Guttate psoriasis



Hereditary haemorrhagic telangiectasia"Osler-Weber-Rendu syndrome" ?AD?condition characterised by multiple telangiectasia over the skin and mucous membranes. 20% cases occur spontaneously without family history.4 4ain diagnostic criteria.If the patient has 2 Possible diagnosis of HHT. If they meet ≥ 3 Definite diagnosis of HHT:Epistaxis Spontaneous, Recurrent nosebleedsTelangiectases multiple at characteristic sites (Lips, Oral cavity, Fingers, Nose)Visceral lesions GIT Telangiectasia +/- Bleeding Anemia Pulmonary A/V malformationsHepatic AVMCerebral AVM Spinal AVMFamily History: 1st-degree relative with HHTEczema: topical steroidsUse weakest steroid cream which controls patients symptomsMildModeratePotentVery potentHydrocortisone 0.5-2.5%Beta- Methasone Valerate 0.025% (Betnovate RD)Clobetasone Butyrate (0.05% ) (Eumovate)Betamethasone valerate (0.1%) (Betnovate)Fluticasone propionate (0.05%) (Cutivate)Clobetasol Propionate 0.05% (Dermovate)Finger tip rule 1 finger tip unit (FTU) = 0.5 g, sufficient to treat a skin area about twice that of the flat of an adult handTopical steroid doses for eczema in adultsArea of skinFingertip units per doseHand and fingers (front and back)1.0A foot (all over)2.0Face and neck2.5An entire arm and hand4.0Back and buttocksFront of chest and abdomen 7.07.0An entire leg and foot8.0Topical steroids prescribed for an adult for a single daily application for 2 weeks:AreaAmountFace and neck15 to 30 gBoth hands15 to 30 gScalp15 to 30 gBoth arms30 to 60 gBoth legs100 gTrunk100 gGroin and genitalia15 to 30 gPompholyx"Dyshidrotic Eczema" A type of eczema affects both the hands (cheiropompholyx) and the feet (pedopompholyx). Precipitated by?humidity (Sweating) and ↑↑temperatures. FeaturesSmall blisters on the?palms and solesPruriticoften intensely itchysometimes burning sensationOnce blisters burst skin may become dry and crackManagementcool compressesemollientstopical steroidsNickel dermatitisNickel is a common cause allergic contact dermatitis Type IV hypersensitivity reaction. It is often caused by jewellery such as watchesIt is diagnosed by a Skin Patch Test.AntihistaminesAntihistamines (H1?inhibitors) are of value in the treatment of allergic rhinitis and urticaria.?Sedating antihistaminesChlorpheniramineAntimuscarinics properties (urinary retention, dry mouth).Non-sedating antihistaminesLoratidineCetirizineMay cause more drowsiness than other drugs in the class.Not preferred for certain ppl like driversPsoriasisCommon (2%) and chronic skin disorder. Red/White, Scaly (Hyperkeratotic/ Hard skin) patches on the skin. ↑↑ Risk of arthritis and CVS disease.Pathophysiology "Multifactorial"Genetic HLA-B13, -B17, and -Cw6. Strong concordance (70%) in identical twinsImmunological Abnormal T cell activity (++) keratinocyte Proliferation Novel group of T helper "Th17" producing IL-17 (Third T-effector cell subset in addition to Th1 and Th2)Exacerbating Factors Triggered by (Strept. Infection)DrugsBeta BlockersACEILithiumAntimalarials (Chloroquine/ Hydroxychloroquine)NSAIDsInfliximabWithdrawal of systemic steroidsSkin Trauma, StressImproved by SunlightRecognised subtypes of psoriasisPlaque psoriasisFlexural psoriasisGuttate psoriasisPustular psoriasisMost common sub-type Well demarcated, Red, Scaly patches Extensor surfaces, Sacrum and Scalp DD. Plaque Psoriasis (Skin is smooth)Transient psoriatic rash (++) by Streptococcal Multiple red, Teardrop lesions on the bodyCommonly on the Palms & SolesManagement of chronic plaque psoriasisRegular emollients ↓↓ scale loss and pruritus1st-line Potent corticosteroid / OD + Vit.D/OD (applied separately, one in the morning/evening)/ 4Ws.2nd-line if no improvement after 8 weeks Vitamin D/ 1*23rd-line if no improvement after 8-12 WsPotent corticosteroid /1*2/ 4 weeks Coal tar preparation/ 1 or 2 daily (Smelly)Short-acting Dithranol can also be used (Smelly)Using topical steroids in psoriasisTopical corticosteroid Skin atrophy, Striae and rebound symptomsSystemic S/E may be seen when potent corticosteroids are used on (large areas > 10%) of the body surface area4 week break before starting another course of topical corticosteroidsPotent corticosteroids < 8 weeks at a timeVery potent corticosteroids < 4 weeks at a timeWhat should I know about vitamin D analogues?Vit. D analogues Calcipotriol (Dovonex), Calcitriol and Tacalcitol↓↓cell division and differentiationS/E uncommon used long-termunlike coal tar and dithranol they do not smell or stain↓↓ scale and thickness of plaques but not the erythemaAvoided in pregnancyThe maximum weekly amount for adults is 100gSteroids in psoriasisTopical steroids are commonly used in flexural psoriasis & mild steroids in facial psoriasis. If steroids are ineffective Vit. D OR Tacrolimus ointment.The scalp, face and flexures prone to steroid atrophy so topical steroids (Not used > 1-2Ws/month)Scalp psoriasisPotent topical corticosteroids/ 1*1/ 4 weeksNo improvement after 4 weeks Different formulation of the potent corticosteroid (Shampoo or Mousse) And/orTopical agents to remove adherent scale (Containing salicylic acid/ Emollients/ Oils) before application of the potent corticosteroidFace, Flexural and genital psoriasisMild or Moderate potency corticosteroid (only) applied 1*1/ 1*2/ maximum of 2 weeksTopical calcipotriol is usually irritant in flexuresSecondary care managementPhototherapyNarrow band U/V "B light" Treatment of choice/ 3 times a weekPhotochemotherapy Psoralen + U/V "A light" (PUVA)S/E Skin Ageing, SQ. cell cancer (not melanoma)Systemic therapy (Arthiritis) Oral Methotrexate first-line. It is particularly useful if there is associated joint diseaseCyclosporineSystemic RetinoidsBiological Agents InfliximabEtanercept TNF alpha antagonist (T.B & Viral hepatitis should be roled out)AdalimumabUstekinumab (IL-12 and IL-23 blocker) is showing promise in early trialsMechanism of action of commonly used drugsCoal Tar probably (- -) DNA synthesisDithranol (- -) DNA synthesis (Wash off after 30 mins) SE/ Burning, StainingCalcipotriol vitamin D analogue ↓↓Epidermal proliferation and restores a normal horny layerChronic plaque psoriasisregular emollients reduce scale loss and reduce pruritusfirst-line: potent corticosteroid OD + Vit D analogue OD (applied separately, one in the morning and the other in the evening/ 4 weeks .second-line: if no improvement after 8 weeks Vit D analogue twice dailythird-line: if no improvement after 8-12 weeks potent corticosteroid applied twice daily / 4 weeks OR Coal tar preparation applied once or twice dailyshort-acting dithranol can also be usedUsing topical steroids in psoriasisTopical corticosteroid therapy may lead to skin atrophy, striae and rebound symptomssystemic side-effects potent corticosteroids are used on large areas e.g. > 10% of the body surface areaa 4 week break before starting another course of topical corticosteroidspotent corticosteroids < 8 weeks at a time very potent corticosteroids < 4 weeks at a timeWhat should I know about vitamin D analogues?Vit D analogues calcipotriol (Dovonex), calcitriol and tacalcitol↓↓ cell division and differentiationadverse effects are uncommonmay be used long-termUnlike coal tar and dithranol they do not smell or stain↓↓ the scale and thickness of plaques but not the erythemathey should be avoided in pregnancythe maximum weekly amount for adults is 100gSteroids in psoriasistopical steroids are commonly used in flexural psoriasis and mild steroids in facial psoriasis. If ineffective vit D analogues or tacrolimus ointment should be used second linethe scalp, face and flexures are prone to steroid atrophy should not be used for more than 1-2 weeks/monthScalp psoriasispotent topical corticosteroids used once daily for 4 weeksif no improvement after 4 weeks Potent corticosteroid (for example, a shampoo or mousse) and/or (agents containing salicylic acid, emollients and oils) before corticosteroid to remove adherent scaleFace, flexutal and genital psoriasisMild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeksSecondary care managementPhototherapyNarrow band ultraviolet B light the treatment of choice. If possible 3 times /weekPhotochemotherapy psoralen + ultraviolet A light (PUVA)adverse effects: skin ageing, squamous cell cancer (not melanoma)Systemic therapyOral methotrexate is used first-line. useful if associated joint diseaseciclosporinsystemic retinoidsbiological agents: infliximab, etanercept and adalimumabustekinumab (IL-12 and IL-23 blocker) is showing promise in early trialsMechanism of action of commonly used drugs:Coal tar ↓↓DNA synthesisCalcipotriol Vit D analogue (reduces epidermal proliferation and restores a normal horny layer)Dithranol ↓↓ DNA synthesis, wash off after 30 mins, S/E: burning, stainingAcanthosis NigricansSymmetrical, brown, velvety plaques (Neck, axilla and groin) "Skin Freckles". Causestype 2 D.MGIT cancerObesityPCOsAcromegalyCushing's diseasehypothyroidismfamilialPrader-Willi syndromeDrugsOral contraceptive pillNicotinic acidPathophysiologyinsulin resistance → hyperinsulinemia → (++) keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1) AlopeciaAlopecia may be divided into scarring (destruction of hair follicle) and non-scarring (preservation of hair follicle)Scarring alopeciaNon-scarring alopeciaTrauma, BurnsRadiotherapyLichen planusDiscoid lupusTinea Capitis Scarring in untreated tinea capitis if a kerion developsMale-pattern baldnessDrugsCytotoxic drugs Carbimazole HeparinOral contraceptive pillColchicineNutritional iron and zinc deficiencyAutoimmune Alopecia AreataTelogen effluviumHair loss following stressful period (surgery)Trichotillomania hair pulling disorderAlopecia areataPresumed autoimmune condition localised, well demarcated patches of hair loss. At the edge of the hair loss small, broken 'exclamation mark' hairsWatchful waiting for spontaneous remission "Hair will regrow" 50% of patients by 1 year, 80-90% eventually. Other treatment options include:Topical or intralesional corticosteroidsTopical minoxidilphototherapydithranolContact immunotherapywigsHirsutism and hypertrichosisHirsutism androgen-dependent hair growth in women, Hypertrichosis androgen-independent hair growthCauses of HirsutismCauses of HypertrichosisPCOS (most common causes of hirsutism) Cushing's syndromeCongenital Adrenal HyperplasiaAdrenal Tumourandrogen secreting ovarian tumourAndrogen therapy.Obesity due to insulin resistanceDrugs PhenytoinCorticosteroidsDrugsMinoxidilCyclosporine DiazoxideCongenital hypertrichosis lanuginose. Congenital hypertrichosis terminalis.Porphyria cutanea tardaAnorexia nervosaAssessment of hirsutism Ferriman-Gallwey scoring system9 body areas (score of 0 – 4)Score > 15 moderate or severe hirsutismManagement of hirsutismWeight loss if overweightCosmetic techniques waxing/bleaching - not available on the NHSCOCPs(Co-Cyprindiol "Dianette") OR Ethinylestradiol and Drospirenone (Yasmin). Co-cyprindiol should not be used long-term ↑↑ VTEFacial hirsutism Topical Eflornithine CI pregnancy and breast-feedingAcne vulgarisUsually in adolescence face, neck and upper trunk Typical lesions "Comedones and Pustules"80-90% of teenagers may persist beyond adolescence (> 25 years 10-15% females and 5% males).Pathophysiology is multifactorialFollicular epidermal hyperproliferation obstruction of the pilosebaceous follicle W keratin plug Activity of sebaceous glands controlled by androgen, although levels are often normal in patients with acneColonisation by the anaerobic bacterium "Propionibacterium Acnes"inflammationClassificationmild Open and closed comedones +/- sparse inflammatory lesionsmoderate widespread non-inflammatory lesions + ↑↑ papules and pustulessevere extensive inflammatory lesions, (Nodules, Pitting, and ScarringTreatmentSingle topical therapy (Topical Retinoids, benzoyl peroxide)Combination topical therapy (Topical Antibiotic, Benzoyl peroxide, Topical retinoid) Oral antibiotics:Tetracyclines lymecycline, oxytetracycline, doxycyclineTetracyclines