Dermamtology - Classroom Notes

DERMATOLOGY Examination of the skin  List common skin signs & their significance Auspitz sign Nail pitting Hutchinson’s sign Nickolsky sign Wickham striae Dennie Morgan Hertov’s sign Onycholysis  pinpoint bleeding when scale is scraped away = Psoriasis discrete 1mm circular depressions (more on fingers) = Psoriasis malignant melanoma under nail bed confirmed by flat irregular pigmented patch on adjacent skin firm sliding pressure  erosions as the dermis & epidermis separate +ve in pemphigus vulgaris, -ve in toxic epidermal necrolysis fine light lines on red papules & plaques (highlight with emollient cream) +ve = lichen planus 2 additional creases in upper eyelid – present in 60% of atopic eczema thinning of the outer 1/3 of eyebrow – 40% of atopic eczema separation of the nail plate from the bed In psoriasis, trauma, chemical exposure & hypothyroidism (ring finger) Examine and describe a cutaneous eruption using dermatological terms correctly Eruption Lesion Pruritus Erythematous Macule Papule Plaque Nodule Scale Crust Wheal Vesicle Pustule Bulla Erosion Ulcer Excoriations Lichenification Rash Any single small area of skin disease Sensation of itching Red Flat, non-palpable area of colour change Small palpable mass (<0.5cm) Flat topped palpable lesion A papule enlarged to >0.5cm Visible white loosening of the outermost skin layer Golden deposit on the surface due to dried plasma Smooth surfaced dermal swelling Small (<0.5cm) papules filled with clear fluid A visible accumulation of pus A blister >0.5cm Partial loss of the surface epithelium, heals without scar Complete loss of surface epithelium, healing  scar Scratch marks Thickening of the skin due to chronic scratching/rubbing Bacterial Infections  Understand what commensal bacteria are. Common skin commensals are Staphylococcus epidermidis Pseudomonas Mycobacteria Propionibacterium (cause acne) Corynebacteri Pseudomonas Aerobe – common in ano/genital/axillae/ears/toe webs Can cause green discolouration (produces pyocyanin (blue/green) and pyoverdin (green/yellow)) Only pathogenic in damaged skin – DONT treat in asymptomatic wounds Can  2o colonisation of ulcers/burns, infection of toe webs or Gr-ve folliculitis (Jacuzzi dermatitis) Rx Topical – flamazine (silver sulphasalazine) or 1% acetic acid soaks Oral – ciprofloxacin Mycobacterium Cutaneous TB (lupus vulgaris) Well demarcated, isolated red/brown plaque Rx – standard TB therapy Tubercuoloid leprosy Isolated hypopigment,  aesthesia & thickened peripheral nerve Due to good host immune response Lepromatous leprosy Widespread - “leonine facies”, thick skin, granulomatous lesions & collapsed nasal septum Due to poor immune response Rx – standard antileprosy Mycobacterium Marinum (fish tank granuloma) Nodule on hand  spreads along lymphatics Rx – minocycline / doxycycline 3 months Spirochaetes Treponema pallidum (syphilis) 1o – asymptomatic, non painful, genital ulcer 2o – asymptomatic erythematous maculo-papular rash on palms & soles Rx – benzylpenicillin IV 14 days if +ve VRDL / TPA test Lyme disease (borrelia burgdorferi) Transmitted by tick bites from woodland animals Annular erythematous rash which migrates through skin F.b. malaise, arthritis, myocarditis, pericarditis, conduction defects, neurological problems Rx – oral doxycycline (100mg bd) for 3 weeks Cornebacterium Eythrasma – overgrowth  red/brown patches (coral pink fluorescence under woods light) Can also cause keratolysis Rx Topical – miconazole cream Oral – erythromycon  Staph Aureus (coag +ve) Should always be considered pathogenic but carriage only important if symptomatic Causes disease by direct invasion of dermis/follicles or by toxin production Ix Skin swabs often +ve Blood cultures only if systemic symptoms / severe sepsis Rx To clear carriage (only temporary protection) Intranasal mupirocin (daily for 5 days) Oral rifampicin (600mg o.d. 7-10 days) Low dose oral clindamycin (150mg o.d. for 3 months) To treat infection Topical mupirocin (bactroban), fusidic acid Oral flucloxacillin (7-14 days) / Erythromycin (10-14 days) IV flucloxacillin 500-1000mg qds 1o staph infections Impetigo  Most common in young children (often on mouth, nose, lips)  Superficial contagoious pyogenic infection  Signs – isolated lesions with yellow crusts, can be regional lymphadenopathy & bullae (if epidermolytic toxin)  Rx – topical mupirocin (some effect), oral fluclox (7-10 days)  Course – rapid resolution within few days of Abx (3-6 weeks without)  Complications – only if streptococcal (scarlet fever, urticaria, erythema multiforme, post-strep glomerulonephritis Ecthyma  Chronic infection with adherant crust & underlying ulceration  Presents as crusted lesion that wont heal  Common on lower leg, buttocks, thighs, face  Can scar  Rx – Oral erthyromycin (14 days) / Fluclox (500mg qds 14 days) / clindamycin  Course – rapid reolution with Abx Folliculitis  Infection of the superficial follicle  small pustules around hair heal w/o scarring  Usually S.Aureus (also pseudomonas, Gr-ve, oils, tar)  Rx – swab + oral flucolx for 2 weeks, chlorhexidine washes may help  Pseudofolliculitis  Apparent folliculitis due to entrapment of hair  foreign body reaction  Can  2o colonisation with staphs  Rx – stop shaving, emollient steroids & Abx, chlorhexidine & erythromycin may help Furunculosis  Acute necrotic infection of a single follicle by S.Aureus  Rx – 14days oral fluclox, mupirocin to clear nasal carriage Carbuncle  Deep infection of multiple follicles with S.Aureus  Most commonly middle age / elderly men, DM, malnutrition, heart failure, drug use, prolonged steroid treatment  Deep seated abscess with multiple drainage sites, fever, pain & tenderness  Common on back of neck, buttocks, thighs and shoulders  Rx – oral fluclox (14 days), exclude DM Sycosis barbae (barber’s rash)  Infection of the facial hair follicles  Usually due to poor hygiene during shaving (dirty razor/shaving brush or towels)  Can spread to adjacent hair follicles  Treat with antibiotics Cellulitis – see streps 2o staph infections infected woulds / ulcers infected atopic eczema Due to toxins Staph Scalded Skin Syndrome (SSSS)  Epidermoltic toxins (ET-A & ET-B)  Usually in infants  Unwell, fever, irritable, widespread erythema  blisters  Rx – supportive + IV fluclox/erthromycin Toxic Shock syndrome (TSS)  TSS1 (80-90%) & TSS2  Unwell. Fever, D&V  circulatory collapse, macular erythema (1-3days), desquamation of hands (10-21 days later), mucosa oedema & ulceration  Rx – if suspected septic shock + rash assume TSS  blood cultures & check with lab, Iv fluclox/erythromycin + ITU support Staphylococcal scarlatina Erythrogenic toxin – mild/initial stage of TSS  Streptococcus (mostly group A) ALWAYS consider pathogenic Ix Skin swabs often +ve  ASO titre (>200u/ml 5-7 days post infection)  Dnase B  NADase Rx Topical – not recommended. Clorhexdine should kill organisms Oral – amoxycillin (500-1000mg qds), penicillin 500mg qds, erythromycin 500mg qds IV – benzylpenicillin 1000-2000mg qds 1o infection Cellulitis, perianal cellulites & necrotising facitis  Can be acute / subacute / chronic infection of loose connective tissue  Most commonly Grp A strep (can also be staph)  Signs – fever, malaise & systemic upset with erythematous, hot, painful, tender limb  Check for – ulcers, tinea pedis, trauma & insect bites  If untreated – blistering & skin necrosis  If reaches deep dermis – necrotising facitis (needs IV Abx & debridement)  Ix – swabs of blisters / entry sites, WCC, ASO, blood culture (but often –ve)  Rx – IV benzylpenicillin (1.2g qds) / Fluclox (1g qds) min 10-14 days  Complications – death (if septicaemia, myocarditis, renal failure), local (skin necorosis, necrotising facitis, abscess, permanent lymphoedema  Prognosis – give low dose pencillin V prophylaxis to prevent recurrence Eryspelas  Usually Grp A strep, can be H.Influezae in children  A form of cellulites but in dermis & upper subcut layers  Common on face, infection from nose/throat/sinus/conjunctivae  Signs – well defined, raised erythema with pain & tenderness + fever & malaise  Ix – nose/throat/conjunctivae if symptoms, FBC & Cultures, look for entry site   Rx – high dose oral/Iv (benpen 1.2g iv qds min 10-14 days), cover H.Influenzae in young Complications – chronic facial lymphoedema & recurrent infections, orbital cellulites can  meningitis & death so MUST be admitted for IV Abx Prognosis – recurrence if predisposition – give 250mg pen V prophylaxis  2o infection atopic excema leg ulcers Due to group A toxins Scarlet fever  2-5d incubation  fever, tonsillitis, painful cervical lymphadenopathy, erythematous rash from day 2 (trunk  legs)  desquamation 7-10 days later  Hypersensitivity  myocarditis, arthritis, osteomyelitis, RF & glomerulonephritis  Ix – FBC (WCC), throat swab,  ASO  Rx – 10-14 day BenzylPenicillin + support Toxic shock like syndrome  Similar to TSS  Ix - +ve blood cultures & swabs  Rx – high dose penicillin & IV gammaglobulin Hypersensitivity to group A antigens Erythema nodosum an acute, nodular, erythematous eruption that usually is limited to the extensor aspects of the lower legs. Assoc with fever, malaise & arthralgia Erythema multiforme Vasculitis Glomerulonephritis Viral Infections  Human papilloma virus Infection of basal keratinocytes  induces proliferation Plantar (1, 2, 4, 57) Soles of feet  discomfort through pressure, more resistant to treatment Common (2) Elevated papules seen on the back of the hand of children, also on face Plane (3) Flat topped, on face / back of hands Filiform Hyperkeratotic papillomatous warts on face, neck, eyelids & skin folds Poor response to topical pains, Rx with electrocautery / curettage Mosaic Confluent crops on hands/feet, very resistant to all treatments Anogenital (6, 11) Predispose to cervical neoplasia, all females should have a smear Prognosis & Rx Most self resolve in months – yrs Topical paints (salicylic / lactic acid = keratolytic) As effective as cryotherapy Daily for 8-12 weeks after bath Cryotherapy Liquid nitrogen (-196oC) – double freeze & thaw cycle (5-30 sec) with 1mm border Very painful & causes blistering Curettage & cautery With disposable curette & electro / silver nitrate for haemostasis LA required Send histology as differential is squamous / melanoma NEVER excise warts as liable to recur in scar Formalin & Podophylin 4% formalin / 10-20% podophyline if no other response  Pox virus Molluscum contagiosum (molluscipox virus I & II) Common in young children / infants esp if atopic dermatitis Crops of small umbilicated papules on trunk with crusting & erythema around Can get 2o infection Self limiting (4-18 months) & contagious – but requires no Rx If Rx for cosmetic / practicality – cryotheapy / podophyline ORF (parapox virus) Farmers, vets, those in contact with animals 5-6 day incubation 2-3cm red/purple papule on fingers (often blisters), can get 2o infection Prognosis – self healing 2-3 weeks, oral fluclox in 2o infection  Herpes simplex I = cold sores, II = anogenital Persists in DRG  asymptomatic shedding & 2o infections possible Cold Sores 1o incubation 5 days On vermillion border (pain & tingling with vesicular eruption) Lymphadenopathy common Rx – topical acyclovir Genital (STD) 1st attack most severe (pain, discomfort, vesicles) Recurrence common Rx – oral acyclovir min 5 days Both types Recurrence common if trauma, UV exposure, URTI, stress, surgery or dermabrasion Complications Gingivomastitis – common in 1-5 yrs, pain, fever, vesicles on mucous membranes Keratoconjunctivitis – superficial corneal ulcer, risk of scarring Bells Palsy – CN VII if nerve affected Eczema herpeticum – HSV + severe atopic eczema  multiple punches out erosions. Admit & system Rx required Erythema multiforme Herpetic Whitlow – herpes in abrasions on skin Disseminating – in immunocompromised  Herpes zoster. Chicken Pox Droplet spread, common in children 14-17 day incubation Infective 2 days before & 5 days after eruption Headache, fever, malaise for 23-48 hrs f.b. vesicles on trunk, face and scalp lasting 10-14 days with crusting & scarring Complications Pregnancy – in 1st 20 weeks – 2% risk neuro, eye & limb defects Pneumonia Hepatitis Encephalitis Disseminated infections Rx – only in adults, immunocompromised & those on steroids – give oral acyclovir 5-7d Shingles Localised reactivation in DRG & schwann cells Pain & tingling for 24-48 hrs  dematomal eruption (infectious) 53% thoracic 20% cervical 15% ophthalmic branch of Trigeminal 11% lumbosacral May disseminate in immunocompromised  haemorrhagic rash Mostly heals without scarring Complications Post herpetic neuralgia (pain >3months) = 30% of adults > 40yrs 2o infection - common – risks of septicaemia & skin necrosis Motor nerve palsy Facial nerve (ramsay hunt syndrome) – ear pain & vesicles in ear Vestibulocochlear nerve – sensorineural deafness, dizzy & vertigo Occular motor palsy Eye complications Uvetis, keratitis and conjunctivitis Encephalitis / meningoencephalits Treatment If within 72 hrs of pain / tingling  oral acyclovir 5 days (800mg od)  Hand, foot and mouth Coxsackie virus (A16, A5, A10) Most commonly infants / young children, can be epidemic in nursery Erythematous vesicles on mouth, palms & soles but usually well Lesions last 5-7 days, self limiting, no Rx required  Pityriasis Rosea (? Due to herpes viruses) Young adults Herald patch (in 80%)– oval erythematos plaque (2-5cm) with scaling  general eruption or erythematous macues on trunk 5-15 days later (asymptomatic/mildly itch) Macules have outer edge or collarette scale Mostly resolve spontaneously, may need mild topical steroid / UVB Fungi & Infestations  Dermatophyte infections Tinea Capitis (scalp) Often in children, transmitted by close contact, sharing brushes etc Commonly M.canis, T.tonsurans Invades hair shaft Signs – alopeci, broken