidly spreading red edematous, tender plaque-like area of skin usually on the lower leg. Often febrile. •May be associated with lymphangitis or lymphadenitis. •Portal of entry is frequently fungal infection between the toes (Tinea pedis). •If facial skin is involved, see Facial erysipelas. •Usually, can clinically distinguish between red indurated demarcated inflamed skin of erysipelas (S. pyogenes) from the abscess of Staph. aureus. Dual infection is rare. Bedside ultrasound may be helpful in detection of deep S.aureus abscess(es). If in doubt, tx for both. Community-associated MRSA can mimic erysipelas; look for loculated purulence.

Bacterial: CELLULITIS (erysipelas) Streptococcus pyogenes (Groups A, B, C, G) S. aureus (rare) Zarbocks: Streptococcus sp, H. flu, Staphylococcus sp Atlas: 1) Clinical dx is based on morphologic features of lesion and clinical setting (i.e. - underlying diseases, travel hx, animal exposure, hx of bite, and age) 2) Confirmed by culture in only 29% of cases in immunoccompetent pts. ~necrotizing fasciitis requires immediate deep bx and frozen-section histopathology Current: 1) Leukocytosis or at least a neutrophilia (left shift) is present from early in the course. 2) Blood cultures may be positive. If a central ulceration, pustule, or abscess is present, culture may be of value. 3) Aspiration of the advancing edge has a low yield (20%) and is usually not performed. Instead, if an unusual organism is suspected and there is no loculated site to culture, a full thickness skin bx taken before Abx are given can be useful. ~Part is cultured and part processed for histologic evaluation w/Gram stain. ~Particularly useful in the immunocompromised pt. ~If a primary source for the infection is identified (wound, leg ulcer, toe web intertrigo), cultures from these sites isolate the causative pathogen in 1/2 of cases and can be used to guide Abx therapy. Although the causative organism can be identified by culturing any drainage or d/c or by needle aspiration, it's probably best to begin tx w/Abx that will cover (see above). Mark the margins of involvement before tx to follow the progression or regression of the area. 1) Mild or early infections may be tx w/ Abx: see Sanford. 2) In severe infections, Abx: see Sanford. 3) If there's poor response to Abx or a necrotizing, soft-tissue infection is suspected: surgical debridement! Sanford: 1) Elevate the involved leg 2) Inpatient parenteral therapy: •PCN G IV OR •Cefazolin IV OR •If PCN or cephalosporin allergic: Vancomycin IV •Tx IV until afebrile; then outpatient PCN V-K po qid AC and HS for a total of 10 days of therapy. 3) For less-ill outpatient therapy: •PCN V-K po qid OR, if PCN allergic: •Azithromycin po x 1 dose then po qd x 4 days OR •Linezolid po bid (expensive) •Tx for a total of 10 days (total of 5 days for Azithromycin) 4) If clinically unclear whether infection is due to S. pyogenes or Staph. aureus, get cultures and start empiric therapy: •Amox or PCN VK or Cephalexin for S. pyogenes and TMP/SMX for Staph. aureus (MRSA) Alternative Regimen 1) Acute bacterial skin and skin structure infections, moderately ill in-patient or out-patient who refuses hospitalization or is unlikely to comply w/a multidose oral regimen, there are 2 very long acting vanco-like drugs: • Dalbavancin IV x 1 then IV one week later (both by 30 min infusion) •Oritavancin IV over 3 hrs Both Dalbavancin and Oritavancin are expensive 2) For suspected S. aureus (fluctuance or pos gram stain): •MSSA (outpatient): Dicloxacillin po qid •MSSA (inpatient): Nafcillin IV or Oxacillin IV •MRSA (outpatient): Doxy po bid or TMP-SMX double strength tab po bid •MRSA (inpatient): Vanco IV Notes: •Mixed infection (Strep. and Staph.) is rare. If S. aureus is present, need incision and drainage. •Usual duration of therapy is 7-10 days. Some tx until pt is afebrile x 3-5 days. •Tx Tinea pedis if present. •Stasis dermatitis due to venous insufficiency can masquerade as bacterial cellulitis/erysipelas; condition is often bilateral, chronic and patient afebrile. No benefit from systemic antibiotics. The only topical therapy w/evidence of benefit is cadexomer iodine gel (Iodosorb et al: expensive) Atlas: ~Systemic high dose Abx tx according to type and sensitivity of microbial organism (see Sanford).

Current Blurb: ~SF blisters filled w/purulent material that rupture easily. ~Crusted superficial erosions. ~Positive Gram stain and bacterial culture. Atlas: ~Occurs adjacent to the site of S. aureus colonization (i.e. nares) ~secondary infection of 1) minor breaks in the epidermis (impetiginization), 2) of preexisting dermatoses, 3) other infections such as eczema hepreticum, or 4) wounds ~crusted erosions characterized by thick, crusted, golden "honey" yellow lesions bacteria colonize unbroken skin and, w/abrasions or bites inoculate the intradermal space, where lesions develop Sanford: •SF bacterial infection due to Streptococcus pyogenes or Staphylococcus aureus. Most frequently occurs in children in hot, humid environments. •S. pyogenes infection manifests as "honey crust" lesions or "punched out" ulcers (ecthyma). •Complications of Strep. impetigo include post-streptococcal glomerulonephritis and rheumatic fever. •Toxin-producing strains of S. aureus cause flaccid fragile bullae: bullous impetigo.

Bacterial: IMPETIGO Streptococcus sp. (Group A causes honey crust impetigo) (Group B, C, G are less common) Staph. aureus (MSSA and MRSA cause bullous impetigo) Clinical findings confirmed by culture ~S. aureus commonly ~failure of oral Abx suggests MRSA ~GAS 1) For Streptococcal impetigo: •(Mupirocin ointment 2% tid or Fusidic acidNUS 2% cream) x 7-12 days OR •Retapamulin 1% ointment bid x 5 days 2) For MSSA bullous impetigo: •(Mupirocin or Retapamulin ointment) or (Dicloxacillin po or Cephalexin po) 3) For MRSA bullous impetigo: •Mupirocin ointment tid or TMP-SMX double strength tab po bid 4) Alternative Regimen •Streptococcal impetigo: Shouldn't need oral Abx as topical therapy is effective. •MRSA bullous impetigo (all po regimens): TMP-SMX-DS OR (Doxycycline or Minocycline) OR (Clindamycin) Atlas: Reduce colonization. Topical abx to infected and colonized sites; systemic Abx 1) Prevention ~benzoyl peroxide wash ~check w/family members for signs of impetigo ~ethanol or isopropyl gel for hands and/or involved sites 2) Topical tx ~mupirocin and retapamulin ointment is highly effective in eliminating S. aureus from the nares and cutaneous lesions 3) Systemic Antimicrobial Tx ~According to sensitivity of isolated organism (see Sanford) Exam Master: 1) For impetigo that is localized and limited to a small area and doesn't have systemic involvement, Bactroban® cream (*Mupirocin*) applied to the affected area TID x 10 days 2) For systemic involvement: oral Abx ~Adults: Dicloxacillin 250 mg or Cephalexin (Keflex®) QID x 5 - 10 days may be administered. ~Peds: cephalexin x 10 days or Augmentin x 10 days

lasts >6 weeks lesions typically wax and wane females > males (2:1) Exam Master ~Urticaria lasting longer than 6 weeks is termed chronic and has an average duration of 12 to 36 months. ~Chronic urticaria (CU) is less prevalent than acute urticaria for all ages. ~Recent studies show that 30% to 50% of cases are autoimmune, involving circulating autoantibodies that lead to degranulation and mediator release from mast cells and basophils.

CHRONIC URTICARIA Idiopathic. Exacerbations can be precipitated by stress. Exam Master: Serum or skin IgE food testing is thus not recommended; however, an autologous serum skin test (ASST) may be helpful. The presence of a 1.5 mm or greater wheal than the control is considered positive. 1) Oral H1 antihistamines ~diphenhydramine (Benadryl) ~hydroxyzine (Vistaril) ~fexofenadine (Allegra) ~cetirizine (Zyrtec) 2) If it doesn't respond initially: H2 antihistamine (added to H1 regimen) ~famotidine (Pepcid) ~ranitidine (Zantac) 3) May require steroids. If there's a concern that urticaria may progress to anaphylaxis, a Rx for an EpiPen s/b given to the pt along w/education regarding how to use it. Exam Master Non-sedating second-generation H1 antihistamines are considered 1st-line therapy. First-generation sedating H1 antihistamines can be used as a 'rescue' medication for 'breakthrough' symptoms or severe cases.

Current Blurb: ~Sudden onset of symmetric erythematous skin lesions with history of recurrence. ~May be macular, papular, urticarial, bullous, or purpuric. ~*"Target" lesions with clear centers and concentric erythematous rings or "iris" lesions* may be noted in EM minor. These are rare in drug-associated EM major. ~EM minor on extensor surfaces, palms, soles, or mucous membranes. EM major favors the trunk. ~most common cause of EM minor: H. simplex ~most common cause of EM major in adults: drugs ~A classic target lesion, found most commonly in herpes-associated EM, consists of 3 concentric zones of color change, most often found acrally on the hands and feet. Not all lesions will have this appearance. ~Drug-associated bullous eruptions in the SJS/TEN spectrum present w/raised purpuric target-like lesions, w/only 2 zones of color change and a central blister, or nondescript reddish or purpuric macules. ~Pain on eating, swallowing, and urination can occur if the appropriate mucosae are involved. Atlas: ~a common rxn pattern of BVs in the dermis w/secondary epidermal changes ~manifests clinically as characteristic erythematous iris-shaped papular and vesiculobullous lesions ~typically involving the extremities (esp the palms and soles) and mucous membranes ~benign course w/frequent recurrences ~most cases related to HSV infection ~recurrences can be prevented by long-term anti-HSV medication ~more severe course in EM major Zarbocks: ~Lesions begin as macules and become papular, and then vesicles and bullae form in the center of the papules. Target or iris lesions are characteristic. ~*Lesions can be localized to the hands and feet or become generalized.* ~*Mucosal lesions (hallmark of EM major) are painful and erode* ~Fever, weakness, and malaise; lungs and eyes may be affected Half of all cases occur in pts <20 yoa Risk Factor: Previous hx of EM is a strong risk factor for subsequent cases. Sanford: •Immune-mediated characteristic skin lesions.

Desquamation: ERYTHEMA MULTIFORME (EM) Most commonly stimulated by viral infection (90%): *H. simplex*, EBV, CMV, adenovirus, HIV Medications are the precipitant in 10% of cases (NSAIDs, Sulfanomides, Anti-seizure drugs, others). Z: can be induced by drugs (phenytoin, barbiturates, PCN, allopurinol) and infections (HSV, Mycoplasma sp.) Idiopathic (50%) 1) Blood tests are not useful for dx. 2) Skin bx is diagnostic. ~Direct immunofluorescence studies are negative. *Z/Atlas:* 1) Avoid precipitating substances, and control herpes outbreaks w/oral valaciclovir or acyclovir. 2) Severely ill pts ~Systemic steroids (prednisone), but effectiveness hasn't been established. Current: 1) General Measures ~TEN is best tx in a burn unit, or hospital setting with similar support. ~Otherwise, pts need not be admitted unless mucosal involvement interferes w/hydration and nutrition. ~Pts who begin to blister s/b seen daily. ~Open lesions s/b managed like 2nd-degree burns. ~Immediate discontinuation of the inciting medication (before blistering occurs) is a significant predictor of outcome. ~Delay in establishing the dx and inadvertently continuing the offending medication results in higher morbidity and mortality. 2) Specific Measures ~The most important aspect of tx is to stop the offending medication and to move pts with >25-30% BSA involvement to an appropriate acute care environment. ~Nutritional and fluid support and high vigilance for infection are the most important aspects of care. ~Recent reviews of systemic treatments for SJS and TEN have been conflicting, but the largest series have failed to show statistically significant benefit w/tx. ~Some data support the use of high-dose corticosteroids (prednisone). If corticosteroids are to be tried in more severe cases, they s/b used early, before blistering occurs, and in moderate to high doses and stopped within days if there's no dramatic response. ~IVIG x 4 days has become standard of care at some centers for TEN cases and can be considered in cases w/>30% BSA involvement. It hasn't been proven to reduce mortality. ~Oral and topical corticosteroids are useful in the oral variant of EM. ~Oral acyclovir prophylaxis of herpes simplex infections may be effective in preventing recurrent herpes-associated EM minor. 3) Local Measures ~Topical therapy is not very effective in this disease. ~For oral lesions, 1% diphenhydramine elixir mixed w/Kaopectate or with 1% dyclonine may be used as a mouth rinse several times daily.

Atlas: ~acute life-threatening mucocutaneous blistering rxns characterized by extensive necrosis and detachment of the epidermis ~they're variants of the same disease and differ only in the percentage of body surface involved ~confluent erythematous purpruic and target-like macules evolve into flaccid blisters and epidermal detachment mostly on the trunk and extremities; there's associated mucous membrane involvement ~fever usually higher in TEN than in SJS ~usually mentally alert; distress due to severe pain ~cardiovascular: pulse may be >120 bpm; BP ~renal: tubular necrosis may occur; acute renal failure ~respiratory and GI tracts: sloughing of epithelium w/erosions Current: *SJS is thought to be a variant of EM ~<10% BSA skin loss TEN is thought to be a severe variant of SJS ~>30% BSA skin loss* ~fever, photophobia, sore throat, mucosal inflammation, sore mouth; cutaneous lesions tend to be concentrated more on the trunk at first; lesions may be painful or may sting ~progression occurs over 4 days: diffuse erythema; morbilliform lesions; necrotic epidermis; wrinkled surfaces; sheetlike loss of epidermis; raised, flaccid blisters (Nikolsky's sign) ~*higher fever and more severe epidermal separation and loss compared w/SJS* ~regrowth takes 3 weeks; delayed in pressure-point areas ~90% of pts have mucosal lesions that are painful and eroding Complications: ~acute tubular necrosis ~erosion in the lungs and gut ~bronchitis Dangers: ~secondary infection ~fluid loss ~electrolyte imbalance may occur in pts of any age or gender

Desquamation: STEVEN-JOHNSONS SYNDROME (SJS) & TOXIC ERYTHEMA NECROLYSIS (TEN) Idiopathic (possibly immunologic response) or drug-induced rxn (sulfonamides, aminopenicillins, FQs, cephalosporins, tetracyclines, phenobarbital, carbamazepine, phenytoin, valproic acid, oxicam, allopurinol, corticosteroids) Labs ~Anemia and lymphopenia ~Bx is diagnostic: full-thickness necrosis of the epidermis and a sparse lymphocytic infiltrate Z: 1) Prompt withdrawal of offending or causative agent. 2) Extensive necrolysis ~transfer to a burn unit for care 3) Tx for fluid and electrolyte imbalance and any complications or infections 4) Tx debate ~Corticosteroids are being debated. If given, they s/b started early in the course of the disease. ~Abx controversy b/c they may be the causative agents. ~IVIG is commonly used, but data doesn't show any improvement in mortality. Atlas: Tx is symptomatic. Systemic tx w/glucocorticoids and high-dose IVIG is advocated by some but still controversial. 1) Early dx and withdrawal of suspected drug(s). 2) Pts best cared for in an intermediate care unit or ICU 3) Manage replacement of IV fluids and electrolytes as for pt w/extensive thermal burn; however, less fluid usually required as for thermal burn of similar extent 4) Systemic glucocorticoids early in the disease and in high doses are reported helpful in reducing morbidity or mortality, but this has been questioned ~late in the disease, they're contraindicated 5) High-dose IVIG halt progression of TEN if administered early; this is questioned by some 6) W/oropharyngeal involvement, suction to prevent aspiration pneumonitis 7) Surgical debridement not recommended 8) Dx and tx complicating infections, including sepsis (fever, hypotension, change in mental status) 9) Tx eye lesions early w/erythromycin ointment Pt education: Wear medical alert bracelet

Current Blurb: ~Firm dermal papule or nodule. ~Overlying black comedone or "punctum." ~Expressible foul-smelling cheesy material. ~May become red and drain, mimicking an abscess. ~common, benign growths of the upper portion of the hair follicle ~common in Gardner syndrome and may be the first stigmata of the condition ~favor the face and trunk and may complicate nodulocystic acne vulgaris ~individual lesions range in size from 0.3 cm to several centimeters ~an overlying pore or punctum is characteristic ~lateral pressure may lead to extrusion of a foul-smelling, cheesy material ~distinguished from lipomas by being more SF (in the dermis not the subcutaneous fat) and by their overlying punctum ~many other benign and malignant tumors may superficially resemble EICs, but all lack the punctum Complications ~EICs may rupture, creating an acute inflammatory nodule very similar to an abscess. ~Cultures of the expressed material will be sterile.

EPITHELIAL INCLUSION CYSTS (EICs) (DDx: Lipoma) 1) Tx is not required if asymptomatic. 2) Inflamed lesions ~I&D or intralesional triamcinolone acetomide 3) Large or symptomatic cysts ~surgical excision is curative

Current Blurb: ~Pruritic, exudative, or lichenified eruption on face, neck, upper trunk, wrists, and hands and in the antecubital and popliteal folds. [*flexural surfaces*] ~Personal or FHx of allergic manifestations (eg, asthma, allergic rhinitis, atopic dermatitis). ~Tendency to recur. ~Onset in childhood in most pts. Onset after age 30 is very uncommon. ~Diagnostic criteria must include pruritus, typical morphology and distribution (flexural lichenification, hand eczema, nipple eczema, and eyelid eczema in adults), onset in childhood, and chronicity. ~Also helpful are: 1) a personal or family history of atopic disease (asthma, allergic rhinitis, atopic dermatitis) 2) xerosis-ichthyosis 3) facial pallor w/infraorbital darkening 4) elevated serum IgE 5) repeated skin infections. ~Itching may be severe and prolonged. ~Rough, red plaques usually w/o the thick scale and discrete demarcation of psoriasis affect the face, neck, and upper trunk. The flexural surfaces of elbows and knees are often involved. ~In chronic cases, the skin is dry, leathery, and lichenified. ~Pigmented ppl may have poorly demarcated hypopigmented patches (pityriasis alba) on the cheeks and extremities. ~In black pts w/severe disease, pigmentation may be lost in lichenified areas. ~During acute flares, widespread redness w/weeping (either diffusely or in discrete plaques) is common. Atlas Blurb: ~An acute, subacute, or chronic relapsing skin disorder. ~Very common in infancy. ~Prevalence peak of 15-20% in early childhood. ~Characterized principally by dry skin and pruritis; consequent rubbing leads to increased inflammation and lichenification and to further itching and scratching (*itch-scratch cycle*). -> *the itch that rashes* ~Often associated w/a person or family hx of AD, allergic rhinitis, and asthma; 35% of infants w/AD develop asthma later in life. ~Associated w/skin barrier dysfunction, IgE reactivity. ~Genetic basis influenced by environmental factors; alterations in immunologic responses in T cells, antigen processing, inflammatory cytokine release, allergen sensitivity, infection. Zarbocks: chronic relapsing skin disorder that begins in childhood many pts also have asthma or allerghic rhinitis (atopy) ~papules and plaques +/- scales; may be associated w/edema, erosion, and crusts ~pruritis and dry, scaly skin; scratching -> lichenification, fissures, and worsening rash; secondary infections most commonly caused by S. aureus ~rash is most common in *flexural surfaces, front an sides of neck, eyelids, forehead, face, wrists, and dorsum of the hands and feet*; generalized in severe disease ~*"white" dermatographism* is characteristic Exam Master: ~Atopic hand dermatitis is probably the most common form of adult atopic dermatitis. ~Pts with history of hand dermatitis before age 15, a history of atopic dermatitis as a child, or persistent eczema or dry, itchy skin on the body as an adult are at increased risk of developing hand eczema as adult. ~These patients exhibit chapping and erythema, but also may develop edema, vesiculation, crusting, scaling, and lichenification. ~Scratching the lesions worsens the inflammation.