avoided in pregnant or breastfeeding women and in children < 12 years of ageErythromycin used in pregnancyMinocycline less appropriate (possibility of irreversible pigmentation)A single oral antibiotic maximum of three monthsTopical retinoid (if not contraindicated) or benzoyl peroxide co-prescribed with oral antibiotics (↓↓ resistance developing).?Topical and oral antibiotics should not be used in combinationGram -Ve folliculitis complication of long-term antibiotic high-dose oral trimethoprim is effective if this occursCombined oral contraceptives (COCP) alternative to oral antibiotics in womenshould be used with topical agentsDianette (Co-Cyrindiol) used Ethinylestradiol + Cyproterone acetateHas anti-androgen properties↑↑↑ VTE compared to other COCPsUsed 2nd-line with counselled about the risksonly be given for 3 months.Retinoids "Oral isotretinoin":?only under specialist supervisionOral retinoid used in the treatment of severe acne. 2/3 of patients long-term remission or cure following a course of oral isotretinoin.Adverse effectsTeratogenicity fshould ideally be using 2 forms of contraception (COCP and condoms)Dryness Skin, eyes and?lips/mouth?The most common S/ENose bleeds (caused by dryness of the nasal mucosa)Low mood (depression and other psychiatric problems are listed in the BNF↑↑ TriglyceridesHair ThinningIntracranial HTN:?isotretinoin treatment should not be combined with tetracyclines for this reasonPhotosensitivityThere is no role for dietary modification in patients with acne.Acne rosaceaChronic skin disease of unknown aetiology. Common with fair-skinned populations >30 YsFlushing, Erythema, Telangiectasia → papules and pustulesFeaturestypically affects nose, cheeks and foreheadflushing is often first symptomtelangiectasia are commonlater develops into?persistent erythema with papules and pustulesrhinophymaOcular involvementBlepharitisKeratitisConjunctivitisMay exacerbate symptoms Drinking alcohol. Sunlight, PregnancyManagementMild symptoms?(↓↓Papules and Pustules, No plaques) Topical metronidazolePredominant flushing but limited Telangiectasia Topical Brimonidine gelMore severe disease especially if Ocular symptomse Systemic antibiotics?Oral tetracycline (Oxytetracycline) erythromycinDaily high-factor sunscreenCamouflage creams may help conceal rednesslaser therapy prominent telangiectasiaRhinophyma referred to dermatologyrighttopEczema herpeticumA severe 1ry infection of the skin by?HSV?1 or 2.?↑↑↑Children W atopic eczema Rapidly progressing painful rash.?Monomorphic blistered punched-out erosions (Circular, Depressed, Ulcerated lesions) usually 1–3 mm in diameter?are typically+/- Fever, Lethargy or Distress.Risk FactorEarly-onset atopic dermatitisHigher total IgE and untreated or undertreated eczema Management Potentially life-threatening children (Urgent sameday referral < 48h) ?admitted?for?IV acyclovirDD. Molluscum Contagiosum Monomorphic umbilicated shiny lesions describe.Warts and Nevi Monomorphic papular lesions.Chickenpox Polymorphic vesicular lesions 'dew drops on a rose petal'Molluscum contagiosumCommon skin infection caused by Molluscum contagiosum virus (MCV), a member of the Poxviridae family.Transmission Directly OR Indirectly (Shared towels and flannels). ↑↑↑children with atopic eczema) W maximum preschool 1-4 years.Lesion Colour Pinkish/ Pearly white papules W Central umbilication (up to 5 mm). (Not painful but might be itchy)Ch.Ch. Lesions appear in clusters in areas anywhere on the body (Except the palms of the hands and the soles of the feet). In children ↑↑ Trunk and in flexures, but anogenital lesions may also occur. In adults Sexual Contact genitalia, pubis, thighs, and lower abdomen. righttopRarely, lesions can occur on the oral mucosa and on the eyelids. ManagementSelf care advice:Reassure self-limiting condition (18 months)lesions are contagious avoid sharing towels, clothing, and baths with uninfected people (siblings)Encourage people not to scratch the lesions If it is problematic, consider treatment to alleviate the itchExclusion from school, gym, or swimming is not necessaryTreatment It is not usually recommended unless troublesome or unsightly, use simple trauma or cryotherapy (Parents' wishes and the child's age)Squeezing (with fingernails) or Piercing (orange stick) following a bath limited to a few lesions at one timeCryotherapy older children or adults, if the healthcare professional is experienced in the procedureEczema or inflammation May develop around lesions prior to resolution.Itching is problematic Emollient and a mild topical corticosteroid (hydrocortisone 1%)Infection (Oedema/ Crusting) Topical antibiotic (Fusidic Acid 2%) Referral may be necessary in some circumstances:HIV +Ve + Extensive lesions? Urgent referral to a HIV specialistEyelid-margin OR Ocular lesions + Red Eye urgent referral to an ophthalmologistAnogenital lesions Referred to Genito - Urinary medicine, for screening for other STIContact dermatitisThere are two main types of contact dermatitisirritant contact dermatitisallergic contact dermatitisCommon Non-allergic reaction due to weak acids or alkalis (detergents). Often seen on the hands. Erythema is typicalCrusting and Vesicles RareUncommon Type IV hypersensitivityOften seen on the head following hair dyes. Presents as an acute weeping eczema (predominately the margins of hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicatedCement is a frequent cause of contact dermatitis. The alkaline nature of cement irritant contact dermatitis Dichromates in cement Allergic contact dermatitisDermatitis herpetiformisAutoimmune blistering skin disorder associated with?coeliac disease. It is caused by?deposition of IgA in the dermis.Itchy, Vesicular skin lesions on the extensor surfaces (Elbows, knees, Buttocks)Skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermisManagementGluten-free dietDapsone Hyperhidrosis Excessive production of sweat. Management Topical aluminium chloride 1st-line. (S/E