Derm

Childhood atopic dermatitis

A type of eczematous dermatitis. Eczema is a group of inflammatory skin conditions characterized by pruritus, erythema, and scale. Chronic, relapsing and remitting, pruritic, inflammatory skin disease with a wide range of severity that is very common in developed countries (20% of kids - usually onset <5yrs, 3% of adults). Pruritus is the primary symptom, and scratching exacerbates the dermatitis. Lesions begin as erythematous papules that coalesce to form erythematous plaques that can weep, crust, or scale. Toddlers and infants generally have eczematous plaques on their cheeks, forehead, scalp, and extensor surfaces. Xerosis is common at all ages. Older children and adolescents have lichenified, eczematous plaques in flexural areas of the neck, elbows, wrists, and ankles. Adults have lichenification in flexural regions and involvement of the hands, wrists, ankles, feet, and face (forehead and around eyes). Lichenification describes skin becoming thick and leathery in response to excessive itching or rubbing. Atopic dermatitis always spares the nasal tip. Patients with acute dermatitis are susceptible to cutaneous infection with Staph aureus and strep pyogenes (group A strep), which often cause hyperacute, weepy flares with pustules or extensive yellow crust. Perform a skin bacterial culture to diagnose and treat with systemic antibiotics (cephalexin). Pityriasis alba mild form of atopic dermatitis of the face, presenting as poorly marginated, hypopigmented, slightly scaly patches on the cheeks, typically in children 3-6yrs old with darker skin. It is more common in spring and summer when normal skin begins to tan. Pityriasis alba generally fades with time but sunscreens can be used to minimize tanning of surrounding skin. Low strength steroids can also be used. 50-80% of kids with atopic dermatosis have another atopic disease. The atopic triad consists of Asthma, atopic dermatitis, and allergic rhinitis. Pathogenesis Genetics, skin barrier dysfunction, impaired immune response, and the environment all play a role. Food allergies are an uncommon trigger (test only with high suspicion or additional symptoms like diarrhea and vomiting). treatment General skin care - tepid baths without washcloths or brushes, pat dry, use mild soaps, apply ointments or thick creams (not lotions) 1-2x daily to whole body within 3 minutes of bathing. Treat acute inflammation with topical corticosteroid ointment (vs. cream). Use low potency steroids for face and folds (and maintenance) and medium for body/limbs (shorter periods). Topical corticosteroid therapy can cause striae, telangiectasias, temporary skin lightening from vasoconstriction, atrophy, and acne. Topical calcineurin inhibitors are 2nd line therapy for atopic dermatitis (because it has a black box warning) that is used for areas that could be damaged by steroids, like on the eyelids. Treat pruritus with antihistamines, especially 1st generation at night (hydroxyzine, dyphenhydramine).

Urticaria/hives

A vascular reaction of the skin characterized by wheals surrounded by a blanchable red halo or flare caused by swelling of the upper dermis. Each papule lasts <12 hours, and the cardinal symptom is pruritis. Most cases are acute (<6 weeks), but some are chronic (>6 weeks). Causes of acute urticaria Post-infection (viral, streptococcal, helminthes), food reactions, drug or infusion reactions (NSAIDs, penicillins, blood products, IV contrast). Detergents and common contact allergens are not triggers of urticaria (except latex) - the process is deeper within the skin rather than triggered by touching something. Chronic urticaria >50% is idiopathic, but causes can be physical (pressure, cold, heat, water, solar, vibration, exercise), cholinergic (physical urticaria from heat or emotion), autoimmune (IgE receptor antibodies causing mast cell degranulation), infectious, medications, or ingestions. Dermatographism is a physical urticaria in which a sharply localized edema or wheal appears within seconds to minutes after the skin has been rubbed, affecting 2-5% of the population. Treat with antihistamines. Immunologic urticaria Antigen binds to IgE on the mast cell surface, causing degranulation and histamine release. Histamine binds to H1 and H2 receptors to cause arteriolar dilation, venous constriction, and increased capillary permeability. Non-immunologic urticaria Direct mast cell degranulation by pharmacologic or physical mechanism. Urticaria is a clinical diagnosis Keep a diary of food and other possible triggers as allergy testing isn't usually helpful. IgE receptor antibody testing is possible in chronic urticaria but doesn't change management. Most cases resolve in 1-3 years but 20% last >5 yrs. Treatment Oral H1 antihistamines are fist line for acute and chronic urticaria. 1st generation cause sedation and have shorter half lives (hydroxyzine or diphenhydramine) - start with low doses at bedtime and avoid other sedating meds 2nd generation are less sedating (loratidine, cetirizine, fexofenadine) - 1-2x daily Conditions that can be mistaken for urticaria Angioedema - like urticaria, antigen binds to IgE on the mast cell surface, causing degranulation and histamine release. Histamine binds to H1 and H2 receptors to cause arteriolar dilation, venous constriction, and increased capillary permeability. But unlike urticaria, this occurs in the deep dermis with subQ swelling. Angioedema commonly affects the face or an extremity (tongue, pharynx, larynx, bowels > hoarseness, dyspnea, GI symptoms). It can be painful or burning, but not pruritic and lasts for several days. Always assess airway, breathing, and circulation due to risk of associated anaphylaxis. Angioedema and/or urticaria can be cutaneous presentations of anaphylaxis - a serious allergic reaction that's rapid in onset and can cause death. Symptoms include chest tightness or SOB, hoarse voice, throat tightness, nausea, vomiting, abdominal pain, and lightheadedness. First line treatment includes epinephrine, IV fluids, and O2.

localized blisters

Blister <1cm diameter Bulla >1cm diameter Erosion/ulceration - unroofed blister crust - dried transudate (serous fluid) Almost anything that causes inflammation in the upper levels of skin can cause a blister. Herpes zoster (shingles) Eruption of latent varicella zoster virus causing dermatomal, unilateral grouped vesicles on an erythematous base. Outbreaks are usually preceded by pain or burning. *Shingles generally occurs only once in the immunocompetent while HSV recurs.* Early treatment with acyclovir or valacyclovir can decrease length of eruption and post-herpetic neuralgia. Herpes simplex 1 and 2 painful, grouped vesicles (can be pustular, white to yellow) on an erythematous base that tend to recur in the same place. HSV1 favors the mouth and nose while HSV2 favors the genitalia, buttocks, and thighs. Perianal erosions or ulcerations in immunosuppressed patients are usually HSV (only erosion may be present at presentation). *Recurrent ulcers on the buttocks or genitals are HSV until proven otherwise.* It can also appear on the fingers of healthcare workers or in others from autoinnoculation. Treat HSV with acyclovir episodically or prophylactically. It can be used during pregnancy and IV acyclovir is available for generalized HSV or VZV in the immunocompromised. Famciclovir and valacyclovir are more expensive but have easier dosing (one dose for episodic treatment). Herpes diagnosis Tzanck prep - bedside scraping and microscopic exam to look for multinucleated giant cells to determine VZV or HSV infection. Tzanck prep can't differentiate the two, however and is unreliable. Viral culture - can be used to diagnose HSV using fluid (not crust), but results take 1-3 weeks. *Direct fluorescent antibody (DFA) test* - differentiates HSV 1 and 2, and VZV using scrapings from the vesicle/erosion for results in 48 hrs. HSV antibody detection detects past exposure, but most have been exposed. Fluid swab for *PCR* is a rapid and sensitive test that differentiates HSV 1 and 2, and VZV (used at UNC). Dyshidrotic eczema (pompholyx) Pruritic vesicopapules on the palms, soles, and sides of the fingers that contain fluid like tapioca pudding. After healing, vesicles can leave behind a mahogany colored mark (post-inflammatory hyperpigmentation). Many patients have a history of atopic dermatitis and coexisting tinea pedis. Dyshidrotic eczema is recurring, often during times of anxiety/stress. Treat with topical steroids. Vesicles by location Dorsal foot - contact dermatitis, insect bites Sides of feet/toes - dyshidrotic eczema Soles - tinea pedis (scaling and interdigital maceration) Balls/heels - friction blisters Mouth/nose/eyes - HSV, bullous impetigo Chest, back (dermatomal) - VZV Fingers - dyshidrotic eczema, contact dermatitis, herpetic whitlow (HSV on fingers) Arms, legs - contact dermatitis Genitalia - HSV History clues Pain precedes onset - HSV, VZV Itch precedes onset - allergic contact dermatitis, dyshidrotic eczema, VZV Trauma precedes onset - friction blister, pressure ulcer, cryotherapy Recurrent blisters - HSV

Bacterial skin infections

Cellulitis Dermal infection presenting as spreading erythematous, non-fluctuant (no pocket of fluid underneath) tender plaque, most often on the lower leg with streaks of lymphangitis spreading from that area to draining lymph nodes. There will be systemic signs of infection - fever, high WBC. Cellulitis can lead to sepsis and death. Risk factors include local trauma (bug bites, wounds), inflammation, edema, systemic infection, or other skin infection. Group A strep and staph. aureus cause 80% of cellulitis. Treat with empiric antibiotic therapy. Give outpatients cephalosporin for group A strep and S aureus. Those with recent exposures or purulent drainage should be given doxycycline, TMP/SMX, or clindamycin to cover community acquired MRSA. Give inpatients vancomycin to cover hospital acquired MRSA. Erysipelas superficial cellulitis with marked dermal lymphatic involvement causing marked edema, generally caused by group A strep. Erysipelas usually affects the lower extremities and face and presents with pain, superficial erythema, and plaque like edema with a sharply defined margin to normal tissue. It can be associated with a high white count (>20,000), chills, fever, headache, vomiting, and joint pain. Treat with oral antibiotics to cover strep (cephalosporin), elevate the involved area, and treat tinea pedis if present (portal of entry for infection). Monitor closely. Abscess a common infection characterized by a localized accumulation of PMNs with tissue necrosis involving the dermis and subcutaneous tissue. Staph. aureus is the most common cause. Abscesses can arise from infection tracking in from the skin surface but are usually deeper than carbuncles and can also be a complication of bacteremia. Clinical features include local pain, swelling, erythema, a fluctuant nodule (pocket of fluid underneath), sometimes spontaneous drainage, and regional lymphadenopathy. Fever, chills, and systemic toxicity are unusual except in patients with concomitant cellulitis. A risk factor for development of this infection is an insect bite, abrasion, or injection drug use. Spontaneous drainage of purulent material often occurs. Otherwise, surgical incision and drainage should be performed if the abscess is fluctuant. Oral antibiotics are usually unnecessary and reserved for cases in which the abscess is not ready for drainage, there are multiple lesions, there is surrounding cellulitis or systemic symptoms such as fever, or the patient is immunocompromised or has other high-risk features such as diabetes. Wound cultures should always be sent incase the patient does not improve with I&D so that you know what antibiotic to give. Patients should be offered HIV testing if they have risk factors. Carbuncle / Furuncle A type of abscess. A furuncle (boil) is an acute, round, firm, tender, circumscribed, perifollicular (around hair follicles) staphylococcal pyoderma that usually ends in central suppuration (puss formation). There can also be lymphatic streaking. A carbuncle is two or more confluent furuncles with separate heads that drain purulent discharge. Some lesions disappear before rupture, but most undergo central necrosis and rupture through the skin, discharging firm, purulent, necrotic debris. Predisposed sites include the nape, axilla, face and buttocks (areas with hair follicles exposed to friction and perspiration), but lesions may occur anywhere. Furuncles/carbuncles are usually caused by Staph aureus. Treatment consists of warm compresses and oral antibiotics (penicillinase-resistant penicillin or a first-generation cephalosporin). Surgical drainage may be required in cases in which spontaneous drainage does not occur and antibiotic treatment does not achieve resolution of the lesion. Bacterial folliculitis Superficial bacterial infection of hair follicles, presenting as small, raised, erythematous, pruritis pustules and papules (<5mm). Folliculitis is generally caused by staph aureus, and genital folliculitis can be sexually transmitted (pustules associated with marked erythema and scaling are probably genital candidiasis). Pseudomonas folliculitis is possible after exposure to a hot tub or swimming pool. Treat folliculitis by cleansing the area with antibacterial soap 3x daily, avoid shaving, and use oral or topical anti-staph agents. superficial pustules rupture spontaneously, but deeper lesions are small abscesses and should be drained. Impetigo Common superficial bacterial skin infection most often in kids 2-5yrs that is contagious among close contacts and usually caused by S. aureus or S. pyogenes. Non-bullous impetigo/ impetigo contagiosum starts as papules surrounded by erythema and progresses to pustules that enlarge and break down to form thick, adherent crusts with a characteristic golden appearance. Bullous impetigo occurs in young children with flaccid bullae with clear yellow fluid that later becomes purulent and ruptures, leaving a thick brown crust and is caused by staph aureus exotoxin. Staph scalded skin syndrome occurs most often in kids <2yrs and adults with renal disease when a focus of infection secretes toxin into the blood, leading to widespread superficial blisters, leading the skin to peel away in sheets. Wound cultures from these erosions are negative. Treat localized impetigo with topical mupirocin ointment. Give cephalosporins or clindamycin for other infections to cover strep and staph. Necrotizing fasciitis Presents as an expanding dusky, edematous, red plaque with blue discoloration. Anesthesia of the affected skin is characteristic. 20% mortality rate, so contact surgery immediately if you suspect it. Treat with widespread debridement and broad spectrum systemic antibiotics for strep/staph. MRI can be helpful, but should not delay surgery. Poor prognostic factors include delayed diagnosis, age 50+, diabetes, atherosclerosis, and infection of the trunk.

