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Common Dermatological Conditions Dr N Samadi IMT1 Royal BromptonSession Layout ● Miscellaneous common conditions ● Dermatological Emergencies ● Skin cancers Not covered ● Childhood rashesAtopic Eczema Recognition Who? Most cases first develop in children < 5. 2 in 3 children grow out of it by their mid teens. How? Multifactorial: Genetics, allergens, infections. Epidermal barrier losses + immunological abnormalities + aggravating factors Diagnosis ● Itchy skin and at least 3 of the following ○ Onset <2 years ○ Past flexural involvement ○ History of generally dry skin ○ Personal history of atopy ot history of atopy in a 1st degree relative ○ Visible flexural dermatitis (if < 4 years on cheeks, forehead & outerside of limbs) Explain that treatment is management rather than cure. Management Avoid triggers e.g. harsh soaps & detergents, Liberal emollient use (3-4x daily) when eczema not that bad as it acts as a barrier and reduces need for topical steroids. Topical steroids if flare is severe. Apply only on active eczematous skin for up to 7 days. Use weakest effective steroid. Topical pimecromilus or tacromilus if not controlled with topical steroid Systemic treatment e.g. azathioprine, ciclosporin or methotrexate in very severe disease For itch: Sedating antihistamines e.g. hydroxizine at nightTopical Steroid Side Effects ● Atrophy ● Striae ● Telangiectasia ● Spread Infection ● Depigmentation ● Contact Dermatitis ● Cushing’s - pituitary/adrenal axis suppression from systemic absorption ● CI: Rosacea, acne, psoriasis (severe), orofacialdermatitisPsoriasis Recognition Who? 75% before age 46 but uncommon in children How? Genetic element (50% risk if both parents have it). Triggers: Stress, infections (strep), skin trauma (Kobner), drugs (lithium, NSAIDs, B blockers, antimalarials). Hyperproliferative epidermis and proliferation & dilatation of blood vessels in dermis + infiltration of inflammatory cells. Diagnosis ● Chronic inflammatory skin condition characterized by scaly erythematous plaques, which typically follows a relapsing remitting course. ● Many types - most common is chronic plaque psoriasis (Also flexural, guttate, psoriatic arthropathy). Management Rx is control rather than cure. Consider psych & ● Emmolients social effects ● Topical corticostroid PLUS Vitamin D ● Phototherapy (Narrowband UVB phototherapy) ● Non-biological oral drugs e.g. Methotrexate, Ciclosporin & Acitretin ● Biological drugs e.g. Infliximab, adalimumab & etanerceptGuttate Psoriasis Recognition Who? Peak incidence 30-40 years How? Precipitated by streptococcal infection 2-4 weeks prior to lesions appearing Diagnosis ● Teardrop, scaly papules on trunk and limbs ● Acute onset over days Management ● Most cases spontaneously resolve within 2-3 months ● No evidence for abx for streptococcal infection ● Topical agents as per psoriasis ● UVB phototherapy ● Tonsillectomy with recurrent episodesPityriasis Rosea Recognition Who? Peak incidence 20-30 years How? Associate with HHV 6 and HHV7 Diagnosis ● Herald patch (usually on trunk) followed by erythematous, oval, scaly patches 1-2 weeks later ● ‘Fir-tree’ appearance ● Minority of patients report preceding viral symptoms Management ● Self-limiting with good prognosis - self-resolves after 6 weeks ● Steroids / emollients / antihistamines to alleviate itch ● UVB therapy in severe / prolonged casesScabies Recognition Who? Children and young adults -. Incidence 6:15 years. Sex ratio 1:1 How? Sarcoptes scabiei mite burrows into skin and lays eggs in the stratum corneum. Intense pruritus caused by a delayed type IV hypersensitivity reaction to mites/eggs 30 days after initial infection. Diagnosis ● Widespread pruritus ● Linear burrows on side of fingers, interdigital webs and flexor aspects of wrist (can affect face and scalp in infants) ● Secondary features (excoriation, infection) due to scratching Management ● Permethrin 5% 1st line ● Malathion 0.5% 2nd line ● Apply to all areas of the skin and leave (8-12 hours permethrin, 24 hours malathion). Reapply if rubbed off. Repeat treatment after 7 days. ● Treat all household and physical contacts at the same time, even if asymptomatic. ● Launder / iron / tumble dry all bedding / towels / clothing ● Be aware that pruritus can persist up to 4-6 weeks post eradocationPityriasis Versicolor Recognition Who? Peak incidence 20-30 years. Sex ratio 1:1 How? Fungal infection caused by Malassezia furfur Diagnosis ● Hypopigmented (or brown or pink) patches on the trunk. More noticeable after suntan. Can have overlying scale, mild pruritus. Management ● Ketoconazole shampoo - Topical