6. Derm Part 2 2024.ppt

DERMATOLOGY PART II Alison Wix, MPA, PA-C Clinical Pharmacology  Folliculitis Inflammation of the hair follicles Most commonly from Staphylococcus aureus Hot tub folliculitis: caused by Pseudomonas Occurs on trunk after hot tub use (bathing suit pattern) The lesions are erythematous pap...

DERMATOLOGY PART II Alison Wix, MPA, PA-C Clinical Pharmacology  Folliculitis Inflammation of the hair follicles Most commonly from Staphylococcus aureus Hot tub folliculitis: caused by Pseudomonas Occurs on trunk after hot tub use (bathing suit pattern) The lesions are erythematous papules or pustules around the hair follicle Typically NOT painful, but they may burn Folliculitis Noninfectious folliculitis Common among people working in hot, oily environments Occlusion, perspiration, and rubbing from tight clothes Pseudofolliculitis Inflamed / ingrown hairs occurring in the beard area “Razor bumps” Type of non-infectious folliculitis Greater risk with African American males Sycosis Bacterial infection of the bearded part of the face Severe, deep-seated, recalcitrant folliculitis with surrounding eczema and crusting Abscesses may form at the site of folliculitis Folliculitis Diagnosis: History and Physical Examination Treatment: Gentle cleansing and mild compresses Protection from offending substances Use of drying agents Mild Cases Topical application of clindamycin or mupirocin (Bactroban) More extensive cases PO Cephalexin (Keflex) Flouroquinolone antibiotic if necessary Hot tub folliculitis is usually self-limiting and resolves without treatment Abscess Localized infection characterized by a collection of purulent material in a cavity Most commonly found in the axilla, buttock, perirectum, or back Formed by necrosis or disintegration of tissue A sterile abscess is one formed without bacterial pathogen Signs and Symptoms: Tender, erythematous, edematous area filled with purulence Abscess Treatment: I&D with packing FIRST CULTURE PO antibiotics Cephalexin (Keflex) Trimethoprim / Sulfamethoxazole (Bactrim) Warm compresses if needed Amoxicillin-clavulanate (Augmentin) 90mg/kg/day 10 days Cephalexin (Keflex) 50 mg/kg/day TID x 10 days (max 500mg/dose) Furuncles and Carbuncles Deep-seated infections of the hair follicles Staphylococcus aureus is the most common pathogen Furuncle is an infection of a single follicle Carbuncle includes more than one infected follicle as a conglomerate mass Signs and Symptoms: Red, hard, tender lesions in hair-bearing areas Progress to become fluctuant and may rupture spontaneously, draining pus and necrotic tissue Furuncles and Carbuncles Treatment: I&D once the lesion is mature Culture Oral antibiotic therapy Same as abscess Warm, moist compresses Pearl: No I&Ds in the “Dangerous Triangle” around the nose Pterygoid Venous Plexus leads to cavernous sinus in the brain Summary Cellulitis Acute, spreading inflammation of the dermis and subcutaneous tissue Causative organisms: H. flu, strep, staph, other Gram (-) species Lesion is not raised May involve localized lymphadenopathy, fever, and malaise Signs and Symptoms: Red, hot, painful, swelling Outline the margins of involvement before treatment Imaging may be helpful if risk of osteomyelitis Cellulitis Treatment Rest, elevation, analgesia PCNs or Cephalosporins initially PO Antibiotics (mild to moderate) Cephalexin (Keflex) Cephalexin (Keflex) TID (max 500mg/dose) Augmentin Amoxicillin-clavulanate (Augmentin) Trimethoprim / Sulfamethoxazole (Bactrim) IV antibiotics (severe) Severe infections or sepsis Failed oral therapy Cefazolin Poor response to antimicrobial therapy or a necrotizing, soft- tissue infection warrants surgical intervention and debridement Erysipelas Superficial bacterial skin infection that includes the upper dermis and extends into the cutaneous lymphatics Signs and Symptoms: Malaise, chills, and high fever approximately 48 hours BEFORE onset of the skin lesions