Ezcematous Eruptions: ATOPIC DERMATITIS (IgE dermatitis, excema, atopic eczema) (DDx: seborrheic dermatitis, contact dermatitis, psoriasis, dermatophytosis) Type I IgE-mediated hypersensitivity rxn 1) *Dx is based on hx in infancy and clinical findings.* 2) Lab studies not routinely done, although cultures for suspected secondary infection may help to guide tx. ~Bacterial Culture: Colonization w/S. aureus is very common in the nares and in the involved skin; almost 90% of pts w/severe AD are secondarily colonized/infected. ~Viral Culture: R/o HSV infection in crusted lesions ~Blood Studies: Increased IgE in serum, eosinophilia, HSV antigen detection for dx of acute HSV infection Z: 1) Antihistamines help to reduce itching 2) Topical corticosteroids are the mainstay of tx ~Systemic corticosteroids s/b avoided. 3) Tacrolimus and pimecrolimus are topical calcineurin inhibitors (immunomodulators) approved for moderate to severe atopic dermatitis. ~Less atrophy w/prolonged use when compared to topical corticosteroids; however, they may carry a potential to cause malignancy. 4) Hydration and topical emollients are key to management. ~Soaps, vigorous rubbing, and irritant clothing such as wool s/b avoided. 5) UVB phototherapy is effective. 6) Severe systemic cases may necessitate cyclosporine. Atlas: ~Acute~ 1) Wet dressings and topical glucocorticoids; topical Abx (mupirocin ointment) when indicated. 2) Hydroxyzine qid for pruritis. 3) Oral Abx (dicloxacillin, erythromycin) to eliminate S. aureus and tx MRSA according to sensitivity as shown by culture. ~Subacute and Chronic~ 1) Hydration (oiled baths or baths w/oatmeal powder) followed by application of unscented emollients (i.e. - hydrated petrolatum) is basic daily tx to counteract xerosis ~12% ammonium lactate or 10% alpha-hydroxyl acid lotion is very effective for xerosis. ~Soap showers only for body folds 2) Topical anti-inflammatory agents ~*glucocorticoids*: most effective but may lead to atrophy; glucocorticoid phobia ~hydroxyquinolone preparations ~tar 3) Minor flare-ups and subacute AD ~Calcineurin inhibitors (tacrolimus and pimecrolimus) are gradually replacing glucocorticoids in most pts 4) Oral H1 antihistamines to reduce itching 5) Severe intractable disease in adults: ~systemic glucocorticoids (otherwise, avoid these) 6) UVA-UVB phototherapy 7) Last resort: ~Cyclosporine tx ~Monitor BP weekly and chemistry panels biweekly 8) Stress management techniques Summary: 1) Baseline therapy of dryness w/emollients 2) Suppression of mild-moderate AD by prolonged topical pimecrolimus or tacrolimus and continued emollients 3) Suppression of severe flares w/topical glucocorticoids followed by pimecrolimus or tacrolimus and emollients 4) Oral and topical Abx to eliminate S. aureus 5) Hydroxyzine to suppress pruritis Pt education: ~Avoid rubbing and scratching ~Use emollients

Current Blurb: ~Erythema and edema, w/pruritus, often followed by vesicles and bullae (in ACD) in an area of contact w/a suspected agent ~Later: weeping, crusting, or secondary infection ~Hx of previous rxn to suspected contactant. ~Patch test w/agent positive (in ACD). ICD: ~80% of cases are due to excessive exposure to or additive effects of primary or universal irritants (eg, soaps, detergents, organic solvents) ~appears red and scaly but not vesicular ~*more common than ACD* ACD: ~most common causes: poison ivy or poison oak; topically applied antimicrobials (esp bacitracin and neomycin), anesthetics (benzocaine); hair-care products; preservatives; jewelry (nickel); rubber; vitamin E; essential oils; propolis (from bees); and adhesive tape. ~occupational exposure is an important cause of allergic contact dermatitis ~weeping and crusting are typically due to allergic and not irritant dermatitis. ~In ACD, the acute phase is characterized by tiny vesicles and weepy and crusted lesions, whereas resolving or chronic contact dermatitis presents w/scaling, erythema, and possibly thickened skin. ~Itching, burning, and stinging may be severe. ~The lesions, distributed on exposed parts or in bizarre asymmetric patterns, consist of erythematous macules, papules, and vesicles. ~The affected area is often hot and swollen, w/exudation and crusting, simulating (and at times complicated by) infection. ~Pattern of the eruption may be diagnostic (eg, *typical linear streaked vesicles on the extremities in poison oak or ivy dermatitis*). ~The location will often suggest the cause: Scalp (hair dyes or shampoos), face (creams, cosmetics, soaps, shaving materials, nail polish), neck (jewelry, hair dyes) ~itching and burning in the affected areas ~in diaper rash, the lesions are within the borders of the diaper ~acute lesions typically are well-demarcated areas of erythema and possibly exudative lesions; vesicles, erosions, and crusts may develop ~chronic lesions show plaques and scaling w/lichenification; satellite papules and excoriations are common ICD vs ACD: ~ICD is a toxic phenomenon: confined to the area of exposure and is therefore always sharply marginalize an never spreads; *most commonly in the hands*; NO papules; configuration is often bizarre or linear ("outside job" or dripping effect) ~ACD is an immunologic rxn that tends to involve the surrounding skin (spreading phenomenon) and may spread beyond affected sites Exam Master 1) ICD ~Irritant hand dermatitis is the most common type of hand inflammation, and is often seen with patients who wash their hands frequently, or use organic solvents or alkaline soaps that make the skin more susceptible to eczema, because they extract water-binding lipids. ~Irritant hand dermatitis presents with dryness, chapping, fissuring, and erythema, especially along the backs of the hands, which become swollen and tender. ~Patients may develop subacute eczematous changes with the skin becoming red, shiny, smooth, and extremely delicate. 2) ACD ~Allergic contact dermatitis of the hands is less common than irritant hand dermatitis. ~In one study, ~15% of patients with hand eczema were found to be sensitive to an allergen at patch testing. ~Common causes of allergic hand dermatitis include allergies to nickel, potassium dichromate, rubber, fragrances in soaps or cosmetics, formaldehyde, or lanolin.

Ezcematous Eruptions: CONTACT DERMATITIS (DDx: impetigo, secondary infection, scabies if generalized itching, atopic dermatitis) Irritant (ICD): chemical irritants (cleaners, solvents, detergents) in contact w/the skin; diaper rash from prolonged contact w/urine, feces, or detergents from washable diapers; *most common form of occupational skin disease* Allergic (ACD): type IV cell-mediated hypersensitivity rxn from occupational or personal contact w/irritants (cleaning supplies, solvents, oils, abrasives, oxidizing or reducting agents, dust, nickel, enzymes, plants) 1) Patch tests that result in similar rxns support the dx. ~After the episode of ACD has cleared, patch testing may be useful if the triggering allergen is not known. 2) Gram stains and/or cultures s/b done if secondary infection is suspected. ~r/o impetigo or secondary infection (impetiginization) Z: 1) Avoid or remove the offending agent. ~Wet dressings w/Burrow's soln (aluminum acetate in water) and *topical corticosteroids* are sufficient in most cases ~Diaper rash: a barrier of petrolatum or zinc oxide is helpful. Keep area clean and dry w/frequent diaper changes and use of disposable diapers. 2) Severe cases may necessitate systemic steroids. ~Prednisone x 2 weeks 3) Chronic lesions can be treated w/topical steroids. 4) Supportive: cleaning w/mild soaps or oatmeal preparations and antihistamines to help alleviate itching General: ~While local measures are important, severe or widespread involvement is difficult to manage w/o systemic corticosteroids b/c even the highest-potency topical corticosteroids seem not to work well on vesicular and weepy lesions. ~Localized involvement (except on the face) can often be managed solely with topical agents. ICD: ~protection from the irritant ~topical corticosteroids ~Exam Master: with lubricants, avoidance of irritation, and use of gloves (cotton under rubber) during washing ACD: ~Local Tx~ 1) Acute weeping dermatitis ~Compresses are most often used. Don't scrub lesions with soap and water. Calamine lotion may be used betw wet dressings, esp for involvement of intertriginous areas or when oozing is not marked. Lesions on the extremities may be bandaged w/wet dressings for 30-60 minutes several times a day. ~High potency topical corticosteroids in gel or cream form (eg, fluocinonide, clobetasol, or halobetasol) may help suppress acute contact dermatitis and relieve itching. This tx s/b followed by tapering of the # of applications per day or use of a mid-potency corticosteroid (i.e. - triamcinolone 0.1% cream) to prevent rebound of the dermatitis. A soothing formulation is 2 oz of 0.1% triamcinolone acetonide cream in 7.5 oz Sarna lotion (0.5% camphor, 0.5% menthol, 0.5% phenol) mixed by the pt. 2) Subacute dermatitis (subsiding) ~Mid-potency (triamcinolone 0.1%) to high-potency corticosteroids (clobetasol, amcinonide, fluocinonide, desoximetasone) are the mainstays of therapy. 3) Chronic dermatitis (dry and lichenified) ~High potency to super potency corticosteroids ointment. ~Systemic Tx~ 1) For acute severe cases, prednisone may be given orally x 12-21 days. ~The key is to use enough corticosteroid (and as early as possible) to achieve a clinical effect and to taper slowly enough to avoid rebound.

Current Blurb: ~"Tapioca" vesicles of 1-2 mm on the palms, soles, and sides of fingers, associated with pruritus. ~Vesicles may coalesce to form multiloculated blisters. ~Scaling and fissuring may follow drying of the blisters. ~Appearance in the 3rd decade, w/lifelong recurrences. ~An extremely common form of hand dermatitis, preferably called pompholyx (Gr "bubble") or vesiculobullous dermatitis of the palms and soles ~Pts often have an atopic background and report flares with stress. ~Pts w/widespread dermatitis due to any cause may develop pompholyx-like eruptions as a part of an autoeczematization response. ~Small clear vesicles stud the skin at the sides of the fingers and on the palms or soles. They look like the grains in tapioca. They may be associated w/intense itching. ~Later, the vesicles dry and the area becomes scaly and fissured. Atlas: ~a special vesicular type of hand and foot dermatitis ~an acute, chronic, or recurrent dermatosis of the fingers, palms, and soles ~sudden onset of many deep-seated pruritic, clear "tapioca-like" vesicles ~large bullae can occur (pompholyx) ~later scaling fissures and lichenification ~itching and when erosions are present pain ~secondary bacterial infection: pustules, cellulitis, lymphangitis, and painful lymphadenopathy ~recurrent attacks are the rule Zarbocks: Generally develops in ppl <40 yoa. Half of those affected have an atopic background. Eruptions follow stress or occur in hot, humid weather. 1) Early disease ~Pruritus is common; pain develops if secondarily infected. ~Sall vesicles in clusters (tapioca appearance) are seen, and occasionally bullae form. 2) Late disease ~Papules, scaling, lichenification, and erosions from ruptured vesicles are seen. ~Painful fissures may develop. Note: There is predilection for the hands in feet.

Ezcematous Eruptions: DYSHIDROSIS (Pompholyx, Vesicular palmar eczema) (DDx: dermatophytosis, bullous tinea, tinea pedis, NSAID-induced eruption) None, except to r/o other things: 1) Culture to r/o secondary infection 2) KOH prep to r/o dermatophytosis and bullous tinea Z: 1) Use wet dressings w/Burrow's soln. ~Large bullae s/b drained but kept intact. 2) Fissures: topical collodion 3) Topical steroids for localized lesions and systemic steroids for severe cases. 4) PUVA in generalized disease. 5) Tx secondary infection w/systemic antimicrobials. Atlas: 1) Topical high-potency corticosteroids, intralesional triamcinolone for small areas. ~if given early in the attack, may help abort the flare and ameliorate pruritus ~important in tx the scaling and fissuring that are seen after the vesicular phase 2) Severe cases: a short course of prednisone 3) Systemic Abx for secondary infection and PUVA either oral or as "soaks" Pt education: ~It is essential that pts avoid anything that irritates the skin ~They should wear cotton gloves inside vinyl gloves when doing dishes or other wet chores, use long-handled brushes instead of sponges, and use a hand cream after washing the hands. Exam Master ~ Numerous tx options are available, including topical steroids w/plastic occlusive dressings x 1-2 weeks. ~Abx (e.g., erythromycin) s/b used only if there's suspected secondary infection.

Current Blurb: ~Chronic itching and scratching. ~Lichenified lesions w/exaggerated skin lines overlying a thickened, well-circumscribed scaly plaque. ~Predilection for nape of neck, wrists, external surfaces of forearms, lower legs, scrotum, and vulva. ~represents a self-perpetuating scratch-itch cycle (a learned behavior that's hard to disrupt) ~intermittent itching incites the pt to scratch the lesions ~itching may be so intense as to interfere with sleep ~dry, leathery, hypertrophic, lichenified plaques appear on the neck, ankles, or perineum ~patches arerectangular, thickened, and hyperpigmented ~skin lines are exaggerated Atlas: ~special localized form of lichenification, occurring in circumscribed plaques ~results from repetitive rubbing and scratching ~lichenification is a characteristic feature of AD, whether generalized or localized ~LSC can last for decades unless the rubbing and scratching are stopped by tx ~occurs in individuals >20 yoa, is more frequent in women, and possibly more frequent in Asians Zarbocks: ~Lichenification is a long-term manifestation of atopic dermatitis due to repetitive scratching and rubbing. ~Skin of pts w/atopic dermatitis is sensitive to minor trauma (touch, rubbing, scratching) ~Lichenification develops as well-circumscribed plaques that are highly pruritic. This sets up a cycle of itch-scratch lesions. ~Solid, firm, thick plaques w/little to no scaling are seen. ~Light touch precipitates a strong desire to scratch. ~Lesions can be single or multiple. Common areas: nuchal area, scalp, ankles, lower legs, upper thighs, exterior forearms, or genital areas ~Black skin more typically shows a follicular pattern of smaller papules rather than larger plaques.

Ezcematous Eruptions: LICHENS SIMPLEX CHRONICUS (Circumscribed Neurodermatitis) (DDx: psoriasis, lichen planus, nummular dermatitis) (no dx listed in Current) Z: 1) KOH prep to r/o fungal infection 2) Bx ~hyperplasia of all components of epidermis ~hyperkeratosis, acanthosis, and elongated and broad rete ridges ~in the dermis, there's a chronic inflammatory infiltrate Z/Atlas: 1) Key to management is stopping the itch-scratch cycle. 2) Occlusive dressing at night (+/- topical steroids or tar preparations can be used for legs and arms) ~Glucocorticoids incorporated in adhesive plastic tape are also effective if left for 24h ~Unna boot: a gauze roll dressing impregnated w/zinc oxide paste is wrapped around a large lichenified area (i.e. - calf) x 1 week 3) intralesional triamcinolone in smaller lesions ~use low doses, otherwise can cause atrophy ~oral hydroxyzine at night may be helpful 4) Antihistamines will reduce itching. Current: 1) lesions in extra-genital regions ~superpotent topical corticosteroids are effective +/- occlusion when used bid for several weeks ~In some pts, flurandrenolide (Cordran) tape may be effective, since it prevents scratching and rubbing of the lesion. ~injection of triamcinolone acetonide suspensions into the lesions may occasionally be curative ~Continuous occlusion w/a flexible hydrocolloid dressing x 7 days at a time for 1-2 months may also be helpful 2) For genital lesions, see the section Pruritus Ani.

small, grouped vesicles coalesce to form coin-shaped plaques w/an erythematous base and clearly demarcated borders crusting and excoriations typically affects young adults and the elderly typically occurs during fall and winter

Ezcematous Eruptions: Nummular dermatitis pruritic inflammatory disorder Z: Chronic disorder that responds to moisturizers or topical steroids Refractory cases: Tar baths or UVB phototherapy

papulopustules form on erythematous bases and may become confluent w/plaques and scales; vermilion border is spared, and satellite lesions are common typically occurs in young women

Ezcematous Eruptions: Perioral dermatitis Culture to r/o staphylococcal infection Z: ~Avoid topical steroids (aggravate lesions) ~Use topical metronidazole or erythromycin or oral minocycline, doxycycline, or tetracycline ~Untreated lesions will fluctuate over time, similar to rosacea.

Current Blurb: ~Dry scales and underlying erythema. ~Scalp, central face, presternal, interscapular areas, umbilicus, and body folds. ~often coexists w/psoriasis ~pruritus is an inconstant finding ~scalp, face, chest, back, umbilicus, eyelid margins, and body folds have dry scales or oily yellowish scurf ~pts w/Parkinson disease, HIV infection, and pts who become acutely ill and are hospitalized often have seborrheic dermatitis. Atlas: ~A very common chronic dermatosis characterized by redness and scaling and occurring in regions where the sebaceous glands are most active (face and scalp, presternal area, in body folds). Mild scalp SD causes flaking (*dandruff*). ~Increased incidence in Parkinson disease and in immunosuppressed pts (HIV/AIDS) ~"Cradle cap" in infants; pityriasis sicca (dandruff) Zarbocks: occurs where sebaceous glands are most active (body folds, face, scalp, genitalia) ~*scattered yellowish or gray, scaly macules and papules w/a greasy look* ~sticky crusts and fissures are found behind the ears (esp in infants); on the scalp, it manifests as cradle cap in infants and dandruff in adults common during infancy and puberty and in young to middle-aged adults Exam Master: ~a common, chronic disorder characterized by greasy scales overlying erythematous patches or plaques ~most common location is in the scalp, where it may be recognized as severe dandruff ~Commonly affected areas on the face are eyebrows, eyelids, glabella, and nasolabial folds ~Pruritus is variable.