antifungal. ● If failure to respond to topical treatment consider alternative diagnosis (e.g. by sending scrapings) with oral itraconazole.Vitiligo Recognition Who? Before age 20-30 How? Autoimmune. Associated with T1DM, Addison’s disease, autoummune thyroid disease, pernicious anaemia, alopecia areata Diagnosis ● Well-demarcated patches of depigmented skin, mostly in peripheries ● Can exhibit Koebner phenomenon ● Sunblock for affected areas Management ● Camouflage makeup ● Topical corticosteroids if applied early ● Topical tacrolimus / phototherapyImpetigo Recognition Who? Peak incidence 1-5 years. Sex ratio 1:1 How? Superficial bacterial infection caused by Staphylococcus aureus or streptococcus pyogenes (GAS). Spread by direct contact with discharged from scabs of an infected person. Highly contagious. Diagnosis ● Golden, crusted skin lesions around the mouth (can develop anywhere on the body but tend to occur on face, flexures, limbs) Management ● Hydrogen peroxide 1% cream ○ New NICE guidelines those not systemically unwell or at high risk of complications, likely aimed at cutting antibiotic resistance ● Topical antibiotics creams ○ Fusidic acid ○ Mupirocin (if suspected fusidic acid resistance or MRSA) ● Oral antibiotics (systemic disease) ○ Flucloxacillin ○ Erythromycin ● School exclusion until all lesions crusted or 48 hours after commencing abx treatmentLichen Planus Recognition Who? Adults between 30-60 years How? Unknown aetiology, probably immune-mediated. Lichenoid drug eruptions (gold, quinine, thiazides. Diagnosis ● Itchy, polygonal, papular rash on palms, soles, genitalia and flexor surfaces of the arms ● Wickham’s striae on the surface ● Koebner phenomenon ● White-lace pattern on the buccal mucosa Management ● Topical steroids ● Benzydamine mouthwash / spray for oral lichen planus ● Oral steroids / immunosuppressionLichen Sclerosus Recognition Who? Most often women >50 (F>M 10:1) How? Cause unclear, likely mixture of genetic, hormonal, irritant, traumatic and infectious components. Diagnosis ● White patches, thickened or crinkled on the skin ● Commonly on non-hair bearing / inner areas of the vulva. Also in perianal region. ● Can be very itchy and sore. Can cause adhesions and scarring ● General measures - wash gently non-soap cleanser, emollients Management ● Topical corticosteroids (potent) ● Oestrogen creams / pessaries ● Tacrolimius ointment ● Topical retinoidShingles Recognition Who? 70+ years How? Reactivation of the varicella-zoster virus - only possible if you have had chickenpox. VZV virus lays dormant in the dorsal root / cranial nerve ganglia, then reactivated by e.g. stress, illness, immunosuppression, skin trauma / burn Diagnosis ● Acute, unilateral, painful, blistreing rash ● Follows a dermatomal distribution (does not cross midline) ● Neuropathic pain Management ● Supportive - Analgesia, calamine lotion, capsaicin, cool compress ● Aciclovir / Famciclovir / Valaciclovir within 72 hours ● Course of oral corticosteroid in conjunction if severe pain ● Primary prevention with herpes zoster vaccine (live vaccine) if > 70 years old Complications Post-herpetic neuralgia - persistent pain in region of rash > 1 month Herpes zoster ophthalmicus - When affects ophthalmic branch of cranial nerve V (may result in irreversible cranial nerve palsy - urgent ophthalm ref) Ramsay-Hunt syndrome - When affects cranial nerve VII (facial nerve) - vesicular lesions in ear, facial/tongue paralysis Encephalitis - 3-4 days after rash, immunocompromised, CN dermatome.Molluscum Contagiosum Recognition Who? Children aged 1-4 years (often with atopic eczema). Sexual transmission in adults How? Molliscum contagiosum virus of the Poxviridae family. Transmitted by close personal contact or contaminated surfaces including rowels. Diagnosis ● Pink / pearly white papules with central umbilication in clusters around the body. Papule contains white, cheesy material. ● In warm, moist aries, armpit, behind knee, groin, genital areas. (Spare palms and soles) Management ● Reassurance (self-limiting) ● Squeezing / piercing ● Cryotherapy ● Referrals ○ If HIV +ve refer to HIV services ○ If eyelid / ocular lesion associated with red eye urgent ref to ophthalmology ○ Adults with anogenital lesions - Refer to GUM & screen for other STISeborrhoeic Dermatitis Recognition Who? Infants, then adults 30-40 years. More common in males 2:1 How? Inflammatory reaction related to proliferation of Malassezia furfur fungus, a normal skin inhabitant. Associations with HIV and Parkinson’s. Diagnosis ● Ezcematous lesions on sebum-rich areas: scalp, periorbital, auricular and nasolabial fold ● May develop