DERM in Primary Care PDF

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Dermatological Disorders in Primary Care A positive KOH examination growth of dermatophyte yeast or mold on culture is diagnostic • hype • Periodic acid Schiff • differentiate type Differential Diagnosis • psoriasis of the nails • chronic paronychia • pseudomonas of the nail (green nail syndrome) •

DISORDERS OF THE NAILS • • •

Acute Paronychia Onychomycosis Select other disorders • Beau’s lines • Onycholysis • subungal hematoma • junctional nevus

Paronychia • Usually results from infection of S. aureus or less commonly by streptococci or pseudomonas • Usually one nail involved • May occur spontaneously or as a result of trauma or manipulation such as nail biting, manicure or hangnail removal Clinical presentation • Acute paronychia is accompanied by the rapid onset of bright red swelling of the proximal or lateral nail fold behind the cuticle. • Painful, tender and throbbing lesion results Treatment • Mild cases warm saline or (Domeboro 1:40)(aluminum acetate) soaks for 10-15 minutes 2-4 x day. • Severe cases-I &D (#11) surgical blade will give rapid relief of pain • Sometimes systemic therapy with antistaphylococcal abx, such as • Dicloxacillin • Cephalosporin may be necessary Onychomycosis (tinea unguium) • Infection of the fingernails or toenails caused by various fungi, yeasts and molds • Tinea Unguium • specifically, to infections caused by dermatophytes such as E. floccosum, T. rubrum and T. mentagrophytes • Yeasts-candida albicans • Molds-aspergillus, fusarium and scopulariopsis • Onychomycosis is more prevalent with increasing age • about 30% of those 70 years or older Distal subungual onchomycosis represents about 90% of all cases. Presents as the following: • Nail thickening and subungual hyperkeratosis (scale buildup under the nail) • Nail discoloration • white, brown, yellow-green, yellow • Nail dystrophy • Onycholysis • nail plate elevation from the nail bed Clinical Manifestations • usually asymptomatic • Infrequently can act as an entryway for more serious bacterial infections of the lower leg especially in diabetics • In superficial white onychomycosis, fungus is superficial and material for scraping can be taken from the dorsal surface of the nail. Diagnosis

Treatment  keep in mind before starting • “prior comorbidity” • Oral therapy • Diagnostic confirmation by KOH or fungal culture • Patient motivation and compliance • Family history of onychomycosis • Patients age & health • Drug cost • Possible drug interactions and side effects •

Terbinafine (Lamisil) • Fungicidal especially against dermatophytes • hepatotoxic • Baseline LFT’s and repeated in 4-6 weeks • Continued clearing even after cessation of therapy • Dosage • 250 mg/day po for 6 weeks for fingernails • 250 mg/day for 12 weeks for toenails • Alternatively pulse dosing 250mg/day for one week monthly for 4 months

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Itraconazole (Sporanox) • Broad spectrum fungistatic • LFT’s same as Lamisil • Dosage 200 mg/day for 6 weeks for fingernails; 12 weeks for toenails • Alternatively pulse dosing with 200 mg twice daily taken with full meals for 7 days of each month) 3 months fingernails, 4 months toenails • Blackbox warning • CHF / cardiac effect • SSx

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Other treatments• Surgical - Laser treatment • Topical agents ineffective-poor nail penetration • However in early distal subungal and superficial white onychomycosis may be used as adjuvant therapy to prevent recurrences after clearing with oral meds • Penlac Nail lacquer topical solution (ciclopirox olamine) • Jublia (efinaconazole 10% solution) good nail penetration • Kerydin (tavaborale) – good acceptance

Dermatological Disorders in Primary Care Subungual hematoma • Trauma • Needle aspiration • Resolve on its own Junctional Nevus • Biopsy? • Nailbed? • At least photo for documentation of growth • Collection of melanocytes • Melanoma? ABSCESSES: Furuncles • Bacterial infection involving an entire hair follicle including subcutaneous tissue. It is characterized by an autoinoculable spread. • Carbuncles are multiple furuncles that develop along contiguous follicle that form large abscess with multiple peaks. • Gram positive bacteria-staph, or MRSA • Common in hairy areas where friction, pressure or moisture present