Psoriasis

Chronic multisystem disease of mainly the skin and joints, affecting 2% of the US population, with onset generally in those 20-30 or 50-60yrs. It waxes and wanes during the lifetime, generally from treatment initiation and cessation rather than spontaneous remission. 33% have a family history. Classification is based on morphology. Pathogenesis Cytokines trigger hyperproliferative state resulting in thick skin and excessive scale. Systemic treatments target these cytokines and immune cells, and trauma can trigger/fuel psoriasis by increasing cytokines (koebner phenomenon). It can sometimes be triggered by steroid withdrawal or infections, esp. strep pharyngitis. 20% of those with psoriasis have arthritis, and nail pitting and oil spots along the edges of the nail are classic for psoriasis. Nail psoriasis can occur with all psoriasis subtypes and indicates higher risk for psoriatic arthritis. Fingernails are involved in 50% and toenails in 35% of those with psoriasis and can involve pitting, onycholysis (separation of nail plate from bed), and subungual hyperkeratosis (abnormal keratinization of distal nail bed). Psoriatic arthritis is a seronegative spondyloarthropathy causing mild to severe symptoms of oligoarthritis, most often in the distal interphalangeal joints. It usually arises in those with psoriasis between 30-50yrs and is not related to skin severity. Those with psoriasis have increased risk for metabolic syndrome, obesity, depression, smoking, and alcohol use. Plaque psoriasis The most common form (80-90%), usually producing mild to moderate disease that is localized or scattered to cover only <5% of BSA. 20% with plaque psoriasis have moderate to severe disease affecting >5% of BSA or affecting crucial body areas (hands, feet, face, genitals). Lesions are scaly, erythematous patches, papules, and plaques that can be pruritic. Can be palmoplantar or appear on the scalp, ears, elbows, knees (extensor surfaces), umbilicus, gluteal cleft, nails, and sites of recent trauma. Chronic plaque psoriasis is typically symmetric and bilateral. Plaques can exhibit the Auspitz sign (bleeding after removal of scale) and/or the Koebner phenomenon (lesions induced by trauma). inverse/flexural psoriasis erythematous plaques in the skin folds (axilla, groin, inframmary), often lacking scale due to moistness of the area. It can resemble a fungal infection, but does not respond to antifungals. Guttate psoriasis drop lesions of 1-10mm salmon-pink papules with fine scale on the trunk and extremities (classically the bellybutton), most often in those 8-25yrs. Guttate psoriasis is often preceded by strep pharyngitis, and there is good chance for long term remission after one episode. Psoriatic erythroderma generalized erythema (bright red) covering 90+% of the body surface area with varying degrees of scaling. It can be associated with fever, chills, and malaise. Hospitalization is sometimes required because of complications like high output heart failure and sepsis. It can be caused or worsened by steroid tolerance or withdrawal (steroids can cause temporary remission, but comes back more severe). Erythroderma can also be caused by atopic dermatitis, cutaneous lymphoma, or underlying malignancy, and a biopsy is needed to distinguish the cause. Manage erythroderma with extensive topical therapy, monitoring fluids/electrolytes, and treating the cause. pustular psoriasis psoriatic lesions with pustules (many PMNs) that can be generalized or palmoplantar, and often triggered by corticosteroid withdrawal. Generalized pustular psoriasis can be life-threatening (requiring hospitalization). Palmoplantar psoriasis can be functionally disabling. Topical Treatment Use topical agents if psoriasis is localized (<5% BSA). High potency topical steroids +/- calcipotriene (vitamin D analog) is first line. Use clobetasol (Class I steroid) for thick skin (eg. knees) or fluocinonide (class II). Topical treatments are more effective when used with occlusion - bandage, saran-wrap, gloves, or socks. Oral steroids are never used with psoriasis because they can cause severe flares with discontinuation. Systemic treatment Systemic treatment (not oral steroids) is used in addition to topical treatment for moderate to severe disease, or limited disease with high impact on QOL (palmoplantar, genital). Systemic treatment includes phototherapy with narrow band UVB light or psoralen plus UVA light (PUVA), which is less carcinogenic than a tanning bed with no systemic side effects. Oral medications include methotrexate (disrupts folic acid metabolism), acitretin, and cyclosporine. Biologic agents used include TNF-alpha inhibitors (infliximab, etanercept, adalumimab), and IL 12/23 blocker (ustekinumab)

Drug reactions

Cutaneous drug reactions are usually inflammatory, generalized, and systemic. Allergy testing is generally not helpful or predictive. Risk factors include being female, prior history of drug reaction, recurrent drug exposure, HLA type (SJS/TEN caused by allopurinol is associated with HLA-B 5801 in Han Chinese), HIV (sulfonamides), and *EBV infection (aminopenicillins).* Immediate reactions - Occur <1hr of the last dose (type I) presenting with urticaria, angioedema, and anaphylaxis. Delayed reactions - occur after one hour but usually >6hrs and occasionally weeks-months after the start of administration (type IV), causing exanthematous eruptions, fixed drug eruption, systemic reactions, and vasculitis. Exanthematous drug eruption 90% of all cutaneous drug eruptions, they are limited to the skin (no mucus membranes) and cause erythematous macules and papules, pruritus and mild fever, usually >2 days after starting the drug (day 8-11) and persisting 2-7 days after stopping. Exanthematous eruptions have no long term complications, but treat with topical steroid and antihistamines. Fixed drug eruption an adverse drug reaction characterized by the formation of a solitary erythematous patch or plaque that will recur at the same site with re-exposure to the drug (takes shorter amt of time to appear with each exposure). Common causes are NSAIDs, tetracyclines, metronidazole, and sulfonamides. FDE often affects the mouth, genitalia, face, and acral areas, with lesions occurring 30min-8 hours after drug ingestion. Early lesions are sharply demarcated erythematous macules evolving into edematous plaques +/- bullae and erosion. healed lesions are dark brown/violet. Lesions are commonly solitary and can become large or can be multiple. Lesions resolve in days to week after stopping the drug. Non-eroded lesions can be treated with a potent topical glucocorticoid ointment and eroded lesions can be treated with an antimicrobial ointment and dressing. Drug-induced hypersensitivity syndrome AKA Drug reaction with eosinophilia and systemic symptoms (DRESS) Characterized by skin eruption (*not mucosal surfaces*) with systemic symptoms (fever) and internal organ involvement (liver, kidney, heart). Patients present with macular exanthem, erythematous centrofacial swelling, fever, malaise, lymphadenopathy, and organ involvement. >70% have eosinophilia. (*When patients present with rash and facial edema, order CBC and LFTs*). Signs and symptoms usually start in the 3rd week of starting a medication or increasing the dose (longer than exanthematous drug eruption, which takes 7-10days) and can persist or recur many weeks after cession of drug. 10% die. Medications that cause DIHS include *allopurinol* (kidney stones), sulfonamides, penicillin, anticonvulsants (phenytoin, carbamazepine, lamotrigine), NSAIDs, and Abacavir (HIV drug). If mild, treat with topical steroids and anti-histamines. Prolonged systemic steroids may be necessary with slow taper. Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) Extensive necrosis and detachment of the epidermis *and mucosal surfaces* (different from DIHS) that is very painful and preceded by 1-3 days of fever, headache, and myalgias. Symptoms begin within 8 weeks of drug exposure and rash is symmetric on the face, upper trunk, and proximal extremities with rapid expansion. Inital erythematous, irregularly shaped, dusky red to pururic macules (atypical targets) progressively coalesce, and the dark centers can blister. the skin eventually detaches in sheets with lateral pressure (Nikolsky sign). Complications include corneal damage, fluid/electrolyte/nutrition problems, secondary infection (bacteremia, sepsis), and mucous membrane stenosis/scarring (OV/Gyn, airway, esophagus). 5-12% die from SJS and >20% die from toxic epidermal necrolysis. Age, comorbidities, and BSA correlate to mortality, usually from sepsis and respiratory failure (sloughing of respiratory epithelium). The most high risk drugs are sulfa antibiotics, allopurinol, tetracyclines, anticonvulsants, and NSAIDs. Diagnose with a punch biopsy. Treat by withdrawing the causative drug and providing supportive care in a burn unit for patients with <25% BSA involvement.