hairs, scale, pustules, lymphadenopathy kerion (boggy purulent plaque due to excess host response Differentials – seborrheoic dermatitis, discoid lupus erythematosus Tine Corporis (body) Usually on non-hairy (glabrous) skin Commonly T.rubrum, M.canis, T.verrucosum Signs – scaly plaque with red border & central healing, spreads centrifugally, itchy Differentials – psoriasis, nummular dermatitis, pityriasis versicolour, pityriasis rosea Tinea Cruris (groin) Commonly T.rubrum Differentials – candidiasis, psoriasis, atopic dermatitis, seborrhoeic dermatitis, erythrasma Tinea Pedis (athletes foot) Commonly T.rubrum, T.mentagrophytes, E.floccosum Complications – 2o infection, cellulites Tinea unguium (nails) Causes similar to pedis Signs – yellow, thickened nails, onycholysis, hyperkeratosis of nail bed Differentials – psoriasis, trauma,moulds Investigations (for all tinea) Woods light (UV>365nm)  green fluorescence Skin scrapings for mycology Nail clippings and subungual debris Hair pluckings / brushed scales Treatments Topical if uncomplicated Azoles (ketoconazole (beware – risk of hepatitis & androgen inhibition), fluconazole) Metabolised by CYP P450 3A Increase effects of coumarins, ciclosporin & phenytoin Decreased effectiveness if on rifampicin Allyamines (terbinafine – 250mg /day systemic, or use as paint) Adverse effects rare Systemic Capitis – griseofulvin 10mg/kg for 6-8 weeks SE – headaches, nausea, photosensitive rash Interacts with phenobarbitone & coumarins Unguium – terinafine 250mg 6 weeks (fingers) or 12 weeks (toes) Or if widespread or immunocompromised patient  Candidiasis Most commonly candida albicans  risk if v.young/old, ill, DM, steroids, Abx or immunosupressed Oral – white curd-like plaque, glossitis, denture stomatitis, angular chelitis Flexural – moist erythema, satellite pustules & erosions Vulvovaginitis / Balanitis – erythema & white discharge Paronichia – swollen red nailfold, common if hands frequently in water Onychomycosis – not common Treatment polyenes (nystatin, amphoteracin) imdiazoles (clotimazole, fluconazole) NOT terbinafine  Know the types of skin conditions that have been attributed to pityrosporum ovale and able to suggest appropriate treatments for these conditions. Pityriasis versicolour Caused by pityrosporum (can also cause seborrhoiec dermatitis and folliculitis Presentation – hyper/hypopigmented macules with fine scales, usually on trunk Treatment – topical antifungals, selenium sulphide shampoo, oral itraconazole (200mg 7d) Repigmentation can take months Recurrence is common Seborrhoeic dermatitis On face, scalp, ears and eyebrows Discrete erythematous and may develop a yellow crust Due to over activity of sebaceous glands Treat with topical steroids Seborrhoeic dermatitis Skin Infestations  Scabies Caused by the scabies louse (sarcoptes scabiei – an arachnida) Signs – itching with burrows (fingers, soles, genitals) and erythematous papules (axillae, groin, genitals, abdo) Rx – topical permethrin (8-12 hrs), malathion (24hrs & repeat 7 days later) & treat contacts Crusted scabies – large nos of mites bec decreased scratching Rx – topical scabicide & ivermethacin  Lice Pediculosis capitis (head lice) Common Itching & popular eruption on scalp and neck, live lice / nymphs if active infection Rx – malathion, permethrin or carbaryl, leave on 12 hrs & repeat 10 days later Fine comb and conditioner also help Pediculosis humanus (body lice) Uncommon in developed world – vector of typhus Pruritus due to louse salivary antigens Rx – wash & dry clothes at high temp, malathion powder, permethrin on clothes & bedding Pthirus pubis (pubic louse) Transmitted by close contact May also affect eyebrows & eye lashes Rx – malthion, permethrin, petrolatum ointment on eyelashes  Fleas Host animals – cats (ctenocephalides felis) and dogs (ctenocephalides canis) Presentation – popular urticaria in clusters / lines, esp on ankles Rx – treat pets, bedding & soft furnishing Acne A chronic inflammatory disease of the pilosebaceous units, characterised by comedomes 85% of children between 12-24 99% on face, 60% on back, 15% on chest  To name the 3 processes involved in the pathophysiology of acne. Comedogenesis – accumulation of “stuff” in the pilosebaceous duct Seborrhoea - increased sebum trying to expel the comedomes Propionobacterium acnes – normal commensal, lives in sebum in duct, causes inflammation  Inflammation – reaction to P.acnes, epidermal barrier function changes, ductal cells secrete cytokines Skin Signs Greasy skin – due to seborrhoea Non-inflammatory Open comedomes – black heads – distended pilosebaceous unit. Opening is impacted with keratin & lipid Closed comedomes – white heads – distended units with no visible opening to the skin, more likely to progress to inflammatory Inflammatory Papules & pustules – superficial units Nodules – can  scarring & tethering  To list 3 different types of acne and explain why differentiating between them are important. Differentials Acne rosacea – women 35-50 Erythema, papules, pustules & telangectasia on nose, cheeks & chin. NO comedomes Increase with sunshine, alcohol & hot drinks (flushing) If severe  gland hypertrophy & sort tissue overgrowth = rhinophyma Rx – low dose oxytetracycline / erythromycin / topical metronidazole. Avoid steroids Perioral dermatitis Eryethamtous papules & pustules on a scaling base, symmetrical around mouth In women 20-35 (due to makeup) Rx – oral tetracycline 250-500mg bd for 8-12 weeks Nodular Acne – severe, deep papules & nodules, scarring common, can be assoc with hydradenitis of axillae & groin Ance Fulimans – complex, nodular acne with systemic fever, malaise & joint pains. Due to immune complex in response to P.acnes Acne Excoriee – clinical signs of scratching, picking and squeezing, usually young girls, underlying acne is mild, may need psychotherapy Occupational Acne – cutting oils, crude tar, in areas where soaked clothing contacts skin. Chloracne – large numbers of white heads due to chlorinated hydrocarbons Tropical Acne – young Caucasians in hot climatee Infantile Acne – 3-12 months, mainly males, monomorphic, low grade inflammation, lasts 2-4 weeks & resolves spontaneously Drug reaction – isoniazid, phenytoin, androgens, anabolic steroids Steroid – monomorphic lesions on trunk in patients on systemic steroids Endocrine – Cushings, PCOS Folliculitis DLE  Know the indication and potential side effects of the following topical treatments: - Benzoyl peroxide No resistance Some anti-inflammatory, decreases cornification, decreases P.Acnes proliferation - - Can  irritation & bleaching Can be used with topical Abx to increase efficacy Antibiotics Erythromycin / clinamycin Well tolerated but can  resistance if used alone Retinoids Expulsion of mature comedomes & inhibits further formation, anti-inflammatory & enhances other agents Use is limited by teratogenicity, erythema & irritation with topical, some photosensitivity