Skin Irritation)Iontophoresis Palmar, Plantar and Axillary hyperhidrosisBotulinum Toxin currently licensed for axillary symptomsSurgery Endoscopic transthoracic sympathectomy (Risk of compensatory sweating)Seborrhoeic dermatitis Chronic dermatitis inflammatory reaction due to proliferation of a normal skin inhabitant (fungus Malassezia furfur). Common (2% general population).FeaturesThe combination (Peri-orbital + Nasolabial scaly rash) associated dandruff is a classical history for seborrhoeic dermatitis.Eczematous lesions on the sebum-rich areas ?Scalp (may cause dandruff).Otitis externa and blepharitis?may developAlopecia is not commonly seen in seborrhoeic dermatitis, but may develop if a severe secondary infection developsAssociated conditions includeHIV p24 antigen testing useful in the early stages for screening. later stages of infection serology for anti-HIV antibodies is most useful.Parkinson's diseaseautoimmune thyroid diseaseScalp disease managementOver the counter preparations containing Zinc Pyrithione ('Head & Shoulders') and Tar ('Neutrogena T/Gel') (1st-line)the preferred second-line agent is ketoconazoleSelenium sulphide + Topical corticosteroid may also be usefulFace and body managementTopical antifungals: (ketoconazoleTopical steroids: best used for short periodsdifficult to treat - recurrences are commonErythrodermaErythroderma is a term used when > 95% of the skin is involved in any kind of rash. Causes of erythrodermaEczemaPsoriasisDrugs GoldLymphomas, LeukaemiasIdiopathicErythrodermic psoriasisMay result from progression of chronic disease Exfoliative phase with plaques covering most of the body. Associated with mild systemic upsetMore serious form is an acute deterioration. Triggering Factors Withdrawal of systemic steroids. Patients need to be admitted to hospital for managementGuttate psoriasis↑↑↑ in children and Adolescents. It may be precipitated by a?Streptococcal infection?(2-4 weeks) prior to the lesions appearing. Features "Tear drop papules" on the trunk and limbsManagementmost cases resolve spontaneously within 2-3 monthsthere is no support the use of antibiotics to eradicate streptococcal infectionTopical agents as per psoriasisUVB phototherapy Accelerate resolutionTonsillectomy may be necessary with recurrent episodesDD. Guttate psoriasis and pityriasis roseaGuttate psoriasisPityriasis roseaProdromeStrept. sore throat 2-4 weeksRespiratory tract infections (Not common in questions)Appearance'Tear drop', scaly papules Trunk and LimbsHerald Patch 1-2 Ws Multiple Erythematous, raised oval lesions with a fine scale confined to the outer aspects of the lesions.?Longitudinal diameters run parallel to the line of Langer. This may produce a 'Fir-tree' appearanceTreatment /?natural historyResolve spontaneously 2-3mTopical agents As psoriasisUVB phototherapySelf-limiting Resolves after around 6 weeksPityriasis RoseaAcute, Self-limiting rash, young adults Herpes Hominis Virus 7/Human Herpis (HHV-7) may play a role. FeaturesNo Prodrome, but?a minority recent viral infectionHerald "Apparent" patch?(usually on trunk) Followed by Erythematous, Oval, Scaly patches(inside the edge) Follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. A 'fir-tree' appearanceSite Thighs, chest, upper arms and neck but usually spares the face.Many drugs have been associated with the pathogenesis including ACEIBarbiturates GoldImatinibisotretinoin,lithiumOmeprazoleCertain antibiotics such as metronidazole.ManagementSelf-limiting - usually disappears after?6-12 weeksPityriasis versicolor"Tinea Versicolor" superficial cutaneous fungal infection caused by?"Malassezia furfur"?(formerly?Pityrosporum ovale). FeaturesTrunk " Most commonly"Patches hypopigmented, pink or brown (hence versicolor). May be more noticeable following a suntanScale is commonMild pruritusPredisposing factorsoccurs in healthy individualsimmunosuppressionmalnutritionCushing'sManagementTopical antifungal ?ketoconazole shampoo?as this is more cost effective for large areasif failure to respond to topical treatment consider alternative diagnoses (send scrapings to confirm the diagnosis) + oral itraconazolePyoderma gangrenosumtypically on the lower limb Initially Small red papule Later Deep, red, necrotic ulcers W Violaceous border+/- systemic symptoms (Fever, myalgiaCauses*idiopathic in 50%IBD UC, Crohn'sRA, SLEMyeloproliferative disordersLymphoma, Myeloid leukaemiasMonoclonal Gammopathy (IgA)1ry Biliary cirrhosisD.M Rare Management↑↑↑ Rapid progression in most patients oral steroids as first-line treatmentOther immunosuppressive therapy (Ciclosporin/ Infliximab) have a role in difficult casesSurgery might worse it / DD.malignancy (referral to a spechialist) Erythema Nodosuminflammation of subcutaneous fat tender, erythematous, nodular lesionsusually occurs over shins, may also occur elsewhere (forearms, thighs)usually resolves (heal without scarring) within 6 weeksCausesInfectionStrept. Cocci Most common identifiable precipitant, especially in children 2-3 W following pharynigitis T.B Chest X-RayBrucellosisSystemic diseaseSarcoidosis Chest X-Ray, ↑↑Ca++ IBDBehcet'sMalignancy/lymphomaDrugsPenicillinsSulphonamidesCOCPPregnancyErythema multiformeHypersensitivity reaction most commonly triggered by infections. It may be divided into minor and major forms. Erythema multiforme major more severe form + Mucosal involvement. FeaturesTarget lesionsinitially (back of the hands / feet) Spreading to the torsoUL > LLPruritus is occasionally seen and is usually mildCausesViruses HSV (the most common cause), Parapox virus (Orf skin disease of sheep and goats)idiopathicBacteriaMycoplasmaStreptococcusDrugsPenicillinSulphonamidesCarbamazepineAllopurinolNSAIDsOral contraceptive pillNevirapineC.T Disease SLEsarcoidosismalignancyErythrasmaGenerally asymptomatic Well defined Flat, Slightly Scaly, Pink or Brown rash (Groin or Axilla). It is caused by an overgrowth "Diphtheroid Corynebacterium Minutissimum"Examination with Wood's light "Coral-Red Fluorescence"?Topical Miconazole or antibacterial are usually effective. More extensive infection Oral erythromycin ImpetigoSuperficial bacterial skin infection ?Staph. Aureus?or?Strept. Pyogenes. 