CELLULITIS Red streaking or tracking • • Purulent drainage in more severe cases • Most common in the extremities • Causative pathogen is usually gram + organisms such as group A beta hemolytic streptococci and S. aureus Treatment • Antimicrobial agent with strong gram + coverage (staph & strep infections) • dicloxacillin or macrolides (azithromycin or clarithomycin) • NSAIDS for discomfort • Antipyretics when fever present Burns • • • •

Risk factors  DM  injection drug use  HIV  close contact with infected individual Signs & Symptoms • Painful • Gradually enlarging rounded furuncle • Erythema of surrounding tissue • clear line of demarcation between affected and unaffected tissue • Fluctuant (presence of pus) in a bacterial infection • “boggy” feel Diagnosis • C&S of purulent drainage Treatment • I&D • Beta lactamase resistant antibiotic with gram positive coverage • Dicloxacillin • First generation cephalosporin • Erythromycin for PCN sensitive • Bactroban (d/c’s in the US) / Mupicocin • Nares • Axillae • anogenital regions for carriers

First degree • Heat injury to some level of epidermis 2nd degree or partial thickness • dermis and above 3rd degree or full thickness • and/or subcutaneous tissue and above More than 75% of burns involve 6% BSA burn 1st de • Tetanus vaccine Partial thickness • Heals best in moist but not wet environment • Bacitracin or Bactroban if not allergic • Silvaderm • Duoderm dressing

Herpes Simplex Virus (HSV) • Recurrent viral mucocutaneous infection spread by skin-to-skin, skin to mucosa or mucosa to skin contact. • HSV-1 has an oral labial predilection • HSV-2 urogenital predilection • However, cross contamination can occur • Etiology • Both virus reside in sensory ganglia • Reactivation occurs in response to: • Minor infection • Physical or emotional stress – most commonly to what is seen • Sun exposure • Unknown triggers • Expression of the virus typically occurs initially in young adulthood

Risk factors • Intimate skin-to-skin or skin-to-mucous membrane contact with infected person. • Transmitted at any time • 70% occurs during asymptomatic viral shedding Signs & Symptoms • Primary outbreak more severe • Neuralgia • burning & stinging, precedes eruption • Small grouped vesicles on erythematous base • Sites of vesicular eruption • Vermillion border of lips, penile shaft, labia, perianal region, buttocks • Vesicles burst, crust, and dry over approx. 1 week • Regional lymphadenopathy, Malaise, Myalgia Differential diagnosis • Chancroid • Syphilis • Pyoderma • Trauma Diagnostic Studies • Tzanck Smear • Direct immunofluorescent antibody slide test • Viral culture • ELISA or Western blot • Frequent outbreaks consider-HIV screening Treatment • Prevention- sunscreen • Prophylactic antiviral agents when risk of triggers is high such as UV light exposure, dental or oral surgery • Acyclovir 200 mg five times daily, 24 hours prior to exposure • Valacyclovir 500mg BID • Famciclovir 250 mg BID • Treatment in immunocompetent patients • Oral forms not typically treated • First genital episode-(7-10 days for all) • Acyclovir 200 mg five times daily or 800 mg TID or • Valacyclovir 1000mg BID or • Famciclovir 250 mg TID • •

Recurrent genital cases typically mild and do not require therapy • reduces duration of outbreak by only 24 hours Suppressive therapy for frequent or severe recurrences-reduces outbreak by 85% • Acyclovir 400 mg BID or • Valacyclovir 500 mg QD or • Famciclovir 125-250 mg BID • Topical therapies not effective in immunocompetent patients

Dermatological Disorders in Primary Care HERPES ZOSTER • Acute vesicular eruption as a result of the varicella-zoster virus. • Follows a typical course and typically occurs only once in most Etiology & Demographics • Typically contracted in childhood as chicken pox • Lies dormant in nerve ganglion • Viral reactivation results in typical disease course-cause unclear • Most common in persons >50 years of age • Unvaccinated persons 85 or > 50% risk of zoster