e.g. Adaptalene – less irritant and anti inflammatory, decreases cornification & P.acnes, can cause skin irritation, avoid in preganacy & breast feeding  Know the indication for and be able to discuss the risk and benefit of the following systemic therapies: - Tetracycline and other antibiotics If moderate – severe / failure of topical treatments / scarring / chest or back involvement Tetracycline / Oxytetracycline – 500mg bd. Must be taken ½ hr b4 food. Not for use in under 12s & pregnant / breast feeding due to teeth & bone deposition, can ppt renal failure. MUST be stopped prior to starting oral retinoids Doxycycline – 100mg bd. Can cause oesophagitis, can take with food, no RF Erythromycin - 500mg bd. Some resistance, GI side effects, Safe in pregnancy Trimethoprim – 300mg bd. Blood disorder/skin rash, not in pregnancy Minocycline – 50mg bd. Hyperpigmentation, vestibular disturbance, hypersensitivity, lupus like syndrome, renal & hepatotoxic, skin & teeth staining To reduce resistance Use BPO 1st line, use combination therapy, avoid using multiple Abx simultaneously, limit Abx use, maintain with BPO / retinoid, retreat with same Abx - Cyproterone acetate - anti androgen in diannette Anti androgen properties so reduces sebum over production Contraindicated in pregnancy, smoking, obesity, HT, hx of thrombosis (VTE risk) SE – headache, weight gain, mood change - Isotretinoin (roaccutane) 0.5-1.0 mg/kg for 4-6 month minimum Very effective, but 20-30% relapse on stopping treatment Decreases comedogenesis, sebaceous gland size & production of P.acnes  antiinflammatory Must be used under dematologist supervision Indicated if – severe, scarring, resistant, rapid releases, psychological / psych disease Contraindicated in pregnancy & breast feeding – must use 2 methods for month before & 3 months after + monthly pregnancy test Toxicity mucocutaneous – dry skin, itching, dermatitis, dry mucosa, epistaxis, skin fragility, hair loss, hair thinning, dry eye (problem with contact lens), photosensitivity increased lipids, deranged LFTs Arthralgia, myalgia, disruption of night vision Initial flare up of acne Some links with depression & suicide  Be able to describe 2 treatment options for scarring. Scars arise from mod-sever acne – can be ice pick or keloid Treat by excision, laser resurfacing (once acne cured) or intralesional steroids for keloids Eczema Vasodilatation  erythema & heat Exudate of plasma & inflammatory cells  oedema Release of inflammatory mediators  pain & itch  Develop a rational method for classifying eczema Acute Dermal vessels v/d  erythema Epidermal oedema  separation of keratinocytes (spongiosis) Inflammatory cells invade dermis/epidermis  oedema Appearance is modified by scratching Sub acute Less spongiosis  less vesicles Epidermal cell malfunction Thickening (acanthosis) Increased keratin (hyper/parakeratosis)  scaling Chronic Marked acanthosis, hyper & parakeratosis  thickened rough “lichenification” with dry, scaly & fissures Persistent vasodilatation & inflammatory cells  erythema  Name the main types of endogenous and exogenous eczema Endogenous Atopic Seborrheic Asteatotic Gravitational Discoid Exogenous Irritant – most people’s skin would respond if in contact for long enough Infective Allergic contact – due to a hypersensitivity – normal skin wouldn’t response  List the main side effects of topical steroids and the measures needed to safeguard against these Tachyphylaxis Tolerance to the vasoconstrictive action of topical steroids  capillaries do not constrict With high potency can occur within 4 days, Takes 4 days to return after stopping therapy. Steroid rosacea In fair-skinned people who already have rosacea Occurs on reducing from prolonged steroid use. Skin Atrophy Thinning of the epidermis and changes in the connective tissue of the dermis. The skin becomes lax, wrinkled, and shiny, visible telangiectasias, hypopigmentation, and prominence of underlying veins. Reversible in most cases but may take months to recover Striae - Stretch Marks In areas where skin touches skin such as the groin and armpits Permanent and irreversible, may be itchy (requiring low dose steroid to relieve. Alteration of Infection Alters the immune response and so the appearance of fungal infections  tinea incognito. Topical Steroid Allergy To a component of the topical steroid base. High risk in those with multiple prescriptions Glaucoma Isolated cases reports of people developing glaucoma after long-term use of topical steroids around the eyes.  Know how to apply topical treatments correctly and familiar with the finger tips unit Should be applied in the direction of the hair 1 finger tip unit is the amount in a single line along the distal phalange of the index finger 1 finger tip unit should be sufficient for one hand area – body plans are available to show how many finger tip units each area requires  Describe the distribution and morphology of atopic, discoid, varicose, pompholyx and seborrhoeic eczema Atopic 15-20% prevalence, improves with age Infants – face & exposed surfaces Children – flexures Increased IgE antibodies, skin prick tests often +ve Diagnosis Itchy skin for the last 12 months + 3 of the following Personal / family history of atopy Visible flexural dermatitis (cheeks < 10yrs) Dry skin in last yr Hx of flexural involvement Early onset (<2yrs) Treatment Education, advise carers, keep nails short (reduce excoriation) Avoid allergens & irritants Use soap substitute Creams (aq), ointments (soft paraffin) bath oils (oilatum) Steroids – v/c and inactivate inflammatory mediators Mild – 1% hydrocortisone bd (sparingly) Mod – hydrocortisone butyrate Potent – betamethasone bd (4-7 days only) Occlusive bandaging (with tar, zinc paste or wet wraps) Antihistamines (if poor sleep) Antibiotics (if bright red with pustules & exudates) – fluclox / erythromycin Topical tacroliums – similar to potent steroid but don’t think skin If all else fails Oral steroids – short term to bring under control UV light Cyclosporin A (check BP, resp function, increased malignancy risk) ? Diet, ? Chinese herbs? Psychological intervention? Complications Of bacteria – staph / strep Viral – molluscum, HSV, Warts, herpeticum Of Treatment – skin thinning, striae, adrenal suppression Eczema herpeticum – virus colonisied eczematous & normal skin  painful puctuate erosions  Rx with oral / IV acyclovir = emergency Seborrheoic eczema Abnormal response to commensal yeast (pityrosporum ovale) Adults - Most common in young men Features Affects areas rich in sebaceous glands (face, scalp, upper trunk) Erythema, scaling, dandruff Folliculitis and flexural variants Treatment Ketoconazole shampoo, imidazole +/- 1% hydrocortisone Often recurs Children First few weeks of life Features Moist shiny erythema in folds Scalp has yellow scales Treatment Emollients, 1% hydrocortisone, +/- antifungal, aq salicylic acid & olive oil for scalp Asteatotic