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See all Premium member Presentation Transcript Dermatology Revision: Dermatology Revision Chris HarlandAims: Aims To pass 4th year exam Hints towards 5th year ClinicalObjectives: Objectives 5 year-Red Specialties handbook 2% of total exam mark: already done! 4 year/GEP-Linked Year 3 ObjectivesGEP ‘Linked Year 3 Objectives: GEP ‘Linked Year 3 Objectives Skin Infection Eczema Psoriasis Skin manifestations of systemic disease Drug reactions Dermatological malignancies Leg ulcers Skin grafts & flaps/Burns managementGEP ‘Linked Year 3 Objectives: GEP ‘Linked Year 3 Objectives Skin Infection Eczema Psoriasis Skin manifestations of systemic disease Drug reactions Dermatological malignancies Leg ulcers Skin grafts & flaps/Burns management)Skin Infection: Skin InfectionSlide7: Herpes simplex infection around the mouthSlide8: Shingles affecting the maxillary division of the trigeminal nerve The diagnosis should be considered in any acute unilateral eruption, dermatomal distribution and especially if there are risk factors e.g. immunosuppressed, elderly patients Slide9: Shingles seen on the neck, affecting one of the cervical rootsSlide10: An important complication of eczema is secondary infection by the herpes virus resulting in eczema herpeticum This is treated with systemic aciclovirSlide11: Eczema herpeticum affecting the face, trunk and limbsSlide12: Molluscum Contagiosum This is caused by the pox virus Classically a pearly pink and umbilicated papule They usually resolve spontaneously, which is preferable to mechanical destruction Slide13: Cellulitis A deep streptococcal infection of the subcutaneous tissue.Patients are usually systemically unwell with pyrexia and malaise. Classically, a poorly demarcated erythematous lesion which can be associated with streaking/red tracks due to spread of infection up the lymphatics, called acute lymphangitis. Treat with intravenous Flucoxacillin and Benzylpenicillin. Patients who are penicillin allergic should have Erythromycin instead.Slide14: Cellulitis affecting the leg and foot The portal of entry here may be athletes foot and one should check between the toes for evidence of thisSlide15: Impetigo A contagious streptococcal or staphylococcal infection Typically produces a golden crusting Treat with topical Fucidin cream +/- oral Flucoxacillin in severe cases Slide16: Scalded Skin Syndrome. There is severe desquamation of the skin and systemic upset Slide17: Scabies of the hand The mite infection is caused by Sarcoptes Scabiei Female burrows into the epidermis and lays eggs. Individuals develop a hypersensitivity to mite excreta and become symptomatic with intense itch Burrows usually occur between fingers but they can be widespreadSlide18: Scabies affecting the finger. Burrows (see arrows) are pathognomonic and are best seen on fingers and palms. The scattered papular lesions are a reaction to the infestation and wheals are commonSlide19: Scabetic nodules in the axilla Scabies commonly affects the hands, feet, breasts and genitalia Extracting the scabies mite and positive identification down the microscope is useful Slide20: Scabies of the foot All family, sexual and household contacts are treated Treatment is with Permethrin. Malathion is used in pregnancy and in very small children Eczema: EczemaSlide22: ECZEMA A type of inflammatory process affecting the skin and due to various factors, both internal and external Eczema = DermatitisSlide23: FEATURES OF ECZEMA SYMPTOMS Itch Painful if fissures Weeping with infection SIGNS Acute erythema, oedema, papules and vesicles Chronic less oedema, lichenification, hyperkeratosis and fissuring Slide24: Severe acute eczema affecting both hands There is erythema, blistering, crusting (scabbing) and bleedingSlide25: Chronic eczematous patch, lichenification Lichenification = thickening of the epidermis due to scratching. Note the accentuation of the skin linesSlide26: Infantile eczema in an overtly miserable infant The skin looks weepy and infected Slide27: Complications Infection Bacterial (Staphylococcus) Viral (Herpes Simplex) in atopic eczema Erythroderma (see later in psoriasis) Side effects from treatments used e.g. allergic contact dermatitis and side effects of steroid abuse including telangiectasia, purpura and atrophy of the skin Slide28: Herpes infection around both eyes Classically, there are closely cropped vesicles or crusted erosions on an erythematous base Involvement of the eyes may lead to corneal scarringSlide29: Herpes infection of the hand with painful vesiclesSlide30: Continued: Treat infections Flucoxacillin for Staphylococcal infections (or topical antibiotic/steroid) Aciclovir for Herpes infections Psoriasis: PsoriasisSlide33: Clinical Patterns Skin Plaque Scalp Flexural Guttate Chronic Palmoplantar pustulosis Acute pustular Erythrodermic Nail psoriasis Joint/arthropathic psoriasis Slide34: Chronic plaque psoriasis, commonest form Well demarcated, red plaque with a scaly silvery surfaceSlide35: Scalp psoriasis. This classically affects the hairline and scale is shed leading to dandruff This can sometimes be difficult to distinguish from bad seborrhoeic dermatitis but psoriasis usually forms thicker scaleSlide36: Nail changes in Psoriasis: Pitting Onycholysis Ridging Subungual hyperkeratosis Salmon patchSlide37: Nail psoriasis. Any nail (usually multiple) can be affected,This slide shows onycholysis which is “lifting off of the nail plate”Slide38: Marked psoriatic nail dystrophy. The presence of psoriasis does not preclude fungal infection and if there is any doubt, one should send samples for microscopy and mycologySlide39: Joint deformity in psoriasis seen here affecting mainly the distal interphalangeal jointsSlide40: ERYTHRODERMA This is when the whole of the skin becomes red and there is little or no scaling Dangers include: poor thermoregulation protein and fluid loss high output cardiac failure secondary infection/septicaemia Some causes: psoriasis eczema drug eruptions pemphigus lymphoma Treatment is supportive and of the underlying causeSlide41: Erythrodermic Psoriasis Psoriasis covers virtually the whole body with widespread erythema and little or no scalingSlide42: Treatment: TOPICAL Emollients, Tar, Salicylic acid, Dithranol Vitamin D analogue (eg. Calcipotriol) Topical steroids PHYSICAL PUVA/UVB therapy SYSTEMIC Cyclosporin (need to monitor renal function and blood pressure) Methotrexate (monitor FBC, LFTs, teratogenic) Vitamin A analogue (Acitretin; teratogenic)Cutaneous manifestations of systemic disease: Cutaneous manifestations of systemic diseaseSlide44: Neurofibromatosis Characterised by multiple skin neurofibromas, skin pigmentation (> 5 café au lait patches) and axillary freckling Slide45: Erythema Multiforme. Target lesions on the hands are typically concentric rings and the centre may be bullous or necrotic. They are fixed lesions unlike in urticariaSlide46: Stevens-Johnson Syndrome Eye changes include conjunctivitis, uveitis and corneal ulceration, so its important to ask for early ophthalmology reviewSlide47: Necrobiosis lipoidica diabeticorum Orange/yellow waxy, atrophic appearance with overlying telangiectasia, often seen over the shins and they may ulcerate Histologically there is partial necrosis of dermal collagen and a histocytic cell responseSlide48: Granuloma Annulare. Flesh coloured, smooth, cobble-stoned, annular lesion with central sparing. They are of variable size and unlike fungal infections there is no flaking. Especially seen over extensor surface of hands They have a similar pathology to necrobiosis lipoidica diabeticorumSlide49: RHEUMATIC CAUSES Systemic sclerosis -Tight shiny facial skin -Telangiectasia -Sclerodactyly -Calcinosis +/- ulceration -Raynaud’s phenomenon Anti-centromere and antinucleolar antibodies +veSlide50: Systemic sclerosis Classically there is beaking of the nose, furrowing of the lips and facial telangiectasia (they are mainly on the cheeks and nose) Most organs may be affected but most frequently the oesophagus and patients can present with dysphagiaSlide51: Sclerodactyly. The skin of the fingers appear tightened and