Cutaneous fungal lesions

Dermatophytes, Malassezia species, and Candida species cause cutaneous superficial infections. Dermatophytoses affect 25% of people worldwide. Dermatophytes include Trichophyton, Microsporum, and Epidermophyton species, which infect keratinized tissues - the stratum corneum and the nail or hair. Tinea is used for dermatophytoses. Diagnosis KOH exam - clean skin with alcohol swab, collect scale with a scalpel blade onto a glass slide, add a drop of KOH and coverslip and head to dissolve the keratin, then look under the microscope for hyphae. Look for parallel lines and septae that cross over an entire cell. Also get a fungal culture because KOH is not that sensitive and it's the only way to definitively identify the organism. Tinea pedis/athletes foot The most common fungal infection in developed countries, generally caused by Trichophyton rubrum. It is hard to permanently cure and can reoccur. Complications include lower leg cellulitis and tinea corporis from autoinoculation. Interdigital type - scaling and redness between the toes, sometimes with maceration (moist, white skin). Moccasin type - sharply marginated scale distributed along the lateral borders of the feet, heels, and soles, with vesicles and erythema sometimes at the margins. Moccasin type is often associated with onychomycosis (chronic nailbed fungal infection) and can present as "one hand, two feet" syndrome, with one hand having fine scale in the creases and nail involvement. Vesiculobullous type - grouped, 2-3mm vesicles or bullae in the arch or instep that can be itchy or painful, caused by delayed hypersensitivity immune response to a dermatophyte. Diagnosis - KOH exam Treatment - dry feet well after bathing, change socks daily, and use open toed shoes when possible. Use foot powder to keep feet dry and keratolytics (urea or salicylic acid), to remove scale. Apply topical antifungals until 2 weeks after resolution. Imidazoles (clotrimazole, miconazole, ketoconazole) are fungistatic. Allylamines (terbinafine, naftifine) are fungicidal. Ciclopirox is fungicidal and fungistatic. Treat onychomycosis with oral terbinafine or azoles for 3+ months (monitor liver function) Tinea corporis/ringworm Dermatophytosis of the body skin, usually the trunk and limbs, causing itching. Distribution is asymmetric, and there is an annular lesion with active border with central clearing. Diagnose with KOH exam using scrapings from the red, scaly margin. Treat as you do tenia pedis. Treat with oral terbinafine or fluconazole for 1-2 weeks for severe or widespread disease (longer if spread into hair follicles). Tinea Capitis Dermatophytosis of the scalp and hair, weakening it and causing it to break as it comes to the surface, leading to "black dots" and patchy alopecic (w/o hair) areas. Tinea capitis is common in black kids (4-8yrs) and spread through direct contact with animals, humans, and fomites. Microsporum canis is the most common cause worldwide, but Trichophyton tonsurans is the most common cause in the US. Tinea capitis can be noninflammatory (black dot, seborrheic), inflammatory (kerion), or both. A kerion is a painful, boggy, inflammatory mass with broken hair follicles that may discharge pus and carries risk of scaring. Tinea capitis can present with postauricular, posterior cervical, or occipital lymphadenopathy. Topical agents are ineffective - treat with griseofulvin or terbinafine granules (shorter treatment course but less effective against M. canis) Tinea cruris/jock itch - similar presentation in the groin or folds (unlike diaper candidiasis, it does not affect labia, scrotum, or penis). tinea manuum - hands tinea facei - face Tinea incognito applying topical steroids to a fungal infection will reduce the inflammatory response, making the lesion appear less prominent, but will allow the fungal infection to spread and go deeper into hair follicles, requiring oral antifungal therapy rather than only topical. Diaper candidiasis Beefy red confluent erosions and marginal scaling in the area covered by a diaper, including skin folds (vs. irritant diaper dermatitis) with satellite papules and pustules (vs. irritant diaper dermatitis). Rash does not improve with barrier creams (zinc oxide paste, petrolatum, triple paste - irritant diaper dermatitis does). Use KOH prep and fungal culture to confirm diagnosis if unsure. Candidal diaper candidiasis occurs when urease enzymes in feces release ammonia from urine, causing acute irritant effect that disrupts the epidermal barrier, allowing entry of candida that's present in feces. Treat with nystatin or imidazole cream/ointment. Oral nystatin can be used if thrush is present or with frequent recurrence. Use hydrocortisone cream/ointment for significant inflammation for a limited time due to risk of atrophy or systemic absorption. Do not use topical steroids, as this can make the infection worse. Not a fungus - irritant diaper dermatitis Erythematous dermatitis limited to exposed areas (not folds) distributed over convex skin surfaces. Infrequent diaper changes and diarrhea predispose infants because chronically moist skin is more easily irritated. treat with barrier creams (zinc oxide paste), frequent diaper changes, looser diapers, treating diarrhea. Candidal intertrigo Candidiasis of large skin folds - groin, armpits, butt crack, under large breasts, under overhanging abdominal folds. Presents as erythematous, eroded areas with satellite papules. Diagnose with KOH, which shows pseudohyphae. Candidal intertrigo burns more than itches (vs. tinea corporis). Risk factors include DM, hot/humid weather, limited mobility, and obesity. Treat with topical antifungals - nystatin and imidazoles (not allylamines). Use systemic imidazoles for extensive disease. Also use hydrocortixone cream to reduce symptoms rapidly, but only use for one week.

Describing morphology

Flat or raised, size, shape (round, geographic), color, borders (sharpness, irregular/regular), texture (scaly), fluid filled, configuration (relation to one another, symmetrical, grouped, dermatomal), distribution (location) Primary lesion - initial lesion Secondary lesion - changes that occur over time or from manipulation (scratching, trauma, infection, healing process) Macules - small (<1cm), flat lesions (eg. tinea vesicolor) usually caused by color chages in the epidermis or upper dermis. Macules indicate that process is confined to the epidermis. They can have secondary changes, like scale or crust. Scale - Visible fragments of the stratum corneum as it is shed from the skin. Scaling usually indicates an epidermal disorder and can result from faulty differentiation of the epidermis (ichthyosis) or accelerated turnover of the epidermis (psoriasis). Crust - Varying colors of liquid debris (serum or pus) that has dried on the surface of the skin. Crusting usually results from trauma to vesicles, bullae, or pustules. Examples: impetigo, secondarily infected dermatitis. Patch - flat lesion >1cm Plaque large (>1cm), plateau-like raised lesion (eg. psoriasis) caused by a proliferation of cells in the epidermis or superficial dermis Tumor/mass - Solid, firm lesions typically > 2 cm that can be above, level with, or beneath the skin surface. Skin tumors, unlike plaques, are solid lesions extending deeper and into the dermis. Examples: tumor-stage mycosis fungoides. Papule - raised lesion <1cm caused by a proliferation of cells in the epidermis or superficial dermis. Nodule - raised lesion >1cm caused by proliferation of cells down to the mid-dermis in which the overlying epidermis looks and feels normal, but there is proliferation of deeper tissues. (eg. dermatofibroma, lipoma, nodular secondary or tertiary syphilis, squamous cell carcinoma.) Vesicles - small (>1cm), raised, fluid-filled lesions. Erosions Secondary lesion from loss of the epidermis that can occur after a vesicle forms and the top peels off. They weep and become crusted but don't usually scar. Ulcer Erosion that involves the dermis and tend to scar. pustule - vesicle filled with pus, which is made of leukocytes and a thin fluid called liquor puris. Bulla -A raised, circumscribed lesion (> 1 cm) containing serous fluid above the dermis (note whether tense or flaccid). Examples: bullous pemphigoid, second-degree burns. Wheal/urticaria - Transient, circumscribed, elevated papules or plaques, often with erythematous borders and pale centers due to dermal edema. Usually resolve within 24 hours. Burrows - Linear or serpiginous (wavy, serpent-like borders) tunnels within the epidermis. (eg. The small and short tunnels of scabies) Telangectasias - Small, superficial blood vessels that become visible because they are dilated. Examples: acne rosacea, chronic radiodermatitis. Petechiae - Small, non-blanching, erythematous macules >0.3 cm (pinpoint to pinhead size), due to rupture of small blood vessels leading to hemorrhage. Ecchymosis Non-blanching, purpuric macules or patches of greater than 3mm due to extravasated blood in the skin. Atrophy - Thinning or depression of skin due to reduction of underlying tissue. Atrophy of the epidermis - thin and wrinkled surface, with thinning and loss of rete ridges on histology. Atrophy of the dermis or subcutaneous fat - depression in the skin with loss of dermal collagen or lipoatrophy (fat cells smaller and closer together) histologically.

Skin basics

Functions Barrier that regulates water loss and protects against mechanical, chemical, and microbial insults. Immunologic barrier that senses and responds to pathogens to prevent infection and cancer (dysfunction can cause inflammation or allergy). Temperature regulation using sweat production and dense superficial microvasculature. Protection from radiation with melanin in the epidermis. Sensory receptors allow for monitoring of environment and mechanoreceptors are important for interacting with physical options. Cutaneous wound repair via coagulation, inflammatory phase, proliferative-migratory phase (tissue formation), and remodeling. Epidermis the topmost layer of skin, consisting mainly of keratinocytes. It takes two weeks for basal cells to reach the startum corneum and 2 more weeks for them to be shed (28 day cycle). From shallow to deep: Stratum corneum - made up of desquamating keratinocytes, or layers of flattened keratinized non-nucleated cells that provide a barrier against trauma and infection. The keratinocytes are held together by lipid mixture that creates a water tight barrier. Stratum granulosum - lipids and the protein filaggrin are produced by keratinocytes in the granular cell layer and are secreted into the extracellular space between the keratinocytes to form a water barrier. (mutations in filaggrin cause atopic dermatitis and asthma) Stratum spinosum - The thickest portion of the epidermis, is has a spiney appearance due to desmosomal junctions that hold the keratinocytes together. Stratum basale - source of epidermal stem cells where cell division occurs. Keratinocytes start at the basal layer and move upwards. (Basal cell carcinoma is the most common form of skin cancer and is composed of cells that resemble basal keratinocyes (but aren't) and present as pearly, erythematous papules or plaques with rolled vorders and telangectasias in sun-exposed areas) Keratinocytes held together by desmosomes (mainly visible in spinous layer). Melanocytes make pigment and transfer it to keratinocytes. Melanocytes Staggered along the basal layer at 1 in 10 keratinocytes to produce and transfer melanin to keratinocytes in the basal layer. All skin types have the same number of melanocytes, but the amount, color, and distribution of melanin differs. Langerhans cells Dendritic cells in the mid-epidermis that recognize, uptake, process, and present antigens to sensitized T cells to induce delayed-type hypersensitivity (eg. contact dermatitis). Immunohistochemical staining is often necessary to see them. Dermis Lies below the epidermis, consisting mainly of fibroblasts, collagen, and elastic fibers. It is 1-4mm thick - much thicker than the epidermis - and contains blood and lymph vessels, nerves, sweat and sebaceous glands, and hair follicles. The papillary dermis is a thin area just below the epidermis, and the reticular dermis is thicker and deeper. Fibroblasts - synthesize and degrade connective tissue proteins in wound healing and scarring (eg. keloids) Mast cells - responsible for immediate-type hypersensitivity reactions in the skin (urticaria/hives). They look like fried eggs and are generally close to blood vessels. Subcutis/panniculus/hypodermis fat and large flood vessels below the dermis that insulates the body, serves as energy supply, cushions and protects skin, and allows for mobility over structures. Pilosebaceous unit Hair follicle, sebaceous glands, apocrine sweat glands, and an erector pilli muscle. Apocrine glands are in the axillary and anogenital areas only and open directly into the hair follicle. Eccrine glands Sweat glands that don't involve a hair follicle and open directly onto the skin surface throughout the body. they help regulate body temperature. Acne vulgaris disorder of the pilosebaceous unit caused by plugging of hair follicle from abnormal keratinization of the upper portion, P. acnes bacteria in the follicle that breaks down the oil to FFA that causes inflammation, hormones/androgens, and sebaceous gland activity (increased by androgens). Erythema nodosum a panniculitis (inflammation of the subcutis) that appears as deep-seated erythematous nodules usually on the shins that can be idiopathic or a reaction to infection, meds, or underlying autoimmune disease (crohn's) Bullous pemphigoid autoimmune blistering disease with autoantibodies to antigens on hemidesmosomes that anchor the basal layer to the dermis, causing tense bullae on an erythematous base. Psoriasis Increased rate of epidermal turnover (hyperproliferation/thickening), which does not allow adequate time for differentiation, leading to scale.