blephariris or otitis externa ● Ketoconazole 2% shampoo Management ● OTC preparations containing zinc pyrithione (Head & Shoulders), and tar (Neutrogena T/Gel) ● Selenium sulphide, topical corticosteroids (for short periods)Acne Rosacea Recognition Who? Adults 30-50 years. More common in females. How? Chronic inflammatory skin condition, primarily of the face. Aetiology unknown. Diagnosis ● Redness, flushing and telangiectasia - can develop into papules and pustules ● Affects nose, cheeks and forehead ● Rhinophyma ● Blepharitis ● Exacerbated by sunlight Management ● Daily sunscreen ● Predominant erythema / flushing - Topical brimonidine (alpha adrenergic agonist temporarily reduces redness) ● Mild-to-moderate papules / pustules - Topical ivermectin ● Moderate-to-severe papules / pustules - Topical ivermectin + doxycycline ● Can refer to derm for laser therapy if not improved with aboveErythema Nodosum Recognition Who? More common in women aged 25-40 years How? Inflammation of subcutaneous fat. Caused by infection (strep, TB, brucellosis), Systemic disease (sarcoid, IBD, Behcet’s), malignancy/lymphoma, drugs (penicillins, sulphomides, COCP), pregnancy Diagnosis ● Tender, erythematous, nodular lesions, typically over the shins ● Resolves within 6 weeks, lesions heal without scarring. Management normally supportive. Management ● Pain management - Rest, Colchicine, NSAIDS, venous compression therapy ● Systemic corticosteroidsDermatitis Herpetiformis Recognition Who? Patients with coeliac disease / gluten sensitivity How? Autoimmune blistering skin disorder. Deposition of IgA in the dermis Diagnosis ● Intensely itchy vesicular skin lesions on extensor surfaces ● Direct immunofluerescence shows deposition of IgA in a granular pattern in the upper dermis Management ● Gluten-free diet ● Dapsone (sulphonamide antibiotic)Bullous Pemphigoid Recognition Who? Peak incidence 70+ years How? Presence of autoantibodies targeting two hemidesmosomal proteins BP180 and BP230 Diagnosis ● Itchy, tense blisters, typically around flexures. Mouth usually spared. ● Skin biopsy - Immunoflourescence shows IgG and C3 at the dermoepidermal junction Management Refer to dermatology for biopsy Oral corticosteroids +/- steroid-sparing immunosuppressive agents e.g. azathioprine / mycophenalate mofetil Topical corticosteroids in mild cases / as adjuvant therapy Blisters usually heal without scarringPemphigus Vulgaris Recognition Who? 50-60 years How? Autoantibodies that target desmoglein proteins, found in the desmosomes (essential in maintaining integrity of skin and mucous membranes) Diagnosis ● Erythematous lesions that transform over time into flaccid blisters, often Nikolsky positive. Can appear anywhere on the body. ● Oral mucosa affected in nearly all cases - painful oral erosions or ulcerations. Other mucosa e.g. nasal, conjunctival, oesophageal, genital can also be involved Management ● Systemic corticosteroids ● Immunosuppressive therapies e.g Azathioptine / Mycophenopate mofetil ● Topical steroids / emollients ● Nutritional supplementation due to painful swallowing Complications Commonly get secondary bacterial infections e.g. cellulitis, impetigo, sepsisErythema Multiforme Recognition Who? Young adults 20-40. Some genetic predisposition. How? Infection - (90% cases) Most commonly HSV-1. Drugs (NSAIDs, sulfonamides, antiepileptics, antibiotics ). Exposures (poison ivy). Systemic disease (IBD, Behcet). Idiopathic. Cytotoxic T-cells inciting apoptosis of keratinocytes. Diagnosis ● Major (mucosal involvement ) vs Minor (no mucosal involvement) ● Raised, papular target lesions in acral distribution (face & extremities) ● Constitutional sx / ocular involvement / urethritis / blister formation uncommon (patient clinically well) Management ● Symptom management (analgesic oral washes, antihistamines, topical steroids) ● Treat the cause / cease medication ● In severe mucosal disease may need hospitalisation for support of oral intake +/- systemic steroidsDermatological EmergenciesStephen Johnson Syndrome / TEN Recognition Who? More common in elderly populations How? Cytotoxic lymphocyte responses against altered keratinocytes via direct cytotoxicity or soluble mediators. More commonly drug or drug/infection combination. Common drug causes - phenytoin, sulphonamides (septrin / co-trimoxazole), allopurinol, penicillins, carbamazepine, NSAIDs Diagnosis ● SJS <10% skin involvement ● TEN > 30% skin involvement ● Flat, macular, ill-defined borders that can progress to vesicles followed by skin sloughing (Nikolsky sign) ● Constitutional sx / ocular involvement / urethritis / blister formation common (patient is clinically