Eczema (without fat) Common in elderly when skin fat is decreased Surface dries out  craquale (like crazy paving) Rx – topical steroids f.b. long term emollients, avoid excessive washing Graviational (static / varices) On lower legs, assoc with poor venous return Rx – emollients + mild-mod topical steroids, compression hosiery. NB – risk of ulceration if severe Discoid Caused by substances affecting skin integrity (chemical damage – alkalia, detergent, water) Most often on hands (hair dressers, nurses, young mums) Most common form of industrial dermatitis Atopic individuals are more susceptible Rx – avoid irritants, wear cotton gloves where possible, emollients & topical steroids Contact dermatitis (allergic) Idiosyncratic type IV hypersensitivity reaction to exogenous substance Usually occurs in industry – nickel is most common, look for distribution pattern, also seen with chromates (builders), epoxy (engineers), rubber (drs), can be a big problem in leg ulcer patients Ix - Patch testing  identify allergens Rx – avoid allergens, emollients, topical steroids Hand dermatitis May be endogenous, irritant or contact (often mixed) Women : men = 2:1 Morphology very variable but if unilateral think fungus Ix – patch testing Rx – v.difficult, often hard to avoid triggers, can  loss of employment Acute – KMnO4 soaks, emollients, topical steroids Chronic – avoid irritants if possible, emollients, steroids, retinoids, attention to hand care Psoriasis A common, genetic inflammatory and proliferative skin disease 1.5-3% prevalence, m=f (F onset 5-9yrs, M onset 15-19 yrs) Aetiology Predisposing - Genetic – 30% +ve family history (70% twin concordance) Aggravating - Environment – trauma, infection, endocrine, drugs (B-blockers, lithium, antimalarials, steroid withdrawal) psychogenic factors, alcohol, smoking Koebner phenomenon – new lesions occurring after local injury (scars, scratches) Pathology Thickened epidermis (16 x normal) Narrowed, elongated rete ridges Absent granular layer Subcorneal microabscesses Lymphocytic infiltrates Decreased cell transit time (28=normal, 3-4 days in psoriasis) Decreased cell cycle time (457=normal, 37.5 hrs in psoriasis) Aggravating factors In approximately 1/3 of people with psoriasis, an injury to the skin (for example a scrape, scratch or bad sunburn), can induce psoriasis in the area of the injury. This is called the “Koebner Phenomenon.” Stress Alcohol Smoking Infections (e.g. Streptococcal infections) Certain drugs. For example; antimalarials, lithium, beta-blockers, antiotensin-converting, enzyme inhibitors, non-steroidal, anti-inflammatory drugs, iodine, digoxin and clonidine, have also triggered or aggravated psoriasis in certain individuals. Plaque psoriasis (90%) Salmon pink, well demarcated, erythematous scaly plaques Losely adherant silvery / white scales Auspitz sign – pinpoint bleeding on scraping of scale Most common on extensor surfaces (elbows, knees, buttocks, knuckles) Guttate psoriasis Mainly on the trunk, scaling is not so prominent Children and adolescents Usually after strep throat infections Clears after 3 months, although often later progresses to plaque psoriasis Pustular psoriasis Generalised (left) Acute onset of sterile pustules on erythema, painful skin & malaise, fever, WCC Localised (right) Palmoplantar pustulosis, but no systemic symptoms Assoc with smoking, onsets later Erythrodermic psoriasis Intense generalised erythema & scaling MUST be admitted for monitoring Risk of hypothermia, high output cardiac failure, sepsis, dehydrated, protein loss Flexural psoriasis Due to friction & maceration Often no scale present Colonisation by yeast & bacteria Psoriatic arthropathy Oligoarticular involvement (knees, ankles, MCPs) Polyarticular – wrist, distal IP joints Spondyoarthropathy – spondylitis & sacroileitis Arthritis mutilians  Know the various topical treatment options and be able to discuss the risk and benefit of each treatment: - Coal tar Messy, limited OPD use, SE folliculitis, irritation - Dithranol Messy, can stain, causes irritation Inhibits keratinocyte proliferation - Only for plaque psoriasis - Vitamin D analogues Clean, so good for out patient use Stimulate differentiation Inhibit DNA synthesis & cell proliferation Calcipotriol binds to skin receptors Can  hypercalcaemia (limited to 100g / week) - Topical steroids Good for facial and flexural psoriasis  Know the various second line treatment options and be able to discuss the risk and benefit of each treatment: - Phototherapy PUVA (UVA & psoralens – photosensitising agent) SE – erythema, pruritus, nausea, long term increased skin cancer risk UVB – narrow band, fewer SE than UVA with similar efficacy Can use with tar / dianthrol / Vit D - Retinoid (actiretin) Vit A suppresses DNA synthesis & cell differentiation SE – teratogenic, hyperlipidaemia, hepatotoxic, dry skin, skeletal changes - Methotrexate Folic acid antagonist, binds to dihydrofolate reductase  inhibits AA synthesis Selectively affects rapidly proliferating cells SE – marrow suppression, liver fibrosis / cirrhosis, teratogenic, many interactions - Cyclosporin Suppression of T-lymphocytes & blocks lymphokine production SE – nephrotoxic, HT, carcinogenic, gum hypertrophy, hypertrichosis Leg Ulceration Venous 80% of leg ulcers are due to venous hypertension Pathology Valves in deep veins lose competency  increased pressure in small venules and capillaries  tissue oedema  hydrostatic pressure  decreased flow  impaired tissue oxygenation & poor wound healing Fibrin is extravasated in oedema fluid  cuff around vessels  further impaired oxygenation Inflammatory mediators (due to hypoxia and infection) released into skin & subcutaneous fat  further tissue damage Predisposing factors Venous disease (DVT, Varicose veins, thrombophlebitis) Childbirth Orthopaedic / abdominal surgery Features Normal foot pulses (unless concurrent arterial insufficiency) Varicose veins Brown discolouration (heamosiderin) Pitting oedema Ulcer – usually on lower 1/3 of leg, mostly medial 2o complications Infection Swab ulcers regularly Superficial (pseudomonal & anaerobes)  slough, exudates & odour, If S.aureus = pain & enlarging with slough. Rx topical antiseptics Cellultis – skin & subcut tissue. Pain, oedema, erythema, blistering, long term risk of lymphoedema with destruction of the lymphatics. Rx aggressive IV Abx until improvement, then oral Dermatitis Irritants – exudates, topical antiseptic Allergens – lanolin, Abx, Cream preservatives Should do a patch test Lymphoedema Due to lymph damage, immobility etc Flexion contractures Of foot due to pain & fibrosis  worsens immobility Treatment General – elevation, exercise, compression, nutrition, treat anaemia, social issues Topical – wash, debride, deslough, antiseptic, antibiotic, dressing & skin care Skin graft – pinch, punch or split skin grafts Systemic – Abx for cellulites, oxypentifyline, antiplatelet, antifibrinolytic, diuretics