CHRONIC SKIN DISORDERS  Acne vulgaris o Pathophysiology  underlying cause; increased sebum production and abnormal desquamation of epithelial cells o Keratin and sebum accumulate in the follicular lining creating a plug (comedo) above the sebaceous gland duct. o The comedo expands resulting in distension of the follicle and a closed comedone (firm, elevated white or yellow papule) forms. o Closed comedone is the precursor to inflammatory lesions associated with acne

Risk Factors • • • Signs & Symptoms • • • • • •

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advancing age Immunosuppression trauma to sensory ganglia Pain along a dermatomal pathway-occurs 48 hours before eruption Grouped vesicles along an erythematous base Unilateral distribution - some lesions may scatter Vesicles erupt, burst, and crust spontaneously over 10 -14 days Regional lymphadenopathy Spread through the leaking fluid of the vesicles • cover the rash • Avoid exposure to the wet vesicles Differential Diagnosis • Poison oak & Ivy • Allergic contact dermatitis • Herpes Simplex virus Diagnostic Studies • Tzanck smear, varicella-zoster virus antibodies, viral culture of lesions

Treatment • • • • • •

Treatment reduces postherpetic neuralgia Immunocompetent patient • treatment 7 days for all regimens Acyclovir 800 mg five times daily or Famciclovir 500 mg TID or Valacyclovir 1000 mg TID Oral corticosteroids for 3 week tapering dose • start at 60 mg QD for pain • Watch out / do not give for DM, OP or gastritis

All patients with corneal involvement: ophthalmology evaluation Postherpetic neuralgia - pain persisting 90 days or more after onset of rash • Capsaicin ointment • Topical lidocaine • Tricyclic antidepressants • Antiepileptic drugs • Regional nerve blocks

  ACNE • • • • • • •

Atopic Dermatitis Psoriasis

Propionibacterium acnes (P. acnes) greatly contributes to the inflammation and irritation associated with acne Hormones • DHT stimulate sebaceous gland size and metabolic rate Increased estrogen will decrease sebum secretion • Birth control pills are sometimes prescribed for management Onset of puberty • severity of acne correlates with level of sex hormones Hyperandrogenism • irreg. menses, hirsutism, unexplained wt gain Comedogenic cosmetics, greasy hair products Medications • corticosteroids, androgens, anabolic steroids, tricyclic antidepressants, SSRI’s, lithium, anti-epilectics,

Treatment • Decrease bacterial load or break down comedo. • Hormonal treatments in females decrease androgen levels • Multidimensional approach most preferred because most pts have inflammatory & noninflammatory lesions • Pt. education- wash with mild cleansers • Noncomedogenic moisturizer & other products such as makeup • Avoid vigorous scrubbing, picking, squeezing • Treatment can take several weeks Medication • Salicylic Acid • Benzoyl Peroxide • Topical antibiotics-inflammatory papules e-mycin and clindamycin most conventional • Oral antibiotics-most commonly prescribed tetracyclines, erythromycin • Topical Retinoids (most well-known)-tazarotene, tretinoin and adapalene • Azelaic Acid • Dapsone • Combination Therapy • e-mycin/BPO • Clindamycin/BPO

Dermatological Disorders in Primary Care •

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• adapalene/BPO Isotretinoin - Accutane • last resort in some • Cannot get pregnant while on treatment - “iPledge” • Use 2 forms of birth control Hormonal treatment (females only) Oral contraceptives decrease androgen levels Spironolactone (not FDA approved for acne) blocks androgen receptors Dietary supplementation Nicotinamide • • Zinc • Diet-high glycemic load foods? In office procedures-intralesional corticosteroids, acne surgery, chemical peels, laser treatment