Pruritus, burning, and tenderness Erysipelas Initially a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque Tender, erythematous, and well demarcated Demarcated borders help differentiate it from other skin infections such as cellulitis Causes: Streptococcus or Staphylococcus Erysipelas Pathophysiology: Bacterial inoculation into an area of skin trauma Portals of Entry Venous insufficiency, stasis ulcerations, inflammatory dermatoses, dermatophyte infections, insect bites, and surgical incisions Facial erysipelas Entry through the nasopharynx Recent streptococcal pharyngitis in 1/3 of cases Erysipelas Diagnosis: Mostly clinical diagnosis  sharply demarcated border Routine blood and tissue cultures are not cost-effective Bacterial cultures from the portal of entry may be helpful with atypical clinical presentations Treatment: Antibiotics Amoxicillin or Cephalexin for mild cases Cefazolin or Ceftriaxone for severe cases and those with systemic symptoms Impetigo Gram (+) bacterial infection of the superficial layers of the epidermis. Two forms: Bullous and non-bullous* Caused by Staphylococcus aureus and group A beta- hemolytic streptococci (GABHS) / Streptococcus pyogenes Non-bullous impetigo occurs in approximately 70% of children younger than 15 years with the infection. Non-bullous Impetigo First noticeable lesion is a papule, 2-5 mm in size Papule  vesicle  honey-yellow, crusted papule or plaque smaller than 2 cm with minimal or no surrounding redness. Non-Bullous Impetigo Bullous Impetigo A vesicle that develops into a superficial, flaccid bulla Fluid becomes turbid  vesicle bursts and develop brown crust Less than 1 cm in diameter on intact skin, with minimal or no surrounding redness. Typically on the trunk Impetigo Treatment Antibiotics MUST provide coverage against both Staphylococcus aureus and Streptococcus pyogenes. MRSA most commonly manifests as folliculitis or abscess Topical antibiotics if localized Bactroban (Mupirocin) ointment x 7-10 days Oral / IV meds if severe or widespread Amoxicillin-clavulanate (Augmentin) Cephalexin (Keflex) * Clindamycin (Cleocin) for PCN allergic Vancomycin Dermatophytosis Superficial fugal infection Can affect the hair, nails, and skin When describing the area of infection, the word tinea (meaning “fungal infection”) is followed by the affected part of the body Clinical Presentation: Presents as an erythematous, annular patch, with distinct borders and central clearing, with a fine scale that covers the patch Symptoms include itching, stinging, and burning Maceration or peeling fissures are common between digits Tinea Pedis Foot Well-demarcated, “mocassin” distribution Erythema, scaling, maceration Can start in feet and move elsewhere “Two feet, one hand” phenomenon Causes: M>F Hot humid weather Excess sweat Occlusive footwear Tinea Pedis Diagnosis: Clinical Treatment: Topical antifungals: Lotrimin Cream Systemic antifungals after failure Tinea Cruris Inguinal Causes Warm, humid environment Obesity M>F Treatment Topical or systemic antifungals: Lotrimin Cream Powders for prevention Tinea Corporis  Trunk, legs, arms, or neck Traditional “ringworm” All ages affected M=F Animal workers at highest risk Trichophhyton rubrum Small to large, round, scaling, sharply marginated, erythematous plaques with a central clearing Treatment: Antifungal: Lotrimin OTC Tinea Unguium Nails AKA onychomycosis Thickening, discoloration and of the nail bed and plate Treatment PO Terbinafine (monitor LFTs) Topical Efinaconazole Tinea Capitis Head Broken hair shafts are seen as black dots with lamp Patches of missing hair Toddlers and school-aged children Transmits by contact Treatment Topicals are ineffective Griseofulvin is drug of choice (DOC) even when only small patches are present Monitor blood work Diagnosis: Dermatophytosis KOH Prep Shows hyphae (spaghetti and meatballs appearance with microscopy) Wood’s Lamp (Ultraviolet light) Look for fluorescence (may be negative) Fungal culture for nails, but can take up to 14 days to grow  General Treatment: Dermatophytosis Topical creams, ointments, lotions, powders, and sprays Usually they are prescribed BID for >/= 4 wks. If there are vesicles, powders help dry the area to help prevent maceration Chronic or resistant infections or nail infection may require oral medications Oral treatment could take up to 3 months Steroids should be avoided Long term use will exacerbate the condition and increase risk of side effects. Local measures including keeping the skin clean and dry, wearing cotton socks and loose-fitting underclothes Long-term antifungals should monitor LFTs  Tinea Versicolor Superficial yeast infection Malassezia furfur Naturally occurring and found on the skin of humans Pathophysiology: Idiopathic as to why this yeast manifests in the spore and hyphal form in some patients M=F More prominent in the summer Affects abdomen and back most frequently  Tinea Versicolor Signs and Symptoms: Hypo or hyperpigmented macules that do NOT tan Tan lesions in fair-skinned, white lesions in darker skin Sharply marginated Round or oval, varying in size, with fine scaling Mostly asymptomatic other than pigment change Notice the infection only during the summer, when their tan is spotted Diagnosis and Treatment: Clinical diagnosis Topical agents – Selenium sulfide lotion or shampoo (i.e. Selsun Blue or Ketaconazole shampoo) Dyspigmentation may continue for months after organism is eradicated, but skin will return to normal  Cutaneous Candidiasis Most frequently from Candida albicans yeast Presents in “intertrigous areas” Infra-mammary folds, inguinal region Signs and Symptoms: Erythema, pruritis, tenderness, pain Worse in warmer weather Diagnosis and Treatment: Initial pustules on erythematous base, become eroded and confluent “satellite lesions” Clinical diagnosis Can obtain wet mount, fungal culture or KOH prep Hyphae, pseudohyphae, budding yeast cells Topical or systemic antifungals pending severity Perlesche Superficial yeast infection around the nasolabial folds AKA Angular Cheilitis Males and Females affected Saliva leaking into folds, stimulating excess yeast growth Symptoms: Itch and burn Treatment: Topical cream (i.e. Ketaconazole cream) Scabies Sarcoptes scabiei Eight–legged mite Microscopic to naked eye Can be found in patients of any age Rarely in infants < 3 months Pearl: Patients who come in complaining of “eczema” between digits.  Scabies Clinical Presentation: Distribution is most common on the hands, genitalia/umbilicus, and axillary areas Concentrated around web spaces between the fingers and toes, around the belt line, or at the edges of socks The lesions are pruritic burrows, vesicles, or nodules with excoriations and crusting Secondary infections (impetiginized) typically are caused by strep or staph Diagnosis: Mites, eggs, or feces found on scraping. Mineral oil slide (live) vs. KOH (kills) + microscopy is confirmative, but NOT always successful  Scabies Treatment: 1% lindane or 5% permetherin in lotion or cream. Applied to the skin from the chin to the bottom of the feet and left on overnight (8 hours minimum), washed off in the morning. The treatment may be repeated in 7 and then again in 14 days Lindane is more toxic and should be avoided in children younger than 2 years, people with extensive dermatitis, and those who are pregnant or lactating Usually guaranteed to kill in 1 attempt (scabicide works on both mites and eggs) Antihistamines or topical steroids may help with the itching All bedclothes and clothing of infected patients and household contacts should be washed  Pediculosis “Lice” 1-3 mm, flat mites with three pairs of legs Females lay 300 nits during a lifetime Nits are opalescent, found on hair shafts, and hatch in about 1 week Transmission is person to person Types Pediculosis capitis infects the scalp (head lice) Pediculosis corporis infects the body