Dermatology without pics

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  • Primary genetic defect in skin barrier function (filaggrin).
  • Care of a patient with SJS/TEN requires:
    Cessation of suspected causative drug(s) – the patient is less likely to die and complications are less if the culprit drug is stopped no later than the day that blisters/erosions appear
    Hospital admission – preferably immediately to an intensive care and/or burns unit as this improves survival, reduces infection and shortens hospital stay
    Nutritional and fluid replacement (crystalloid) by intravenous and nasogastric routes – reviewed and adjusted daily
    Temperature maintenance – as body temperature regulation is impaired
    Pain relief – as pain can be extreme
    Sterile handling and reverse isolation procedures
    Skin care:
    topical antiseptics e.g. silver nitrate or chlorhexidine, (but not silver sulfadiazine as it is a sulfa drug)
    dressings such as gauze with petrolatum or non-adherent nanocrystalline-containing gauze
    biosynthetic skin substitutes can reduce pain
    avoid using adhesive tapes
    preferable not to remove the dead skin; leave the blister roof as a ‘biological dressing’
    daily examination and skin culture to detect bacterial infection
    Eye care:
    daily assessment by ophthalmologist,
    frequent eye drops/ointments (antiseptic, antibiotic, cortisone)
    Mouth care:
    mouthwashes
    topical oral anaesthetic
    Lung care:
    may include aerosols, bronchial aspiration, physiotherapy
    may require intubation and mechanical ventilation if trachea and bronchi are involved
    Urinary catheter because of genital involvement and immobility
    Psychiatric support for extreme anxiety and emotional lability
    Physiotherapy to maintain joint movement and reduce risk of pneumonia
    Regular assessment for infection including of skin, mucous membranes, catheter sites:
    Staphylococcal infection is common; gram negative infection may also arise
    appropriate antibiotic should be given if infection develops
    prophylactic antibiotics are not recommended and may even increase the risk of sepsis
  • Dermatology without pics

    1. 1. Dermatolgy Dr Alistair Brown
    2. 2.       Descriptive terms in dermatology Common skin conditions Skin cancer Emergency Dermatology Infections MCQs
    3. 3. What are you describing? Pruritus  Lesion – altered area of skin  Rash – eruption  Naevus – localised malformation of tissue structure.  Comedone – plug in a sebaceous follicle containing sebum – may be open (blackhead) or closed (whitehead). “The patient has a rash…” 
    4. 4. Where is it? Generalised – all over body  Widespread – extensive  Localised – one area of skin  Flexural – body fold eg groin, axilla  Extensor – eg knees, shins  Pressure areas – sacrum, buttocks, ankles, heels.  Dermatome – skin supplied by single nerve  Photosensitive areas – sun exposed. “The patient has a widespread rash affecting their torso” 
    5. 5. What colour is it?      Erythema – redness (due to inflammation and vasodilation) blanches on pressure. Purpura – red or purple colour (due to bleeding into the skin or mucous membranes) does not blanch to pressure. Petechiae (small pinpoint macules) and ecchymoses (larger bruise like patches) Hypopigmentation (pityriasis vesicolor) De-pigmentation (vitiligo) Hyperpigmentation (melasma)
    6. 6. Configuration       Discrete Confluent – lesions merge together Linear Target Annular Discoid
    7. 7. What shape is it?        Macule – flat area of altered colour Patch – larger area of altered colour Papule – solid raised lesion <0.5cm in diameter Nodule – Solid raised lesion >0.5cm diameter Plaque – palpable raised lesion >0.5cm Vesicle – raised clear fluid filled lesion <0.5cm diameter. Bulla – raised clear fluid filled lesion >0.5cm diameter.
    8. 8. Test Yourself        Macule Patch Papule Nodule Plaque Vesicle Bulla
    9. 9. http://www.dermnetnz.org/dermatit is/atopic.html
    10. 10. Atopic Excema       Itchy papules and vesicles on an erythematous base. Affects face and extensor in infants, flexor aspect children and adults. Occurs in early childhood, usually resolves. Risk factors: fhx of atopy, assoc asthma, allergic rhinitis etc) Exacerbating factors: infections, allergens (chemical, food, dust, pets), sweating, heat, stress. Complications: secondary bacterial/viral infection
    11. 11. Management     Avoid exacerbating agents Frequent emolients Topical steroids for flares Antihistamine for symptomatic relief
    12. 12. http://www.dermnetnz.org/scaly/p soriasis-general.html
    13. 13. Psoriasis   A chronic inflammatory disease hyperproliferation of keratinocytes and inflammatory cell infiltration. Chronic plaque – most common     (Other types: guttate, seborrhoiec, flexural, pustular, erythrodermic) 2% of population Precipitants: trauma, stress, infection, drugs, alcohol Signs and symptoms:      Well demarcated lesions with erythematous base, and silver scaly plaques Affecting extensor surfaces and scalp Auspitz sign 50% nail changes (pitting, onycholysis) 5-8% associated arthropathy (symmetric polyarthritis, asymmetrical oligomonoarthritis, distal interphalangeal disease, spondyloarthropathy, athritis mutilans.)