1ry infection or a complication of an existing skin condition (Eczema Scabies or insect bites) ↑↑↑children, particularly during warm mon Sites Face, flexures and limbs not covered by clothing. Spread Direct contact with discharges from the scabs of an infected person. The bacteria invade skin through minor abrasions.Mainly by the hands, but indirect spread via toys, clothing, equipment and the environment may occur. The incubation period between 4 to 10 days.Features'Golden', crusted skin lesions typically found around the mouthvery contagiousManagementLimited, localised diseaseTopical fusidic acid first-lineTopical retapamulin 2nd-line if fusidic acid has been ineffective or is not toleratedMRSA Should be considered in hospital stay and following surgery.Not susceptible to (fusidic acid or retapamulin) Topical Mupirocin (Bactroban) should, therefore, be used in this situationExtensive diseaseoral flucloxacillinoral erythromycin if penicillin-allergicchildren should be excluded from school until the lesions are crusted and healed or 48 hours after commencing antibiotic treatmentBullous pemphigoidAutoimmune D causing sub-epidermal blistering of the skin. 2ndry antibodies against Hemidesmosomal proteins (BP180 and BP230)↑↑common in elderly patients. Features Itchy, Tense Flisters typically around flexuresUsually heal without scarringmouth is usually spared*In reality 10-50% degree of mucosal involvement in exam will not be mentioned a classic DD Pemphigoid and Pemphigus.Skin biopsyimmunofluorescence shows IgG and C3 at the dermoepidermal junctionManagementReferral to dermatologist for biopsy and confirmation of diagnosisOral corticosteroids are the mainstay of treatmentTopical corticosteroids, immunosuppressants and antibiotics are also used. Pemphigus vulgarisAutoimmune disease Abs against?Desmoglein3 (Cadherin-type epithelial cell adhesion molecule). ↑↑ Ashkenazi Jewish population.FeaturesMucosal ulceration?"Common" Oral involvement "50-70%".Skin blistering "flaccid" Easily ruptured vesicles on touch and bullae painful but not itchy. May develop months after the initial mucosal symptoms. "Nikolsky's" spread of bullae following application of horizontal, tangential pressure to the skinBiopsy Acantholysis ManagementSteroids are first-lineImmunosuppressants Bullous Pemphigoid No mucosal involvement + Hemidesmosomal proteins Pemphigus Vulgaris Mucosal involvement + Ab against Desmoglein3 KeratoacanthomaBenign epithelial tumour ↑↑↑ common with advancing age and rare in young people. Features Looks like a Volcano or craterInitially a smooth dome-shaped papule rapidly grows to crater centrally-filled with keratin (Brown/Yellow color)Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar.Urgently excised difficult clinically to exclude SQ. cell carcinoma. Removal also may prevent scarring. Keloid scarsTumour-like lesions arises from C.T of a scar and extend beyond the dimensions of the original woundpredisposing factorsEthnicity ↑↑↑ Dark skinAge ↑↑ young adults, rare in the elderlyCommon sites (Sternum Shoulder Neck Face Extensor surface of limbsTrunk)Keloid scars ↓↓↓ likely if incisions are made along relaxed skin tension lines.TreatmentEarly keloids may be treated with intra-lesional steroids (Triamcinolone)Excision is sometimes requiredLanger lines used to determine the optimal incision line have been shown to produce worse cosmetic results than when following skin tension linesKoebner phenomenon Skin lesions which appear at the site of injury. It is seen in:PsoriasisVitiligoWartsLichen planusLichen sclerosusMolluscum contagiosumActinic keratosesActinic, or solar, keratoses (AK) is a common premalignant skin lesion develops due to chronic sun exposure. FeaturesSmall, and flat might develop Erythematous and rough to touchCrusty or Scaly, lesionsPink, Red, brown or the same colour as the skinTypically on sun-exposed areas (Temples of head, Back of hnds) FarmersMultiple lesions may be presentManagement Prevention of further risk sun avoidance, sun creamFluorouracil Cream typically a 2 to 3 week courseThe skin will become red and inflamed Topical hydrocortisone is given following fluorouracil to help settle the inflammationTopical Diclofenac mild AKs. Moderate efficacy but much fewer side-effectsTopical Imiquimod: trials have shown good efficacyCryotherapyCurettage and cauteryLentigo malignaA type of melanoma in-situ ?flat brown pigmentation with irregular edge progresses slowlyAt some stage become invasive causing lentigo maligna melanoma.Malignant melanomaSuperficial spreadingNodularLentigo malignaAcral lentiginousFrequency70% of cases2nd commonestLess commonRare formTypically affectsArms/ legs/ back/ chestyoung peopleThe most aggressiveSun exposed skin Middle-aged Chronically sun-exposed skin Older peopleMelanoma in-situ progresses slowly May invasive lentigo maligna melanoma.Nails, palms or soles African Americans or Asians> 40 (Male = Female)AppearanceA growing moles with diagnostic features Red or black lump bleeds or oozesA growing mole with diagnostic features Frackles in face & Scalp present for long time ChangeSubungual pigmentation on palms/Feet (Hutchinson's sign) extension of the nail bed, matrix and nail plate pigmentation to the adjacent cuticle and proximal or lateral nail folds.Other rare forms of melanoma Desmoplastic melanomaAmelanotic melanomaMelanoma arising in other parts of the body such as ocular melanoma.The main diagnostic (major criteria)Change in sizeChange in shapeChange in colour2ry features (minor criteria)Diameter >6mmInflammationOozing or bleeding↓↓sensationPrognostic factorsThe invasion depth of a tumour (Breslow depth) single most important prognostic factor Breslow Thickness5 year survival< 1 mm95-100%1 - 2 mm80-96%2.1 - 4 mm60-75%> 4 mm50%TreatmentSuspicious lesions Excision biopsy (The lesion should be removed in completely as incision biopsy can make histopathological assessment difficult.Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required Margins of excision-Related to Breslow thicknessLesions 0-1mm thick1cmLesions 1-2mm thick1- 2cm (Depending upon site and pathological features)Lesions 2-4mm thick2-3 cm (Depending upon site and pathological features)Lesions >4 mm thick3cmFurther treatments Sentinel LN mapping, Isolated limb perfusion and block dissection of regional LN groups should be selectively applied.Erythema ab igneSkin disorder caused by over exposure to infrared radiation. Characteristic features Reticulated, Erythematous patches + Hyper pigmentation & Telangiectasia. A typical history Elderly women who always sits next to an open fire.(or presentation in Winter ↑↑exposure to heat)Complication If the cause is not treated SQ. cell skin cancer.SQ. cell carcinoma of the skinMetastases are rare (2-5%). arising in chronic wounds The most common malignancy of the lip and mostly occurring on the lower lip "90%" (DD. Basal cell Carcinoma)SCCs arising in a chronic scar? ↑↑ aggressive so early diagnosis and biopsy are important to prevent metastatic disease. Non- healing painless chronic wounded (Scarred or inflamed skin skin overlying focus of osteomyelitis, scars, radiotherapy scars and venous ulcers.?Risk factors Excessive exposure to sunlight / psoralen UVA therapyActinic keratoses and Bowen's diseaseImmunosuppression (following?renal transplant, HIV)Smoking especially lips Long-standing leg ulcers (Marjolin's ulcer)Genetic conditions (Xeroderma pigmentosum, Oculocutaneous albinism)Treatment< 20mm in diameter Surgical excision (Biopsy) with 4mm margins if lesion Tumour >20mm margins 6mm. Mohs micrographic surgery after confirming diagnosis may be used in high-risk patients and in cosmetically important sites.PrognosisGood PrognosisPoor prognosisWell differentiated tumoursPoorly differentiated tumours < 20mm diameter20mm in diameter < 2mm deep4mm deepNo associated diseasesImmunosupression for whatever reasonBasal cell carcinomaOne of the three main types of skin cancer "Rodent Ulcers" slow-growth and local invasion W rare metastasis BCC is the most common type of cancer in the Western world. FeaturesMany types most common "Nodular BCC", which is described hereSun-exposed especially the head and neck (Majority of lesions)initially pearly, Flesh-coloured Papule with Telangiectasiamay later ulcerate leaving a Central 'Crater'/DepressionMorphemic basal cell carcinoma firm/rough/waxy patches often on the cheeks.?ReferralGenerally, if a BCC is suspected,?a routine referral should be madeAn excision biopsy is not necessary as it is a clinical diagnosis Management Mohs Surgical removal Confirms diagnosis + treat the lesion (removing it fully until clear margins are present.curettagecryotherapyTopical cream: imiquimod, fluorouracilRadiotherapySystemic mastocytosisResults from a neoplastic proliferation of mast cells. FeaturesUrticarial Pigmentosa - produces a wheal on rubbing (Darier's sign)FlushingAbdominal painMonocytosis on the blood film.Diagnosis↑↑serum tryptase levelsUrinary Histamine urinary 5-HIAA levelsVenous ulcerationVenous ulceration is typically above the medial malleolusDD. Ongoing infection is not a common cause of non-healing leg ulcers.InvestigationsAnkle - Brachial pressure index (ABPI) non-healing ulcers to assess for poor arterial flow (If abnormal referral to the vascular surgeons) 'Normal' ABPI (0.9 - 1.2) < 0.9 indicate arterial disease. >1.3 may also indicate arterial disease (False -Ve results 2ry to arterial calcification (D.M)Managementcompression bandaging, usually 4 layers (Only treatment real benefit)If the ulcer fails to heal referral for consideration of biopsy to exclude a malignancy oral Pentoxifylline Peripheral vasodilator, improves healing rateSmall evidence base supporting use of flavinoidslittle evidence hydrocolloid dressings/ Topical growth factors/ U/S therapy/ Intermittent pneumatic compressionVitiligoAutoimmune condition loss of melanocytes and depigmentation of the skin. (1%) population (20-30 years). Featureswell-demarcated patches of depigmented skinthe peripheries tend to be most affectedTrauma may precipitate new lesions (Koebner phenomenon)Associated conditionsType 1 D.MAddison's diseaseAutoimmune Thyroid disordersPernicious anaemiaAlopecia areataManagementSunblock for affected areas of skinCamouflage make-upTopical corticosteroids may reverse the changes if applied earlyTopical tacrolimus and Phototherapy (caution needs to be exercised with light-skinned patients)Lichen planusLichen planus is a skin disorder of unknown aetiology, most probably being immune-mediated. FeaturesPlanus Purple,?Pruritis,?Papular,?Polygonal violaceous may coalesce rash on flexor surfaces. Sclerosis Itchy white spots typically seen on the vulva of elderly mon Sites palms, soles, genitalia and flexor surfaces of armsShape Polygonal with a 'white-lines' pattern on the surface (Wickham's striae)Oral involvement "Common" 50% (white-lace pattern )on the buccal mucosaNails thinning of nail plate, longitudinal ridging."Koebner Phenomenon " may be seen (new skin lesions appearing at the site of trauma)Lichenoid drug eruptions - causes:GoldQuinineThiazidesManagementTopical Steroids "Topical clobetasone butyrate" the mainstay of treatmentBenzydamine mouthwash or spray oral lichen planusExtensive lichen planus oral steroids or immunosuppressionLichen sclerosusInflammatory condition affects the genitalia and ↑↑common in elderly females leads to atrophy of the epidermis with white plaques formingFeatures Itch is prominentDiagnosisusually made on clinical grounds but a biopsy may be performed if atypical features are present.Patients under routine follow-up will need a biopsy if:?Suspicion of neoplastic change (Persistent area of hyperkeratosis/ Erosion or Erythema/ New warty/ Papular lesions)Fails to respond to