Necrotizing soft tissue infections

Injury or trauma leads to inflammation (dolor, calor, rubor, tumor) followed by pain out of proportion to exam, fever, chills, fatigue, vomiting, septic shock and death. NSTIs usually only happen in immunocompromised patients - diabetes, kidney disease, cancer, HIV, etc. Fournier's gangrene - NSTI in the perineum from aerobes and anaerobes in the GI tract Ludwig's angina - submandibular/sublingual necrosis from polymicrobial organisms from the orgal cavity. Necrotixing faciitis - fascia necrosis Myositis, myonecrosis - muscle necrosis Type 1 - polymicrobial type 2 - monomicrobial (usually strep pyogenes) Most common causes Strep pyogenes (group A strep) - gram positive, purple cocci in chains, inoculated through breaks in the skin. Vibrio vulnificus - gram negative rod associated with trauma in marine or brackish water Aeromonas hydrophila - gram negative rod associated with trauma in fresh or brackish water Clostridium perfringens - spore forming, gram positive anaerobe bacilli with endospores within them (tennis racket appearance) that are associated with vehicle accidents contaminated with soil Staphylococcus aureus - gram positive, cocci in grape clusters and the cause of community acquired MRSA Treatment Treat all NSTI with early surgery and debridement, broad spectrum antibiotics: Beta lactam + beta lactamase inhibitor, or carbapenem for mixed aerobes + anaerobes. Vancomycin for S. aureus Beta lactam + beta lactamase inhibitor + clindamycin for Group A strep (penicillin disrupts peptidoglycan synthesis and the cell wall, allowing clindamycin to enter and inhibit protein/toxin synthesis) Staph vs. Strep Both are gram positive Staph is catalase positive, strep (and enterococcus) is catalase negative Staph aureus is coagulase positive Staph epidermidis and staph saprophyticus are coagulase negative Strep poygenes (group A) and strep agalactiae (group B) are beta hemolytic. Strep pneumoniae and viridans strep are alpha hemolytic. Enterococcus is gamma hemolytic. Strep pneumoniae Gram positive, lancet shaped diplococci with a polysaccharide capsule that causes upper respiratory tract infections, pneumonia, bacteremia, and meningitis. It is optichin antibiotic sensitive (P disk) and alpha hemolytic. Viridans strep make up 50% of bacteria in the mouth and are the most common cause of infective endocarditis. Viridans is optichin resistant (P disk) and alpha (sometimes gamma) hemolytic. Strep pyogenes (group A) Gram positive, purple cocci in chains that are beta hemolytic and cause bacterial pharyngitis, cellulitis, impetigo, NSTI and toxic shock syndrome. Strep pyogenes can also cause rheumatic fever and glomerulonephritis. It is bacitracin (A-disk) sensitive. Virulence factors: M protein sticking out of the hyaluronic acid capsule is antiphagocytic and varies between strains, some cross reacting with cardiac tissue, causing rheumatic fever (resembles cardiac tissue so autoantibody response develops). Group A strep also releases hyaluronidase that degrades subQ tissue and streptokinase that activates plasminogen to destroy clots - bot of which create a plane along which bacteria can spread. Exotoxins include erythrogenic toxin (scarlet fever rash), streptolysins (beta hemolysis), pyogenic exotoxin A (STSS superantigen that causes toxic shock syndrome), and exotoxin B (NSTI-causing strains). Pyogenic infections include pharyngitis, cellulitis, and NSTIs. Toxigenic infections include scarlet fever and toxic shock syndrome. Immune mediated diseases include rheumatic fever, and acute glomerulonephritis. Treat group A strep with beta lactam, beta lactamase inhibitor, and clindamycin. Strep agalactiae (group B) Beta hemolytic, bacitracin (A-disk) resistant bacteria that colonize the female genital tract and cause neonatal meningitis and sepsis.

Cutaneous manifestations of systemic disease

Light chain (AL) amyloidosis/ primary systemic amyloidosis Plasma cell dyscrasia (abnormal proliferation of monoclonal population) produces monoclonal light chains that deposit in multiple organ systems, sometimes related to underlying Waldenstrom's, multiple myeloma, or MGUS (monocolonal gammopathy of undetermined significance). AL amyloidosis can present initially in one organ system, most often as asymptomatic proteinuria or nephropathy, but also restrictive cardiomyopathy, peripheral neuropathy, carpal tunnel syndrome, or heptomegaly. Cutaneous findings include macroglossia, pinch purpura (capillary fragility on face, eyelids), waxy thickening, and infiltrated nodules and plaques, especially periorbitally. Only 25% have clinically evident skin involvement. Serum and urine protein electrophoresis can detect circulating light chains, but diagnosis requires biopsy of affected organ(s) to reveal amyloid as apple green birefringence using congo red staining. Manage AL amyloidosis by treating plasma cell dyscrasia. Systemic sarcoidosis systemic inflammatory disease characterized by hyperactivity of cell-mediated immunity, affecting the lungs in 90% and skin in 33% (usually symmetric red-brown papules and plaques). It's more common in blacks and females. Biopsy shows non-caseating granulomas. Any organ can be involved, so patients need a chest Xray, PFTs, eye exams, ECG/Holter, +/- echocardiogram. Cardiac disease causes up to 25% of deaths, often suddenly. Lofgren's syndrome is sarcoidosis with erythema nodosum, hilar adenopathy, fever, migrating polyarthritis and acute iritis and has a better long term prognosis than other forms. Systemic sarcoidosis can remit spontaneously but there is no cure. Control with corticosteroids, antimalarials, minocycline, and immunomodulators. Necrobiosis lipoidica Necrotizing skin condition associated with diabetes in up to 65% (but <5% with diabetes have it) and often affecting young and middle-aged adults. It may be a microangiopathy or collagen disorder. Necrobiosis lipoidica is characterized by yellow-brown, atrophic, telangiectatic plaques with an elevated violaceous rim, usually pretibial. It can have a flame like appearance. It is often symptomatic but ulcerations following trauma can be very painful and decreased sensation and hypohidrosis may occur. Topical steroids are first line treatment. Sweet's syndrome/ Acute febrile neutrophilic dermatosis Fever and malaise with abrupt onset erythematous plaques with occasional vesiculation, commonly on the head, neck, and upper extremities but can be anywhere (even internal organs). AFND usually occurs in women ages 30-60yrs and is idiopathic in 50%. Triggers include infection (usually upper respiratory strep), malignancies (acute myelogenous leukemia), and other chronic inflammatory disorders. Sweet's syndrome persists for weeks to months if untreated, so treat underling infection/disease and give systemic corticosteroids for rapid improvement. Erythema nodosum The most common form of panniculitis, with tender nodules on the anterior lower legs without ulceration lasting 4-6 weeks and recurring in 1/3 of patients. 50% are idiopathic, but triggers cause a delayed hypersensitivity response to infections (strep), antibiotics, oral contraceptives, pregnancy, or chronic inflammatory diseases. Erythema nodosum is more common in women 10-30yrs old. Diagnosis is usually clinical (biopsy atypical cases), and systematic symptoms include arthritis, arthralgia, malaise, and fever. Treat with NSAIDs and underlying systemic disease if possible. Calcific Uremic arteriolopathy (calciphylaxis) Associated with ESRD in most patients, it starts with painful, violaceous, subQ nodules and plaques and progresses to chronic, painful ulcers +/- retiform purpura, typically on the lower extremities and trunk (less often on digits or genitals). Biopsy demonstrates arteriolar calcification. Surgical debriedment improves survival, and sodium thiosulfate can help sometimes. Kidney transplant can lead to resolution. Patients should not take vitamin D, calcium, or warfarin. Survival at 1 year is 48%, worse in proximal disease.

Infestations and bites

Pediculosis capitis (lice) Pediculus humanus causes scalp pruritus +/- posterior cervical lymphadenopathy. Adult lice or nits are most common on the proximal hair shafts of the occipital scalp and are not movable along the hair shafts. It is more common in children and less common in blacks. Adults live 30 days on the scalp, 1-2 days off and eggs hatch in 8-12 days and are viable 10 days off the scalp. OCT permethrin lotion is available but resistance can occur, in which case topical ivermectin and malathion prescriptions can be used. Sarcoptes scabiei (scabes) Spread by direct contact and less commonly fomites, presenting 3-4 weeks after exposure, most often in the finger webs, waistline, umbilicus, breasts, axilla, scrotum, and penis. They create linear markings (burrows) 1-10mm in length. Diagnose with skin scraping with mineral oil prep to look for mites, eggs, or scybala (feces) under the microscope. First line treatment in patients over 2 months old is 5% permethrin cream applied from the neck down and left on overnight. Crusted scabies is a severe, very contagious variant in the disabled and immunocompromised, requiring 2 doses of oral ivermectin 2 weeks apart (do not use in pregnant or lactating women). Ivermectin can cause diarrhea, itching, joint pain, and skin irritation. Bedbugs Cimex lectularis live in furniture and mattress seams, can live 1 year without feeding, and can cause a distinct odor. Bites (edematous papules) can be multiple in a linear array and occur on open skin surfaces rather than creases like scabies. their saliva contains vasocilators, anti-platelet agents, and blocks factor X to Xa conversion, sometimes causing bites to bleed. Bites resolve in 1-2 weeks. Topical corticosteroids can be used for itching and antibiotics for secondary infection. Arachnid bites Latrodectus (black widow) Tegeneria (Hobo spider) Loxosceles (brown recluse) - found in the midwest and SE in dark areas, they have a violin-shaped dark brown mark on the cephalothorax. The initial wound can progress to necrosis from sphingomyelinase in the venom and deep ulcer formation (rule our MRSA). Patients can have flu-like symptoms and rarely hemolysis, renal failure, anemia, and/or hypotension. Manage with supportive care, bandages, cool compresses, and pain control.

Zoonoses

Pediculus humanus The head/body louse transmits Rickettsie species, causing typhus (vs. typhoid fever that is caused by Salmonella enterica serovar Typhi through food/water), which presents with headache, malaise, and fever. Brucella species gram negative rods that colonize cattle, bison, elk, goats, sheep, and pigs and are transmitted via ingestion of unpasturized milk products or through skin (during butchering). Brucella are facultative intracellular bacteria that can survive within macrophages and disseminate via the blood stream. Their LPS triggers systemic inflammation and granulomas can form in the liver, spleen, kidneys, and other organs. Brucellosis is most common in the Mediterranean and can cause fever, generalized lymphadenopathy, mild splenomegaly, and tenderness in sacroiliac joints. Patients have low hematocrit and Hb, elevated WBC (mainly PMNs), and elevated liver enzymes. Brucella cultures require 3 week incubation (so don't have time to grow normally). Treat with doxycycline (penetrates cells) and streptomycin or rifampin for 6 weeks. Francisella tularensis Small, gram negative rod that infects rabbits, deer, and rodents and is transmitted between animals by ticks and flies. Humans are infected via a vector or cutaneous exposure to infected animal tissue, causing tularemia. It is also a bioterrorism agent, as inhalation causes high mortality pneumonitis. Tularemia presents with fever, erythematous pustules that form 3-5 days after infection and ulcerate 2-4 days later, painful lymphadenopathy with granulomas, low hematocrit and Hb, high WBC (mainly PMNs), and normal liver enzymes (in contrast to Brucella). Only 10-50 bacteria are needed for infection, so BSL-3 containment is required for cultures and Francisella is difficult to culture, so diagnose using serologic testing - a 4x rise in IgG antibodies against F. tularensis antigens confirms diagnosis. Treat with streptomycin, gentamycin, or doxycycline for 10-14 days. Yersinia pestis Small, gram negative rod with bipolar staining with clearing in the middle (safety pins) that grows best in vitro at 20-25C (cold). Y. enterocolitica and Y. pseudotuberculosis are GI pathogens that lack Y. pestis virulence factors. Cause of the plague, occurring most often today in SE Asia, Subsaharan Africa, and Peru, and most prevalent in the US in the west - transmitted by prairie dogs. Bubonic plague is transmitted by fleas, and infection spreads to lymph nodes, causing death in 50% if untreated. Septicemic - Yersenia Pestis in the blood. Pneumonic plague is spread via respiratory transmission (bioterrorism or respiratory droplets) or can result from septic emboli from the bloodstream. Pneumonic plague is the deadliest form, killing 100% if untreated. Patients present with fever, painful buboes (enlarged nodes), petechial hemorrhages, high ESR, WBC (PMNs), and liver enzymes and bilirubin. Virulence factors include: Glycoprotein-based extracellular capsule (F-1 antigen), endotoxin (LPS), and exotoxins, and YOPS - Yersenia outer surface proteins that are secreted via type 3 secretion to inhibit immune responses by forming a channel between the host cell and the bacteria and pumping enzymes through. They replicate explosively and spread to lymph nodes, disseminate via bloodstream where they are engulfed by monocytes (but not killed), trigger SIRS (systemic inflammatory response syndrome) with endotoxin, and can lead to lobar pneumonia if spread to the lung. Diagnose with culture - yersinia grow well on standard media and have fried egg appearance with raised centers. Treat yersenia pestis with streptomycin (outside US) or Gentamycin or fluoroquinolones in the US. Bartonella henslea Gram negative rod part of the normal oral flora of cats with low virulence potential, causing self-limited infection in immunocompetent people. bartonella is spread by cat scratches or bites and causes fever, enlarged nodes on the same side as the scratch in those who are immunocompetent. Immunocompromised hosts (AIDS) can develop bacillary angiomatosis, lesions in the skin or internal organs, so treat with azithromycin antibiotics. Coxiella burnetti Gram negative, spore forming, intracellular bacteria w/o an arthropod vector that causes Q-fever via inhalation of spores in urine, feces, placental tissue, amnion of infected cattle, sheep, and goats. Bacillus anthracis Gram-positive, spore forming rod in chains that causes anthrax (common in animals, rare in humans). Human infection is acquired via cutaneous exposure, inhalation, or ingestion. Cutaneous disease causes a pigmented eschar - necrotic lesions surrounded by edema caused by bacterial toxins. Inhalation disease (wool-sorters disease) results in dissemination from the lung to mediastinal lymph nodes, leading to hemorrhagic mediastinitis, pleural effusions, septic shock, and death from the toxins. Rabies Bullet shaped, enveloped, negative sense RNA Rhabdoviridae virus. Rabies is transmitted by animal bites (rabbit, fox, dog) from saliva or neural tissue to mucosa or non-intact skin. Bite in the extremities leads to rabies in 15%, vs. 60% if the bite is on the head. The virus replicates at the wound, enters peripheral nerves, and spreads retrograde to the brain and then anterograde to the periphery, including salivary glands (hydrophobia). Toxoplasma gondii Parasites that cause toxoplasmosis. Cats are the definitive hosts (where T. gondii can sexually reproduce), and infective oocysts in their feces can infect humans and other mammals (intermediate hosts), where they form cysts in the muscle and brain. the immunocompromised and pregnant women are at most risk (TORCHES infection - pregnant women shouldn't change litter boxes).