    14. 14. Management     Avoid precipitants. Topical therapy – vit d analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, salicylic acids. Phototherapy (extensive disease) Systemic – methotrexate, oral retinoids, ciclosporin, mycophenolate mofetil, biologics (adalimumab, etanercept, infliximab and ustekinumab)
    15. 15. http://www.dermnetnz.org/acne/ac ne-vulgaris.html
    16. 16. Acne Vulgaris     Inflammation of pilosebaceous follicle – face, chest, upper back. Hormonal – increased sebum productiomn, abnormal follicular keratinisation, p. acnes colonisation and inflammation. Non inflammatory lesions - open and closed comedones, inflammatory lesions – papules, pustules, nodules, cysts. Complications – post inflammatory hyperpigmentation, scarring, deformity, psychosocial impact.
    17. 17. Management   Topical – benzoyl peroxide, topical antibitics, topical retinoids. Oral oral antibiotics eg tetracycline’s  Females – OCP – dianette  Oral retinoids – isotretinoin, severe acne 
    18. 18. http://www.dermnetnz.org/lesions/ basal-cell-carcinoma.html
    19. 19. Basal cell carcinoma    Locally invasive tumour of epidermal keratinocytes “pearly papule” with surface telangectasia and rolled edges, may have ulcerated centre. Risk factors         uv exposure Sunburn as a child Skin type 1 Male Immunosuppresion Previous hx of skin cancer Genetic predisposition Management    Surgical Radiotherapy Other: cryotherapy, curretage and cautery, topical photodynamic therapy, imiquimod cream.
    20. 20. http://www.dermnetnz.org/lesions/bo wen.html
    21. 21. Squamous cell carcinoma    Invasive malignant tumour of epidermal kertinocytes or appendages with potential to metastasise. Risk factors: sun exposure, pre-malignant skin condistions eg. Actinic keratoses, chronic inflammation (leg ulcers), immunosuppression, genetic predisposition, smoking. Treatment:     Surgical excision Moh’s micrographic surgery Radiotherapy Chemotherapy – metastatic disease
    22. 22. http://www.dermnetnz.org/lesio ns/melanoma.html
    23. 23. Malignant melanoma   Invasive malignant tumour of epidermal melanocytes with metastatic potential. ABCDE approach        Asymettry Border Colour Diameter Evolution Symptoms – bleeding, itch Risk factors:         Atypical moles Large numbers of moles Skin type 1&2 Severe sun burn <14 Fhx Sun exposure Previous melanoma immunosuppression
    24. 24. Management  Surgical excision Excision biopsy  WLE +/- sentinel node biopsy  If node positive – axillary clearance  If further nodes positive – staging    Intensive followup Palliative options – aim to reduce macroscopic disease burden.
    25. 25. Emergencies  http://www.dermnetnz.org/reactions/angioede ma.html
    26. 26. Urticaria, Angioedema, Anaphylaxis     Causes – food, drugs, insect bites, contact eg latex, autoimmune, hereditary (angiodema), etc Urticaria – swelling superficial dermis – raises epidermis causing itch wheals. Angiodema – deeper swelling involving dermis and subcutaneous tissue – tongue and lips. Anaphylaxis – bronchospasm, facial and laryngeal oedema, hypotension, can start with angiodema and urticaria.