adequate treatment.Extra genital LS + features suggesting an overlap with morphoeaPigmented areas to exclude an abnormal melanocytic proliferation;2nd-line therapy is to be used.ManagementTopical steroids and emollientsFollow-up:↑↑risk of vulval cancerDD. Candida ?May cause pruritus + white plaques but lesions would not seen on her inner thighLivedo reticularisPurplish, Non-blanching, Reticulated rash? caused by obstruction of the capillaries resulting in swollen venules. CausesIdiopathic (most common)Polyarteritis NodosaSLECryoglobulinaemiaAPL syndromeEhlers-Danlos SyndromeHomocystinuriaPruritusConditionNotesLiver diseaseHistory of alcohol excessStigmata of chronic liver disease spider naevi, bruising, palmar erythema, gynaecomastiaDecomposition ascites, jaundice, encephalopathyIron deficiency anaemiaPallorOther signs koilonychias/ Atrophic Glossitis/ Post-Cricoid webs/ Angular StomatitisPolycythaemiaPruritus particularly after warm bath'Ruddy Complexion'GoutPeptic ulcer diseaseChronic kidney diseaseLethargy & pallorOedema & weight gainHypertensionLymphomaNight sweatsLymphadenopathyHSMFatigueOther CausesHyper- and hypothyroidismD.MPregnancy'Senile' pruritusUrticariaSkin disorders Eczema, Scabies, Psoriasis, pityriasis roseaPyoderma gangrenosumtypically on the lower limbsinitially small red papulelater deep, red, necrotic ulcers with a violaceous bordermay be accompanied systemic symptoms e.g. Fever, myalgiaCauses*idiopathic in 50%inflammatory bowel disease: ulcerative colitis, Crohn'srheumatoid arthritis, SLEmyeloproliferative disorderslymphoma, myeloid leukaemiasmonoclonal gammopathy (IgA)primary biliary cirrhosisManagementthe potential for rapid progression is high in most patients and most doctors advocate oral steroids as first-line treatmentother immunosuppressive therapy, for example ciclosporin and infliximab, have a role in difficult cases*note whilst pyoderma gangrenosum can occur in diabetes mellitus it is rare and is generally not included in a differential of potential causesPorphyria cutanea tardaThe most common hepatic porphyria. Inherited defect in Uroporphyrinogen Decarboxylase Acquired caused by Hepatocytes damage (Alcohol/ Hepatitis C/ Oestrogen).FeaturesClassically Photosensitive rash + Blistering + Skin fragility (Tear easily) on the face and dorsal aspect of hands (most common feature)HypertrichosisHyperpigmentationInvestigationsUrine ↑↑uroporphyrinogen and pink fluorescence of urine under Wood's lampSerum iron Ferritin level to guide therapyManagementChloroquineVenesectionpreferred if iron ferritin > 600 ng/mlScabies"Sarcoptes scabiei"? spread by prolonged skin contact. Affects children and young adults.?The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus due to a delayed type IV hypersensitivity reaction to mites/eggs (30 days after the initial infection).Featureswidespread prurituslinear burrows on the side of fingers, interdigital webs and flexor aspects of the wristInfants face and scalp may also be affected2ry features are seen due to scratching: excoriation, infectionManagementPermethrin 5% is first-lineMalathion 0.5% is second-linepruritus persists for up to 4-6 weeks post eradicationAppropriate guidance on use Avoid close physical contact with others until treatment is completeall household and close physical contacts treated at the same time, even if asymptomaticlaunder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill off mites.Apply the insecticide to all areas (face and scalp). Patients should be given the following instructions:apply the insecticide cream or liquid to cool, dry skinpay close attention areas between fingers and toes, under nails, armpit area, creases of the skin (Wrist & Elbow)leave on the skin for 8-12 hours for permethrin, or for 24 hours for malathion, before washing offreapply if insecticide is removed during the treatment period, e.g. If wash hands, change nappy, etcrepeat treatment 1 week laterCrusted (Norwegian) scabiesPatients with suppressed immunity, especially HIV.?The crusted skin will be teeming with hundreds of thousands of organisms.?Ivermectin is the treatment of choice and isolation is essentiall Skin disorders associated with malignancyParaneoplastic syndromes associated with internal malignancies:Skin disorderAssociated malignanciesAcanthosis NigricansGastric cancerAcquired ichthyosisLymphoma Acquired hypertrichosis lanuginosaGIT and lung cancerDermatomyositisOvarian and lung cancerErythema gyratum repens ('wood-grain' pattern?)Concentric, Erythematous (flat\ slightly raised bands W wavey white scale in at the edge of erythemaLung cancerErythrodermaLymphomaMigratory ThrombophlebitisPancreatic CancerNecrolytic Migratory ErythemaGlucagonomaPyoderma gangrenosum (Bullous & Non-bullous forms)Myeloproliferative disordersSweet's syndromeHaematological malignancy ( Myelodysplasia tender, purple plaques)TylosisOesophageal cancerSkin disorders associated with pregnancyMelasmaAtopic eruption of pregnancyPolymorphic eruption of pregnancyPemphigoid GestationisFlat, symmetrical, brown-pigmented patch Cheeks, Forehead, Nose and upper lip May resolve a few months after monest skin disorder in pregnancyEczematous, Itchy red No specific treatment is neededPruritic condition associated in last trimester1st appear in abdominal striaeManagement depends on severity: Emollients, Mild potency topical steroids and oral steroids may be usedPruritic blistering lesionsIn peri-umbilical region later spreading to the trunk, back, buttocks and arms2nd or 3rd trimester and rarely 1st pregnancyOral corticosteroids are usually requiredShin lesionsErythema NodosumPyoderma GangrenosumPretibial MyxoedemaNecrobiosis Lipoidica diabeticorumErythema nodosumSymmetrical, Erythematous, Tender, nodules which heal without scarringmost common causes are Streptococcal infections, Sarcoidosis, IBD and Drugs (Penicillins, Sulphonamides, Oral contraceptive pill)Pyoderma gangrenosuminitially small red papule later deep and necrotic ulcers with a