ATOPIC DERMATITIS • Inherited type I (immunoglobulin E-mediated hypersensitivity of the skin. • “Itch that rashes” • Persistent xerosis • unpredictable, with flares and remissions • Asian • personal history of asthma, hay fever, allergic rhinitis • Triggers • synthetic fabrics, alcohol, certain foods, overexposure to dry, cold weather, hot, humid conditions that predispose to sweating. • Distribution of lesions • flexural folds, neck, wrists, ankles, eyelids, lips, scalp, hands Treatment • Nonsteroidal Topical skin Barriers • Atopiclair, MimyX, Eletone • Topical Steroids First line therapy in AD. • Fluticasone twice weekly applied to areas involved in flares • Topical Calcineurin Inhibitors • anti-inflammatory effect without side effects of topical corticosteroids. Block Tcell activation pathway. • Eladil cream or Protopic ointement • Ointment – greasier but better than lotion or cream • Tacrolimus ointment (0.03%) also supplied as 0.1% can be used on facial and eyelid eczema • Pimecrolimus cream (1%) • Both may cause a transient burning sensation • Antihistamines • major value is sedative effect • diphenhydamine • Presence of pustules within areas of dermatitis may indicate a secondary infection, usually S. Aureus. • Prescribe dicloxacillin, erythromycin Patient Teaching • Bathing tips: • Helpful: removes crusts, irritants and decreases stress • Not longer than 10 minutes • Mild soap • Dove, Cetaphil lotion cleanser • Apply lotions after bathing

Vaseline jelly, Eucerin, Aquaphor, Cetaphil, Lubriderm, Moisturel Wear cotton, avoid overheating or sweating • Avoid environmental allergens, house dust mites •

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PSORIASIS • Inflammatory skin condition immunologically based • Alteration of cell kinetics of keratinocytes with a shortening of the cell cycle resulting in 28x the normal production of epidermal cells. • Rapid skin cells – sunburn looking skin • Psoriasis is a T-cell driven disease. Most current therapies are directed at the suppression of responsible T cells. • Protein or fluid loss • Types: • Plaque • Guttate • Pustular • Erythrodermic • Psoriatic arthritis Risk factors • Genetics: 40% of people with psoriasis have a positive family history for the disease. • At least 9 chromosomal loci linked to psoriasis. • Environmental and behavioral triggers: • Smoking • Obesity • Medications • Lithium • Antimalarials • beta blockers • Infection • streptococcal infection can trigger guttate psoriasis Psoriasis: Plaque • Erythematous, pruritic papules with a silvery-white scale. • Plaques can be localized or general • Can occur anywhere on the body; found on palms & soles, scalp, nails, perianal & genital regions. • Facial area not usually seen. Psoriasis-Guttate • Occasionally preceded by group A beta-hemolytic streptococcal pharyngitis. • Should be promptly treated with appropriate antibiotic • PCN • E-mycin • for group A beta-hemolytic stretococcus. Treatment  UVB phototherapy or natural sunlight. • High potency class 1, 2, or 3 steroids

Dermatological Disorders in Primary Care Psoriasis: Pustular • Rare, characterized by pustules on normal or inflamed erythematous skin. • Unknown pathogenesis. No precipitating factors. • May or may not have had stable plaque psoriasis in the past. • Suggested triggers steroids, drugs • Pustules are sterile, eruption generalized. • Relapses and remission may occur over a period of years. Psoriasis: Erythrodermic • Inflammatory psoriasis that often affects most of the body surface. • Least common type • may occur in association with pustular psoriasis • Clinical signs • severe redness, desquamation of skin • Skin looks “sunburned” • Tachycardia pruritis, pain, changes in body temp • Edema (esp around ankles) • Treatment: • Hospitalization Psoriasis: Arthritic • Inflammatory arthritis associated with psoriasis • Occurs in 6-40% (average 30%) of patients with psoriasis, depending on population studied. • Prevalence increases with increasing BSA affected. • Arthritis typically develops 7-10 years after onset of psoriasis, at an average age of 36 years. • Rheumatoid factor negative • May be progressive, severe deforming. • Clinical features • Stiffness • Pain • Swelling • Tenderness of joints, ligaments and tendons • Nail disease is common • Dactylitis (sausage digit) is common, affects fingers and toes • Subluxation of the small bones • Onycholysis of the nails Psoriasis: National Psoriasis Foundation Coverage and Severity  Mild: less than 3% BSA  Moderate: 3-10% BSA  Severe: >10% BSA *1% = surface area of the hand •

Psoriasis covering < 5% of body surface can be managed by PCP.