Ezcematous Eruptions: SEBORRHEIC DERMATITIS Hereditary diathesis, but Malassezia furfur may play a pathogenic role. Z: 1) UV radiation is helpful ~lesions improve during the sumer and flare during the fall and winter 2) Cradle cap ~Tx w/olive oil compresses and baby shampoo or ketoconazole shampoo or cream or w/hydrocortisone 3) Dandruff ~Acute flare-ups: Use shampoos containing selenium or zinc ad ketoconazole shampoo ~Severe cases: tar shampoos or topical steroids 4) Other areas ~ketoconazole shampoo or topical steroids ~blepharitis is tx w/gently scrubs using baby shampoo; f/u w/a suspension of sulfa and/or steroid preparation or ketoconazole cream if needed Current: 1) Scalp ~Shampoos that contain zinc pyrithione or selenium are used daily if possible. These may be alternated with ketoconazole shampoo (1% or 2%) used twice weekly. ~refractory cases: combination of shampoos ~for milder cases and scalp psoriasis: Tar shampoos ~Topical corticosteroid solutions or lotions are then added if necessary and are used bid. (See tx for scalp psoriasis) 2) Facial ~Mainstay of therapy is a mild corticosteroid (hydrocortisone 1%, alclometasone, desonide) used intermittently and not near the eyes. ~If the disorder can't be controlled w/intermittent use of a mild topical corticosteroid alone, ketoconazole (Nizoral) 2% cream is added bid. ~Topical tacrolimus (Protopic) and pimecrolimus (Elidel) are steroid-sparing alternatives. 3) Non-hairy areas ~Low-potency corticosteroid creams (ie, 1% or 2.5% hydrocortisone, desonide, or alclometasone dipropionate) are highly effective. 4) Intertriginous areas ~Apply low-potency corticosteroid lotions or creams bid x 5-7 days and then once or twice weekly for maintenance PRN. ~Ketoconazole or clotrimazole cream may be a useful adjunct. ~Tacrolimus or pimecrolimus topically may avoid corticosteroid atrophy in chronic cases. 5) Eyelid Margins ~"Marginal blepharitis" usually responds to gentle cleaning of the lid margins nightly PRN, w/undiluted Baby Shampoo using a cotton swab. Exam Master: ~low-potency topical glucocorticoids in conjunction with a topical antifungal agent (ketoconazole cream or ciclopirox cream) is often effective ~scalp may benefit from antidandruff shampoos or high-potency topical glucocorticoid solutions for the control of severe scalp involvement.

~chronic venous insufficiency leads to edema, stasis dermatitis, hyperpigmentation, fibrosis, and ulceration ~varicose veins, SF phlebitis, and venous thrombosis commonly occur before skin changes ~women > men (3:1) (pregnancy exacerbates both venous insufficiency and stasis dermatitis) ~pts complain of heaviness or aching in the legs, which is aggravated by standing and relieved w/walking ~dermatitis of lower legs and feet manifests w/inflammatory papules, scales, and crusts; stippled pigmentation develops, and excoriations are common

Ezcematous Eruptions: Stasis dermatitis 1) Doppler studies, sonography, or venography will confirm chronic insufficiency. 2) Bx of lesions shows dilated vessels, tortuous veins, edema, and fibrin deposition. Z: 1) Chronic venous insufficiency: ~compression stockings ~sclerosis of varicose veins helps to prevent further dermatitis, but recurrence is common 2) Vascular bypass or angioplasty may benefit severely compromised areas, but results are only fair. 3) Ulcers: ~chronic tx

Current Blurb: ~Itching and burning in hairy areas. ~Pustules in the hair follicles. inflammation of hair follicles pseudofolliculitis = ingrown hairs occurring in the beard area ~lesions are erythematous papules or pustules; usually not painful, but may burn ~sycosis is severe, deep-seated, recalcitrant folliculitis w/surrounding eczema and crusting ~abscesses may form at the site of folliculitis Sanford: •Infection of the hair follicle w/purulent exudate in the epidermis. •Need to distinguish from non-infectious etiologies, e.g., pseudofolliculitis barbae (foreign rxn to ingrown hair in beard).

Folliculitis S. aureus (most common) P. aeruginosa (inadequately chlorinated swimming pools, whirlpools, and hot tubs) Aeromonas hydrophila (following water exposure) C. albicans (after Abx exposure, glucocorticoid therapy or DM) Reports of folliculitis and SQ abscesses from rapid growing atypical mycobacteria after exposure in nail salons, foot whirlpool baths. Etiology: M. chelonae; M. fortuitum Malassezia furfur non-infectious type is common among people working in hot, oily environments (engine workers on ships, machinists, or anyone working in a hot, dirty environment) occlusion, perspiration, and rubbing from tight clothes Z: 1) Gentle cleansing and mild compresses help. ~Protection from offending substances and use of drying agents also help. 2) Mild cases: ~Topical application of clinda or erythromycin works well ~Mupirocin (Bactroban) ointment also may be used 3) More extensive cases ~oral Abx 4) Hot tub folliculitis ~usually resolves w/o tx ~severe or recalcitrant cases may be tx w/a FQ Sanford: 1) Usually self-limiting; no therapy indicated. Hot packs for comfort. 2) Avoid shaving involved area. 3) See specific therapy for M. fortuitum and M. chelonae. 4) Alternative Regimen •Could use Mupirocin ointment if staphylococcal etiology. •Could use antifungal topical cream/ointment if Candida suspected or proven. Note: •In AIDS patients, consider eosinophilic folliculitis.

Current Blurb: ~Severe pruritus of vulva, anus, or body folds. ~SF denuded, beefy-red areas +/- satellite vesicopustules. ~Whitish curd-like concretions on the oral and vaginal mucous membranes. ~Yeast and pseudohyphae on microscopic exam of scales or curd. ~Itching may be intense. ~Burning is reported, particularly around the vulva and anus. ~Lesions consist of superficially denuded, beefy-red areas in the depths of the body folds such as in the groin and the intergluteal cleft, beneath the breasts, at the angles of the mouth, and in the umbilicus. ~The peripheries of these denuded lesions are superficially undermined, and there may be satellite vesicopustules. ~Whitish, curd-like concretions may be present on mucosal lesions. ~Paronychia may occur.

Fungal: (Mucocutaneous) CANDIDIASIS 1) Direct microscopy ~KOH prep visualizes pseudohyphae and yeast forms 2) Culture ~Identifies species of Candida ~Presence of C. albicans doesn't make the dx ~Sensitivities to antifungal agents can be performed on isolate in cases of recurrent infection ~R/o bacterial secondary infection 1) General Measures ~Affected parts s/b kept dry and exposed to air as much as possible. ~If possible, discontinue systemic antibiotics. 2) Nails & Paronychia ~Apply clotrimazole solution 1% bid. ~Alternative: Thymol 4% in ethanol applied once daily 3) Skin ~Apply nystatin ointment or clotrimazole cream 1%, either w/hydrocortisone cream 1% bid. ~Gentian violet 0.5% solution is economical and highly effective in treating cutaneous candidiasis (and also mucosal disease), but the purple discoloration represents a cosmetic issue in some pts. 4) Vulvular and Anal Mucosal Membranes ~For vaginal candidiasis, single-dose fluconazole is effective. ~Intravaginal clotrimazole, miconazole, terconazole, or nystatin may also be used. ~Long-term suppressive therapy may be required for recurrent or "intractable" cases. ~Non-albicans candidal species may be identified by culture in some refractory cases and may respond to oral itraconazole bid x 2-4 weeks. 5) Balanitis ~Most frequent in uncircumcised men, and Candida usually plays a role. ~Topical nystatin ointment is the initial tx if the lesions are mildly erythematous or superficially erosive. ~Soaking w/dilute aluminum acetate for 15 minutes bid may quickly relieve burning or itching. ~Chronicity and relapses, esp after sexual contact, suggest reinfection from a sexual partner who s/b tx. ~Severe purulent balanitis is usually due to bacteria. If it's so severe that phimosis occurs, oral Abx (some w/activity against anaerobes) are required; if rapid improvement does not occur, urologic consultation is indicated. 6) Mastitis ~Lancinating breast pain and nipple dermatitis in breastfeeding women may be a manifestation of Candida colonization/infection of the breast ducts. ~Oral fluconazole daily can be dramatically effective. ~Topical gentian violet 0.5% is also useful in these cases.

Atlas: ~occurs in moist, occluded areas (interdigital, diaper area, occluded skin) ~many pts have predisposing factors 1) Candidal Intertrigo ~pruritis, tenderness, pain ~initial pustules on erythematous base become eroded and confluent ~subsequently, fairly sharply demarcated, plycyclic, erythematous, eroded patches w/small pustular lesions at the periphery (satellite pustules) ~inframammary or submammary, axillae, groins 2) Interdigital ~most common in obese elderly ~initial pustule becomes eroded, w/formation of SF erosion or fissure ~webspace usually betw 3rd and 4th fingers; maceration in feet webspace 3) Diaper Dermatitis ~irritability, discomfort w/urination, defecation, changing diapers ~erythema, edema w/papular and pustular lesions ~erosions, collarette-like scaling at the margins of lesions ~genital and perianal skin, inner aspects of thighs and buttocks 4) Occluded Skin ~under occlusive dressing, under cast, on back in hospitalized pt 5) Follicular Candidiasis ~small, discrete pustules in Ostia of hair follicles ~usually in occluded skin •SF Candida infection of the epidermidis. •Presents as erythematous plaques and erosion which may have satellite papulopustular lesions in warm, moist skin folds. •Risk factors: infants (diaper rash), obesity, diabetes, immunosuppression.

Fungal: CANDIDIASIS (Cutaneous) Candida albicans Clinical findings confirmed by direct microscopy or culture 1) Direct microscopy ~KOH prep visualizes pseudohyphae and yeast forms 2) Culture ~Identifies species of Candida ~Presence of C. albicans doesn't make the dx ~Sensitivities to antifungal agents can be performed on isolate in cases of recurrent infection ~R/o bacterial secondary infection Sanford: 1) Primary Regimen •Miconazole 2% solution, lotion, cream or powder bid OR •Clotrimazole 1% solution, lotion, or cream bid OR •Nystatin lotion, cream, or powder bid 2) Alternative Regimen •Fluconazole once daily in refractory cases Atlas: 1) Prevention ~Keep intertriginous areas dry, wash w/benzoyl peroxide bar, and use imidazole powder 2) Topical Antifungals ~Nystatin, azole, or imidazole cream 3) Oral Antifungals ~Nystatin (suspension, tablet, pastille) ~Eradicates bowel colonization ~May be effective in recurrent candidiasis of diaper area, genitals, or intertrigo 4) Systemic Antifungal Agents ~fluconazole tablets or oral suspension; parenteral for IV infusion ~Itroconazole capsules, oral solution, ketoconazole tablets, amphotericin B IV for severe disease

•Thrush: creamy white patches overlying inflamed mucosa of buccal and pharyngeal mucosa, palate, and tonsils. •Erythematous variant with flat erythematous lesions. •Angular cheilitis w/erythematous fissures in the corners of the mouth.

Fungal: CANDIDIASIS (Thrush) Candida albicans Other non-albicans Candida sp. 1) Mild disease: •Clotrimazole troches 5x/day x 7-14 days OR •Nystatin suspension or pastilles qid x 7-14 days 2) Moderate-severe disease and/or HIV-positive patient: •Fluconazole x 7-14 days 3) Alternative Regimen •Itraconazole solution x 7-14 days •Posaconazole bid x 3 days, then qd x 7-14 days •Voriconazole x 7-14 days •Caspofungin loading dose, then IV or Micafungin IV or Anidulafungin IV loading dose, then IV x 7-14 days •Amphotericin B x 7-14 days Note: •HIV-positive patients: Antiretroviral therapy (ART) is recommended to prevent recurrent disease. •Suppressive therapy in select immunocompromised patients with recurrent disease: Fluconazole 3x/week. •Dysphagia or odynophagia is predictive of esophageal candidiasis.

•Vaginal or vulvar irritation, burning, or pruritus. •Cheesy, white d/c with white plaques on vaginal mucosa. •Swelling or erythema of the perineum. Exam Master ~Pt who presents w/a malodorous d/c and intense itching, has the S&S of trichomoniasis. ~Trichomoniasis is associated w/a greenish-gray, frothy, often malodorous d/c. ~75% of the male partners of the infected pts harbor the organism. ~Characteristic "strawberry spots" can be seen on the cervix and vagina.

Fungal: CANDIDIASIS (Vulvovaginitis) Candida albicans most common Other Candida sp. Clinical suspicion confirmed by KOH prep of scraping from mucosal surface. 1) Uncomplicated: Topical azole therapy: •Butoconazole 2% cream HS x 3 days or 2% cream SR x 1 OR •Clotrimazole vaginal tabs (2 HS x 3 days) or 1% cream HS x 7 days (14 days may ↑ cure rate) or vaginal tab x 7 days or vaginal tab x 1 OR •Miconazole vaginal suppository (1 HS x 3 days) or vaginal suppository x 7 days or 2% cream HS x 7 days OR •Terconazole vaginal tab (1 HS x 3 days) or 0.4% cream HS x 7 days or 0.8% cream intravaginal x 3 days •Tioconazole 6.5% vaginal ointment x 1 dose Fluconazole 150 mg po x 1 dose 2) Complicated (immunocompromised, recurrence, severe disease, or non-C. albicans species): •Topical azole therapy as above for ≥ 7 days •Fluconazole x 2-3 doses 3) Alternative Regimen (Candida glabrata infection): •Topical Flucytosine cream 17% alone or in combination w/Amphotericin B cream (3%) intravaginal daily x 14 days •Topical boric acid, gelatin capsule intravaginal daily x 14 days Note: Recurrent vulvovaginal candidiasis: consider induction therapy w/10-14 days of topical or oral azole, followed by Fluconazole once weekly x 6 months. Atlas: 1) Azole Creams or Suppository 2) consider systemic therapy if recurrent ~fluconazole tablets or oral suspension; parenteral for IV infusion ~Itroconazole capsules, oral solution, ketoconazole tablets, amphotericin B IV for severe disease 3) tx sexual partners

~SF fungal infection that can affect the hair, nails, and skin ~when describing the area of infection, the word tinea ("fungal infection") is followed by the affected part of the body •tinea pedis (foot) •tinea cruris (groin) •tinea corporis (trunk, legs, arms, or neck) •tinea barbae (beard) •tinea unguium (nails) •tinea manuum (hand) •tinea facialis (face) •tinea capitis (head) ~erythematous, annular patch w/distinct borders and a central clearing; a fine scale usually covers the patch ~itching, stinging, and/or burning; maceration or peeling fissures are common betw the digits ~nails present w/a thickening discoloration and onychomycosis of the nail bed and nail plate ~tinea capitis: broken hair shafts are seen as black dots ~a kerion (indurated, boggy, inflammatory plaque studded w/pustules) can appear w/any of these infections but cost commonly is found w/tinea capitis; it represents an intense inflammatory rxn to SF dermatophytes)

Fungal: DERMATOPHYTOSIS 3 most common dermatophytes affecting humans: Trichophyton, Microsporum, Epidermophyton spp Most common in the industrialized world: Trichophyton rubrum KOH prep s/b done to confirm the presence of fungus Z: 1) Wide selection of topical creams, ointments, lotions, powders, and sprays. ~use bid x 4+ weeks ~if vesicles are present, powders help to dry the area and to prevent maceration 2) Chronic or resistant infections or nail infection: ~may require oral griseofulvin, itraconazole, terbinafine, or ketoconazole ~tx may take 3 months 3) Kerions ~fluconazole or griseofulvin 4) Compliance and monitoring are very important! ~Advise pts taking griseofulvin not to use alcohol in any form b/c it may cause a rxn similar to that w/disulfiram (Antabuse): flushing, HA, N&V, sweating, weakness, vertigo, CP, dyspnea, confusion ~Pts w/hepatic disorders s/b monitored closely when using oral antifungal meds ~If the pt will be on these meds for a long period (i.e. tx tineau unguium for several months): monitor liver enzymes (make sure to get a baseline) 5) Steroids s/b avoided ~Long-term use will exacerbate the condition and increase the risk of side effects. 6) Local measures ~keeping the skin clean and dry ~wearing cotton socks and loose-fitting underclothes

Current Blurb: ~Velvety, tan, or pink macules or white macules that do not tan. ~Fine scales that are not visible but are seen by scraping the lesion. ~Central upper trunk the most frequent site. ~Yeast and short hyphae observed on microscopic examination of scales. ~hypo or hyperpigmented macules that do not tan ~most pts are asymptomatic and notice the infection only during the summer, when their tan is spotted due to localized areas of yeast overgrowth ~not contagious ~most common area involved: upper trunk Sanford: •Fine, scaly rash w/patches of discolored skin w/sharp borders commonly found on back, underarms, upper arms, chest, and neck. •Skin may appear lighter than surrounding healthy skin; in African Americans, either hypo- or hyper-pigmentation •R/o erythrasma. Exam Master: ~hypopigmented scaly patches w/a few reddish-brown hyperpigmentation

Fungal: Tinea Versicolor (Pityriasis Versicolor) *Malassezia furfur* (a yeast found on the skin of humans) Not sure why this yeast manifests in the spore and hyphal form in some pts, causing disease. KOH prep of scrapings will show hyphae and spores (*spaghetti and meatballs*) Wood light exam will show orange fluorescence Z: 1) Daily applications of selenium sulfide shampoo from the neck to the waist ~Leave it on for up to 15 min x 7 consecutive days ~Can be repeated monthly for maintenance therapy as necessary 2) Less popular topical methods of tx as well as oral tx w/ketoconazole ~Shouldn't shower for 18 hrs after taking oral ketoconazole (b/c it works by being delivered to the skin surface thru the pt's sweat) 3) Newer imidazole creams, lotions, and solutions are effective but expensive. Sanford: 1) Limited disease: •Ketoconazole 2% shampoo daily x 3 days; can use 2-3 times/wk for maintenance/prevention •Selenium sulfide 2.5% shampoo: daily application while bathing for 1-2 weeks, can use 2-3 times/wk for maintenance/prevention 2) Extensive disease: •Fluconazole 300 mg x 1 dose, repeat in 14 days 3) Alternative Regimen •Itraconazole x 7 days

Tender inflammatory nodules or abscesses form. Lesions aren't related to hair follicles. Open comedones and sinus tracts form and may drain purulent material. +/- fibrosis, scarring, and contractures (severity is variable) affects females betw puberty and menopause (axillary disease) > males (anogenital disease) Risk Factors: obesity, hx of acne, apocrine duct obstruction, and bacterial infection; appears to be a genetic tendency Sanford: •a chronic follicular disease that occludes hair follicles in the skin of the axilla, inguinal area, perianal, perineal and infra-mammary areas. •Presents as painful, inflamed nodules. Exam Master: ~The age of onset begins at puberty, and it affects girls/women more than boys/men. ~*The initial lesions appear as red inflammatory nodules and/or abscesses that are very tender.* ~They may resolve, or they may drain purulent material. ~The lesions may reoccur in the same area. ~Their distribution is localized to the axillae, breasts, anogenital area, and groin. ~They may have a unique *double comedone* appearance that is highly characteristic of this disorder.