only if another comorbidity Arterial 5-10% of all ulcers Diagnosis Hx – smoking, rest pain, claudication, other ischaemic disease OE – decreased / absent pulses, decreased dopplers, cool limb, atrophic, hairless, poor capillary refill, painful, punched out Treatment Local – clean & debride, treat infection, stop smoking, graft if possible Surgical – embolectomy, endarterectomy, bypass, amputation Vasculitic Uncommon but may show systemic disease Diagnosis Multiple small painful ulcers on the legs & feet with areas of purple/black necrosis & purpura Histopathology shows vasculitis Aetiology Inflammatory – SLE, rheumatoid, polyarteritis nodosa, HSP, pyoderma gangrenosum Small vessel occlusion – septic emboli, cellular debris, hyperviscosity, Neoplastic Neuropathic Sensory neuropathy  decreased sensation  minor repeated trauma e.g. DM, leprosy, syphilis, paraplegia, motor neuropathy (decreased movement & perfusion) Diabetic Very common & multifactorial (small vessel disease, neuropathy & infection) Neoplastic Skin tumour  necrosis  non healing ulcer Benign and malignant melanocytic lesions  Know the different types of benign melanocytic naevi. Ephilides (macule = freckle) Increased melanin without increased melanocytes Well demarcated round/oval/irregular light pigmentation on sun exposed areas More common in blonde / ginger people, fade with age and fluctuate with IV exposure Uncountable Lentiginies (macules) Epidermal hyperplasia with increased melanin +/- increased basal melanocytes Solar lentigo Occur in adulthood in sun exposed areas Darken with UV but don’t fade Countable, darker and larger than ephilides Lentigo simplex (see pic) Occur in childhood, No relation to sun exposure May affect mucosa (lips, genitals) Increased melanocytes in basal layer Melanocytic naevi Melanocytes that fail to migrate / mature Congenital (see pic) 1% of poplulation small naevi (<1.5cm), larger than acquired slightly raised & will become more elevated as the child grows Bathing trunk naevi (>1.5cm) = 12% lifetime malignancy risk, excise + yrly checks Mongolian bluespot = melanocytes in the dermis, common in asians, benign Acquired Develops after birth, usually <25yrs Junctional – brown, macular, nests of melanocytes at dermoepidemal junction Compound (see photo) – warty lighter brown papules, some melanocytes in dermis Dermal – skin/light brown smooth dome shaped with melanocytes mainly in dermis Halo – undergoing regression (see picture) Blue – melanocytes in the dermis, in the extremities  List the risk factors for the development of malignant melanoma. 50% of melanomas arise from naevi (picture = dysplastic naevus) colour change / irregular colour irregular shape 1cm diameter itching Bleeding for no reason Risk factors Moles – have a risk of turning to melanoma Previous self/family history UV exposure Early (childhood) sun exposure & blistering sunburn Race – Caucasians are at high risk, very rare in afro/carribean Fair skin & hair colour– linked with race Immune deficiency – AIDS, transplant patients  Seborrhoiec keratosis (basal cell papillomas) Harmless growth on skin in elderly, often pigmented Age related – usually start to appear at 40yrs Not infectious and do not become malignant  Be familiar with the different sub-types of melanoma. In situ melanoma – Neoplastic melanocytes throughout the epidermis but not invasive Superficial spreading Common in young-middle age (legs in women, trunk in men) Macule with irregular border, may have had slow horizontal growth, later become nodular Nodular On any site of the body, usually in older people, poor prognosis Blue/black/red/amelanotic nodule, ulcerated, bleeding, developed rapidly Lentigo Maligna Melanoma Usually on the face of the elderly, arise within a lentigo maligna (Lentigo Maligna – Neoplastic melanocytes along the basal layer which may become invasive – see picture) Acral lentigionous melanoma Usally on palms/soles/nails (hutchinsons sign) Can occur in asian / afrocarribeans Higher incidence in over 20s (increases with age) Amelanotic melanoma Absent / minimal visible pigment, often detected late  Be able to discuss prognosis and management with patients. Management – excision 1cm margin for every 1mm depth invasion Prognosis (5 yr survival) Depends on breslow thickness (depth in mm from granular cell layer) In situ = 100% <1.5mm = 90% 1.5-3.0mm = 60% >3.0mm = 40%  Be able to give appropriate sun protection advice. Avoid being outside in the heat of the day (11-4) Wear minimum factor 30 sunscreen, reapply regularly esp after swimming Where possible cover up and wear a broad brimmed hat Non Melanoma Skin Cancers and benign skin tumours Most common Ca – 2-5% incidence Risk is cumulative with sun / UV exposure  Describe the clinical features of the following premalignant and malignant lesions: - Actinic (solar) keratoses Pre-malignant lesion for SCC Occur due to long term sun exposure, very common esp. in fair skin 80% on back of hands, forearms, head & neck Risks – increasing age, male, outdoor occupation/hobby Appearance – small single/multiple scaly erythematous/brown papules <1cm, may be rough,sore, itchy, pain, cosmetic problem Treatment 25% spontaneously disappear Cryotherapy – 95-100% cure rate 5FU – will show sub clinical AK  sore & unsightly Curettage & cautery – excellent cure rate & cosmetic result Excision – only if diagnosis in doubt Photodynamic therapy – can be painful, recurrence variable - Bowen’s Disease Asymptomatic, slow growing, usally solitary Welll demarcated, scaly erythematous plaque Commonly on legs, head & neck, women>men Differentials – psoriasis, discoid eczema, lichen simplex, AK, superficial BCC, SCC Treatment – 5FU, Cryo, Curettage, excision, radio, photodynamics - Basal cell carcinoma (including the different sub-types) 80% of non-melanoma skin cancer Generally slow growing, locally invasive, mets are very rare Mostly on sun exposed sites in Caucasians (mostly head and neck) Increase with increasing age, UV exposure, in males and fair skin Presentation Well defined erythematous, pearly nodule / plaque May be a central ulcer with a rolled edge & telangectasia May bleed, crust, separate and bleed again as a non healing sore Can behave as a rodent ulcer – eat through skin, muscle, bone and meninges Ix Biopsy to confirm Superficial Erythematous patch/plaque usually on trunk with fine scale & telangectasia May be ulcerated, show central fibrosis or have poorly defined border Differentials – nummular eczema, psoriasis, Bowens, tinea or mycosis Nodular Round/spherical/oval/dome papule/nodule With pearly, translucent appearance & soft-firm consistency Slow growth, may ulcerate / appear cystic Differentials – intrademal naevus, sebaceous hyperplasia Treatment Curettage & cautery – if small well defined BCC – 92-97% cure, 60% if recurrent Cryotherapy – excellent cosmetic result, 94-100% cure but blisters Surgical excision – 5mm margin  95% cure