Localized Therapies Topical Steroids-Class I-VII potency Class 1-Temovate (Clobetasol propionate) Class II Topicort Class III Cutivate Class IV Kenalog, Westcort Class V Kenalog, DesOwen Class VI DesOwen Class VII Hytone, Cortizone 10 Keratolytic Agents-Salicylic Acid 6% Topical Vitamin D3- Calcipotriene 0.005% (Dovonex cream), Calcitriol (Vectical) Topical Retinoids -Tazarotene 0.05%, 0.1% cream/gel (Tazorac cream/gel) Topical Immunomodulators-Tacrolimus ointment 0.03%, 0.1% Tar Preparations-Estar, PsoriGel, Doak Tar oil Source:Goodheart’s Photoguide to Common Skin Disorders.Philadelphia, PA, Wolters Kluwer; 2009

Phototherapy • Useful for moderate-severe plaque psoriasis not responsive to topical RX • Narrowband UVB • Safest, most effective • UVB fewer side effects than UVA, tried first, can be combined with oral retinoid derivative (ReUVB) to decrease dosage of UVB radiation to skin. • Often combined with topical treatment • UVA • Used with methoxsalen known as PUVA (psoralen). • Administered in Dermatologist office • Increases risk of skin cancer Conventional Systemic Therapies • Methotrexate: Plaque, erythrodermic or generalized pustular • Most commonly prescribed systemic therapy • Recommended for treatment of moderate or severe psoriatic arthritis • Adult dose is 2.5 mg/week PO initially, then 12.5-25 mg/week depending on response. • Limitation is hepatotoxicity • CBC, monthly liver and renal function blood tests should be ordered. • Cyclosporine (Neoral, Sandimmune) • Useful for short term RX of significant exacerbations • Recommended to treat severe psoriasis after failure of >1 other systemic therapy • Initial: 2 to 5mg/kg/day divided doses • Acitretin (Soriatane) erythrodermic, generalized pustular • Often used with UV light • General takes 3-6 months for response • Initial: 25 mg/day PO then increase. • Maintenance: 20-50 mg/day PO • Teratogen • no pregnancy during and for three years after D/C

Dermatological Disorders in Primary Care

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Phosphodiesterase Type-4 Inhibitor • Apremilast (Otezla) (oral tablet) • Moderate to severe plaque psoriasis • Most common side effects • first two weeks and resolved with continued use • Diarrhea, nausea & headache • Can increase risk of depression • Weight loss 5-10% has been reported IL-17A Inhibitor • Secukinumab (Cosentyx) (injectable) • Moderate to severe plaque psoriasis • Most common side effects-nasopharyngitis, diarrhea, URI

BIOLOGIC AGENTS for the Treatment of Moderate to Severe Psoriasis • Interact with specific targets in T-cell mediated inflammatory processes and have an anti-inflammatory effect • TNF Inhibitors • Humira (Adalimumab)-Dosing-80 mg SQ, followed by 40 mg SC every other week. • Enbrel (Etanercept)-Dosing- 50 mg twice weekly for 12 weeks, then 50 mg sc each week. • Remicade (Infliximab)-Dosing- 5mg/kg IV at week 0, 2, 6, then every 8 weeks. • IL-12/23 Antagonist • Stelara (Ustekinumab)-Dosing- 45 or 90 mg SQ at week 0 and 4,then once every 12 weeks. Psoriasis and risk of comorbidities • Psoriasis is a potentially multisystem disorder • Patients with psoriasis have a 50% increased risk of mortality • Increased risk for MI, CAD, metabolic syndrome • Require annual TB skin test and TIV vaccination for patients treated with biologics • Screen for and treat aggressively CV comorbidities and risk factors • Schedule annual physical exam and labs (glucose, lipid measurements)...