unwell) Management ● Stop precipitating factor ● Supportive care (replace volume loss and electrolyte derangement) - often on ITU ● IV Immunoglobulins, immunosuppressive agents e.g. ciclosporin / cyclophosphamide, plasmapheresisErythroderma Recognition Who? M>F (3:1). Pre-existing skin disease / systemic condition associated with erythroderma. How? Drug eruption. Atopic dermatitis, psoriasis, Sezary syndrome (cutaneois T-cell lymphoma), Graft vs Host disease, HIV Diagnosis ● Widespread reddening of the skin due to inflammatory skin disease. Associated with exfoliation (also known as exfoliative dermatitis) ● Affects 90% or more of the skin surface. ● Heat loss leads to hypothermia, fluid loss leads to electrolyte abnormalities and dehydration, secondary skin infection, hypoalbuninaemia from protein loss and increased metabolic rate. ● Discontinue unnecessary medications Management ● Monitor fluid balance and body temperature ● Maintain skin moisture with wet wraps, other types of wet dressings, emollients and mild topical steroids. ● Antibiotics for bacterial infection ● AntihistaminesDermatological CancersBasal Cell Carcinoma Recognition Who? Most prevalent in elderly males How? UV exposure, immunosuppression Diagnosis ● Nodular - Pearly nodule with rolled edge + telangiectasia ● Superficial - Scaly red plaques with smooth raised edges. ● Lesions are on sun-exposed sites ● Slow growth and local invasion - metastasis very rare ● Risk factors - Sun exposure, repeated sunburn, previous skin cancer Management Excision often management of choice Other options - Cryotherapy - Curettage - Radiotherapy - Photodynamic therapy Topical imiquimoid or fluorouracilActinic Keratosis Recognition Who? Fair-skinned, elderly population How? Dysplastic epidermal lesions as a result of chronic UV radiation exposure. Diagnosis ● Small, crusty or scaly lesions on sun-exposed areas of the skin ● Pink, red, brown or skin-coloured ● Histology shows atypical keratinocytes in lower ⅓ epidermis ● Sun protection Management ● Fluorouracil cream - causes redness and inflammation that might need to be managed with topical hydrocortisone ● Topical diclofenac ● Topical imiquimod ● Cryotherapy ● Curettage and cauterySquamous Cell Carcinoma Recognition Who? Most common in elderly males How? >90% cases due to numerous DNA mutations in multiple somatic genes e.g. mutations in p53 suppressor gene caused by exposure to UV exposure Diagnosis ● Enlarging, scaly or crusted lumps, usually arising within pre-existing actinic keratosis or intraepidermal carcinoma. On sun-exposed sites. Grow over weeks/months. Can ulcerate. Can be painful. ● Metastases rare but occur in 2-5% cases ● Histology shows nests of squamous epithelial cells arising from the epidermis and extending into the dermis ● Excision with a 3-10mm margin of normal tissue around visible tumour. May need flap / skin Management graft ● Shave / curettage / electrocautery for low-risk tumours on trunk and limbs ● Aggressive cryotherapy for small, low risk tumour ● Mohs micrographic surgery for large facial lesions with indistinct margins / recurrent tumours / cosmetically important sites ● Radiotherapy if inoperable / patient unsuitable for surgery / adjuvant.Keratoacanthoma Recognition Who? Fair-skinned older males with history of chronic sun exposure How? Arises from the infundibulum of hair follicle, specific pathogenetic mechanisms unclear. Diagnosis ● Solitary, dome-shaped nodule with central keratin-filled crater, predominantly in sun-exposed sites Management ● Spontaneous remission within 3 months, often leaves scar ● Often urgently excised as difficult to differentiate from SCCMalignant Melanoma Recognition Who? Childhood (rare), Early-onset (F>M, lower extremity, intermittent sun exposure), Late-onset (M>F, head and neck, accumulated sun exposure) How? Uncontrolled proliferation of melanocytic stem cells that have mutated. Acquired ‘sporadic’ mutations more common (UV exposure). Germline ‘inherited’ mutations passed down from parents. Diagnosis ● Superficial melanoma (55-60% of all melanomas) Breslow thickness - ○ Asymmetry of shape and colour measurement (in mm) ○ Border irregularity, including smudgy or ill-defined margin ○ Colour variation and change from the surface of the ○ Different (formerly diameter) skin to the deepest ○ Evolving (enlarging, changing) component of the ● Nodular melanoma (10-15% of all melanomas) melanoma Deeper thickness = ○ Elevated worse prognosis ○ Firm to touch ○ Growing Management ● Wide local excision ● Systemic therapy - biologics / immune-modulating therapy ● Radiation therapy Thank you! Your feedback is greatly appreciated!