HIDRADENITIS SUPPURATIVA disease of the apocrine gland areas (axilla, anogenital, and scalp) •Abnormal skin cell development and shedding •Caused by follicular obstruction w/subsequent sterile inflammation. •Bacterial infection is not a primary event, but secondary bacterial infection can occur. Culture for secondary bacterial infection Zarbock's: 1) Lesions tx w/intralesional triamcinolone, incision and drainage of abscesses, and excision of sinus tracts. 2) Oral abx are given until lesions resolve; prednisone is added if the lesions are severe and s/b tapered >2 weeks. 3) Severe cases, especially in the anogenital area, may benefit from psychological support. Sanford: All regimens based on clinical experience. Refrain from smoking and lose weight if obese. Tx varies w/stage of dz: 1) Stage 1: Localized disease w/o sinus tracts or scarring •Topical Clindamycin 1% lotion bid reduces frequency of abscess formation •Anecdotal reports of benefit from intralesional triamcinolone 2-5 mg 2) Stage 2: Recurrent abscesses w/sinus tracts and scarring •Reports of benefit from combination of Clinda + Rifampin 3) Stage 3: Diffuse (severe) disease with multiple interconnected sinus tracts and scarring •Some reports of benefit from cyclosporine therapy. 4) Alternative Regimen •Surgical management may be curative for either individual scarred lesions or severe stage 3 disease. Several techniques used. •Recent use of laser therapy, especially for Stage 1 disease *Pt education: •Need daily use of antiperspirants. •Avoid tight clothing and high humidity. •Some advocate antiandrogens: in women, estrogen contraceptive + spironolactone; in men, dutasteride.

Tiny hairs ("exclamation hairs") are typically found. Loss can be patchy, involve only the scalp (alopecia totalis), or include the entire body (alopecia universalis). Atlas: ~a localized loss of hair in round or oval areas w/no apparent inflammation of the skin ~non-scarring; hair follicle intact; hair can regrow ~clinical findings: hair loss ranging from solitary patch to complete loss of all terminal hair Exam Master: ~may see nail pitting

Hair & Nails: ALOPECIA AREATA Idiopathic. Hair loss that may be seen in thyroiditis, pernicious anemia, SLE, or Addison's disease. (Atlas: not needed though) 1) ANA to r/o SLE 2) RPR test to r/o secondary syphilis 3) KOH prep to r/o tinea capitis Z: It may respond to systemic steroids, but relapse is common. Atlas: ~intralesional triamcinolone effective for limited number of lesions 1) General ~Tx directed at inflammatory infiltrate. No curative tx is currently available. ~In many cases, the most important factor in management of the pt is psychological support from dermatologist, family, and support groups. ~Pts w/extensive scalp involvement may prefer to wear a wig or hairpiece. 2) Glucocorticoids ~Topical: superpotent agents not usually effective ~*Intralesional injection: few and small lesions can be tx w/intralesional triamcinolone acetonide* ~Induction of allergic contact dermatitis: dinitrochlorobenzene, squaric acid dibutylester, or diphencyprone successful, but local discomfort due to ACD and swelling of regional lymph nodes ~Oral PUVA: variably effective, worth a trial in pts who are highly distresses; entire body must be exposed Exam Master: ~Treatment of alopecia areata includes watchful waiting for patients with a few small patches of involvement. Patients with limited involvement have a very good prognosis, usually returning to normal hair growth and distribution. ~Other patients with a little more involvement, or those who are upset by their bald patches, can be treated with intralesional injection of steroid (triamcinolone acetonide) to stimulate hair growth. ~A more extensive involvement of the scalp is treated with anthralin, photochemotherapy, topical allergens, or topical minoxidil. ~Systemic steroids will cause hair growth, but the new hair will only last as long as the steroid therapy, thus this treatment is not often used.

Loss of hair that's variable and unpredictable. Atlas: ~*Pattern hair loss is the most common type of progressive balding.* ~In males, pattern/extent of hair loss varies from bitemporal recession, to frontal and/or vertex thinning, to loss of all hair except that long the occipital and temporal margins ("Hippocratic wreath") 1) Skin: ~Most pts present w/complaints of gradually thinning hair or baldness. ~Scalp skin is normal. In young women, look for signs of virilization (acne, excess facial or body hair, male-pattern escutcheon). W/advanced pattern hair loss, scalp is smooth and shiny; orifices of follicles are barely perceptible w/the unaided eye. 2) Hair ~hair in areas of pattern hair loss becomes finer in texture (shorter in length, reduced diameter) ~in time, hair becomes vellus and eventually atrophies compleletly 3) Distribution ~Men usually exhibit patterned loss in the frontotemporal and vertex areas ~Women also lose scalp hair according to the male pattern, but hair loss is far less pronounced 4) Systemic ~In young women w/AGA, look for signs of virilizatoin (clitoral hypertrophy, acne, facial hirsutism) and, f present, r/o endocrine dysfunction.

Hair & Nails: ANDROGENETICA ALOPECIA (Males: androgenetic alopecia, male-pattern baldness, common baldness; Females: hereditary thinning, female-pattern baldness) Occurs thru the combined effect of: 1) Genetic predisposition 2) Action of androgen on scalp hair follicles Clinical dx is made on the hx, pattern of alopecia, and family incidence of AGA. Skin bx may be needed in some cases. Zarbocks: 1) Recent onset and smaller areas of hair loss ~Minoxidil solutions are most effective ~Finasteride may also be effective. Side effects: loss of libido, ED Atlas (see p.766 for explanation): 1) Oral Finasteride 2) Topical Minoxidil 3) Antiandrogens (women only) 4) Hairpiece 5) Surgery ~hair transplantation ~scalp reduction/rotation flaps Exam Master Pts w/androgenetic alopecia who have no evidence of a hyperandrogen state s/b tx w/topical minoxidil, finasteride, or hair transplant.

indicates infection w/fungi or yeast Sanford: •Fungal infection of the fingernail or toenail. •Main patterns include distolateral subungual, proximal subungual (associated with immunosuppressive condition, HIV), SF and total dystrophic. Atlas: ~nails lose protective and manipulative function ~complications: pain in toenail w/pressure from shoes, predispose to secondary bacterial infections, ulcerations of the underling nail bed ~complications occur more commonly in the growing population of immunocompromised individuals and diabetic pts ~most occur on the feet, esp on the big toes ~simultaneous occurrence on toenails and fingernails isn't common

Hair & Nails: ONYCHOMYCOSIS (Tinea Unguium) Dermatophytes (Trichophyton rubrum and T. mentagrophytes) account for most of cases Rarely candida and molds can cause disease 1) Clinical dx is never adequate. 2) Clinical findings confirmed by finding fungal forms in KOH prep, nail clipping, and/or isolation of pathogenic fungus on culture. Sanford 1) Primary Regimen ~Fingernail~ •*Terbinafine* x 6 weeks (79% effective) •Itraconazole x 2-3 months (~60-70% effective) ~Toenail~ •*Terbinafine* x 12 weeks (66-76% effective) •Itraconazole x 3-4 months (~60% effective) 2) Alternative Regimen ~Fingernail~ •Fluconazole x 3-6 months (~50% effective) ~Toenail~ •Fluconazole x 6-12 months (~50% effective) •Efinaconazole (Jublia) 10% solution applied once daily x 48 weeks for the topical tx of toenail onychomycosis due to T. rubrum and T. mentagrophytes •Tavaborole (Kerydin) 5% solution applied once a day x 48 weeks Atlas (see p.809): 1) Debridement 2) Topical Agents 3) Systemic Agents ~terbinafine ~itraconazole (approved) in dermatophytes and Candida ~fluconazole (not approved) in dermatophytes and Candida ~ketoconazole (not approved) 4) Secondar prophylaxis ~antifungal cream, lotion, or powder daily ~antiseptic gels: ethanol or isopropyl alcohol ~pedicures/manicures: make sure instruments are sterilized or individuals have their own

inflammation of the nail fold erythema, swelling, and throbbing pain may extend into the proximal nail fold and eponychium Sanford: •Cutaneous infection of the hand, cuticle or fingers usually occurring near or around the nail. •Often results from thumb sucking, nail biting, manicuring, other trauma.

Hair & Nails: PARONYCHIA Bacterial: S. aureus, Gram-negative rods Fungal: Candida sp. Viral: H. simplex (Whitlow), Orf 1) Bacterial •Incision and drainage; culture •TMP-SMX-DS 1-2 tab po bid while waiting for culture result 2) Fungal •Topical Amphotericin B, Clotrimazole, Econazole, Miconazole, or Nystatin tid/qid x 7-14 days OR •Ketoconazole x 14 days •Ciclopirox olamine 1% cream/lotion; apply topically bid x 7-14 days 3) Viral •Acyclovir x 10 days •Famcicloviror Valacyclovir x 7-10 days

Sanford: •Homelessness. Poor personal hygiene. Sharing a bed. •Lice live in clothing, especially the seams. Leave clothing for blood meal. •Lice can serve as vector for trench fever, typhus, or relapsing fever. •Main host complaint is itching.

Insects/Parasites: PEDICULOSIS (Body Lice) Pediculus humanus humanus (Pediculus humanus corporis) Dx is by visual identification of louse in clothing. SANFORD 1) Primary Regimen •5% Permethrin cream to entire body skin. Leave in place 6-8 hours. Only one application. •Problem is the clothing. Either heat wash (149º F), dry clean or discard. If clothing washed, dry iron - especially seams. Rarely, nits on body hair. 2) Alternative Regiman •Ivermectin on days 0, 7 and 14 reported successful in an outbreak in a homeless shelter ATLAS 1) Decontamination of clothing and bedding ~hygiene measures 2) Delousing ~pyrethrin, permethrin, malathion

Sanford: •Lice infestation of the scalp; presents with pruritis. Most common in children. Occurs worldwide. Do not carry any disease. •Adult louse free and crawls on scalp and hair; eggs (nits) appear white and on hair shaft near scalp. •Most often asymptomatic; reaction to saliva of louse can cause itching.

Insects/Parasites: PEDICULOSIS (Head Lice) Pediculus humanus capitis 1) Sanford: ~Diagnosis by visualizing live organism. ~Suggest use of wet combing: wet hair w/hair conditioner, use fine-toothed comb (nit comb), start at scalp level with pressure, comb entire scalp twice (sensitivity 91%). 2) Atlas: ~Clinical findings, confirmed by detection of lice. ~Louse comb increases chances of finding lice. ~Nits alone aren't diagnostic of active infestation. Nits within 4mm of scalp suggest active infestation. ATLAS 1) Topically applied insecticides ~permethrin, malathion, pyrethrin, piperonyl, butoxide 2) Systemic ~oral ivermectin SANFORD Topical ~Most drugs kill adults but not the eggs; hence re-treatment in 7-10 days usually necessary to kill newly hatched lice prior to their laying eggs. ~Regardless of topical tx , remove nits w/nit comb initially and repeat in 7-10 days. 1) *Pyrethrins and permethrin* still 1st choice although increasing resistance recognized: •Permethrin 1% cream rinse (OTC as Nix or generic); prescription strength is 5% but no more effective than the OTC 1%. •Shampoo, dry hair, apply permethrin & leave in place 10 minutes, then rinse. Repeat in 7-10 days. •Pyrethrins w/piperonyl butoxide (OTC as Rid or generic) •Apply to dry hair for 10 minutes, shampoo, repeat in 7-10 days •A failure to respond may indicate drug resistance. 2) Malathion lotion 0.5% (includes terpineol) (Ovide) •Kills both adults and eggs •Apply to scalp for 8-12 hours before rinsing •2nd treatment in 7 days sometimes needed •Malodorous, more expensive, but more efficacious than Permethrin; compliance only 50% 3) Spinosad, 0.9% suspension (Natroba) [expensive] • Apply to affected area of dry hair for 10 minutes and then wash off; repeat in 7 days if needed 4) Benzyl alcohol (Ulesfia) •5% lotion applied to dry hair for 10 minutes & then rinsed off. Repeat in 7 days. 5) Ivermectin 0.5% lotion (Sklice) [expensive] •Kills adults; causes death of newly hatched lice within 48 hrs •Approved for infants >6 months old •Convenient: Apply to dry hair and scalp for 10 minutes and then rinse Oral 1) Ivermectin •Can repeat after 8 days if live lice persist •Alternative if lice resistant to topical therapy •Do not use in pregnancy or in children weighing <15 kg 2) TMP-SMX x 10 days •TMP-SMX combined with topical Permethrin. TMP-SMX kills vitamin B-producing bacteria in gut of louse. Note: •Geographic variations in resistance of lice to Permethrin. •Finding nits (eggs) w/o lice doesn't always mean infection is present. Nits can remain visible for months after eradication of live lice. •Kids w/head lice can return to school after 1st topical tx. Pt Education: •Wash hats, scarves, coats and bedding in hot water and dry in hot dryer for 20 or more minutes •Wash combs and brushes and vacuum room of the patient

Current Blurb: ~Pruritus with excoriation. ~Nits on hair shafts; lice on skin or clothes. ~Occasionally, sky-blue macules (maculae ceruleae) on the inner thighs or lower abdomen in pubic louse infestation. 1-3mm flat creatures w/3 pairs of legs females lay 300 nits during a lifetime nits are opalescent, found on hair shafts, and hatch in about 1 week transmission is person to person ~pruritis is variable in severity; excoriations may become secondarily infected ~lice are visible but often difficult to find; nits are more readily seen on the hair shafts

Insects/Parasites: PEDICULOSIS (Lice) Pediculus humanus capitis infects the scalp (head lice) P. humanus var. corporis infects the body Phthirus pubis infects the pubic area (crabs) Specimens can be viewed under the microscope to confirm the dx. Z: 1) Prevention is key; avoid sharing contact item (hats, hairbrushes, etc) ~All contacts s/b examined. 2) Topical insecticides are effective. ~1st line tx: *permethrin*, pyethrins, and *malathion* ~alternative: ivermectin 3) Special combs help to remove nits ~Petroleum jelly or other occlusive materials may help suffocate the lice. 4) Reapplication in 7-10 days is recommended to kill any newly hatched lice.

Sanford: •Sexually transmitted lice infestation involving pubic area. Can spread to eyelashes (Pediculosis ciliaris). •Common to have another STD; test at time of diagnosis. Atlas: Manifested clinically by mild-mod pruritus, papular urticarial, and excoriations

Insects/Parasites: PEDICULOSIS (Pubic Lice, Crabs) Phthirus pubis (crab louse) Pediculosis pubis Pediculosis ciliaris (eyelash) Visualization of live adult lice, nymphs, or nits (eggs) attached to pubic (or other) hair to dx active infestation. SANFORD 1) Permethrin 1% cream, or Pyrethrins with piperonyl butoxide • Apply to pubic and perianal skin, thighs, trunk and axillae. Wash off after 10 minutes. •Evaluate for retreatment after 7 days. •If patient unlikely to return, advise empiric retreatment 2) Whether topical or oral therapy, remove visible nits (eggs) with fine-toothed nit comb or tweezers. 3) Pediculosis ciliaris (eyelash infestation): •Apply petrolatum or occlusive ophthalmic ointment to lid margins bid. •After 8-10 days, mechanically remove lice and nits. •If normal removal fails, Ivermectin 1 week apart. 4) Alternative Regimen ◾Malathion 0.5% lotion to pubic and perianal skin, thighs, trunk and axillae. Wait 8-12 hours before washing off. Malodorous. ◾Ivermectin x 1 dose then repeat in 2 weeks. Don't use during pregnancy or for children weighing <15 kg. Note: •Tx sexual contacts within the previous 30 days. •Don't use Lindane; toxicities include seizures and aplastic anemia. •Wash bedding and clothing in hot water and dry at ≥ 130ºF. ATLAS 1) Topically applied insecticides ~permethrin, malathion, pyrethrin, piperonyl, butoxide 2) Systemic ~oral ivermectin 3) Decontaminate bedding and clothing. 4) Tx sex partners.

Current Blurb: ~Generalized very severe itching. ~Pruritic burrows, vesicles and pustules, esp on finger webs and in wrist creases. ~Mites, ova, and brown dots of feces visible microscopically. ~Red papules or nodules on the scrotum and on the penile glans and shaft are pathognomonic. Atlas: ~SF epidermal infestation by S. scabiei hominis; chronic undiagnosed scabies is the basis for the expression "7 year itch" ~pruritus often w/minimal cutaneous findings; burrows under stratum corneum ~scabetic nodules: eczematous dermatitis; hyperinfestation (crusted or hyperkaratotic or Norwegian scabies) ~pruritus is intense, widespread, usually sparing head and neck ~itching often interferes w/or prevents sleep ~pruritus may be absent w/hyperinfestation ~rash ranges from no rash to generalized erythroderma ~pts w/atopic diathesis scratch, producing eczematous dermatitis ~some pts experience pruritus for many months w/no rash ~tenderness of lesions suggests secondary bacterial infection Zarbock: ~Distribution is most common on the hands, genitalia, and axillary areas. Lesions are often seen in the web spaces betw fingers and toes, around the belt line, or at the edges of socks. ~Lesions are pruritic burrows, vesicles, or nodules w/excoriations and crusting. ~Secondary infections typically are caused by GAS. Any age, but rarely in infants <3 months

Insects/Parasites: SCABIES Infestation w/Sarcoptes scabiei (8-legged mite) Dx: *Clinical findings, confirmed (if possible) by microscopy (identification of mites, eggs, or mite feces).* 1) Microscopy (Positive microscopy is confirmative but not always successful.) ~Highest yield in identifying a mite is in typical burrows on the finger webs, flexor aspects of wrists, and penis ~A drop of mineral oil before scraping facilitates yield. ~3 findings are diagnostic: S. scabiei mites, eggs, and fecal pellets ~Exam Master: *The most readily available test is examination of skin scrapings under low power magnification.* Note: Dx easily missed and s/b considered in a pt of any age w/persistent generalized severe pruritus. Z: 1) Use 1% lindane or 5% permethrin in a lotion or cream. ~Applied to the skin from the chin to the bottom of the feet and is left on overnight (8 hrs), and then washed off in the morning. ~Tx s/b repeated in 7 days. 2) Antihistamines or topical steroids may help relieve the itching. 3) Lindane is more toxic and s/b avoided in children <2 yoa, ppl w/extensive dermatitis, and those who are pregnant or lactating. SANFORD 1) Primary Regimen ~Immunocompetent~ •Permethrin 5% cream (ELIMITE). Apply to entire skin from chin down to and including toes. Also, under fingernails and toenails. Leave on 8-14 hours. Repeat in 1-2 weeks. Safe for children age >2 months. •Reapply to hands after handwashing. ~Norwegian or crusted scabies in immunocompromised patients, HIV/AIDS~ •Ivermectin on days 1, 15 and 29 + Permethrin 5% cream daily x 7 days and then twice weekly until cured. 2) Alternative Regimen •Ivermectin on day 1; second dose in 1-2 weeks if sx persist Pt education: •Antihistamines may help reduce itching. •Secondary streptococcal infections can occur. •Treat close contacts. •Wash and dry linens and clothing of infected pts and household. ATLAS Principles of tx: tx infested individuals and close physical contacts at the same time, whether or not sx are present; application s/b to all skin sites 1) Recommended Regimen ~*permethrin 5% cream* applied to all areas of the body ~lindane (g-Benzene hexachloride) 1% lotion or cream applied thinly to all areas of the body from the neck down; wash off thoroughly after 8 hrs Note: Lindane shouldn't be used after bathing or by pts w/extensive dermatitis, pregnant or lactating women, or children >2 yoa. Mite resistance exists. Low cost. 2) Alternative Regimen ~Topical: crotamiton 10%, sulfur 2-10% in petrolatum, benzyl benzoate 10% and 25%, benzyl benzoate w/sulfiram, malathion 0.5%, sulfram 25%, ivermectin 0.8% ~Systemic: oral ivermectin Note: Not approved by FDA. Don't use in infants, young children, or pregnant/lactating women.