Petechiae, purpura, and vasculitis

Purpura red-purple color from extravasation of blood into skin or mucous membranes that can be palpable or non-palpable (macular). Macular purpura is petechiae if <3mm, and ecchymoses if >5mm (bruise). Macular purpura is generally non-inflammatory while palpable purpura is a sign of vascular inflammation (vasculitis) and can be primary or secondary to an underlying disease. Palpable purpura is the hallmark lesionof leukocytoclastic vasculitis (small vessel vasculitis). Purpura does not blanch when pressed with a glass slide (diascopy), unlike erythema secondary to vasodilation. Purpura can result from hyper or hypo coagulable states, vascular dysfunction, and extravascular causes. Ask patients about a family history of bleeding/thrombotic disorders (von Willebrand), drugs or meds that could affect platelets (aspirin, warfarin), and medical conditions (liver disease) that can alter coagulation. Get a CBC with diff and PT/PTT. Actinic (senile) purpura Easy bruising with extravasated erythrocytes and increased perivascular inflammation due to sun damage Scurvy Insufficient vitamin C intake (diets, alcoholism), increased requirements (medications), or increased loss of vitamin C (dialysis) leads to easy bruising, perifollicular petechiae, keratotic plugging of hair follicles with corkscrew hairs, and hemorrhagig gingivitis because vitamin C is required for normal collagen structure. Low vitamin C leads to skin and vessel fragility. Disseminated intravascular coagulation (DIC) Results from unregulated intravascular clotting resulting in depletion of clotting factors and bleeding. Patients present with petechiae and purpura as well as systemic signs of infection/sepsis - fever, tachycardia, hypotension, tachepnea. WBCs are high, and there is decreased fibrinogen and increased PT, and PTT. Purpura fulminans is petechiae and large ecchymotic patches on the extremities. Neisseria meningitidis is one cause - a gram negative diplococcus. Rocky mountain spotted fever Most commonly fatal tickborne infection in the US, caused by Rickettsia rickettsii. There are initially faint macules on the wrists or ankles that spread and become petechial on the trunk, extremities, palms, and soles. The classic triad is fever, rash, and history of tick bite (but most patients don't have them all - elderly often lack rash). Palpable purpura (vasculitis) Small vessel vasculitis (leukocytoclastic vasculitis) produces palpable purpura and urticarial lesions in rare cases. Henoch-Schonlein purpura is an example, but small vessel vasculitis can also be idiopathic, malignancy, rheumatologic, infection, or medication. Small to medium vessel vasculitis causes subQ nodules, purpura, and FIXED livedo reticularis (aka livedo racemosa) and includes ANCA associated vasculitidies (Churg-Strauss syndrome, microscopic polyangiitis, wegener granulomatosis) and essential cryoglobulinemic vasculitis. Medium vessel vasculitis can cause ulceration and necrosis and includes polyarteritis nodosa. Large vessel vasculitis can cause claudication, ulceration, and necrosis and includes giant cell arteritis and takayasu arteritis. Diseases can involve more than 1 type of vessel and vessels in other organs. Evaluate vasculitis with a CBC with platelets, ESR (systemic vasculitis has sed rates >50), ANA (positive suggests presence of connective tissue disorder), ANCA (Wegener granulomatosis, microscopic polyarteritis, drug-induced, Churg-Strauss), Complement (low suggests mixed cryoglobulinemia, urticarial vasculitis, or lupus), and urinalysis (renal involvement). Henoch-Schonlein Purpura (HSP) Common systemic vasculitis in children (3-15yrs) characterized by palpable purpura, arthritis, abdominal pain, and kidney disease. HSP occurs most often in winter because it is brought on by viral or bacterial infection. Diagnosis is made clinically +/- a skin biopsy, which shows leukocytoclastic vasculitis in postcapillary venules (small vessel disease). Direct immunoflourescence of the biopsy shows *Immune complexes in vessel walls contain IgA deposition - the diagnostic feature.* Rule out strep infection with ASO or throat culture. After diagnosis, perform urinalysis and BUN/Cr to test kidney function and stool guaiac for GI involvement. HSP in adults suggests underlying malignancy. Most children recover completely, but progressive renal disease is possible, esp in adults. Treatment is supportive +/- prednisone. Polyarteritis Nodosa Potentially systemic necrotizing vasculitis of medium-sized arteries characterized by painful subQ nodules, which can ulcerate +/- livedo reticularis. PAN can be cutaneous only or systemic (skin, peripheral nerves, kidneys, joints, GI tract) and can be associated with HBV, HCV, HIV, and parvo B19. Nerve involvement presents with paresthesias and decreased sensation and reflexes and is called mononeuritis multiplex. Kidney involvement can present with urine sediment positive for increased protein, RBCs, WBC, and tubular casts. ESR and CRP will be high and skin biopsy from a subQ nodules will show inflammation of medium sized arteries. PAN is chronic, lasting months to years, with exacerbations and remissions. Local wound care should be applied for any ulcerations. Prednisone and other immunomodulation may be needed if severe.

Skin Cancer

Risk factors Those with large/giant congenital nevi (>20cm in an adult) have an increased risk for developing melanoma - 5-10% will (refer to dermatology for monitoring). Those with 5+ atypical nevi or atypical mole syndrome are also at increased risk. 10% of melanomas are familial, often caused by CDKN2A (atypical mole syndrome) and CDK4, p53, BRCA2, and others. Dermoscopy Magnification used to examine lesions for asymmetry, irregular borders, large diameter (>6mm), multiple colors, and evolving/change. Benign nevi tend to share a similar pattern in an individual (signature nevus), and melanoma and other cancers usually have a different pattern. Atypical nevi Difficult to distinguish clinically and histologically from melanoma. Atypical nevi are not precancerous, but patients with >5 are at increased risk and should see a dermatologist and perform regular skin self-exams. Patients with >100 acquired nevi, those with 2+ first degree relatives with history of melanoma, and those with history of melanoma should also see a dermatologist. Atypical mole syndrome is characterized by >50 nevi that usually appear near puberty and continue, significantly increasing the risk for developing melanoma in an atypical mole or normal skin. Biopsy is performed if melanoma is suspected, but don't remove all atypical nevi. Biopsy Before biopsy, take a photo or record landmarks incase later excision is needed. Biopsy the entire lesion (except on face or cosmetically sensitive areas) so that you know there is no melanoma in the remaining lesion and you know the Breslow depth - the most important prognostic information. Melanoma Usually asymptomatic, developing de novo or within a pre-existing nevus, usually in sun exposed areas. They usually appear as a pigmented papule, plaque, or nodule and can bleed, be eroded, or crusted with a history of change. It is the most common cancer in women 25-29yrs old. Melanoma is caused by melanocytes, often from cumulative UVB and UVA exposure. Risk increases with age, fair skin, >100 acquired nevi, immunosuppression, personal history or 2+ 1st degree relatives with melanoma, UV exposure, and genetic syndromes. Breslow depth is the most important prognostic factor for survival and management. Ulceration, mitotic rate, lymph involvement, and metastases are also prognostic factors. Superficial spreading type - the most common type, usually on the back in men or the back/legs in women, with tumor growth primarily horizontal Nodular type - rapid, vertical growth (greater breslow depth) Lentigo maligna type - slow, horizontally progressing tumor mainly in elderly patients in areas of chronic sun exposure Acral lentiginous - more common in darker skin tones and often large because diagnosis is delayed by misdiagnosis (as callous or wart). Amelanotic type - can be confused with psoriasis, dermatitis, basal/squamous cell carcinoma Melanoma <1mm Breslow depth requires surgical excision for treatment. If >1mm, sentinel node biopsy is performed with node dissection if positive. Regular skin exams with a dermatologist are needed for life, along with continued sun protection. Ipilimumab is a monoclonal antibody that binds CTLA-4 that normally suppresses immune responses, triggering immune reaction to melanoma and improving survival and quality of life. BRAF inhibitors (vemurafinib, dabrafenib) are monoclonal antibodies that target mutated BRAF with V600E or V600K mutations that are present in 40-50% of melanomas, improving quality of life and increasing survival for a short period before resistance develops. Actinic Keratosis Premalignant lesions that can progress to squamous cell carcinoma, caused by keratinocyte mutations (p53) induced by UV damage and more common with fair skin, immunosuppression, increased age, or genetic predisposition. They present as gritty erythematous macules or thin plaques on sun-exposed areas and are often more easily felt than seen. If thick, tender, or >6mm, there is higher risk for SCC. Actinic cheilosis presents on the lips, often the lower lip, and should be biopsied if there are persistent ulcerations or indurated areas. Treat an isolated lesion with liquid nitrogen cryotherapy, or large areas with topical 5-FU or imiquimod creams or photodynamic therapy. Squamous cell carcinoma It can present in a wide variety of forms, is friable, and can sometimes be pruritic. Caused most commonly by UV-induced mutations, especially p53, in keratinocytes. Chemical exposures like arsenic can also contribute. SCC is most common in sun exposed sites of fair skinned patients. Metastasis risk is higher and there is worse prognosis for larger diameter lesions (>2cm), deeper (>4mm) and recurrent tumors, tumors in bone/muscle/nerve, location on scalp/ears/nose/lips, tumor arising in scars/ulcers/genitals, immunosuppressed patients, and tumors caused by arsenic ingestion. SCC in situ (aka Bowen's disease) are circumscribed pink/red patches or thin plaques with scaly or rough surface, with keratinocyte atypia confined to the epidermis and not invading into the dermis (it is invasive when it involves the dermis). SCC in situ can be treated with curette and desiccation or with 5-FU cream, imiquimod cream, or photodynamic therapy when excision is contraindicated. Surgical excision is needed for invasive SCCs. Radiation may be used in poor surgical candidates. Basal cell carcinoma Most common skin cancer with the same risk factors as SCC. It arises from nonkeratinizing keratinocytes that originate in the basal layer, due to UV radiation causing PTCH (tumor suppressor gene) mutation. BCC is locally invasive, with very rare metastasis. Nodular BCC - most common subtype, presenting as pearly papule or nodule with rolled border and telangiectasias, most often on the head and neck. Unlike SCC, it does not have scale. Superficial BCC - presents with pink/transucent color, telangiectasia, and slightly rolled border and can be a thin, scaly plaque. It can be confused with SCC in situ or actinic keratosis, so diagnosis is histological. Ulcerated, pigmented, and morpheaform (scar-like) forms can also occur. Treat BCC with curette and dessication, cryosurgery (not done often), excision with 3-4mm margins, or Mohs micrographic surgery. Imiquimod cream, 5-FU cream, or photodynamic therapy can be used for superficial BCC. Radiation for non-surgical candidates. Mohs Micrographic Surgery Used to treat BCC and SCC to minimize recurrence rates and maximally conserve tissue. Visible tumor is removed and the underside of the removed area is examined histologically for tumor cells. Areas where cancer is found are mapped to the excision site, and more tissue is removed until no cancer is seen under the microscope. Mohs is often used on the nose, ears, eyes, lips, scalp, and hands for infiltrating, sclerosing, morpheaform, or micronodular BCC subtypes as well as tumors that are large, recurrent, or have indistinct borders.