shiny due to fibrosis. There are telangiectasia also seen here affecting the handsSlide52: Vitiligo Areas of pigment loss are symmetrical and are often annular in outline, but can be various shapes Usually initially affect fingers, hands, face and genitalia Exhibits the Kobner reaction, with the development of lesions at traumatized sitesSlide53: Graves disease and vitiligo Tests will include those for thyroid function and autoantibodiesSlide54: Kaposi Sarcoma They are blue/black palpable and discrete lesions seen over the skin and in the mouthSlide55: Kaposi Sarcoma affecting the palateSlide56: Kaposi Sarcoma affecting the back in a young manSlide57: Lupus Pernio Classically, purplish/red palpable lesions, especially seen over the nose, cheeks and earlobesSlide58: MISCELLANEOUS Erythema Nodosum F>M, young adults Causes: -Sarcoidosis -Streptococcus (preceding URTI) -Tuberculosis, Leprosy -Drugs (Sulphonamides, OCP, Penicillin) -Inflammatory Bowel Disease -Behcets Syndrome (Orogenital ulcers, uveitis, arthritis, meningoencephalitis, colitis) -Idiopathic It presents with tender, erythematous nodules especially over the legs and is associated with fever, arthralgia and malaise Treatment is of the underlying cause Slide59: MISCELLANEOUS Urticaria (hives, “nettle-rash”) Common Pink, itchy or burning swellings (wheals) can occur anywhere on the body. Individual lesions last for less than 24hrs but new lesions can continue to appear elsewhere Classified as acute or chronic (urticaria persisting for >6 weeks) The majority are idiopathic but other causes include - physical (cold, heat) - autoimmune (hyperthyroidism) - drugs - SLESlide60: Dermatitis Herpetiformis More common in Caucasians Any age, peak 20-30s Associated with Gluten sensitive enteropathy Histologically there are subepidermal blisters and immunofluorescence shows fixed IgA in dermal papillae. There is no circulating autoantibody Treatment is lifelong with a gluten free diet. Dapsone can also be given to these patients (side effects include methaemoglobinaemia and haemolytic anaemia)Slide61: Dermatitis Herpetiformis Intensely pruritic, symmetrically distributed, erythematous papules and vesicles over the extensor surfaces of elbows, knees, forearms, buttocks and face/scalpSlide62: Dermatitis Herpetiformis affecting the buttocks Slide63: Dermatitis Herpetiformis affecting the extensor surface of both kneesSlide64: VESICO – BULLOUS DISORDERSSlide65: Blister is a circumscribed skin lesion containing fluid Vesicle <0.5cm blister Bulla >0.5cm blister Slide66: Bullous Pemphigoid Affects the older patient Histologically there are subepidermal blisters with the defect in the dermo-epidermal junction. Immunofluorescence shows IgG and C3 binding to the dermo-epidermal junction in a linear fashion. Circulating IgG is present in the serum Treatment is initially with moderate doses of systemic steroids and this can be stopped after several years (? role of steroid sparing agents)Slide67: This is the histology of a patient with Bullous Pemphigoid. The defect is in the dermo-epidermal junction and the blister space is filled with eosinophils (note the pink cytoplasm)Slide68: Bullous Pemphigoid Tense blisters on an erythematous pruritic base, usually affecting upper arms and thighsSlide69: Pemphigus Affects adults 40-60s Biopsy shows intraepidermal vesicles with keratinocytes floating free in the blister cavity (acantholysis) Immunofluorescence shows IgG fixed against intercellular desmosomes between keratinocytes. Circulating IgG is found in the serum Treatment is initially with high dose systemic steroids and in the long-term a steroid sparing agent e.g. Azathioprine Slide70: Bullous Pemphigus It usually begins in the oral mucosa and is characterised by flaccid vesicles which are fragile and burst readily producing eroded areas on the face, scalp, neck and chest Nikolsky sign positive is when a shearing stress on normal skin can cause new erosions to formSlide71: There are eroded areas on the chest wall and a positive Nikolsky sign due to fragility of the blisters Slide72: Pemphigus affecting the oral mucosaSlide73: Pemphigus Vulgaris Drug reactions: Drug reactionsDermatological malignancies: Dermatological malignanciesSlide76: SKIN TUMOURS Melanoma Non-Melanoma (SCC, BCC, others)Slide77: MALIGNANT MELANOMA Relatively uncommon, but recent increase in incidence Usually occurs on sun-exposed sites vulnerable to episodic exposure and sunburn (backs in men and legs in women) More common: -fair/freckled skin -large number of moles -atypical, large moles -family/personal previous history Slide78: Mackie’s Guide for Malignant Melanoma: Major signs - change in shape - change in size - change in colour Minor signs - inflammation - crusting/bleeding - diameter >7mm - altered sensation e.g. itch ABCD: Asymmetry, Border, Colour, DiameterSlide79: Its important to pick up early as prognosis is directly related to tumour thickness (Breslow) Thin lesions <1.5mm Thick lesions > 3.5mmSlide80: Various forms of melanoma: Nodular melanoma Superficial spreading melanoma Acral melanoma Subungual melanoma (melanoma seen under the nail and spread to the skin produces Hutchinsons sign) Amelanotic melanoma (often there is a rim of pigment and can present late) Lentigo maligna (pre-malignant melanoma)Slide81: Superficial Spreading Melanoma. This is the most common variety, which initially grows horizontally before becoming raised. Note the irregular edge, non-uniform pigmentation and large sizeSlide82: Superficial spreading melanoma This is Clark’s level 1 (in situ i.e. no invasion) There are fuzzy edges and non-uniform colour Slide83: Nodular melanoma. There is a nodular component and they are more aggressive than the superficial variety as their growth is mainly verticalSlide84: Afro-Caribbean people rarely get melanomas but when they do it is usually on their hand or sole of their foot- Acral melanomaSlide85: Satellite lesions are indicative of cutaneous metastasis and advanced stagesSlide86: Lentigo maligna This is a non-invasive form of melanoma and consists of proliferating malignant melanocytes Typically flat, brown, irregularly pigmented area on elderly, sun-damaged face It spreads along the skin insidiously and the presence of nodules indicate invasionSlide87: Treatment Wide excision of the malignant melanoma Prognosis 97% (Breslow <0.78mm) 90% (Breslow <1.5mm) 40% (Breslow >3mm) Sentinel node biopsy: Sentinel node biopsy Staging procedure First draining lymph node Early treatment if lymph spread Prognosis?Slide89: Basal cell carcinoma at the nasolabial fold There is a pearly, translucent edge especially when the skin is stretched and also overlying telangiectasia Slide90: Nodular BCC on the nose Treatment options for BCCs include: excision radiotherapy curettage and cautery The treatment option depends on the location, size of the BCC and any previous treatmentsSlide91: Squamous cell carcinoma of the lip. Slide92: Marjolins Ulcer SCC arising from a venous ulcer Treatment options for squamous cell carcinoma include: excision radiotherapySlide93: There are multiple pigmented naevi on this woman’s back. Can you spot the melanoma? Multiple dysplastic naevi and melanoma found in families (dysplastic naevus syndrome) represents a high risk of melanoma and they should be screened periodically for melanoma Leg ulcers: Leg ulcersLeg ulcers: Leg ulcers Venous Arterial Diabetic Sickle cell Pressure/decubitus Tumours Neuropathic (eg leprosy) Traumatic Infections (eg Buruli ulcer)Slide96: Erosion UlcerSlide97: Venous ulcer -medial malleolus -pitting oedema -haemosiderin (brown) -eczema -varicose veins -lipodermatosclerosis Slide98: Sickle cell ulcerSkin grafts/flapsBurns management: Skin grafts/flaps Burns managementGEP ‘Linked Year 3 Objectives: GEP ‘Linked Year 3 Objectives Skin Infection Eczema Psoriasis Skin manifestations of systemic disease Drug reactions Dermatological malignancies Leg ulcers Skin grafts & flaps/Burns management)GOOD LUCK!: GOOD LUCK! To pass 4th year exam Hints towards 5th year Clinical You do not have the permission to view this presentation. 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