violaceous borderidiopathic in 50%, may also be seen in IBD, connective tissue disorders and myeloproliferative disordersPretibial myxoedemasymmetrical, erythematous lesions seen in Graves' diseaseshiny, Orange peel skinNecrobiosis lipoidica diabeticorumD.M + Shiny, painless areas of yellow/red skin Lesion + TelangiectasiaGranuloma annularePapular lesions that are often slightly hyperpigmented and depressed centrallytypically occur on the dorsal surfaces of the hands and feet, and on the extensor aspects of the arms and legsA number of associations have been proposed to conditions such as D.M.Skin disorders associated with diabetesPyoderma gangrenosum D.M it is rare and is often not included in a differential of potential causesNecrobiosis lipoidicashiny, painless areas of yellow/red/brown skin typically on the shinoften associated with surrounding telangiectasiaInfectioncandidiasisstaphylococcalNeuropathic ulcersVitiligoLipoatrophyDiabetic dermopathy Red papules progress to small, round, atrophic hyperpigmented skin lesions, usually on the shins. It is associated ↑↑age & ↑↑duration of diabetes.Granuloma annulare* Papular lesions slightly hyperpigmented + Depressed centrallySkin disorders associated with tuberculosisPossible skin disordersLupus Vulgaris Commonest 50% of cases Indian face and is common around the nose and mouth (Erythematous flat elevate then ulcerate) Erythema NodosumScarring AlopeciaScrofuloderma breakdown of skin overlying a tuberculous focusVerrucosa cutisGummaStevens-Johnson syndromeSevere systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction. Delayed-hypersensitivity reaction involving T-cells (Same for toxic epidermal Necrolysis). FeaturesRash is typically maculopapular with target lesions being characteristic. May develop into vesicles or bullaeMucosal involvementSystemic symptoms fever, ArthralgiaCausesPenicillinSulphonamides (Co-Traimoxazole)AllopurinolNSAIDsOral contraceptive pillAnti –Epileptics Lamotrigine, carbamazepine, phenytoinManagement Hospital admission is required for supportive treatmentToxic epidermal NecrolysisPotentially life-threatening skin most commonly 2ndary to a drug reaction. Scalded appearance over an extensive area. TEN might be severe end of a spectrum of skin disorders (Erythema multiforme & Stevens-Johnson S).FeaturesSystemically unwell pyrexia, tachycardic+ Ve "Nikolsky's sign" the epidermis separates with mild lateral pressureDrugs induce TENPhenytoinCarbamazepinePenicillinsSulphonamidesAllopurinolNSAIDsManagementstop precipitating factorSupportive care Often in ICUIV immunoglobulin 1st-lineImmunosuppressive agents (ciclosporin and cyclophosphamide) PlasmapheresisPellagraNicotinic acid (Niacin/ Vit. B3) deficiency. Causes Alcoholics ↑↑ commonIsoniazid?therapy (- -) conversion of tryptophan to niacin).FeaturesDermatitis?(Brown, Scaly rash on sun-exposed sites if around neck "Casal's Necklace" DiarrhoeaDementia/ Depression low mood, irritability, apathy and anxiety, Delusions, psychosis, drowsiness and comaDeath if not treatedZinc deficiencyDestruction or malfunction of gut mucosa and malabsorption. Total Parenteral nutrition FeaturesCognitive impairmentAlopeciaGeophagia (ingesting clay/soil)Perioral dermatitis: red, crusted lesionsAcrodermatitis Herpetiformis Peri - Orificial dermatitis.Short statureHSMHypogonadismFungal nail infections"Onychomycosis" is fungal infection of the nails. Caused byDermatophyte "Fungal Infection" "Trichophyton Rubrum" "90% of cases"yeasts CandidaNon-dermatophyte mouldsRisk factors D.M/ ↑↑ age.Features'unsightly' nails are a common reason for presentationThickened, rough, Opaque nails are the most common findingDifferential diagnosisPsoriasisRepeated traumaLichen PlanusYellow nail syndromeInvestigationNail clippingsScrapings of the affected nailFalse -Ve rate for cultures are around "30%" repeat samples may need to be sent if the clinical suspicion is highManagementAsymptomatic?and the patient is not bothered by the appearance do not need to be treated if it isDiagnosis confirmed by microbiology before starting treatmentDermatophyte infectionOral Terbinafine? 1st-line with oral itraconazole as an alternativeFingernail infections 6 weeks - 3 months Toenails treated for 3 - 6 monthsTreatment is successful in around 50-80% of peopleCandida?infection:Mild disease Topical Antifungal (Amorolfine) More severe oral itraconazole for 12 weeksTopical treatment is given Fingernails 6 months for Toenails? 9-12 months TineaDermatophyte fungal infections. Three main types of infection are described depending on what part of the body is infectedTinea capitis - scalpTinea corporis - trunk, legs or armsTinea pedis - feetTinea capitis (scalp ringworm)Tinea corporis (ringworm)Tinea pedis (athlete's foot)Cause of scarring alopecia mainly in childrenUntreated Raised, pustular, spongy/boggy mass called "kerion"CauseTrichophyton Tonsurans?"Commonest"Microsporum Canis? (Cats or Dogs)Diagnosis: Microsporum canis? green fluorescence under Wood's lampTrichophyton? do not readily fluoresce under Wood's lamp. Scalp scrapings "Most useful"Management Trichophyton Tonsurans? Terbinafine Microsporum Griseofulvin Topical ketoconazole shampoo first two weeks to reduce transmissionCauses Trichophyton Rubrum?Trichophyton Verrucosum?(contact with cattle)Well-defined annular, Erythematous lesions with pustules and papules Treated with oral fluconazoleItchy, peeling skin between the toescommon in adolescenceOnycholysisDescribes the separation of the nail plate from the nail bed. CausesIdiopathic↓↓ peripheral circulation (Raynaud's)Trauma Excessive manicuringInfection especially fungalSkin Disease Psoriasis, DermatitisSystemic disease Hyper- and HypothyroidismYellow nail syndromeSlowing of the nail growth characteristic thickened and discoloured nails seen in yellow nail syndrome. AssociationsCongenital LymphoedemaPleural EffusionsBronchiectasisChronic sinus infections ................
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