The Red Face

Seborrheic dermatitis Common inflammatory reaction to Malassezia yeast that thrives on seborrheic (oil producing) skin, presenting as erythematous scaling patches on the scalp, hairline, eyebrows, eyelids, central face, nasolabial folds, external auditory canals, or central chest. Seborrheic dermatitis can be hypopigmented, especially in dark skin types and is often worse in patients with HIV or neurologic disorders (parkinson's). Treat flares on the face with low-potency topical steroids (desonide) or ketoconazole cream. Use antidandruff shampoo on the scalp and chest (ketoconazole, selenium sulfide, zinc, pyrithione), leaving it on the skin 10 minutes before rinsing. Infantile seborrheic dermatitis is called "cradle cap" and presents as diffuse, yellowish greasy scale throughout the scalp, also from mallasezia species. It can affect the neck, folds, and diaper area with intense erythema. Baby shampoo can be used for gentle removal, but don't use ketoconazole. Rosacea Erythema and telangiectasias +/- papules and pustules typically on the mid face (nose and cheeks) and occasionally the brow, chin, eyelids, and eyes (grittiness, redness, irritation). It can be distinguished from acne vulgaris by it's lack of comedones and from lupus by its involvement in the nasolabial folds. Rosacea can also present with rhinophyma (dermal sebaceous gland hyperplasia of the nose). Ocular rosacea includes keratitis, blepharitis, and conjunctivitis. Rosacea flares with alcohol, sunlight, spicy foods and hot drinks. Therapy is life-long and treatment includes topical metronidazole, sodium sulfacetamide, azelaic acid, and sulfur cleansers. Oral antibiotics (doxycycline) can be used for pustular and papular lesions or ocular symptoms. All patients should wear sunscreen. Lasers can treat erythema. Isotretinoin can be used in severe cases, and surgery can be used to treat rhinophyma (ablative laser). Perioral dermatitis/ steroid rosacea perioral erythema and papules sparing the area near the vermilion border (pink line of the lips) often preceded by topical steroid use or steroid inhalers. Treat with tetracyclines or a macrolide for 1 months. Allergic contact dermatitis Delayed-type hypersensitivity reaction (type IV) that occurs when susceptible patients become sensitized to an allergen in contact with their skin. Itch can precede onset. Allergic contact dermatitis of the eyelid is often caused by transfer from the hands (cosmetics, metals, topical meds, poisonivy). Treat with desonide cream - a low potency topical steroid. Test for allergens using a patch test - apply common allergens in square patches for 2 days and remove them to observe any reactions that appear 2-14 days later. Irritant contact dermatitis Causes 80% of contact dermatitis via direct skin toxicity from a substance - detergents, harsh chemicals, frequent hand washing. It is not related to immune response or allergy, so everyone is susceptible.

Dermatologic therapy basics and topical steroids

The efficacy of topical medication is related to the strength of the active ingredient, anatomic location, vehicle, and concentration of the medication (foam, cream, oil, ointment, solution, spray, and gels. Ointment lubricating, occlusive, greasy (eg. vaseline). Use for smooth, non-hairy skin with dry, thick or hyperkeratotic lesions (NOT on hairy and intertringinous/skin to skin areas). cream less greasy and can have drying effects. Creams are not occlusive, can sting, and are more likely to cause irritation due to preservatives and fragrances. Creams are used for acute exudative inflammation in intertriginous areas. Lotion pourable liquids that are less greasy, and less occlusive, penetrating easily with little residue. Those with alcohol can have a drying effect on an oozing lesion. Lotions can be used in hairy areas. Oils less stinging that lotions or solutions, used on the scalp, especially for those with coarse or very curly hair. Gel jelly like substance that can contain alcohol and is greaseless. Gel is the least occlusive and dries quickly. Gel is used for acne, exudative inflammation (acute contact dermatitis), and on the scalp or other hairy areas without matting. Foams spreads readily and easier to apply, but more expensive. Foams are used for hairy areas with inflammation. Sprays aerosols (rarely used) and pump sprays Topical corticosteroids Produce an anti-inflammatory response in the skin for conditions characterized by hyperproliferation, inflammation, and immunologic involvement and can also provide symptomatic relief for burning or pruritic lesions. Corticosteroids are organized into classes based on their potency, which is inherent to the molecule rather than the concentration. Ointments are inherently stronger than creams or lotions. Local side effects include skin atrophy, telangiectasias, striae, acne, steroid rosacea, and hypopigmentation. Reduce the risk by using the least potent steroid for the shortest time possible. Systemic side effects are rare. Class I super high potency corticosteroids, including clobetasol are used for severe dermatoses over nonfacial and nonintertriginous areas (scalp, palms, soles, thick plaques on extensor surfaces). Limit use to <3 weeks. Class II - High potency corticosteroids including fluocinonide Class III-V - Medium potency corticosteroids, including triamcinolone. Classes II-V are used for mild to moderate nonfacial and nonintertriginous areas (OK on flexural surfaces for limited periods). limit use to 6-8 weeks and then intermittent on an as-needed basis. Class VI-VII Low potency corticosteroids, including desonide and hydrocortisone, used for large areas and on thinner skin (face, genitals, intertriginous areas). Estimating amount to prescribe The quantity of a topical medication dispensed from a 5mm nozzle placed on the pad of the index finger from the distal tip to the DIP joint is one fingertip unit (FTU) = 500mg, which treats 2% of the body surface area. The size of the patient's palm is 1% of their body surface area. It takes 30 grams to cover the average adult body once When writing Rx for BID use for one month, the face requires 30-45 grams, extensor surfaces of both arms require 120-150 grams, and widespread lesions on the trunk, legs, and arms require 1-2lbs. Body surface area is divided up into areas of 9% surface area: head and neck, posterior or anterior surface of upper trunk, posterior or anterior surface of the lower trunk, one arm, posterior or anterior surface of one leg. The genitals make up 1%. When prescribing a topical medication include the generic name, vehicle, concentration, directions, amount, and number of refills.

generalized, extensive blisters

Chicken pox Primary varicella zoster infection causes diffuse vesicles on erythematous base in various stages of healing that can be extensive and severe, especially in adults. Disseminated reactivated zoster can be identical in the immunosuppressed. Diagnose Chicken pox by PCR, DFA, culture of Tzank. Pemphigus vulgaris Autoantibodies to desmogleins 1 and 3 (in desmosomes) between keratinocytes, causing superficial bullae and erosions, usually in the elderly. Diagnose with direct immunoflourescence and consult dermatology. In immunoflourescence, antibodies of a paralesional biopsy are stained so that there is intercellular staining between keratinocytes. Bollous pemphigoid Autoantibodies to hemidesmosomes cause deep, tense bullae on a pruritic, urticarial base, leading to a split between the basement membrane and basal layer, usually in the elderly. Diagnose with BPAG2 antibodies found with direct immunoflourescence (leads to linear staining along the basement membrane) and consult dermatology. Drug eruptions Appear acutely and can lead to vesicles, bullae, and large erosions. Consult dermatology.

Fungi, dermatophytes, and yeast

Dermatophytes Group of keratinophilic fungi infecting skin, hair, and nails. Superficial infections are called ringworm or tinea. Fungal virulence factors include keratinases, proteases, and lipases that disrupt skin structures, causing inflammation. Candida albicans yeast Colonizes normal skin, but overgrowth can cause superficial infection with epithelial damage. Predisposing factors include anything that disrupts the innate immune system - antibiotics, steroid therapy, diabetes, and obesity. Candida can cause invasive, systemic infection in immunocompromised.

skin-related viral infections

Enveloped RNA viruses Measles (rubeola) and Rubella (german measles) are included in the MMR vaccine Non-enveloped DNA viruses Parvovirus V19 (fifth disease) HPV (warts) - small, double stranded, circular DNA genome. Enveloped DNA viruses HHV 6/7 (roseola) Varicella zoster (latency in trigeminal and dorsal root ganglia - chicken pox, shingles) HSV1 and 2 (latency in neurons - herpes) KSHV/HHV8 (latency in lymphoid cells) Poxvirus (molluscum contagiosum) Zostavax - shingles vaccine live, attenuated virus given to all 60yrs or older except immunocompromised people or pregnant women. It reduces shingles/zoster by 51%.

Normal skin flora and defenses

Gram positive bacteria predominate, especially in dry areas. Gram negatives are more prevalent in moist areas (armpits, groin, near mucus membranes). Most organisms are in the superficial layers of the stratum corneum and the upper parts of hair follicles. Staph. epidermidis is the most common aerobic bacteria in the skin. Staph. aureus colonizes the nose, perineum, and vulva and is very common on patients with atopic dermatitis. P. acnes is a diphtheroid and anaerobe prevalent in areas with sebaceous glands and the cause of acne. Gram negatives include enterobacter, klebsiella, and E. coli. Group A Strep. Pyogenes and group B strep. agalactiae are both beta-hemolytic and inhibited by lipids, so they are NOT common on normal skin. Strep. viridans and Strep. pneumoniae are alpha hemolytic and are common in the mouth (rarely spreading to skin). Immune response Keratinocytes have TLRs that recognize antigens and secrete proinflammatory cytokines and chemokines to recruit non-resident immune cells. They also secrete antimicrobial peptides (AMPs) including beta-defensins and LL37 that lay along the skin surface and insert into bacterial cell membranes to form pores. Bacteria have trouble developing resistance to these peptides because they work in a haphazard way. The skin's defenses are enhanced by normal skin flora, Staph. epidermidis - Dendritic cells sample the S. epi antigens, present them to CD8+ Tcells, inducing release of IL-17. Keratinocytes respond by enhancing their barrier function and limiting pathogen invasion. Hygiene hypothesis Dysregulated innate immune response results in chronic cutaneous inflammation, like in atopic dermatitis - reduced antimicrobial peptides lead to increased infections with S. aureus > S. epidermidis, and chronic inflammation allows bacterial and viral infections. More diverse skin flora correlate with disease remission. Atopic dermatitis is more common in developed countries and urban environments, in those late to begin school, and with higher SES, suggesting reduced microbial colonization may play a role.

Acne

Open comedo - blackhead closed comedo - whitehead Acne vulgaris disorder of pilosebaceous follicles that generally begins age 8-12 (first sign of puberty), peaks at 15-18, and resolves by 25yrs. Acne vulgaris affects 90% of adolescents and there is often family history (number, size, and activity of sebaceous glands is inherited). 12% of women and 3% of men have acne until their 40s, and women may have their first outbreak at 25-30yrs. Acne vulgaris is related to hormones (androgens), sebaceous gland activity (increased by androgens), plugging of hair follicles from abnormal keratinization, and P. acnes in the hair follicle that metabolizes lipid to free fatty acids that cause inflammation. Comedonal acne vulgaris - open and closed comedones inflammatory acne vulgaris - papules and pustules Nodulocystic acne vulgaris - nodules and cysts. All forms vary from mild to severe and can cause scarring or post-inflammatory hyperpigmentation. Treat mild comedonal acne with a topical retinoid +/- topical BPO, and add topical clinca/erythromycin for mild papules/pustules. Moderate papulopustular or mild nodular acne should also use oral antibiotics (mino or doxycycline). Severe/scarring nodular acne should be treated with isotretinoin (acutane). All topical treatments take 4-6 weeks to work. Women with acne caused by excess androgens (eg. PCOS) can be treated with spironolactone.