~Generally, pt will begin to feel pain 3 hrs after a bite; systemic sx begin 4-6 hrs after the bite. ~An acute necrotic injury to the skin lasts 10-15 days. ~Black widows can cause a neurologic overstimulation (i.e. - muscle aches, spasms, rigidity). These spiders aren't prevalent today. Brown recluse can cause a significant rxn: ~Single bite is accompanied by an infarct of skin caused by rapid blood coagulation within the vessels. ~Lesion is a sinking macule, pale gray in color, slightly eroded in the center, and has a halo of very tender inflammation and hemorrhage. ~Lesion can extend to the muscle and be as large as the palm of the hand. Sanford: •Bite wound from spiders. •Most necrotic ulcers attributed to spiders are probably due to another cause, e.g., cutaneous anthrax or S. aureus (MRSA) infection. Infection associated w/spider bites is overdiagnosed. •Spider bite is painful; cutaneous anthrax infection is not painful. •Black widow bite may be confused with "acute abdomen". •Brown recluse spider habitat limited to the US (South Central and desert Southwest states).

Insects/Parasites: SPIDER BITES Although all spiders in the US are venomous, only a few can puncture the human skin. Most important = brown recluse (Loxosceles reclusa). Most bites occur while the pts is sleeping or dressing in the morning after the spider had crawled into the clothing during the night. Z: 1) *Most bites can be managed w/local care and analgesics.* 2) Neurologic manifestations of black widow bites are tx w/*diazepam and calcium gluconate.* 3) Brown recluse bites may be tx locally w/wound cleansing and analgesia. ~Extensive debridement has not proven to be beneficial. ~Usually, the wound decreases significantly in 5-10 days. 4) Antivenin rarely is indicated and not readily available. Current: 1) Black Widow ~Pain may be relieved w/parenteral opioids or muscle relaxants (eg, methocarbamol). ~Calcium gluconate 10% IV may transiently relieve muscle rigidity, though its effectiveness is unproven. ~Latrodectus antivenom is very effective, but b/c of concerns about acute hypersensitivity rxns (horse serum-derived), it's often reserved for very young or elderly pts or those who don't respond promptly to the above measures. Horse serum sensitivity testing is required. 2) Brown Recluse ~B/c bites occasionally progress to extensive local necrosis, some authorities recommend early excision of the bite site, whereas others use oral corticosteroids. ~Anecdotal reports have claimed success w/dapsone and colchicine. ~All of these tx remain of unproved value. Sanford: 1) Black widow (Latrodectus): •No antibiotic therapy indicated •Diazepam or calcium gluconate is helpful to control pain, muscle spasm. •Evaluate need for tetanus prophylaxis. 2) Brown recluse (Loxosceles): •Bite usually self-limited and self-healing. •No therapy of proven efficacy. Note: Brown recluse spider bite: •Dapsone is often used despite marginal supportive data. •Dapsone causes hemolysis (check for G6PD deficiency). Can cause hepatitis; baseline and weekly liver panels suggested.

"a black spot" acquired hyperpigmentation disorder of sun-exposed areas and may be associated w/pregnancy or w/oral contraceptives or other meds hyperpigmented macular areas evolve rapidly over weeks color usually is uniform young females

MELASMA (CHLOASMA) Wood's lamp examination accentuates the hyperpigmented macules Sunblock is essential. 1) 3% hydroquinone solution in combo w/0.025% tretinoin gel 2) alternative: 4% hydroquinone and glycolic acid in a cream base may be used

Atlas: ~multifocal systemic tumor of endothelial cell origin ~4 clinical variants: classic/European KS, endemic African KS, immunosuppressive therapy-related KS, and HIV/AIDS-related KS ~Stage- and variant-dependent localized and/or generalized disease: patches, plaques, and nodules ~Systemic involvement: mainly GI tract ~Responds to radiation and chemo. ~Mucocutaneous lesions are usually asymptomatic but are associated w/significant cosmetic stigma. ~At times, lesions may ulcerate and bleed easily. ~Large lesions on palms or soles may impede function. ~Lesions on the LEs that are tumorous, ulcerated, or associated w/significant edema often give rise to mod-severe pain. ~Urethral or anal canal lesions can be associated w/obstruction. ~GI involvement rarely causes sx. ~Pulmonary KS can cause bronchospasm, intractable coughing, SOB, and progressive respiratory failure. Sanford: •Viral DNA found in all KS tumors •Infection precedes KS •Seropositivity rate predicts KS rate •Virus latent in most cells; lytic in <5% of cells •Targets spindle cells

Neoplasms: KAPOSI SARCOMA *HHV8*; also called Kaposi's sarcoma-associated herpesvirus (KSHV) ATLAS ~Skin bx ~Imaging for internal organ involvement SANFORD •Clinical appearance & then biopsy •HHV8/KSHV serology; can now quantitate HHV8 in plasma by PCR Sanford: 1) Immune reconstitution (improvement) w/ effective ART leads to: •Reports of clearance of HHV8 from circulating cells (60-80% response rate) •Protease inhibitors have anti-tumor activity in mice & patients 2) Suggest oncology consultation for best local and systemic therapy Atlas: ~Goal is to control sx of the disease, not cure. 1) Classic KS ~responds well to radiotherapy of involved sites 1) African-endemic KS ~ when symptomatic, responds best to systemic chemo 3) Immunosuppressive drug-related KS ~regresses or resolves when drug dosages are reduced or discontinued 4) HIV-AIDS-associated KS ~usually responds to a variety of local therapies ~for extensive mucocutaneous involvement or visceral involvement, chemo is indicated ~all of this in addition to HAART

Current Blurb: ~May be flat or raised. ~S/b suspected in any pigmented skin lesion w/recent change in appearance. ~Examination w/good light may show varying colors, including red, white, black, and bluish. ~Borders typically irregular.

Neoplasms: MELANOMA Histologic dx 1) Treatment of melanoma consists of excision. ~After histologic dx, the area is usually reexcised w/margins dictated by the thickness of the tumor ~Thin low-risk and intermediate-risk tumors require only conservative margins of 1-3 cm. ~More specifically, surgical margins of 0.5-1 cm for melanoma in situ and 1 cm for lesions < 1 mm in thickness are recommended. 2) Sentinel lymph node bx (selective lymphadenectomy) using preoperative lymphoscintigraphy and intraoperative lymphatic mapping is effective for staging melanoma pts w/intermediate risk w/o clinical adenopathy and is recommended for all pts w/lesions >1 mm in thickness or w/high-risk histologic features. ~Referral of intermediate-risk and high-risk pts to centers w/expertise in melanoma is strongly recommended. ~Identifying the oncogenic mutations in pts w/advanced melanoma may be important in their tx. ~The long-term use of beta-blockers may reduce the risk of progression of high-risk melanoma.

Current Blurb: ~Non-healing ulcer or warty nodule. ~Skin damage due to long-term sun exposure. ~Common in fair-skinned organ transplant recipients.

Neoplasms: SCC *The preferred tx is excision.* ~Electrodesiccation and curettage and x-ray radiation may be used for some lesions, and fresh tissue Mohs is recommended for high-risk lesions (lips, temples, ears, nose) and for recurrent tumors. ~F/u for must be more frequent and thorough than for BCC, starting at every 3 months, w/careful examination of lymph nodes. ~In addition, palpation of the lips is essential to detect hard or indurated areas that represent early SCC. ~All such cases must be bx. ~Multiple SCCs are very common on the sun-exposed skin of organ transplant pts. The intensity of immunosuppression, not the use of any particular immunosuppressive agent, is the primary risk factor in determining the development of skin CA after transplant. The tumors begin to appear after 5 yrs of immunosuppression. Voriconazole tx appears to increase the risk of development of SCC, esp in lung transplant pts. Regular dermatologic evaluation in at-risk organ transplant rts is recommended. Biologic behavior of skin CA in organ transplant recipients may be aggressive, and careful management is required. ~Other forms of immunosuppression (i.e. - chronic lymphocytic leukemia, HIV/AIDS, and chronic iatrogenic immunosuppression) may also increase skin CA risk and be associated w/more aggressive skin CA behavior.

~abscess in the sacrococcygeal cleft associated w/subsequent sinus tract development ~painful, fluctuant area at the sacrococcygeal cleft more common in hirsute and obese individuals males > females (4:1) rare: pts >40 yoa Sanford: •"nest of hair" disease •an inflammatory process in the skin and SQ tissue •vast majority of cysts are at the cephalad end of the intergluteal cleft •Pts can present w/asymptomatic painless cysts or sinus openings, acute abscesses, or chronic persistent drainage.

PILONIDAL DISEASE (pilonidal cyst) Anaerobes, mixed aerobes and anaerobes Thought to result from a congenital failure to separate the ectoderm from the mesoderm with resultant trapping of "skin rests" under the surface of the skin. Sanford: 1) Surgical excision or incision and drainage. 2) Abx is adjunctive: •Mild: Amox-Clav bid •More Severe: Pip-Tazo IV or (Metronidazole IV + Ceftriaxone IV) Follicle removal may be required, w/unroofing of sinus tracts

Current Blurb: ~Examine at-risk patients on admission to hospital and daily thereafter. ~Pressure ulcers should be described by one of six stages: Stage I: Blanchable hyperemia. Stage II: Extension through epidermis. Stage III: Full thickness skin loss. Stage IV: Full thickness wounds with extension into muscle, bone, or supporting structures. Stage V: If eschar or slough overlies the wound, the wound is unstageable. Stage VI: Suspected deep tissue injury is an area of discolored or blistered skin.

PRESSURE ULCERS see Current pp.92-93

Current Blurb: ~Usually, abrupt onset of widespread, symmetric erythematous eruption. ~May mimic any inflammatory skin condition. ~Constitutional symptoms (malaise, arthralgia, HA, and fever) may be present. ~As is well recognized, only a minority of cutaneous drug reactions result from allergy. ~True allergic drug rxns involve prior exposure, an "incubation" period, rxns to doses far below the therapeutic range, manifestations different from the usual pharmacologic effects of the drug, involvement of only a small portion of the population at risk, restriction to a limited # of syndromes (anaphylactic and anaphylactoid, urticarial, vasculitic, etc), and reproducibility. ~*Rashes are among the most common adverse reactions to drugs* and occur in 2-3% of hospitalized pts. ~Amoxicillin, TMP-SMZ, and ampicillin or PCN are the most common causes of urticarial and maculopapular rxns. ~TEN and SJS are most commonly produced by sulfonamides and anticonvulsants. ~Phenolphthalein, pyrazolone derivatives, tetracyclines, NSAIDs, TMP-SMZ, and barbiturates are the major causes of fixed drug eruptions. 1) Simple drug eruptions ~involve an exanthem, usually appear in the 2nd week of drug therapy, and have no associated constitutional or lab findings. ~abx (including the penicillins and quinolones) are the most common causes 2) Complex drug eruptions (drug-induced hypersensitivity syndromes) ~occur during the 3rd week of tx on avg and have constitutional and lab findings: fevers, chills, hematologic abnormalities (especially eosinophilia), and abnormal liver or kidney function. ~mnemonic for complex eruptions is *"DRESS" (DRug Eruption with Eosinophilia and Systemic Sx*) ~most common causes are the long-acting sulfonamides, allopurinol, and anticonvulsants; use of anticonvulsants to tx bipolar disorder and chronic pain has led to an apparent increase in these rxns ~in pts of certain races, polymorphisms of antigen presenting MHC loci increases risk for the development of severe drug eruptions ~coexistent reactivation of EBV, HHV-6, or CMV is often present and may be important in the pathogenesis of these complex drug eruptions

Papulosquamous Diseases: DRUG ERUPTION (Dermatitis Medicamentosa) 1) Routinely ordered blood work is of no value in the dx of simple drug eruptions. 2) In complex drug eruptions, the CBC, liver biochemical tests, and renal function tests s/b monitored. Skin bx may be helpful in making the dx. 1) General Measures ~systemic manifestations are tx as they arise (eg, anemia, icterus, purpura) ~Antihistamines may be of value in urticarial and angioneurotic rxns ~Epi IV or SQ s/b used as an emergency measure ~In drug-induced hypersensitivity syndromes (DRESS), systemic corticosteroids may be required 2) Local Measures ~SJS/TEN w/extensive blistering eruptions resulting in erosions and SF ulcerations, which demand hospitalization and nursing care as for burn pts, develops in some DRESS pts.

Current Blurb: ~Pruritic, violaceous, *flat-topped* papules w/fine white streaks and symmetric distribution. ~*Lacy or erosive lesions of the buccal and vaginal mucosa; nail dystrophy* ~Commonly seen along linear scratch marks (Koebner phenomenon) on anterior wrists, penis, legs. ~Histopathologic examination is diagnostic. ~an inflammatory pruritic disease of the skin and mucous membranes characterized by distinctive papules w/a predilection for the flexor surfaces and trunk ~*3 cardinal findings: typical skin lesions, mucosal lesions, and histopathologic features of band-like infiltration of lymphocytes in the upper dermis* ~most common drugs causing LP-like rxns: sulfonamides, tetracycline, quinidine, NSAIDs, HCTZ ~Allergy to mercury and other metal containing amalgams can trigger oral lesions identical to LP ~Itching is mild to severe ~Lesions are violaceous, flat-topped, angulated papules, up to 1 cm in diameter, discrete or in clusters, w/very fine white streaks (Wickham striae) on the flexor surfaces of the wrists and on the penis, lips, tongue as well as buccal, vaginal, esophageal, and anorectal mucous membranes ~Papules may become bullous or eroded ~The disease may be generalized ~Mucous membrane lesions have a lacy white network overlying them that may be confused w/leukoplakia ~Presence of oral and vaginal LP in the same pt is common ~Pts w/both these mucous membranes involved are at much higher risk for esophageal LP ~The Koebner phenomenon (appearance of lesions in areas of trauma) may be seen. ~A special form of LP is the erosive or ulcerative variety, a major problem in the mouth or genitalia. ~SCC develops in 5% of pts w/erosive oral or genital LP and may occur in esophageal LP. Atlas: ~an acute or chronic inflammatory dermatosis involving skin and/or mucous membranes ~characterized by flat-topped, pink to violaceous, shiny, pruritic polygonal papules (see 4P's below) ~predilection for flexural aspects of arms and legs, can become generalized ~in the mouth, milky-white reticulated papules; may become erosive and even ulcerate ~main sx: pruritus; in the mouth, pain Zarbocks: acute or chronic inflammatory dermatitis that occurs in adults females > males *4P's: purple polygonal pruritic papule* ~Lesions are flat-topped, shiny, violaceous papules w/fine white lines on the surface (Wickham's striae). They typically are grouped and most commonly occur on the flexor aspect of the wrists, lumbar area, eyelids, shins, and scalp. Koebner's phenomenon is seen. ~Mucosal lesions occur on the vaginal mucosa, glans and penis, and in the mouth. They usually are very painful and often ulcerate. ~Variants include follicular, vesicular, actinic, and ulcerative lesions. ~Lesions may affect hair (scarring alopecia) or nails (destruction of nail fold and nail bed w/longitudinal splintering).