    27. 27. Management     ABC approach – call for help if concerned. Urticaria only – antihistamines Angioedema and severe urticaria – corticosteroids and antihistamines. Anaphylaxis – get help! Adrenaline 0.5 mg IM = 0.5 mL of 1:1000  Antihistamine – chlorphenamine  Corticosteroids 
    28. 28. q=stevens+johnson+syndrome+der m+nz&oq=steven&aqs=chrome.1.69 i57j69i59l2j0l3.3052j0j4&sourceid=chr ome&espv=210&es_sm=122&ie=UT F-8
    29. 29. Stevens-johnson syndrome and Toxic epidermal necrolysis •Primarily a drug reaction: sulfonamides (eg cotrimoxazole), NSAIDs, Carbamazepine, Phenytoin, Phenobarbital, Valproic acid, Lamotrigine. •Can also be caused by infections: HSV, mycoplasma. •Prodromal illness – fever, cough, sore throat, general malaise followed by abrupt onset macular or purpuric blistering rash. •Prominent mucosal involvement, at least 2 of: •Eyes (conjunctivitis) – red, sore, sticky •Lips/mouth (cheilitis, stomatitis) – red crusted lips, mouth ulcers •Oesophagus – causing difficulty eating •Upper respiratory tract (trachea and bronchi) – causing cough and respiratory distress •Genital area and urinary tract – ulcers •Gastrointestinal tract – causing diarrhoea. •SJS <10%BSA TEN>30% BSA •Mortality 5-12% SJS, >30%TEN •Management – stop drug cause, supportive – preferably burns unit
    30. 30. http://www.dermnetnz.org/reactions /erythroderma.html
    31. 31. Erythroderma     Exfoliative dermatitis involving >90% of skin surface. 20-40% mortality. Treat cause – eg. atopic dermatitis, psoriasis, blistering diseases (pemphigus and bullous pemphigoid), cutaneous T-cell lymphoma Supportive management – fluid loss, elctrolyte imbalance, hypothermia, high output cardiac failure, capillary leak, prevention of secondary infection. Prognosis depends on cause, mortality 20-40%
    32. 32. http://www.dermnetnz.org/bacteria l/necrotising-fasciitis.html
    33. 33. Necrotising fasiitis • Rapidly spreading infection of the deep fascia with secondary tissue necrosis • Group A haemolytic strep or mixed anaerobic and aerobic bacteria. • Risk factors – abdominal surgery, diabetes, immunosuppression, age, malignancy • BUT 50% occur in previously healthy individuals • Pain disproportionate to signs, erythematous blistering necrotic skin, systemically unwell with fever and tachycardia, subcutanceos emphysema (crepitus). • Urgent surgical debridement and antibiotics
    34. 34. http://www.dermnetnz.org/viral /eczema-herpeticum.html
    35. 35. Excema Herpeticum • Caused by HSV infection superimposed on a skin condition most commonly atopic eczema. • Extensive papules and erosions with systemic fever and malaise • Management – antivirals (aciclovir) +/- abx for secondary bacterial infection • Complications – Encephalitis, DIC, opthalmic involvement, rarely death
    36. 36. http://www.dermnetnz.org/bact erial/impetigo.html
    37. 37. Impetigo     Streptococcus pyogenes and/or Staphylococcus aureus Enlarging pustules and round, oozing patches +/- golden yellow crusts. Exposed areas such as the hands and face, or in skin folds particularly the armpits. Management:    Antiseptic or antibiotic ointment eg. Fusidic acid Oral antibiotics  Avoid spread     Avoid close contact with others. Affected children must stay away from school until crusts have dried out. Use separate towels and flannels. Change and launder clothes and linen daily.
    38. 38. http://www.dermnetnz.org/arthr opods/scabies.html
    39. 39. Scabies     Itchy rash on trunk and limbs, finger webspaces, wrist, spares the scalp Burrow tracts can be seen Diagnosis on microscopic examination of tracts. Treatment (all contacts simultaneously!) 25% Benzyl benzoate lotion, applied daily for 3 days  5% Permethrin cream, left on for 8-10 hours  0.5% Aqueous malathion lotion, left on for 24 hours 
    40. 40. MCQs Atopic Eczema True or False A. a family history of atopy B. If occurs early and defined has bad prognosis C. In children it is common on cheeks D. In adults more common on flexor area E. Pruritis is absent
    41. 41. MCQ 2  What skin condition is this likely to be? -  Atopic dermatitis Tinea corporis Psoriasis Vitiligo Scabies What else should you examine?
    42. 42. MCQ 3  True or False which of the following are known risk factors for melanoma? Sun bed use  Xeroderma pigmentosum  Smoking  Ciclosporin  Living in the South West  Obesity 
    43. 43. MCQ4  How would you manage this patient? Imiquimod cream  Watch and wait  Punch biopsy of the lesion for histology  Take a picture and review in 3months to see if it has grown  Surgically remove with a 2mm margin for histology  WLE with a 2-3cm margin 
    44. 44. MCQ 5  A 60 year old woman presents with raised, erythematous lesions on the limbs and blistering in the mouth and eyes. She had been taking a number of drugs prescribed by her GP. Which may be responsible for her presentation?  nifedipine paracetamol paroxetine prednisolone Sulphasalazine  What is the most important first management?     
    45. 45. MCQ 6       A 22 year old male presents with generalised pruritus of six weeks duration. Examination reveals little except for erythematous papules between the fingers. Which of the following therapies would be most appropriate for this patient?  astemizole calamine lotion chlorpromazine ciprofloxacin permethrin cream
    46. 46. MCQ 7       Which of the following is a recognised feature of psoriasis?  angular stomatitis iridocyclitis Koebner Phenomenon loss of hair response to chloroquine

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