Papulosquamous eruption (red scaly rash)

Pityriasis rosea acute exanthematous eruption mainly in young people (10-35yrs) related to HHV6 infection. Patients can sometimes have flu-like symptoms (malaise, GI upset, upper respiratory symptoms, fever, lymphadenopathy, sore throat). The rash classically starts as a single annular erythematous 2-10cm patch with peripheral scale and central clearing (herald patch) and spreads quickly over the body with oval salmon-colored patches (darker with dark skin) with minor scale, sparing the palms and soles. The oval patches follow skin tension lines on the back (Xmas tree sign). Pityriasis rosea is self limiting, with 50% resolving in 5 weeks and >80% resolving by 8 weeks without treatment. Those who request treatment can use topical steroids and antihistamines (macrolides and acyclovir may help). Secondary syphilis Primary syphilis begins with a painless chancre, and secondary phase begins weeks later with malaise, fever, headache, stiff neck, myalgias, arthralgias, runny nose and eyes, and mental changes, along with a rash on the palms and soles. The rash is often round to oval papules and plaques on the trunk and extremities, or can be a papulosquamous eruption similar to pityriasis rosea (or many other forms). *Involvement of the palms and soles is characteristic, with round macules that may have collarettes of scale.* Skin biopsy can be helpful for diagnosis using immunostaining for T. pallidum. Confirm with serologic tests for syphilis (rapid plasma reagin). Treat with intramuscular benzathine penicillin G. Nummular dermatitis multiple coin-shaped eczematous plaques on the extremities and trunk that may be scaly but lack the central clearing seen with tinea corporis (fungal infection) and is KOH negative. Nummular dermatitis is very pruritic (distinguishing it from psoriasis) and can have weeping, cracking, vesicles, or crusts. Pathology shows spongiotic dermatitis. Treat with fluocinonide ointment (class II steroid), as you would atopic dermatitis or any other eczema. Apply lotions (emollients) 2x per day to prevent dry skin. Asteatotic dermatitis/ xerotic eczema flaking, pruritic skin progressing to cracked skin that looks like a lake bed and is itchy and stinging, usually on the lower legs, flanks, and arms in the elderly. Treat with high potency topical steroid.

Benign skin lesions

Seborrheic keratosis Benign superficial (epidermal) growth common after age 30 that can arise on all body surfaces except the palms and soles. They are often multiple, can be extensive, and don't go away. Color can vary from black, tan, white, pink and texture can be velvety or verrucous (wart-like), often with a stuck-on, waxy appearance. They may be curetted, frozen, or electrodessicated if irritated or cosmetically bothersome. When excoriated, a pink base is revealed. Small, dark, SKs in dark skinned individuals are called dermatosis papulosa nigra, and occur in 30% of blacks. They can be removed by snipping or electrodessication, but freezing causes dyspigmentation. Stucco keratoses are small, white-gray SKs that pepper the dorsal feet and ankles of older whites. Nevus (pl. Nevi) Umbrella term for a group of benign, circumscribed overgrowth of normal skin/tissue cells. They usually appear before age 30yrs. Acquired nevi can start as brown macules and papules in children and progress to skin colored or pink papules with age and they can become more raised or pedunculated, but symmetry and diameter should stay consistent. Those that develop after age 50 should raise suspicion of melanoma. A symmetric shape, regular border, uniform color, small size (diameter <6 mm) are features that help distinguish a nevus from melanoma. Eg. melanocytic nevus ("mole" - increased proliferation of melanocytes), vascular nevi, epidermal nevi, connective tissue nevi. Acrochordons/skin tags fleshy papules arising in axillae, neck, groin, and eyelids that are skin colored to brown and often pedunculated. They are caused by genetics, obesity, friction, and can mark insulin resistance (consider screening blood glucose or HbA1c when they present with acanthosis nigricans). Skin tags can be removed with snipping (pressure or aluminum chloride for bleeding), liquid nitrogen for lighter skin types, or electrodessication. They can sometimes fall off on their own. Acanthosis Nigricans velvety, hyperpigmented plaques and warty-papules in the axillae, groin, neck, and/or anogenital region, often associated with diabetes mellitus or insulin resistance, obesity, medications, or internal malignancies. Cherry Angioma small (< 5mm), red-to-purple, dome-shaped papule usually located on the trunk that are benign capillary neoplasms that do not blanch. Most people start getting them around age 30yrs and they don't go away. Occasionally they can bleed or thrombose, mimicking melanoma. Histologically, they are a well circumscribed, sometimes lobular proliferation of capillaries with slightly thickened walls. Dermatofibroma benign, spindle cell dermal proliferation that looks like a wad of scar tissue histologically. They are common on the legs and often multiple, induced by minor trauma (shaving). they have a firm, scar-like texture and a peripheral rim of darkening pigment is common. Pinching either side of the dermatofibroma tends to cause it to dimple down (dimple sign) from the scar-like tethering to the dermis. Solar lentigines/lentigo AKA sun/age/liver spot A brown, sharply circumscribed macule resembling a freckle caused by sun damage that is not malignant or premalignant (but reflects history of sun exposure and thus skin cancer risk). Histologically, an increased number of melanocytes or melanin is found in the basal layer of the epidermis. Unlike ephelides (freckles), lentigo borders are usually regular and sharp, there is downward thickening of the epidermis between dermal papillae, and they do not fade with cessation of sun exposure. Treat with sun protection, bleaching creams, liquid nitrogen, chemical peels, or lasers. Sebaceous hyperplasia Sebaceous (oil) gland overgrowth causes skin-colored or slightly yellow, umbilicated (central dell) papules, often on the forehead and face that slowly arise over years. Removal is cosmetic. Differentiate from basal cell carcinoma (can be skin colored papules) by yellow color, umbilication, multiple similar papules, no telangiectasia, and not friable (no bleeding, scabbing). Biopsy may be necessary. Keloid Overgrowth of scar tissue beyond the original scar site, most common in blacks in the upper trunk and earlobes. They can be itchy or tender, and sometimes cosmetically disfiguring. Excision only causes recurrence of an even larger keloid - instead use intralesional steroid injection. Epidermal inclusion cyst Mobile subQ nodule, often with an overlying punctum (opening/point), that arises from a hair follicle (although sometimes referred to as sebaceous cysts). Debris collects within a sac, leading to discharge of foul smelling, cheesy white material. Complete surgical excision is the only way to be rid of the lesion, although they are benign and require no treatment. There is risk for rupture and abscess formation, which may require incision and drainage. Unlike a bacterial abscess, ruptured EICs are usually sterile and don't require oral antibiotics (but still require incision and drainage). Milia tiny (1-2mm), white/yellow keratin-containing epidermoid cyst with no central puncta often on the face that can be easily extracted without scarring. Almost 1/2 of newborns have some milia, which tend to resolve. But milia in adults often persists. Pilar cysts A benign cyst commonly found in the scalp, appearing as a flesh-colored, firm but malleable nodule or tumor. They arise from the middle part of the epithelial lining of a hair follicle, or the outer root sheath, which produces keratin that accumulates as the contents of the cyst. No treatment is necessary, but the cyst (with its epithelial lining) can be removed surgically. Histology shows a cyst lined by squamous epithelium that shows abrupt keratinization without a granular cell layer. The cyst is filled with homogenous keratin. Lipoma collections of fat under the skin, usually stabilizing at a few cm in diameter. They are often solitary and occur in the trunk and proximal extremities (or if familial, can be multiple and begin early in childhood, AD). Lipomas can sometimes be tender.

infectious skin bacteria

Staph. aureus and Strep. pyogenes (group A strep) have toxic shock toxins (superantigens/Mitogen) that stimulate massive polyclonal expansion (rather than specific monoclonal expansion targeting that antibody) of T cells and a cytokine storm. Staph. Aureus In addition to toxic shock toxins has exfoliative toxins that disrupt normal skin structure, causing staphylococcal scalded skin syndrome (babies) and intraepidermal splitting (exotoxins A-D cleave desmoglein). S. aureus can have some resistance to antimicrobial peptides by releasing enzymes that degrade them and by repelling them with a negative charge at their surface. Rickettsia rickettsii obligate intracellular gram negative tick born cause of rocky mountain spotted fever Neisseria meningitidis gram negative, encapsulated colonizer of the nasopharynx that can cause disseminated infections like meningitis Treponema pallidum sexually transmitted spirochete causing secondary syphilis rash

dark and light rashes

Tinea Versicolor Fungal infection that causes pigmentary changes and scaling in the epidermis (scaling is often not visible until rubbed with a finger or scalpel blade). The lesions appear as patches with fine scale and can be pink, tan, white, or sometimes hyperpigmented usually on the neck, trunk, upper arms (rarely the face). Caused by the yeast Pityrosporum orbiculare (called Malassezia furfur when in the infectious hyphal form). Fungal enzymes produce compounds that inhibit melanin production (often asymptomatic except that affected areas do not tan). Microscopically, a KOH preparation shows a combination of short fungal hyphae and yeast forms in a "spaghetti and meatballs" (unlike other fungal infections, there are TONS for spores and hyphae on the slide). Treat with anti-dandruff shampoos like selenium sulfide, pyrithione zinc, or ketoconazole daily for 2 weeks - apply to affected areas before showering for 15 minutes and then rinse. Use 1-2x weekly to prevent recurrence. Ketoconazole creams used 2x daily for 2 weeks can be used for limited disease, or one time oral fluconazole or ketoconazole for widespread/recurrent disease. Scaling stops within days but pigment alteration takes weeks-months to recover. Melasma/chloasma Patchy (reticulated) light to dark brown pigmentation of the face, usually in women and running in families. Melasma is associated with hormonal changes - pregnancy, birth control pills, hormone replacement. It worsens with UV exposure and is treated with sun avoidance, daily sunscreen with SPF 30+ and broad spectrum coverage, and hydroquinone 4% cream 2x daily. If this fails, triple topical therapy, lasers, or chemical peels may be used. Minocycline pigmentation Brown or blue-grey deposition after months to years in some patients taking minocycline due to direct deposition of the drug or increased melanin production. It's first noticeable on the alveolar ridge, palate, and sclera, so discontinue if seen. It can involve the bones and thyroid but is harmless. It can occur in scars, on shins, or diffusely and may not fade after discontinuation. Amiodarone and antimalarials (hydroxychloroquine and chloroquine) can also cause hyperpigmentation Stasis dermatitis Eczematous eruption occurring with venous insufficiency and leg edema that can be acute or chronic and can be weepy (distinguish cellulitis - pain, unilateral, fever, and not recurrent). Extravasation leads to brown pigment (permanent) and petechiae and venous ulcers can result, especially on the medial malleolus. Inflammatory rash can also occur due to extravasation of WBCs. Reduce edema with elevation and compression stockings and use class I and II topical steroids to control inflammation. Avoid topical antibiotics because 1/2 develop allergic contact dermatitis (esp to neomycin and bacitracin). Postinflammatory hyperpigmentation Darkening of the skin at or around sites of injury or inflammation, especially in those with olive or slightly darker complexion. Pigmentation takes months to years to fade. Postinflammatory hypopigmentation can also occur, and pigmentation may return slowly Vitiligo Autoimmune attack on melanocytes, often in areas of trauma (knees, elbows, fingers, mouth, eyes, genitalia. It can be associated with other autoimmune disorders (especially if presenting in older adults). A Wood's light exam can be used to increase contrast between pigmented and depigmented areas. Treat with potent topical steroids (triamcinolone for face and class I or II for other areas) or tacrolumus ointment, phototherapy (narrow band UVB, UVA), and cosmetic cover-ups. Steroid hypopigmentation Skin lightening from potent topical or intralesional corticosteroids (eg. joint injections), more often in darker skin types. Pityriasis alba mild form of atopic dermatitis that causes light patches on children's faces that generally goe away in a few years. Like all atopic dermatitis, moisturization is key. Sunscreens minimize tanning to limit the contrast between involved and normal skin. Consider low strength topical steroid if sunscreen and moisturizers fail.