Pediculosis pubis infects the pubic area (crabs) Pediculosis Clinical Presentation: Pruritus is variable in severity Excoriations may become secondarily infected Visible, but often difficult to find Nits are more readily seen on the hair shafts Pediculosis  Pediculosis Diagnosis and Treatment: Specimens can be viewed under the microscope to confirm the diagnosis Prevention is key Avoid sharing contact items such as hats, brushes, etc. All contact items should be examined Topical insecticides are effective Permethrin 1% Special combs help to remove nits Reapplication in 7-10 days may be recommended to kill any newly hatched lice Lyme Disease Tick-borne, inflammatory disorder Caused by the spirochete Borrelia burgdorferi Transmitted via deer tick bite Hallmark Early EXPANDING skin lesion, Erythema Migrans (EM) May be followed weeks to months later by neurologic, cardiac, or joint abnormalities Stages Early Disseminated Late Symptoms of Lyme Disease Early Stage (1-4 weeks) Erythema Migrans with SINGLE lesion only Fever, myalgia, headache, fatigue, arthralgia Disseminated Stage (1-6 months) Erythema Migrans with single or multiple lesions Carditis Nerve Palsy Septic Arthritis Fever, myalgia, headache, fatigue, arthralgia Late Stage (>6 months) Chronic mono/oligoarthritis Fever, myalgia, headache, fatigue, arthralgia  43 Erythem a Migrans Erythema Migrans Early stage Lyme disease Most common tick-borne disease in U.S. / Europe Transmitted by deer tick bite More common in spring / summer months in wooded areas Incidence of disease is higher when tick attaches for longer than 72 hrs “Bulls-eye” approximately 1 wk after tick bite (can be solid) Flu-like symptoms (fevers, chills, adenopathy, muscle aches, HAs, fatigue) Diagnosis of Lyme Disease Early Stage (1-4 weeks) Clinical diagnosis ONLY ELISA and Western Blot 75% are negative Disseminated Stage (1-6 months from bite) ELISA and Western Blot and clinical diagnosis 70% positive with multiple EM 95% positive with CNS/cardiac involvement EKG to check for block Late Stage (>6 months from initial infection) ELISA and Western Blot 100% positive Treatment of Lyme Disease Amoxicillin or Doxycycline for 8 yoa Prophylactic for ALL ages within 72 hours of tick removal Doxycycline 4mg/kg PO x 1 dose if 45kg Treatment of Lyme Disease Early Amoxicillin 90mg/kg PO BID x 14 days Doxycycline 100mg PO BID OR 2mg/kg PO (max dose 100mg/dose) BID x 10 days Disseminated Stages Amoxicillin 90mg/kg PO BID x 14 days Doxycycline 100mg PO BID OR 2mg/kg PO (max dose 100mg/dose) divided BID x 14 days Late Stage Amoxicillin 90mg/kg PO BID x 28 days Doxycycline 100mg PO BID OR 2mg/kg PO (max dose 100mg/dose) divided BID x 28 days  Erythema Multiforme (EM) Allergy-mediated cutaneous condition Causes Induced by drugs Sulfonamides, phenytoin, barbiturates, PCN, allopurinol Following infections Herpes simplex, mycoplasma species Idiopathic (50% of cases) Half of all cases occur in patients < 20 yrs old Previous history of EM is a strong risk factor for subsequent cases Pathophysiology: Mostly unknown, herpes-associated EM appears to represent the result of a cell-mediated immune reaction associated with herpes simplex virus (HSV) antigen Erythema Multiforme Signs and Symptoms: Continuum of lesions: Macules  papules  vesicles  bullae May be “Bullseye” appearing like erythema migrans Lesions can be localized to the hands and feet or become generalized. Fever, weakness, malaise Lesions are painful and can erode Minor – no involvement of mucosa Major – involvement of mucosa Lungs and eyes may be affected Treatment: Avoid target causes Systemic steroid therapy Erythema Nodosum Acute inflammatory (immune) reaction Involving subcutaneous fat Appearance of painful nodules on lower legs Causes: Infection Medications / drugs Sarcoidosis Strep Erythema Nodosum Signs and Symptoms: Painful and tender lesions + fever, malaise, arthralgias (typically ankle joints) Diagnosis: Blood work shows increased ESR, CRP, leukocytosis ? Bacterial culture – group A strep CXR – r/o sarcoidosis  Erythema Nodosum Treatment: Symptomatic Bed rest Anti-inflammatories Spontaneous resolution typically occurs in ~6 weeks New lesions may erupt during this time Pearl: Lesions never break down or ulcerate, and they heal without scar formation Stevens-Johnson Syndrome (SJS) & Toxic Epidermal Necrolysis (TEN) Muco-cutaneous blistering reactions Most often caused by a drug reaction SJS thought to be severe variant of EM (erythema multiforme) TEN is severe variant of SJS M=F Any age Pathogenesis thought to be an immunologic response Dangers Infection, fluid loss, and electrolyte imbalance  SJS/TEN Widespread epidermolysis and blistering Keratinocyte apoptosis occurs Organized series of biochemical reactions leading to cell changes and death Signs and Symptoms: Fever, sore throat and sore mouth Painful, blister-like lesions appear Erythema, necrosis of epidermis, loss of layers like sheets (+Nicolsky’s sign) SJS: 30% total skin loss SJS/TEN Diagnosis and Treatment: Biopsy Remove underlying agent Treatment for symptomatic relief Similar to burn units +/- Steroids IV fluids IVIG SJS/TEN Staphylococcal Scalded-Skin Syndrome (SSSS) Staph infection (typical in infancy) Produces exfoliative toxins Secondary to conjunctivitis, (otitis media) OM, nasal colonization, bullous impetigo Signs and Symptoms: Tender, erythematous areas on skin +/- low grade fever Irritability Ill-defined sandpaper appearance on skin Later deepens, skin more painful, superficial sloughing occurs SSSS Diagnosis: Bacterial culture to r/o infection Clinical +Nicolsky’s sign Treatment: Oral antibiotics Baths and compresses Hydration (severe cases via IV) Usually resolves without scarring Spider Bites All spiders in the US are venomous Only a few can puncture the skin Most bites occur while sleeping or dressing in the morning after the spider crawled into the clothing during the night Signs and Symptoms: Feel pain ~3 hours after bite Systemic symptoms begin 4-6 hours after bite Acute necrotic injury to the skin lasts 10-15 days Spider Bites Black widows Can cause a neurologic overstimulation (e.g, muscle aches, spasms, rigidity) These spiders are not as prevalent Brown recluse Loxosceles reclusa Single bite  infarct of skin caused by rapid blood coagulation within the vessels Lesion is a sinking macule, pale gray in color, slightly eroded in the center, and has a halo of very tender inflammation and hemorrhage Lesions can extend to the muscle and be as large as the palm of the hand Spider Bites Spider Bites Treatment: Most bites can be managed with local care and analgesics Neurologic manifestations of black widow bites can be treated with diazepam and calcium gluconate Brown recluse bites may be treated locally with cleansing and analgesia Extensive debridement has not been proven to be beneficial Typically, wound decreases significantly in 5-10 days Antivenom rarely is indicated and is not readily available Antibiotics for infection Alopecia “Loss of hair” Androgenic alopecia Male pattern baldness Common slow, progressive form of hair loss Has a genetic component Extent is variable and unpredictable Treatment: Topical Minoxidil solutions are most effective in persons with recent onset and smaller area of hair loss Oral Finasteride may be alternative Alopecia Areata Immune mediated Nonscarring hair loss Sudden, rapid hair loss in circular, discrete areas Hair loss can be patchy Tiny (vellous) hairs are typically found Treatment Topical cream: desoximetasone (topicort) Injectable steroids: triamcinolone Treatment is painful AND relapse is common Other types of Alopecia Alopecia Totalis Involve entire scalp Alopecia Universalis Include the entire body Traction Alopecia Involve “pampered” areas of scalp Mechanically induced secondary to bending follicle Extensions or weaves Can be permanent Alopecia areata totalis