Papulosquamous Diseases: LICHEN PLANUS (DDx: psoriasis, lichen simplex chronicus, GVH disease, syphilis, leukoplakia) lichen planus-like eruptions may occur in GVH disease, malignant lymphoma, and drug rxns 1) *Bx and direct immunofluorescence* confirm the dx. ~Erosive oral lesions require biopsy and often direct immunofluorescence for dx since LP may simulate other erosive diseases. 2) Screening for Hep C s/b considered due to the higher prevalence of anti-hepatitis C virus antibodies in pts w/LP. Z: 1) Topical steroids w/occlusive dressings are used. 2) Intralesional steroids or topical tretinoin us used for severe localized lesions. 3) Oral lesions: cyclospirne mouthwash 4) Severe, painful cases: systemic therapy (cyclosporine, corticosteroids, or retinoids) 5) Generalized eruptions: psoralens + UVA (PUVA) radiation therapy Current: 1) Topical Therapy ~Superpotent topical corticosteroids applied bid are most helpful for localized disease in non-flexural areas. ~Alternatively, high-potency corticosteroid cream or ointment may be used nightly under thin pliable plastic film. ~Topical tacrolimus appears effective in oral and vaginal erosive LP, but long-term therapy is required to prevent relapse. If tacrolimus is used, lesions must be observed carefully for development of CA. Since absorption can occur thru mucous membranes, serum tacrolimus levels s/b checked at least once if widespread mucosal application (>5-10 cm2) is used. ~If the erosive oral LP lesions are adjacent to a metal containing amalgam, removal of the amalgam may result in clearing of the erosions. 2) Systemic Therapy ~Corticosteroids may be required in severe cases or in circumstances where the most rapid response to tx is desired. ~Unfortunately, relapse almost always occurs as the corticosteroids are tapered, making systemic corticosteroid therapy an impractical option for the management of chronic LP. ~NB-UVB, bath PUVA, oral PUVA, and the combination of an oral retinoid + PUVA (re-PUVA) are all forms of phototherapy that can improve LP. ~Hydroxychloroquine po bid can also be effective in mucosal LP. Atlas: *topical and systemic glucocorticoids, cyclosporine* ~Local Therapy~ 1) Glucocorticoids ~*cutaneous lesions: topical glucocorticoids* w/occlusion ~*symptomatic cutaneous or oral mucosal lesions and lips: intralesional triamcinolone* 2) Cyclosporine and Tacrolimus Solutions for severely symptomatic oral LP ~Systemic Therapy~ 1) Cyclosporine for very resistant and generalized cases 2) Glucocorticoids ~Oral prednisone for pts w/symptomatic pruritis, painful erosions, dysphagia, or cosmetic disfigurement 3) Systemic Retinoids (Acitretin) ~adjunctive measure in severe (oral, hypertrophic) cases ~Other~ 1) PUVA Photochemotherapy in pts w/generalized LP or cases resistant to topical therapy 2) Mycophenolate mofetil, heparin analogues (enoxaparin) in low doses; azathioprine Exam Master: Topical glucocorticoids with intralesional triamcinolone (pt also had oral lesions)

Current Blurb: ~Oval, fawn-colored, scaly eruption following cleavage lines of trunk. ~Herald patch precedes eruption by 1-2 weeks. ~Occasional pruritus. ~a common mild, acute inflammatory disease that's 50% more common in females ~young adults are principally affected, mostly in the spring or fall ~concurrent household cases have been reported ~Itching is common but is usually mild. ~lesions consist of oval, fawn-colored plaques up to 2 cm in diameter. ~centers of the lesions have a crinkled or *cigarette paper* appearance and a collarette scale (i.e. - a thin bit of scale that is bound at the periphery and free in the center); only a few lesions in the eruption may have this characteristic appearance ~Lesions follow cleavage lines on the trunk (*Christmas tree pattern*), and the proximal portions of the extremities are often involved ~A variant that affects the flexures (axillae and groin), so called inverse pityriasis rosea, and a papular variant, esp in black pts, also occur ~An initial lesion (*herald patch*) that's often larger than later lesions often precedes the general eruption by 1-2 weeks. The eruption usually lasts 6-8 weeks and heals w/o scarring. Atlas: ~an acute exantheatous eruption w/a distinctive morphology and often w/a characteristic self-limited course ~initially, a single (primary or "herald") lesion develops, usually on the trunk ~1-2 weeks later, a generalized secondary eruption develops in a typical distribution pattern (Christmas tree) ~entire process remits spontaneously in 6 weeks Zarbocks: characterized by a herald patch, which precedes widespread symmetrical papular eruption ~May be mild URI-like prodrome before the onset of the rash. ~Herald patch is a solitary round or oval pink plaque w/a raised border and fine adherent scales in the margin. It typically precedes the rash by a week or so. ~Rash begins to appear on the trunk as round or oval, salmon-colored, slightly raised papular and macular lesions usually 1 cm in diameter. ~Long axis of each lesion usually follows the natural skin folds, giving a *Christmas tree-like distribution*. It's usually confined to the trunk. ~In the beginning, the lesions are covered w/a fine scale that desquamates, leaving an inverse collarette scale around each lesion. ~Pityriasis rosea usually lasts for 3-8 weeks and disappears spontaneously.

Papulosquamous Diseases: PITYRIASIS ROSEA (DDx: syphilis, tinea corporis, seborrheic dermatitis, tinea versicolor) Idiopathic, but *reactivation of HHV-7 and HHV-6* are the most probable cause 1) Dx is made by finding one or more classic lesions. 2) A serologic test for syphilis s/b performed if at least a few perfectly typical lesions aren't present and esp if there are palmar and plantar or mucous membrane lesions or adenopathy (suggestive of secondary syphilis) 3) For the nonexpert, an RPR (rapid plasma reagin) test in all cases is not unreasonable. Atlas: Symptomatic 1) oral antihistamines and/or topical antipruritic lotions for relief of pruritus 2) topical glucocorticoids 3) may be improved by UVB phototherapy or natural sunlight exposure if tx is begun in 1st week of eruption 4) short course of systemic glucocorticoids Z: 1) None indicated other than lotions or emollients for the scales. 2) UVB phototherapy may be helpful if started during the 1st week of eruption. 3) Lotions, antipruritics, or oral antihistamines may help if itching is bothersome. Current: 1) *often requires no tx* 2) In Asians, Hispanics, or blacks (in whom lesions may remain hyperpigmented for some time), more aggressive management may be indicated.Treatment is, otherwise, only indicated if the pt is symptomatic. No tx has been demonstrated efficacious in pityriasis rosea in adequately controlled and reproduced trials. Most dermatologists recommend UVB treatments, or prednisone as used for contact dermatitis for severe or severely symptomatic cases. For mild to moderate cases, *topical corticosteroids* of medium strength (triamcinolone 0.1%) and oral antihistamines may also be used *if significant pruritus is bothersome.*

Current Blurb: ~Silvery scales on bright red, well-demarcated plaques, usually on the knees, elbows, and scalp. ~*Nail findings: pitting and onycholysis* (separation of the nail plate from the bed). ~Mild itching (usually). ~May be associated with *psoriatic arthritis* ~Psoriasis patients are at increased risk for metabolic syndrome and lymphoma. ~Histopathology not often useful, can be confusing ~often no sx, but itching may occur and be severe ~Favored sites include the scalp, elbows, knees, palms and soles, and nails ~lesions are red, sharply defined plaques covered w/silvery scales ~glans penis and vulva may be affected ~Occasionally, only the flexures (axillae, inguinal areas) are involved ~Fine stippling ("pitting") in nails is highly suggestive ~Pts w/psoriasis often have a pink or red intergluteal fold ~Not all pts have findings in all locations, but the occurrence of a few may help make the dx when other lesions are not typical. ~Some pts have mainly hand or foot dermatitis and only minimal findings elsewhere ~There may be associated arthritis that's most commonly distal and oligoarticular, although the rheumatoid variety w/a negative rheumatoid factor may occur. ~The psychosocial impact of psoriasis is a major factor in determining the tx of the patient. Atlas: ~a chronic disorder w/polygenic predisposition and triggering environmental factors (bacterial infection, trauma, or drugs) ~several clinical expressions; typical lesions are chronic, recurring, scaly papules, and plaques; pustular eruptions and erythroderma occur ~clinical presentation varies among individuals: only a few localized plaques to generalized skin involvement ~psoriatic erythroderma in psoriasis involving the entire skin ~psoriatic arthritis in 10-25% of pts Zarbocks: Chronic, inflammatory, scaling condition of the skin that also may involve the mucous membranes. Earlier the onset, the more severe. Psoriasis in HIV+ pts can be very severe and resistant to tx. ~Psoriasis patches usually are raised, pink to red papules and plaques w/distinct margins and loosely adherent *silvery scales*. Peeling away a scale produces specks of bleeding from the capillaries (Auspitz's sign). ~Patches most often are found on the scalp and the *extensor surfaces* of the elbows and knees but can be found anywhere on the body. ~Pruritis is common. Scratching leads to more lesions (Koebner's phenomenon). ~Pts w/extensive disease also have nail involvement: tiny pits and ridges, are separated from the nail bed (onycholysis), and oil spots; discoloration and crumbly nails ~Psoriatic arthritis occurs in 5-10% of pts. It involves the distal joints of the hands and feet, typically is asymmetric, and may be present w/o skin lesions. ~Sx are usually mild, but the lesions are unsightly and interfere w/ADLS. Variants ~*Psoriasis vulgaris*: most common type; involves chronic recurring scaling papules and plaques. ~Psoriatic erythroderma: lesions involve the entire skin surface; this variant is exfoliative and serious ~Guttate psoriasis: acute eruption of typical and atypical lesions in a disseminated pattern; it spares the palms and soles and often appears after strep pharyngitis ~Pustular psoriasis (von Zumbusch's syndrome)" an abrupt, life-threatening condition characterized by widespread pustules that coalesce to form lakes of pus; fever, malaise, and leukocytosis are seen Affects 2% of the population Most pts have localized psoriasis, but more severe forms exist.

Papulosquamous Diseases: PSORIASIS A greatly enhanced epidermal cell turnover (to a rate 28x normal). A genetic predisposition exists, although only about 1/3 of the pts have family members w/the condition. Dx made by hx and appearance. Z: 1) Mild cases ~topical corticosteroids and topical Vit D perparations (calcipotriene) 2) Systemic steroids help, but the disease often will flare after withdrawal. 3) Coal tar or salicylic acid preparations and occlusive dressings are effective in controlling or removing scales. 4) Moderate cases ~May respond to tazarotene gel (topical retinoid) 5) More serious cases ~UVB phototherapy, PUVA, and methotrexate have been effective but carry risks of skin CA, cataracts, and hepatotoxicity ~Avoid methotrexate in immunocompromised pts, as it's a potent immune suppressant. ~Methotrexate is contraindicated in pregnancy. It's widely distributed in maternal tissues and can persist in the liver for up to 3-4 months after exposure. Therefore it should be *stopped at least 3 months before conception*. A period of at least 2 years between stopping oral retinoids and pregnancy is recommended. ~Pulmonary toxicity of the folate antimetabolite methotrexate (MTX) is seen with both high- and low-dose treatment and may present with acute or chronic symptoms. Either symptomatic or asymptomatic radiographic lung damage may be due to inflammation, infection, or MTX related neoplasia. It is recommended that a chest radiograph be obtained prior to initiating MTX treatment. ~The investigations that are mandatory before starting MTX therapy consist of a CBC, serum transaminase levels, serum creatinine with computation of creatinine clearance, and CXR. In addition, serological tests for the hepatitis viruses B and C and a serum albumin assay are recommended. In patients with a history of respiratory disease or current respiratory symptoms, LFTs with determination of the diffusing capacity for carbon monoxide are recommended. Folate supplementation can be given routinely to patients treated with MTX for RA. In practice, a minimal dosage of 5 mg of folic acid once a week with the methotrexate dose, is appropriate. 6) Pustular psoriasis ~May respond to acitretin (synthetic retinoid) +/- UV ~This is also helpful in erythroderma and psoriatic arthritis but is teratogenic. 7) Severe recalcitrant disease ~Cyclosproine may be effective, but recurrence after cessation is common. Current: ~There are many therapeutic options in psoriasis to be chosen according to the extent (body surface area [BSA] affected) and the presence of other findings (i.e. arthritis). ~Certain drugs, such as beta-blockers, antimalarials, statins, and lithium, may flare or worsen psoriasis. ~Even tiny doses of systemic corticosteroids may lead to severe rebound flares of their disease when they're tapered. *Never use systemic corticosteroids to tx flares of psoriasis.* ~In general, pts with moderate to severe psoriasis s/b managed by or in conjunction w/a dermatologist. See p.129 for further info Exam Master: ~If the lesions are limited to the extremities, treatment includes *topical fluorinated glucocorticoids. The appropriate tx is soaking the areas in water, removing the scales, applying glucocorticoids to wet skin, and covering the area w/plastic wrap overnight.* ~Topical retinoids, salicylic acid, and cyclosporine See Atlas p.59-61 ~Topical fluorinated glucocorticoids

[see p.262 also] Most pts who develop this complication have an inability to change position and, thus, sustain long periods of uninterrupted pressure, w/subsequent tissue ischemia. Greatest risk: pts w/spinal cord injury National Pressure Ulcer Advisory Panel: Stage I: Intact skin w/erythema that blanches Stage II: Partial-thickness skin loss; may present as abrasion, blister, or shallow crater Stage III: Full-thickness skin loss extending to the SQ tissue but not beyond the fascia; crater +/- undermining of adjacent tissue Stage IV: Full-thickness skin and SQ tissue loss w/extension into muscle tendons, bone, or joint capsule Atlas: Stage I: Nonblanching erythema of intact skin Stage II: Necrosis, SF or partial-thickness involving the epidermis and/or dermis. Bullae -> necrosis of dermis (black) -> shallow ulcer Stage III: Deep necrosis, crateriform ulceration w/full-thickness skin loss; damage or necrosis can extend down to, but not thru, fascia Stave IV: Full-thickness necrosis (-> ulceration) w/involvement of supporting structures such as muscle and bone. May enlarge to many centimeters. +/- tenderness. Borders of ulcers may be undetermined.

Pressure Ulcers (Decubitus Ulcers) linked to pressure and shear forces over bony prominences Quantitative wound culture is essential to differentiate betw colonization and true infection. 1) Tx should encompass a multimodal approach that includes removal of the pressure source, supplemental nutritional support, and surgical intervention. 2) Reconstructive procedures are performed only after tissue cultures show that there's no evidence of infection. 3) Tx can include skin grafts or rotational flaps. 4) Abx s/b reserved for those pts who manifest clinical signs of septicemia. Atlas: 1) Stage I & II: ~Topical abx (not Neomycin) under moist sterile gauze may be sufficient for early erosions ~Normal saline wet-to-dry dressings may be needed for debridement. 2) Stage III & IV: ~Surgical management: debridement of necrotic tissue, bony prominence, removal, flaps, and skin grafts. 3) Infectious Complications ~Prolonged course of antimicrobial agent depending on sensitivities, w/surgical debridement of necrotic bone in osteomyelitis.

Atlas: ~dermatophytic trichoycosis of the scalp, predominantly in preadolescent children ~clinical presentations vary widely: non-inflammatory scaling; scaling and broken-off hairs; severe, painful inflammation w/painful, boggy nodules that drain pus (kerion) and result in scarring alopecia 1) Noninflammatory infection ~scaling ~diffuse or circumscribed alopecia ~occipital or posterior auricular adenopathy ~"gray patch" tinea capitis~ ~partial alopecia, often circular in shape, showing numerous broken-off hairs, dull gray from their coating of arthrospores ~fine scaling w/fairly sharp margin ~hair shaft becomes brittle, breaking off at or slightly above scalp ~small patches coalesce, forming larger patches ~inflammatory response minimal, but massive scaling ~+/-several or many patches, randomly arranged ~Microsporum species may show green fluorescence w/Wood's lamp 2) "Black Dot" Tinea Capitis ~broken-off hairs near the scalp give appearance of "dots" (swollen hair shafts) in dark-haired pts ~dots occur as affected hair breaks at surface of scalp ~tends to be diffuse and poorly circumscribed ~low-grade folliculitis may be present ~resembles seborrheic dermatitis 3) Kerion ~inflammatory mass in which remaining hairs are loose ~boggy, purulent, inflamed nodules, and plaques ~usually painful; drains pus from multiple openings, like honeycomb ~hairs don't break off but fall out and can be pulled w/o pain ~follicles may d/c pus; sinus formation; mycetoma-like grains ~thick crusting w/matting of adjacent hairs ~a single plaque is usual, but multiple lesions may occur w/involvement of entire scalp ~frequently, associated lymphadenopathy is present ~heals w/scarring alopecia 4) Favus ("honeycomb") ~early cases show perifollicular erythema and matting of hair ~later, thick yellow adherent crusts composed of skin debris and hyphae that are pierced by remaining hair shafts ~fetid odor ~little tendency to clear spontaneously ~often results in scarring alopecia •Itchy, red, raised, scaly patches often sharply defined. •Redder margins than centers creates impression of a ring.

Tinea Capitis Trichophyton tonsurans Microsporum canis (N. America; other sp. elsewhere) 1) Wood's Lamp ~T. tonsurans doesn't fluoresce 2) Direct Microscopy ~skin cales contain hyphae and arthrospores 3) Fungal Culture ~growth of dermatophytes usually seen in 10-14 days 4) Bacterial Culture ~r/o bacterial infection, usually S. aureus of FAS Sanford: 1) Adult •Terbinafine x 2-4 weeks 2) Pediatric (>2 yoa): •Terbinafine (wt-based dosing) x 2 weeks 3) Alternative Regimen •Itraconazole x 4 weeks OR •Fluconazole x 8-12 weeks OR •Griseofulvin (microsize formulation) x 6-8 weeks (adult) or until hair regrows (child). Note: •Durations of therapy are for T. tonsurans; treat for approximately twice as long for M. canis. All agents have similar cure rates (60-100%) in clinical studies. •Serious but rare cases of hepatic failure have been reported in pts receiving Terbinafine and should not be used in those w/chronic or active liver disease. •Addition of topical Ketoconazole or selenium sulfate shampoo reduces transmissibility. Exam Master S/b tx w/oral griseofulvin or terbinafine + 2.5% selenium sulfide or ketoconazole shampoo.

Current Blurb: ~*Ring-shaped (annular) lesions w/an advancing scaly border and central clearing or scaly patches with a distinct border.* ~On exposed skin surfaces or the trunk. ~Microscopic examination of scrapings or culture confirms the diagnosis. ~lesions are often on exposed areas of the body (i.e. - face and arms) ~hx of exposure to an infected cat may occasionally be obtained, usually indicating Microsporum infection. ~Trichophyton rubrum is the most common pathogen, usually representing extension onto the trunk or extremities of tinea cruris, pedis, or manuum ~Itching may be present. ~*In classic lesions, rings of erythema have an advancing scaly border and central clearing * Atlas: ~*scaling, sharply marginated plaques* ~*peripheral enlargement and central clearing* produce annular configurations w/concentric rings or arcuate lesions; fusion of lesions produces gyrate patterns ~single and occasionally scattered multiple lesions

Tinea Corporis or Tinea Circinata (Body Ringworm) Trichophyton rubrum, T. mentagrophytes, Epidermophyton floccosum Dx may be confirmed by KOH preparation or culture. 1) Primary Regimen •Terbinafine 1% cream (Lamisil AT) apply bid x 1 week •Butenafine 1% (Lotrimin Ultra) apply once daily x 2 weeks 2) Alternative Regimen Topical •Naftifine HCl 1-2% cream or gel apply once daily x 2 wks •Imidazoles (clotrimazole, ketoconazole, econazole, etc.) apply bid x 2-4 weeks Systemic •Terbinafine x 2 weeks •Ketoconazole x 4 weeks •Fluconazole 1x/wk x 2-4 weeks •Griseofulvin (microsize formuation): Adults x 4-6 weeks; Peds x 2-4 weeks Note: Can often be cured w/topical tx alone. Systemic tx can be reserved for severe or refractory infection, recurrent infection, or in immunocompromised patients. Serious but rare cases of hepatic failure have been reported in pts receiving Terbinafine and should not be used in those w/chronic or active liver disease. Atlas: 1) Topical agents ~imidazoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole, sulconazole, sertaconazole) ~allylamines (naftifine, terbinafine) ~naphthionates (tolnaftate) ~substituted pyridine (ciclopirox olamine) 2) Systemic Antifungal Agents ~terbinafine tablet (allylamin) = most effective ~itraconazole capsules, oral solution, IV ~fluconazole tablets, oral suspension, IV ~ketoconazole tablets Current: 1) Local Measures ~responds to most topical antifungals (OTC: miconazole, clotrimazole, butenafine, and terbinafine) ~Terbinafine and butenafine require shorter courses and lead to the most rapid response ~Ts s/b continued for 1-2 weeks after clinical clearing. ~Betamethasone dipropionate with clotrimazole (Lotrisone) is not recommended. ~Long-term improper use may result in side effects from the high-potency corticosteroid component, esp in body folds. ~Cases of tinea that are clinically resistant to this combination but respond to topical antifungals w/o the topical corticosteroid can occur. 2) Systemic Measures ~Griseofulvin (ultramicrosize) bid x 4-6 weeks ~Itraconazole as a single week-long pulse of 200 mg daily is also effective. ~Terbinafine x 1 month is an alternative.