rate (bigger margin if >2cm) Mohs Micrographic surgery – more precise excision, costly, time consuming but 99% cure rate Radiotherapy – useful but provides no histology, 90% cure 5-flurouracil – for non critical sites & low risk, 5% cream  inflammatory response  destroyed but will leave a sore Photodynamic therapy – topical photosensitiser f.b. activating light  phototoxic reaction  kills tumour, only used in trials -  Squamous cell carcinoma 20% of NMSC Risks – ageing, recreational outdoor UV exposure, fair skin, ionising radiation, arsenic, smoking, immunocompromised Common on head, neck, hand dorsum, legs Can arise in areas of SLE, old scars, sinus tracts, chronic ulcers & lupus vulgaris (all  higher mets rate) or arise from precursor areas – actinic keratoses (AK) or Bowens disease (BD) – also high mets rate Features firm, flesh toned endo/exophytic indurated papule/nodule “non healing lump” – sore, painful, oozes, bleeds can rapidly expand may be smooth, scaly, ulcerated, crusted or hyperkeratotic If infected = malodour & fungating Ix Biopsy for thickness & invasion Prognosis 75-90% (25% if metastatic) Worse if on ear, lip, >2cm, thicker, non sun exposed area, chronic inflammation, poorer differentiation, host immunosupression, mucosal or perineural invasion Treatment Excision – if well defined = 4mm margin (more if >2cm) = 95% fully removed Curettage & cautery – if <1cm, well differentiated, slow growing & on sun exposed site. Do 2-3 cycles Radiotherapy – if surgery unacceptable / morbidity high Recurrence – 95% local recurrence & mets detected in 5 yrs Describe the clinical features of the following benign lesions: - Dermatofibroma Benign overgrowth of cells in the dermis – most common on legs Can have good blood supply  red/yellow or black if necrotic Linked with insect bites / mild injury to area, many have no history Treatment not usually required – can be removed for cosmesis - Epidermoid and pilar cysts (sebaceous cysts) Epidermoid and pilar cysts look like small smooth lumps under the skin surface. Benign (non-cancerous) and usually cause no harm or problems. If required, they can be removed easily by a small operation done under local anaesthetic. Complications Infection  red, inflamed and painful. Rx Abx Leakage - 'toothpaste' like material if the cyst is punctured or damaged. 'Horn' may grow on the skin over the cyst. - Neurofibroma May arise at any level in the spinal cord, typically, from the posterior nerve roots. They lie extramedullary and are slowly growing and benign. Presentation - slowly advancing spastic paraparesis with a unilateral band of pain and distorted sensation at the level of the lesion. Cafe au lait spots may be seen in the skin with neurofibromas because of their are association with multiple neurofibromatosis. Complete operative removal is feasible but at the sacrifice of the nerve root at the origin of the lesion. Neurological deficit is minimised by overlap from adjacent nerve roots. - Haemangioma (including pyogenic granuloma) “a congenital benign skin lesion consisting of dense, usually elevated masses of dilated blood vessels". May present as a birthmark Most will disappear over time. 10% of Caucasians. F:M = 3-5:1 Hemangiomas can be vivid superficial lesions (often referred to as "Strawberry Marks"), or they can appear as a bluish swelling if they are under the skin. Sometimes they can be both superficial and deep. Approximately eighty percent are located on the face and neck, with the next most prevalent location being around the liver area. - Keratoacanthoma Starts as a small papule  rapid growth Dome shaped papule with crater core filled with keratinous material Telangectasia often visible Often spontaneously involutes Risks – sun exposure, chronic exposure to tar, pitch and petroleum oils Diagnosis – histology required to distinguish from SCC The Skin & Systemic Disease  Be aware of the cutaneous manifestations of diabetes, thyroid disease and systemic lupus erythematosus Diabetes Necrobiosis lipoidica 40-60% of people with this will develop DM, but not very common in DMs Necrosis of the connective tissue with lymphocytic and granulomatous infiltrate Degenerating collagen is replaced with lipid Usually over shin, but can occur anywhere Granuloma annulare Localised popular lesions on the hands and feet (may occur elsewhere) May be multipe/single and may be partially/wholly annular Some necrobiosis with histocytes forming palisades + giant cells and lymphocytes More common in womn and under 30s Is harmless and self limiting but is assoc with IDDM Diabetic dermopathy Multiple hyperpigmented atrophic macules on the legs Typical lesions are depressed (atrophic) and appear to have post-inflammatory hyperpigmentation. Histology sections may demonstrate red blood cell extravasation and capillary basement membrane thickening. Patients can usually relate antecedent trauma or inflammation and sometimes precipitating lesions coexist with the atrophic ones. Skin infections, leg and foot ulcers Mentioned in other sections of these notes Thyroid disease Hypothyroidism Dry skin, oedema of eyelids and hands, absence of sweating, coarse thin hair, pale ivory skin, brittle poorly growing nails, purpura, bruising and telangectasia Hyperthyroidism Soft, thickened skin, pretibial myxoedema, increased sweating (palms & soles), thinning of scalp hair, diffuse pigmentation, rapidly growing nails, palmar erythema and facial flushing Pretibial myxoedema Sign of increased TSH Areas of non-pitting oedema appear on the anterior or lateral aspects of the legs or in sites of old or recent trauma Lupus erythematosus Systemic Lupus Erythematosus (SLE) Female : Male = 8 :1 Acute erythematous eruption bilaterally on the malar area of face (butterfly rash) Can also be photosensitivity, hair loss, mouth ulcers, discoid plaques and vasculitis Systemic changes are fever, arthritis, renal involvement Subacute Lupus Erythematosus Variant in 10% of SLE Non scarring erythematous plaques mainly on face, hands and arms Systemic involvement less than SLE High incidence of neonatal lupus to children of affected mothers 60% have antinuclear factors, 80% have anticytoplasmic antibodies Discoid Lupus Erythematosus (DLE) Well defined photosensitive inflammatory lesions with atrophy and hyperkeratosis of follicles  nutmeg grater feel Mainly on face & other areas exposed to sun, worse in summer months Antinuclear antibodies are very rare Rx with steroids & immunosupressants Liver disease Obstructive Jaundice Jaundice & pruritus (due to bile salt deposits in the skin) Improvement in colour and itching with Cholestryramine (binds bile salts) Liver failure Vascular changes – spider naevi, palmar erythema (due to diffuse telangectasia) Leukonykia – is linked with hypoalbuminaemia Porphyria Cutenea Tarda – bullae, scarring and hyperpigmentation in sun exposed areas Cirrhosis Xanthomas – deposits of fatty material in the skin & subcutaneous tissues, can be found on extensors of knees & elbows, on Achilles tendon or generalised Asteotosis – dry skin with a crazy paving pattern  Be aware of the cutaneous manifestations of internal cancers, e.g. acanthosis nigricans, acquired ichthyosis, pyoderma gangrenosum and dermatomyositis Acanthosis nigricans Velvety, light-brown-to-black, markings usually on the neck, under the arms or in the groin. Most often associated with obesity & insulin resistance Can be associated with lymphomas and adenocarcinoma of the stomach Acquired Ichthyosis Areas of rough, dry skin, with scaling on the scalp, and with overgrowth on palms & soles Can be assoc with Hodgkin & Non-Hodgkin lymphoma, lung, breast, ovarian and cervical cancer. May also be linked to marrow transplantations, SLE, and drug reactions Pyodermal Gangrenosum An area of non-specific inflammation & pustules  break down to form a necrotic ulcer with hypertrophic margins Can be underlying vasculitis Assoc with Crohn’s disease, RA, abnormal gamma globulins and leukaemia Dermatomyositis Commonly carcinoma of breast, lung, ovary & GI Local erythema with a purple hue (heliotrope) mainly on eyelids, cheek & forehead. May also occur on dorsum of fingers Will fade away if tumour excised Assoc with muscle weakness (with electromyographic changes & inflammatory infiltrate)  Be able to diagnose erythema nodosum and suggest a list of possible triggers Erythema nodosum Immunological reaction pattern. Tender nodules on shins. May be idiopathic, or caused by infection - streptococcal, primary TB, coccidiomycosis, drugs such as sulphonamides, oral contraceptives, systemic disease such as sarcoid, Bechets, ulcerative colitis. Ix: history, examination, chest x-ray, throat swab, ASO titre Erythema Multiforme Skin reaction pattern, characterised by target lesions at acral sites. May be idiopathic. Mild forms often due to herpes simplex. Drugs - sulphonamides, anticonvulsants, allopurinol, penicillin. With blisters = Stevens Johnson syndrome Severe with large bullae at edges of target lesions Often drug related (penicillin and anticonvulsants) Assoc with cough with purulent sputum, headache, malaise and arthralgia  Be able to recognise a vasculitic rash and suggest a list of possible triggers Inflammation around dilated capillaries and small blood vessels a variable clinical picture with red macules & papules with necrosis & bruising Usually over legs and arms In children is often pupuric (e.g. HSP with nephritis) Systemically can affect renal, joint, GI and CNS Causes Infection – strep, hepatitis Drugs – many inc sulphonamide, penicillin, phenothiazines and phenacitin Chemicals – insecticides, weed killers, phenolic compounds Connective tissue disease – SLE, RA Lymphoma and leukaemia Dysproteinaemias Drug eruptions  Be able to recognise skin eruptions such as urticaria and toxic epidermal necrolysis which may be caused by drugs Urticaria Itchy red wheal Oedema, vasodilatation and cellular infiltrate of lymphocytes, polymorphs and histiocytes May preceed - vasculitis, pemphigoid, dermatitis herpetiformis Can be physical urticaria Dermatographism – due to histamine release on light pressure Cold/heat urticaria Solar urticaria – reaction to sunlight exposure Cholinergic – after exertion, stress or exposure to heat Aquagenic – occurs on contact with water Non physical urticaria Food – fish, dairy, eggs, chocolate, nuts, strawberry, pork, tomato Food additives – dyes, sodium benzoates Salicylates – in medicines and foods Infection – bacterial, viral and protozoal Systemic – autoimmune, collagen, carcinoma Contact – may occur with many things Papular – insect bites Inhalants – house dust, animal danders Management Eliminate all possible causes Antihistamines & H2 blockers (e.g. cimetidine) Adrenaline –for acute attacks, esp if angioedema of resp tract Systemic corticosteroids only in acute cases Toxic epidermal necrolysis Rapidly evolving mucocutaneous reaction Widespread erythema, necrosis, and bullous detachment of the epidermis resembling scalding Complications Epithelial loss results in vulnerability to bacterial and fungal infections and predisposes to septicemia. Mucosal membranes are affected to a varying extent and can cause GI hemorrhage, respiratory failure, ocular abnormalities, and genitourinary lesions. Significant fluid loss from extensive skin lesions as well as an inability to tolerate oral intake can lead to hypovolemia, acute tubular necrosis, and shock. Causes Sulfonamide antibiotics Anticonvulsants (phenobarbital, phenytoin, carbamazepine, valproic acid) Oxicam nonsteroidal anti-inflammatory drugs (NSAIDs) Allopurinol Antiretroviral medications Corticosteroids  Know the appropriate skin care for patients with skin failure Treatment of drug rashes Stop drug Consider measures to reduce drug in system Symptomatic Oral steroids controversial Avoid drug in future Label medical records Skin Failure Loss of normal temperature control with inability to maintain the core body temperature, and failure to prevent percutaneous loss of fluid, electrolytes and protein, with resulting imbalance, and failure of the mechanical barrier to prevent penetration of foreign materials Consequences of acute skin failure Altered haemodynamics – peripheral V/D & increased cutaneous flow (erythema & oedema) + increased blood volume and cardiac output to compensate  high output cardiac failure Altered thermoregulation – hypothermia is very common, although there may be fever due to infection and release of interleukins Metabolic abnormalities – BMR increases to compensate for hypothermia  hyperglycaemia & glycosuria (due to pancreatitis & decreased insulin due to stress & infection). Shivering also uses up resources Fluid & electrolyte imbalance – total water loss via skin is 400ml/day, this increases greatly in skin failure due to increased transepidermal loss. If fluid replacement is not adequate  dehydration and hyperosmolar but decreased urine output  low Na+ & high K+ with raised urea & creatinine. If blistering further fluid is lost. Loss of nutrients – mainly protein (shed scales, increased BMR, decreased hepatic function). Impaired absorption and utilisation of Iron & B12 + increased cell turnover  anaemia Peripheral oedema – due to increased capillary leakage (with shift to extravascular space), hypoalbuminaemia, cardiac failure and inflammation Pulmonary complications – aspiration pneumonia if severely ill. Altered immune function – lymphopenia, neutropenia and thrombocytopenia with impaired chemotaxis & phagocytosis Infection – damaged barrier function  colonisation & systemic entry, compounded by poor immune function DVT – due to prolonged immobilisation Care of patients with acute skin failure Nursing care Monitoring hemodynamic changes Fluid, electrolyte balance and nutrition Prevention of complication (e.g. sepsis) Prompt identification of risk factors Topical therapy.