Acne medications

Topical acne treatments take 2-3 months to cause an effect and mild skin irritation is common. Moisturizers or reduced frequency of application can limit side effects. Examples of topical treatments include benzoyl peroxide, topical antibiotics, and topical retinoids. Benzoyl peroxide (BPO) topical medication with both antibacterial and comedolytic (breaks up comedones) properties that is available as an Rx or over the counter. BPO can bleach hair, fabric, or carpet and can irritate skin (discontinue if severe). Topical antibiotics Used to reduce P. acnes and inflammation in inflammatory acne. Topical antibiotics are also used with BPO to avoid resistance in treatment of mild to moderate acne and rosacea. Erythromyxin 2% solution/gel and clindamycin 1% lotion/solution/gel/foam are used for acne or rosacea. Metronidazole .75% or 1% cream/gel is used for rosacea. Topical retinoids Tretinoin, all trans retinoic acid used for acne vulgaris, photodamaged skin, fine wrinkles, and hyperpigmentation, but can cause dryness, pruritis, erythema, scaling, and photosensitivity. Don't apply topical retinoids at the same time as benzoyl peroxide because BPO oxidizes tretinoin. Oral antibiotics Tetracycline, doxycycline, minocycline used for moderate to severe inflammatory acne and combined with BPO to prevent antibiotic resistance. Oral minocycline can be used for systemic sarcoidosis and rosacea. All can cause GI upset, tetracycline and doxycycline can cause photosensitivity, and minocycline can cause vertigo and hyperpigmentation. Oral antibiotics shouldn't be used during pregnancy or in those <8yrs old, but they don't interfere with hormonal contraception. Oral isotretinoin a retinoic acid derivative used for severe, nodulocystic acne failing other therapies. It's usually given in a single 5-6 month course and NEVER during pregnancy (teratogen). Female patients must be enrolled in an FDA-mandated prescribing program to use the medication and must use 2 forms of contraception during treatment and 1 month after. Isotretinoin can cause xerosis (dry skin), cheilitis (chapped lips), elevated liver enzymes, and hypertriglyceridemia. Those with severe acne can suffer mood changes and depression. Severe headache can be a manifestation of the uncommon side effect pseudotumor cerebri.

Topical antifungals and oral antihistamines

Topical antifungals can be fungistatic or fungicidal, but do not treat infection of the hair or nail (require systemic treatment). They are preferred for most superficial fungal infections of limited extent because they are low cost, effective, easy to use, and have a low potential for side effects or drug interactions. Imidazoles are fungistatic, used to treat candida and dermatophytes, and include ketoconazole (Rx and OTC), econazole, oxiconazole, sulconazole, clotrimazole (Rx and OTC), and Miconazole (OTC). Allylamines and benzylamines are fungicidal, more effective for dermatophytes than candida, and include Naftifine, Terbinafine (OTC), and Butenafine Polyenes are fungistatic in low concentrations, are better for candida than dermatophytes, and include nystatin. Oral antihistamines The most widely used agents for pruritis and chronic urticaria. For most pruritic dermatoses other than urticaria, 1st generation H1 antihistamines work mainly through sedative effect rather than anti-histaminic properties. First generation H1 antagonists are sedating due to anticholinergic side effects (memory impairment, confusion, dry mouth, blurred vision), limiting their dose but helping as a sleep aid. Caution should be used with elderly patients due to increased fall risk, CNS, and anticholinergic effects. 1st generation antihistamines include Diphenhydramine (OTC), hydroxyzine (Rx, generic), and chlorpheniramine (OTC). 2nd generation H1 antagonists are minimally sedating and require less frequent dosing. They include cetirizine, loratadine, and fexofenadine.

Skin diseases for specialists

Type I neurofibromatosis AD disease (50% de novo) characterized by skin and neurologic anomalies due to mutations in neurofibromin 1. 69-90% of patients have neurofibromas, >90% have cafe-au-lait macules, 80% have axillary/inguinal freckling (Crowe's sign), and 25% have plexiform neurofibroma (very specific - feels like bag of worms). Cafe-au-lait macules are oval-shaped, tan to brown patches with regular borders and uniform pigmentation that become more noticeable through the fist decade. >90% have Lisch nodules in the iris, 10-15% have optic gliomas, 30-50% have learning difficulties, and skeletal dysplasias and pheochromocytoma (catecholamine secreting tumor) are also associated. Treat symptomatic or rapidly changing neurofibromas with excision, regularly screen patients for optic gliomas and pheochromocytoma. Tuberous sclerosis AD disorder with incomplete penetrance (75% de novo) with cutaneous lesions + peripheral/CNS neoplasms caused by mutations in TSC1 (hamartin gene product) and TSC2 (tuberin gene product). 80% have facial angiofibromas (usually symmetric and bilateral), almost all have hypomelanotic macules (ash leaf spots), 50% have Shagreen patch, and 30-60% have periungual fibromas. Shagreen patch (aka connective tissue nevi or collagenoma) can be hyperpigmented or hypopigmented with a leather-like/pigskin surface. Periungual fibromas (Koenen's tumor) are smooth, firm, flesh-colored lumps that emerge from the nail folds, most often around the toenails. 70% have gingival fibromas and almost all have dental enamel pits. Retinal hamartomas, myocardial rhabdomyomas, seizures, mental deficits, and multiple bilateral angiomyolipomas (90%), and renal carcinoma are also common. Evaluate and monitor tuberous sclerosis with neurodevelopmental/behavioral evaluations, ophthalmologic exam, cranial CT or MRI, EEG/ECG, and renal US. Pyoderma gangrenosum Uncommon, chronic, recurrent cutaneous ulcerative skin disease related to underlying systemic disease in 50%, including inflammatory bowel and hematologic malignancy. 50% are idiopathic. Lesions begin as a large papulopustule and progress to ulceration, usually in the lower legs. They are triggered by skin injury and can occur after surgery or debridment (i.e. pathergy; suspect pyoderma gangrenosum when wounds break down 2-3 days after surgery). To diagnose, exclude infection with cultures and biopsy. Treat with local and systemic corticosteroids, with immunomodulation for more resistant lesions. Look for and treat underlying systemic disorders (colonoscopy, hematological studies, skin biopsy). lichen Sclerosus Inflammatory disease that leads to ivory-white scar-like atrophy often associated with pain, fissures, and pruritus. It can lead to destructive scarring, vaginal or urethral stenosis. Extragenital lichen sclerosus is less common and causes ivory white plaques. Anogenital makes up 85% of cases and can cause severe pain and pruritus or be asymptomatic (can be mistaken for abuse). Treat with clobetasol ointment (class I corticosteroid) for 12-24 weeks. Delusions of parasitosis An isolated, fixed false belief of infestation with parasites, causing sensations of biting, crawling, stinging and sometimes visual hallucinations. Patients are often functional in other aspects of life. Patients usually present in their 50s-60s and may have excoriations, lichenification, or ulcerations that are self-induced. This is different than Morgellon's disease, in which patients think their sores contain fibers extruding from the skin (sores often caused by delusions of parasitosis). Treat delusions of parasitosis with antipsychotic medication - Pimozide and risperidone are not FDA approved but are helpful. Infantile hemangioma Benign proliferations of endothelial tissue appearing in the first weeks of life and proliferating for 6-24 months before involuting. They are the most common tumors in infants, and females and premees are at highest risk. They can be superficial (bright red), deep (blue-purple), or both. Ulceration can lead to pain and infection, and there can be disfigurement due to size and location. PHACES syndrome consists of large, facial, often dermatomal hemangiomas - Posterior fossa and brain malformations, Hemangioma, Arterial anomalies of cervical and cerebral vessels, Cardiac defects, Eye anomalies, and Sternal defects. Diffuse neonatal hemangiomatosis involves the skin and viscera with risk of high output cardiac failure. Treat neonatal hemangiomas with observation if low risk or with beta blockers (propranolol - first line) or systemic corticosteroids (second line) or vincristine (third line) if large, disfiguring, or ulcerating. Port wine stain Congenital capillary malformation causing well-demarcated red macules and patches that typically present at birth. Size remains stable but develops darker color and cobblestoned texture and nodules with age. PWS are most often on the face, but can be anywhere. Treat with laser therapy at a younger age for better outcome. Sturge-Weber syndrome - PWS in the V1/V2 distribution associated with leptomeningeal angiomas, developmental delay, seizures, ocular abnormalities, and tissue overgrowth. Spinal dysraphism - associated with midline lumbosacral PWS. PWSs are different from nevus simplex/salmon patches (angel kiss on forehead or stork bite on the neck) in newborns, which are more prominent when crying and face between 1-3yrs. Kaposi sarcoma Neoplasm of endothelial cells linked to HHV8, presenting as dark, violaceous plaques or nodules most often in those with AIDS or transplants. There can be systemic and internal organ involvement. Prevent with HAART therapy. Use destructive treatments for limited disease. Systemic chemo is used for symptomatic or advanced systemic disease. Hidradenitis suppurativa (acne inversa) Inflammatory disorder of the hair follicle causing abscesses, nodules, and sinuses - epithelialized tunnels with multiple connections to the skin surface. Commensal bacteria may play a role, along with hormones around puberty, starting in the teens or 20s and lasting many years. Female gender, family history, smoking and obesity are risk factors, but it is not related to infection or hygiene. Hidradenitis suppurativa has very high morbidity - linked to depression, employment problems, and sexual dysfunction. Unpredictable disease flairs require urgent and emergent visits. Long term antibiotics can be anti-inflammatory. OCPs and spironolactone may be helpful in women. Adalimumab and other systemic anti-inflammatories can be used. Incision and drainage is used for acute symptom relief and wide excision can be used in severe disease.

Warts and Molluscum Contagiosum

Verruca vulgaris Hyperkeratotic, exophytic (growing outward), dome-shaped papules or nodules that are most common on the fingers, dorsal hands, knees, or elbows but can occur anywhere. They can have punctate black dots representing thrombosed capillaries and can koebnerize (spread with skin trauma). Verruca vulgaris occurs in 20% of school-aged children and is also common in young adults, equally in males and females. It's caused by HPV viruses with subtypes determining wart morphology. HPV is transmitted by skin-skin contact or contaminated surfaces/ovjects. Patients can spread it from a lesion to uninfected skin. HPV infects the basal keratinocytes of cutaneous and mucosal epithelium. Verruca vulgaris - common warts Verrucae planae - flat warts that are skin-colored or pink, smooth-surfaced, slightly elevated, and flat-topped papules. They are common on the dorsal hands, arms, and face. Palmoplantar verruca - thick, endophytic papules with central depression and sometimes pinpoint black dots representing thrombosed blood vessels. Plantar warts can be painful when walking. condylomata acuminata - external genital warts are sessile (no stalk or pedunculation) and exophytic and can be broad-based papules or large confluent plaques on the external genitalia, perineum, perianal, inguinal fold, or mons pubis. Condylomata acuminata are generally caused by HPV types 6 and 11 (vs. high grade intraepithelial neoplasia from 16 and 18). Gardasil protects against 6, 11, 16, and 18. Immunosuppression from HIV or organ transplant can lead to persistent, extensive infection. Destructive therapies include cryotherapy, laser, electrocautery with curettage, and surgical debulking. Imiquimod is a topical toll-like receptor 7 (TLR-7) and TLR-8 agonist that stimulates the immune response (causes inflammation). Verruca/wart treatment Most will spontaneously resolve in 1-2yrs without scar, so choose therapy with low toxicity and scarring risk (or watchful waiting). Most are destructive or aim to simulate immune response to HPV. There is no antiviral therapy for cure and recurrence is high. Cryotherapy - use of liquid nitrogen to destroy the lesion. Side effects include post-inflammatory pigment alteration (hypopigmentation with darker skin types), scar, pain, blister, and nail dystrophy. Molluscum contagiosum Benign, skin-limited, usually asymptomatic poxvirus infection occurring usually in children with 2-20 discrete, 5mm, flesh colored to translucent, dome shaped papules, some with central umbilication. MC is usually on the trunk, face, and extremities or can be sexually transmitted on the external genitals. It's associated with eczematous eruption in 10% and spreads through direct contact or fomites (objects that carry infection), but isolation isn't necessary. Those with eczema and immunocompromise can have more widespread and prolonged eruptions. MC usually resolves in months, but treatment can reduce spreading and transmission, especially when genital. Destructive methods include cryotherapy, curettage, and cantharidin (blister beetle extract). Imiquimod and topical retinoids can be helpful. Treat associated dermatitis with topical steroid.