Current Blurb: ~Marked itching in intertriginous areas, usually sparing the scrotum. ~*Peripherally spreading, sharply demarcated, centrally clearing erythematous lesions.* ~May have associated tinea infection of feet or toenails. ~Laboratory exam w/microscope or culture confirms diagnosis. ~lesions are confined to the groin and gluteal cleft. ~Intractable pruritus ani may occasionally be caused by a tinea infection. ~Itching may be severe, or the rash may be asymptomatic. ~Lesions have sharp margins, cleared centers, and active, spreading scaly peripheries. ~Follicular pustules are sometimes encountered. ~Area may be hyperpigmented on resolution. Atlas: ~subacute or chronic dermatophytosis of the upper thigh and adjacent inguinal and pubic regions ~"Always" associated w/tinea pedis, the source of the infection ~large, scaling, well-demarcated dull red/tan/brown plaques ~central clearing

Tinea Cruris (Jock Itch) Trichophyton rubrum, T. mentagrophytes, Epidermophyton floccosum 1) Hyphae can be demonstrated microscopically in KOH preparations. 2) The organism may be cultured. Sanford: 1) Primary Regimen •Terbinafine 1% cream (Lamisil AT) apply bid x 1 week •Butenafine 1% (Lotrimin Ultra) apply once daily x 2 weeks 2) Alternative Regimen Topical •Naftifine HCl 1-2% cream or gel apply once daily x 2 wks •Imidazoles (clotrimazole, ketoconazole, econazole, etc.) apply bid x 2-4 weeks Systemic •Terbinafine x 2 weeks •Ketoconazole x 4 weeks •Fluconazole 1x/wk x 2-4 weeks •Griseofulvin (microsize formuation): Adults x 4-6 weeks; Peds x 2-4 weeks Note: Can often be cured w/topical tx alone. Systemic tx can be reserved for severe or refractory infection, recurrent infection, or in immunocompromised patients. Serious but rare cases of hepatic failure have been reported in pts receiving Terbinafine and should not be used in those w/chronic or active liver disease. Atlas: 1) Prevention ~after eradication minimize reinfection w/showe shoes and antifungal powders 2) Topical Antifungal Agents ~imidazoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole, sulconazole, sertaconazole) ~allylamines (naftifine, terbinafine) ~naphthionates (tolnaftate) ~substituted pyridine (ciclopirox olamine) 3) Systemic Antifungal Agents ~terbinafine tablet (allylamin) = most effective ~itraconazole capsules, oral solution, IV ~fluconazole tablets, oral suspension, IV ~ketoconazole tablets Current: 1) General Measures ~Drying powder (eg, miconazole nitrate [Zeasorb-AF]) can be dusted into the involved area in pts w/excessive perspiration or occlusion of skin due to obesity. 2) Local Measures ~Terbinafine cream is curative in >80% of cases after once-daily use x 7 days. 3) Systemic Measures ~Griseofulvin ultramicrosize bid x 1-2 weeks is reserved for severe cases. ~1 week of itraconazole or terbinafine can be effective.

Current Blurb: ~Most often presenting with asymptomatic scaling. ~May progress to fissuring or maceration in toe web spaces. ~Itching, burning, and stinging of interdigital web; scaling palms, and soles; vesicles of soles in inflammatory cases. ~The fungus is shown in skin scrapings examined microscopically or by culture of scrapings. Atlas: ~often unilateral, most commonly on the dominant hand ~usually associated w/tinea pedis

Tinea Manuum

Current Blurb: ~Most often presenting with asymptomatic scaling. ~May progress to fissuring or maceration in toe web spaces. ~Common cofactor in lower leg cellulitis. ~Itching, burning, and stinging of interdigital web; scaling palms, and soles; vesicles of soles in inflammatory cases. ~The fungus is shown in skin scrapings examined microscopically or by culture of scrapings. ~an extremely common acute or chronic dermatosis ~itching, burning, or stinging ~Pain may indicate secondary infection w/complicating cellulitis. ~*Interdigital tinea pedis is the most common predisposing cause of lower leg cellulitis in healthy ppl* ~Regular exam of the feet of diabetic pts for evidence of scaling and fissuring and tx of any identified tinea pedis may prevent complications. ~has several presentations that vary w/location. ~On the sole and heel, tinea may appear as chronic noninflammatory scaling, occasionally w/thickening and fissuring. This may extend over the sides of the feet in a "moccasin" distribution. ~often appears as a scaling or fissuring of the toe webs, perhaps w/sodden maceration; as the web spaces become more macerated, the KOH preparation and fungal culture are less often positive because bacterial species begin to dominate. ~there may also be grouped vesicles distributed anywhere on the soles, generalized exfoliation of the skin of the soles, or nail involvement in the form of discoloration and thickening and crumbling of the nail plate

Tinea Pedis (Athlete's Foot) Trichophyton rubrum, T. mentagrophytes, Epidermophyton floccosum KOH and culture does not always demonstrate pathogenic fungi from macerated areas. 1) Primary Regimen •Terbinafine 1% cream (Lamisil AT) apply bid x 2 weeks •Butenafine 1% (Lotrimin Ultra) apply once daily x 4 weeks OR bid x 2 weeks 2) Alternative Regimen Topical •Naftifine HCl 1-2% cream or gel apply once daily x 2 wks •Imidazoles (clotrimazole, ketoconazole, econazole, etc.) apply bid x 2-4 weeks Systemic •Terbinafine x 2 weeks •Ketoconazole x 4 weeks •Fluconazole 1x/wk x 2-4 weeks •Griseofulvin (microsize formuation): Adults x 4-6 weeks; Peds x 4-8 weeks Note: Can often be cured w/topical tx alone. Systemic tx can be reserved for severe or refractory infection, recurrent infection, or in immunocompromised patients. Serious but rare cases of hepatic failure have been reported in pts receiving Terbinafine and should not be used in those w/chronic or active liver disease. Current: 1) Local Measures ~Macerated Stage~ ~*Burrow's wet dressing*: aluminum subacetate solution soaks for 20 minutes bid. ~Broad-spectrum antifungal creams and solutions (containing imidazoles or ciclopirox instead of tolnaftate and haloprogin) will help combat diphtheroids and other gram-positive organisms present at this stage and alone may be adequate therapy. ~If topical imidazoles fail, 1 week of once-daily topical allylamine (terbinafine or butenafine) will often result in clearing. ~Dry & Scaly Stage~ ~Use any of the antifungal agents listed in Table 6-2. ~addition of urea 10-20% lotion or cream may increase the efficacy of topical tx in thick ("moccasin") tinea of the soles. 2) Systemic Measures ~Griseofulvin may be used for severe cases or those recalcitrant to topical therapy. ~If the infection is cleared by systemic therapy, the pt s/b encouraged to begin maintenance with topical therapy, since recurrence is common. ~Itraconazole x 1-2 weeks or terbinafine x 2-4 weeks may be used in refractory cases.

Current Blurb: ~Eruptions of evanescent wheals or hives. ~Itching is usually intense but may on rare occasions be absent. ~Special forms of urticaria have special features (dermatographism, cholinergic urticaria, solar urticaria, or cold urticaria). ~Most incidents are acute and self-limited over a period of 1-2 weeks. ~Chronic urticaria (episodes lasting >6 weeks) may have an autoimmune basis.

URTICARIA & Angioedema

Current Blurb: ~Pain along the course of a nerve followed by grouped vesicular lesions. ~Involvement is unilateral; some lesions (<20) may occur outside the affected dermatome. ~Lesions are usually on face or trunk. ~Direct fluorescent antibody positive, esp in vesicular lesions. Atlas: ~characterized by unilateral dysethesia (pain, tenderness, paresthesia in the involved dermatome); a vesicular or bullous eruption limited to a dermatome(s) innervated by a corresponding sensory ganglion ~postherpetic neuralgia is a major morbidity Sanford: •Effective tx is most evident in pts >50 yoa •Must begin tx within 3 days of onset of rash. •Herpes Zoster (Shingles) becoming more common in those receiving anti-TNF antibody therapy •Immunization results in 25-fold decrease in infection rate •Tx options for post-herpetic neuralgia •Increasing recognition of increased risk of stroke in the 6 months after an episode of H. zoster. Oral antivirals during clinical infection may have a protective effect

VARICELLA-ZOSTER VIRUS INFECTIONS: Herpes Zoster (Shingles) Herpes zoster virus (Varicella zoster virus) 1) Prodrome Stage: ~suspect zoster in older or immunocompromised pts w/unilateral pain 2) Active Vesiculation ~clinical findings usually adequate ~may be confirmed by Tzanck test, DFA, or viral culture to r/o other HSV infection 3) Postherpetic Pain Syndrome ~by hx and clinical findings Sanford: 1) Immunocompetent •Valacyclovir po tid x 7 days OR •Famciclovir tid x 7 days OR •Acyclovir po 5x/day x 7-10 days •Add Prednisone taper (21 days total) in pts >50 yoa to decrease discomfort during acute phase of infection. Does not decrease incidence of post-herpetic neuralgia. 2) Immunocompromised •Not severe: Acyclovir po 5x/day x 7 days •Severe (>1 dermatome, CN V or disseminated): Acyclovir IV (infusion over 1 hr) x 7-14 days 3) Alternative Regimen: Immunocompromised (not severe): •FamciclovirNAI x 7 days OR •ValacyclovirNAI x 7 days •NAI = not an approved indication. Atlas: 1) Prevention: vaccination ~shouldn't be given to HIV positive pts 2) Antiviral Therapy ~oral famciclovir or valaciclovir ~severly immunocompromised: IV acyclovir ~acyclovir resistant: IV foscarnet 3) Supportive Therapy ~bed rest, sedation, pain management w/narcotic analgesics ~moist dressings 4) Postherpetic Neuralgia ~gabapentin, pregabalin, tricyclic antidepressants (i.e. - doxepin), capicin cream topically ~nerve block Exam Master: Peds: The correct response is symptomatic treatment and prevention of secondary infection. ~Shingles is an acute infection caused by the varicella-zoster virus. It is less common in children than in adults, but has been documented in children as young as 1 week old. ~The onset of pain often precludes the typical vesicular eruption. The lesions often begin nearest to the CNS and extend peripherally. The involvement of the ophthalmic branch of the trigeminal nerve may involve the cornea and zoster of the maxillary division of the trigeminal nerve produces vesiculation of the palate, uvula, and tonsillar area. Herpes zoster in children is generally mild. ~In a normal child, symptomatic tx and prevention of secondary infection are the mainstays of tx. ~Oral acyclovir may be necessary in pts w/ophthalmic disease or w/disseminated zoster due to immunosuppression. ~IV varicella-zoster IG may be used within 48-72 hrs of exposure for the tx of immunocompromised pts and those w/disseminated disease. ~Oral cephalexin would be indicated in pts that develop a secondary bacterial infection.

macules of hypopigmentation may occur focally, segmentally, or in a generalized pattern can be very psychologically distressing, esp in dark-skinned pts any age every race males = females Exam Master: Positive antiparietal cell antibodies ~The clinical presentation is suggestive of vitiligo with associated Grave's disease. This is not an unusual presentation since up to 30% of pts with vitiligo have been found to have thyroid disorders such as Grave's disease. ~S&S of Grave's disease, which is typified by hyperthyroidism due to circulating thyroid stimulating immunoglobulins (TSIs), include heat intolerance, unexplained weight loss, irritability, diplopia, tachycardia, proptosis, fine tremors, onycholysis, pretibial myxedema, and a diffusely enlarged thyroid gland. ~Laboratory investigations of patients with Grave's disease usually reveal positive thyrotropin receptor antibodies (TSIs), decreased thyrotropin levels, elevated free T4, and free T3 levels. ~Investigations of patients with vitiligo reveal a total absence of epidermal melanoctyes in a skin biopsy of the vitiliginous areas. This is thought to be autoimmune related since vitiligo patients have a high incidence of melanocyte antibodies. In addition, around 50% of patients with vitiligo have circulating autoantibodies such as antiparietal cell antibodies and antithyroglobulin antibodies. The latter are also usually present in patients with Grave's disease, even in the absence of vitiligo. ~Patients with vitiligo can also develop *leukotrichia* or depigmentation of hair. This whitening or graying of the hair can affect the hair on the scalp, eyebrows, eyelashes, beard, and even pubic and axillary hair. ~Other features of vitiligo include increased sweating in the amelanotic macules and patches that have intact sensation. ~As vitiligo affects all melanocytes, even those in the membranous labyrinth of the inner ear, patients with vitiligo can develop hearing problems and hypoacusis. In addition, depigmentation can develop in the choroid of up to 40% of patients with vitiligo, and 5% of vitiligo patients can develop iritis but the color of the iris (plural irides) does not change.

VITILIGO Idiopathic. Destruction of melanocytes can be associated w/thyroid disease, pernicious anemia, DM, and Addison's disease 30% of pts report a FHx Sunscreens, cosmetic cover-up products or repigmentation therapies under the direction of an experienced dermatologist may be used. Atlas p.289 Exam Master: The treatment of vitiligo is determined by the size, number, and location of the depigmented macules and patches. 1) Localized vitilgo ~topical corticosteroid: fluticasone propionate, clobetasol propionate, or triamcinolone ~Other treatment modalities used for patients with a few localized macules or patches include topical calcineurin inhibitors (pimecrolimus or tacrolimus) and topical psoralens (PUVA light therapy) 2) vitiliginous patches affecting >20% of their skin. ~Oral 8-methoxypsoralen with ultraviolet A therapy (PUVA) light therapy or systemic psoralen photochemotherapy 3) extensive vitiligo that involves >50% of their skin. ~Depigmentation with p-(benzyloxy) phenol Minigrafting together with split skin grafts are some of the surgical interventions used for the management of vitiligo. Minigrafting is not the most appropriate intervention for this patient since these surgical interventions are recommended for patients with localized vitiligo with stable activity.

Current: ~small (0.2-0.6 cm) macules or papules (flesh-colored, pink, or slightly hyperpigmented) that feel like sandpaper and are tender when the finger is drawn over them ~occur on sun-exposed parts of the body in pts of fair complexion ~considered premalignant, but only 1:1000 lesions per year progress to become SCC Zarbocks: ~type of keratoderma (a generalized thickening of the horny layer of the epidermis) ~thickened lesions progress very slowly to SCC; can also progress to a cutaneous horn

Verrucous Lesions: ACTINIC KERATOSIS (solar keratoderma) [Benign Neoplasm] premalignant condition caused by cumulative exposure to the sun and is more prevalent in fair-skinned ppl 1) *Liquid nitrogen* can be used successfully to tx keratodermas. ~lesions crust and disappear in 10-14 days 2?) Electrodessication and curettage also are effective. 3?) Mild acid tx and application of onsel's soln (ferric subsulfate soln) have been used. 4) *5-Fluorouracil* (applied topically bid x 2-4 weeks) is effective, but pts must be warned that their lesions will look worse before they look better. ~rub into the lesions morning and night until they become first red and sore and then crusted and eroded (usually 2-3 weeks) ~Carac (0.5% fluorouracil) may be used once daily for a longer period (4 weeks to several months) ~Keratoses may clear with less irritation. ~Imiquimod 5% cream applied 2-3 timesweekly x 3-6 weeks is the more costly alternative 5) Photodynamic therapy can be effective in refractory cases and reduces the duration of tx 6) Any lesions that persist s/b evaluated for possible bx.

Current: ~benign plaques, beige to brown or even black, 3-20 mm in diameter, w/a velvety or warty surface ~*Appear to be stuck or pasted onto the skin.* ~extremely common (esp in the elderly) and may be mistaken for melanomas or other types of cutaneous neoplasms Zarbocks: ~type of keratoderma (a generalized thickening of the horny layer of the epidermis) ~benign plaque, beige to brown or black, w/a velvety, warty surface that appears* "stuck on"* ~lesions are more common in older ppl Atlas: ~most common of the benign epithelial tumors ~lesions are hereditary; don't appear until age 30 and continue to occur over a lifetime, varying in extent from a few scattered lesions to literally hundreds in some very elderly pts ~lesions range from small, barely elevated papules to plaques w/a warty surface and a "stuck on" appearance ~lesions are benign; can become irritated or traumatized, w/pain and bleeding; SCC s/b ruled out

Verrucous Lesions: SEBORRHEIC KERATOSIS [Benign Neoplasm] Zarbocks: 1) Liquid nitrogen can be used successfully to tx keratodermas. 2) Electrodessication and curettage also are effective. 3) Mild acid tx and application of onsel's soln (ferric subsulfate soln) have been used. 4) 5-Fluorouracil (applied topically bid x 2-4 weeks) is effective, but pts must be warned that their lesions will look worse before they look better. Current: Although they may be frozen with liquid nitrogen or curetted if they itch or are inflamed, no tx is needed. Atlas: ~Don't require tx except for cosmetic reasons. ~Cryosurgery w/liquid nitrogen spray works only in flat lesions, and recurrences are possibly more frequent ~Best approach is curettage after slight freezing w/cryospray, which also permits histopathologic exam.

Current: ~a relatively benign pruritic disease characterized by tense blisters in flexural areas, usually remitting in 5-6 yrs, w/a course characterized by exacerbations and remissions ~most affected persons are >60 yoa (often in their 70s or 80s), and men are affected twice as frequently as women ~appearance of blisters may be preceded by urticarial or edematous lesions for months ~oral lesions are present in about 1/3 of affected persons ~various forms: localized, vesicular, vegetating, erythematous, erythrodermic, nodular Atlas: ~a bullous autoimmune disease usually in elderly pts ~pruritic papular and/or urticarial lesions w/large tense bullae ~subepidermal blisters w/eosinophils ~C3 and IgG at epidermal basement membrane, antibasement membrane IgG autoantibodies in serum ~autoantigens are keratinocyte hemidesmosome proteins ~often starts w/a prodromal eruption (urticarial, papular lesions) and evolves in weeks to months to bullae that may appear suddenly as a generalized eruption ~initially mod-severe pruritus; later, tenderness of erodes lesions ~no constitutional sx, except in widespread, severe disease Zarbocks: ~May be a prodrome of urticarial or papular lesions. ~Bullae are large, tense, oval, or round and contain serous or hemorrhagic fluid. They rupture less easily than in pemphigus. ~Typically, bullae collapse and crust; at times, bleeding erosions occur. ~*Axillae, thighs, groin, and abd commonly affected.* Mucous membrane lesions are less severe and less painful than in pemphigus vulgaris. Typically occurs in pts in 6th decade of life Exam Master: ~autoimmune disorder that affects structural protein of the skin ~Common occurrence betw 60-80 yoa, and it often appears on the lower legs. ~Initial sx include moderate to intense pruritus ~lesions are usually urticarial, papular, and erythematous; they evolve in weeks to months to large, tense bullae.

Vesicular Bullae: BULLOUS PEMPHIGOID Autoimmune disorder: autoantibodies, complement fixation, neutrophil, and eosinophils cause bullous formation. *Bx and direct immunofluorescense confirm dx.* 1) Light microscopy shows a subepidermal blister. ~neutrophils in "Indian-file" alignment at dermal-epidermal junction 2) Direct immunofluorescence ~IgG and C3 are found at the dermal-epidermal junction Z: 1) Systemic prednisone may be given at high doses until remission, then at lower dose for maintenance. 2) Azathioprine may be added. 3) Mild cases or localized recurrences ~Topical steroids Atlas: *Topical and systemic glucocorticoids and other immunosuppressives.* 1) Systemic prednisone until clear ~either alone or combined w/azathioprine 2) refractory cases: IVIG, plasmapheresis 3) milder cases: ~sulfones (dapsone) 4) low-dose methotrexate is effective and safe in elderly 5) in very mild cases and for local recurrences ~topical glucocorticoid or topical tacrolimus therapy may be beneficial 6) tetracycline +/- nicotinamide has been reported to be effective in some cases

Atlas: ~*mucosal HPV infections are the most common STIs seen by dermatologists* ~HPV present in the birth canal can be transitted to a newborn during vaginal delivery and can cause external genital warts and respiratory papillomatosis ~warts: barely visible papules to nodules to confluent masses occurring on anogenital skin or mucosa and oral mucosa; external genital warts on external genitalia, perineum; cervix ~dysplasia of anogential and oral skin and mucosa ranging from mild-severe to SCC in situ; invasive SCC can arise within SCCIS; most commonly in cervix, anal canal •Warts: external genital, cervix, vaginal, urethral, anal, skin papillomas. •HPV vaccine can prevent infection w/commonly involved serotypes •Associated w/head and neck CAs: HPV 16, other serotypes.

Viral: CONDYLOMA ACUMINATUM (Genital Warts) Papillomaviruses Clinical dx Occasionally confirmed by bx Sanford: 1) External genital warts Pt applied: •*Podofilox* (0.5% solution or gel): apply 2x/day x 3 days, 4th day no therapy, repeat cycle 4x •Imiquimod 5% cream: apply once daily HS 3x/week x up to 16 weeks •Sinecatechins: apply to external genital warts only 3x/day until effect or adverse effect Provider administered: •Cryotherapy with liquid nitrogen; repeat q1-2 weeks •Podophyllin resin 10-25% in tincture of benzoin. Repeat weekly PRN •Trichloroacetic acid (TCA): repeat weekly PRN •Surgical removal. 2) Cervical: Need evaluation for evolving neoplasia. Gynecological exam. 3) Vaginal: Cryotherapy w/liquid nitrogen or TCA 4) Urethral: Cryotherapy w/liquid nitrogen or Podophyllin resin 10-25% in tincture of benzoin 5) Anal: Cryotherapy w/liquid nitrogen or TCA or surgical removal. Advise anoscopy to look for rectal warts 6) Skin papillomas: Topical α-lactalbumin. Oleic acid (from human milk) applied 1x/day x 3 weeks Notes: •Podofilox: Inexpensive and safe (pregnancy safety not established). Mild irritation after tx. •Imiquimod: Mild to moderate redness & irritation. Topical imiquimod effective for tx of vulvar intraepithelial neoplasms. Safety in pregnancy not established. •Cryotherapy: blistering and skin necrosis common. •Podophyllin resin: Must air dry before treated area contacts clothing. Can irritate adjacent skin. •Sinecatechins: Avoid exposure to mucous membranes (vagina, rectum, mouth, eyes). •TCA: Caustic. Can cause severe pain on adjacent normal skin. Neutralize w/soap or sodium bicarbonate. Atlas: Goal of tx is removal of warts and reduction of S&S. No therapy can eradicate HPV or prevent cervical or anogenital CA. Selection of tx s/b guided by preference of pts. 1) Prevention ~condoms ~HPV vaccine 2) Pt-applied agents ~Imiquimod 5% cream, podophylox 0.5% solution 3) Clinician Administered Therapy ~cryosurgery ~podophyllin resin 10-25% ~trichloroacetic acid 80-90% ~surgical removal ~elecrtodesiccation

Current Blurb: ~Recurrent small grouped vesicles on an erythematous base, especially in the orolabial and genital areas. ~May follow minor infections, trauma, stress, or sun exposure; regional lymph nodes may be swollen and tender. ~Viral cultures and direct fluorescent antibody tests are positive. Atlas: ~whether first symptomatic or recurrent, may "typically" present clnically w/grouped vesicles arising on an erythematous base on keratinized skin or mucous membrane; most HSV infections are "atypical" w/patch(es) of erythema, small erosions, fissures, or subclinical lesions that shed HSV ~following primary infection, HSV persists in sensory ganglia for the life of the pt, recurring w/lessening in immunity ~in healthy individuals, recurrent infections are asymptomatic or minor, resolving spontaneously or w/antiviral therapy ~w/host defense defects, mucocutaneous lesions can be extensive, chronic, or disseminate to skin or viscera Sanford: •Mucocutaneous, oral labial Herpes simplex infection. •Fever blisters. •Start tx w/prodrome symptoms (tingling/burning) before lesions appear.

Viral: HERPLES SIMPLEX (Cold or Fever Sore) HSV-1 1) Confirmed by viral culture or antigen detection ~*Tzank Smear* ~seroconversion diagnoses first-episode infections ~antibodies may take 2-6 weeks to develop ~recurring herpes can be r/o if seronegative for HSV antibodies 1) Oral regimens •Valacyclovir x 1 day •Famciclovir x 7 days (HIV pts only) 2) Alternative Regimen ◾At first sign of prodrome: Famciclovir 1500 mg one dose or 750 mg q12h x 1 day ◾Topical regimens (less preferred): •Penciclovir 1% cream q2h during day x 4 days •Acyclovir 5% cream 6x/day (q3h) x 7 days (approved for HIV patients only) Note: Symptoms reduction •Oral regimens: Valacyclovir (1 day), Famciclovir (2 days), Acyclovir (½ day) •Topical regimens: Penciclovir (1 day); Acyclovir (½ day) Atlas: 1) Prevention ~Avoid skin-to-skin contact during outbreaks. 2) Topical Antiviral Therapy ~Minimal efficacy ~Acyclovir 5% ointment ~Penciclovir 1% cream while awake for recurrent orolabial infection 3) Oral Antiviral Therapy Drugs ~Acyclovir, *valacyclovir*, famciclovir 4) Recurrences

Current Blurb: ~Recurrent small grouped vesicles on an erythematous base, especially in the orolabial and genital areas. ~May follow minor infections, trauma, stress, or sun exposure; regional lymph nodes may be swollen and tender. ~Viral cultures and direct fluorescent antibody tests are positive. Atlas: ~chronic STD characterized by symptomatic and asymptomatic viral shedding Sanford: •Initial and recurrent episodes. •Pregnancy considerations: •Acyclovir is safe even in the 1st trimester. •No proof that Acyclovir at delivery reduces risk/severity of neonatal herpes. •In contrast, C-section in women with active lesions reduces risk of transmission. •Increased risk of dissemination to include severe, and even fatal, hepatitis. •For recalcitrant pseudotumoral anogenital herpes, type 2, in HIV patients, see Comment.

Viral: HERPLES SIMPLEX (Genital Herpes) HSV-2 1) Confirmed by viral culture or antigen detection ~Tzank Smear ~seroconversion diagnoses first-episode infections ~antibodies may take 2-6 weeks to develop ~recurring herpes can be r/o if seronegative for HSV antibodies 1) Primary (initial episode) •Acyclovir 400 x 7-10 days OR •Valacyclovir x 7-10 days OR •Famciclovir x 7-10 days 2) Subsequent recurrent episodes ~Immunocompetent~ •Acyclovir x 2 days or x 5 days OR •Famciclovir x 1 day or x 5 days OR •Valacyclovir x 3 days or x 5 days ~Immunocompromised, HIV~ •Acyclovir x 5-10 days OR •Famciclovir x 5-10 days OR •Valacyclovir x 5-10 days Alternative Regimen 1) For severe cases only: Acyclovir IV x 5-7 days 2) Acyclovir-resistant HSV: Foscarnet IV x 7 days 3) Chronic suppression (daily): Immunocompetent or Immunocompromised/HIV •Acyclovir, Famciclovir, OR Valacyclovir Atlas: 1) Prevention ~Abstain from sexual activity while lesions are present ~Condom use 2) 1st Episode ~Oral antivirals: Acyclovir 3) Recurrances ~Oral antivirals: Acyclovir, valacyclovir, or famciclovir 4) Maintenance Therapy ~Oral antivirals: acyclovir, valcyclovir, or famciclovir 5) Severely Immunocompromised ~IV or oral acyclovir 6) Acyclovir Resistant ~IV foscarnet

Current: ~presents as single or multiple dome-shaped, waxy papules 2-5 mm in diameter that are umbilicated ~Lesions at first are firm, solid, and flesh-colored but upon reaching maturity become soft, whitish, or pearly gray and may suppurate. ~principal sites of involvement: face, lower abd, genitals ~lesions are autoinoculable and spread by wet skin-to-skin contact; in sexually active individuals, they may be confined to the penis, pubis, and inner thighs and are considered an STI. ~common in pts w/AIDS, usually w/a helper T cell count <100/mcL; extensive lesions tend to develop over the face and neck as well as in the genital area. Atlas: ~self-limited epidermal viral infection ~skin-colored papules; often umbilicated ~few to myriads of lesions ~host defense defects: large nodules w/confluence ~in healthy ppl, resolves spontaneously common in children but can affect adults ~in adults, lesions are commonly in the groin areas and on lower abdomen ~virus can be transmitted during sexual activity ~immunocompromies pts (i.e. - HIV), lesions can be larger and more widespread, including predominance on the head and neck lesions manifest as discrete, flesh-colored, waxy, *dome-shaped umbilicated papules* over the face trunk and extremities 3-6mm and appear in groups *a white curd-like or yellow caseous material can be expression from under the depression of the lesion*

Viral: MOLLOSCUM CONTAGIOSUM poxvirus 1) *Clinical dx* ~central umbilication of the dome-shaped lesion 2) Bx lesion in HIV disease if disseminated invasive fungal infection is in the DDx Z: 1) *tx usually not necessary (self-limited disease)* 2) if therapy is indicated, local destruction of individual lesions either by: ~1st line: curettage ~cryotherapy, ~electrodessication ~acid or exfoliative peel Note: These tx can be painful. Current: 1) best tx is by curettage or applications of liquid nitrogen as for warts (but more briefly) ~When lesions are frozen, the central umbilication often becomes more apparent 2) Light electrosurgery w/a fine needle is also effective. 3) Estimated that individual lesions persist for ~2 months. ~They're difficult to eradicate in pts w/AIDS unless immunity improves ~However, in AIDS, w/highly effective antiretroviral treatment, molluscum don't need to be tx b/c they usually spontaneously clear. Atlas: ~Office-based tx include curettage, cryosurgery, and electrodessication ~Imiquimod 5% cream may be effective Exam Master: The condition is self-limited and usually resolves in 6 - 9 months. In immunosuppressed patients, the lesions may number in the hundreds. Given the self-limited nature of the disease, no tx is usually the best option in healthy children. For irritated or infected papules, tx may be accomplished w/gentle curettage. Application of liquid nitrogen or cantharidin may be used as well, but carry with them the possibility of subsequent scarring.

Current Blurb: ~Exposure 14-21 days before onset. ~Fever and malaise just before or with eruption. ~Rash: pruritic, centrifugal, papular, changing to vesicular ("*dewdrops on a rose petal*"), pustular, and finally crusting. Atlas: ~characterized by successive crops of pruritic vesicles that evolve to pustules, crusts, and sometimes scars ~primary infection occurring in adulthood may be complicated by pneumonia and encephalitis Sanford: •Vaccination has markedly reduced the incidence of VZV infections and associated morbidity

Viral: VARICELLA-ZOSTER VIRUS INFECTIONS (Chickenpox) Varicella-zoster virus (VZV) Clinical dx 1) Immunocompetent host, chickenpox ~Child age 2-12 years~ •No treatment is an option for mild-moderate disease •Valacyclovir or Acyclovir x 5 days (start within 24 hrs of rash) for pts at increased risk of moderate or severe varicella; chronic cutaneous or pulmonary diseases; chronic salicylate tx (increased risk of Reye's syndrome) ~Adolescent, young adults~ •Acyclovir x 5-7 days (start within 24 hrs of rash) OR •ValacyclovirNAI x 5 days ~Pregnancy (3rd trimester), pneumonia~ •Acyclovir po or IV x 5 days 2) Immunocompromised •Acyclovir IV (infused over 1 hour) x 7 days Alternative Regimen Prevention, post-exposure prophylaxis Since <5% of cases of varicella but >50% of varicella-related deaths occur in adults >20 yoa, the CDC recommends a more aggressive approach in this age group: •1st, Varicella-zoster immune globulin (VZIG) is recommended for post-exposure prophylaxis in susceptible persons at greater risk for complications (immunocompromised: HIV, malignancies, pregnancy, and steroid therapy) ASAP after exposure (<96 hrs). •If varicella develops, initiate tx quickly (<24 hrs of rash) w/Acyclovir. Some would tx presumptively w/Acyclovir in high-risk pts. •Susceptible adults should be vaccinated. Check antibody in adults w/neg or uncertain hx of varicella (10-30% will be Ab-neg.) and vaccinate those who are Ab-negative. •Susceptible children should receive vaccination. Recommended routinely before age 12-18 months but OK at any age. ATLAS 1) Immunization 2) Symptomatic Therapy ~antihistamines lotions; avoid antipyretics due to risk of Reye syndrome 3) Antiviral Agents ~Decrease severity of course if given within 24 hrs of onset ~Neonates: acyclovir ~Peds (2-18 yoa): valaciclovir or acyclovir ~Adolescents?: Valaciclovir ~Immunocompromised: Valaciclovir, acyclovir, or famciclovir ~Severely immunocompromised: IV acyclovir ~Acyclovir resistant: Foscarnet IV

Current Blurb: ~Verrucous papules anywhere on the skin or mucous membranes, usually no larger than 1 cm in diameter. ~Prolonged incubation period (average 2-18 months). Spontaneous "cures" are frequent (50% at 2 years for common warts). ~"Recurrences" (new lesions) are frequent. ~common, plantar, and genital warts are caused by HPVs. ~Typing of HPV lesions is NOT a part of standard medical evaluation except in the case of genital dysplasia. ~Genital HPV types are divided into low-risk and high-risk depending on the likelihood of their association with cervical and anal CA. ~There are usually no sx. ~Tenderness on pressure occurs w/plantar warts; itching occurs w/anogenital warts. ~Flat warts are most evident under oblique illumination. ~Periungual warts may be dry, fissured, and hyperkeratotic and may resemble hangnails or other nonspecific changes. ~Plantar warts resemble plantar corns or calluses. Atlas: ~cutaneous warts are discrete benign epithelial hyperplasia w/varying degrees of surface hyperkeratosis ~cutaneous warts are manifested as minute papules to large plaques ~lesions may become confluent, forming a mosaic ~extent of lesions is determined by the immune status of the host Zarbocks: ~skin warts can be flat or SF; plantar warts are deeper; surface is rough, resembling tiny heads of cauliflower ~warts of the oral cavity or larynx can be life threatening if they block the airway ~anogenital warts occur almost exclusively on the squamous epithelial of the external genitalia and perianal area ~cervical warts (esp HPV types 16 and 18) are a risk factor for dysplasia, which may progress to cervical CA

Viral: VERRUCAE (Warts) HPV (>100 serotypes) replicates in cutaneous and mucosal epithelium (growth remains local and regress spontaneously) Common warts can arise on any skin surface. Genital warts (condylomata) are spread thru sexual contact. Dx usually made on clinical findings. W/host defense defects, HPV-induced SCC at periungual sites or anogenital regions s/b r/o by lesional bx. 1) Microscopic study ~characteristic hyperplasia and hyperkeratosis ~koilocytotic squamous cells are present 2) Presence of HPV is confirmed by immunofluorescence ~Molecular probes can detect HPV in cervical tissue Z: 1) Spontaneous regression is typical over time. 2) Type, location, and age of pt dictate tx. ~Extent of lesions, pt's motivation, and pt's immunologic status also affect tx choice. 3) Salicylic acid plasters can be effective for common warts. ~Cryosurgery or electrodessication can be effective but risks scarring. 4) Imiquod (Aldara) is a topical therapy that pts can apply at home, but compliance is a problem. 5) Intralesional interfereon also may be effective if other treatments fail. 6) Anogenital warts ~trichloroacetic acid or topical podophyllin ~may require many applications 7) Surgical excision is successful, but recurrence is common 8) Vaccine ~16 & 18: cervical CA ~8 & 11: warts Atlas: Aggressive therapies (often painful, scarring) are usually avoided b/c of recurrence. Plantar warts that are painful b/c of their location warrant more aggressive therapies. 1) Small lesions: 10-20% salicylic aid and lactic acid in collodion 2) Large lesions: 40% salicylic acid plaster x 1 week, then application of salicyclic acid-lactic acid in collodion 3) Imiquimod Cream ~at sites that aren't thickly keratinized, apply 1/2 strength 3x per wk ~persistent warts may require occlusion ~hyperkaratotic lesions on palms/soles s/b debrided frequently; imiquimod used alternatively w/a topical retinoid (i.e. - tazarotene topical gel) may be effective 4) Hyperthermia for Verruca Plantaris ~hyperthermia w/hot water immersion x 20 minutes or 3/ weekly for up to 16 tx 5) cryosurgery ~if pts have tried home therapies and liquid nitrogen is available 6) electrosurgery ~more effective than cryosurgery but greater chance of scarring ~EMLA cream can be used for anesthesia for flat warts ~lidocaine injection is usually required for thicker warts, esp palmar/plantar lesions 7) CO2 laser surgery ~may be effective for recalcitrant warts but no better than cryosurgery or electrosurgery 8) surgery ~single, nonplantar verruca vulgaris ~curettage after freon freezing ~not indicated in that these lesions are epidermal infections