My Dermatology

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My Dermatology
2012-01-21 12:53:15
Eczema psoriasis lesions

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  1. Define psoriasis
    A chronic, relapsing and remitting scaling skin disease
  2. What is the pathogenesis of psoriasis?
    • T-cell mediated autoimmunity
    • Abnormal T cell infiltration releases cytokines = increased keratinocyte proliferation
  3. What are some co-morbidities of psoriasis?
    • Psoriatic arthritis: Arthritis in 30% of chronic psoriasis
    • Metabolic syndrome
    • Liver disease
    • Depression
  4. What are the frequent ages of onset of psoriasis?
    Between 20-30 and 50-60
  5. Outline the common clinical presentation of psoriasis
    • Discrete, circular, pink patches/plaques from hyperkeratosis
    • Found on extensor surfaces, scalp, buttocks (trauma sites)
    • Nail features; onycholysis, pitting
  6. Describe the subtypes of psoriasis
    • Plaque: Pink/red scaly plaques
    • Guttate: 'Raindrop' like, very small, circular plaques on trunk. Related to strep throat
    • Pustular: Diffuse redness with blisters on palms and feet soles + exfoliation
    • Erythromdermic: Generalised redness, extreme keratosis
  7. What factors affect the treatment choice for psoriasis?
    • Severity
    • Patient choice
    • Patient capability
    • Related arthropathy
  8. Outline the treatment choices for psoriasis
    • Topical creams
    • Phototherapy
    • Acitretin
    • Methotrexate
    • Ciclosporin
    • (in order of toxicity)
  9. Outline the pathophysiology of eczema
    • Inherited abnormalities in the skin; irregular fillagrin expression
    • Creates a 'barrier defect'
    • Increased permeability reduces antimicrobial function
  10. Describe some endogenous causes of eczema?
    • Atopic: Allergy = itchines. Managed with moisturisers + antihistamines, maybe topical steroids
    • Seberrhoiec: Yeast infection; anti-fungal shampoo and moisturiser given
    • Varicose: Vein incompetence = hydrostatic pressure = stretched dry skin. Compression socks
  11. What are common causes of exogenous eczema?
    • Contact allergies the main cause; nickel, chromate, cobalt, fragrance etc.
    • Photosensitivity due to drugs
  12. What is native joint septis arthritis?
    • A medical emergency, where one of the patient's joints becomes infected.
    • Loss of cartilage and osteoarthritis
  13. What is the clinical presentation of septic arthritis?
    • Single or polyarticular
    • Inflammation
    • Fever
    • Knee and hip
    • Can develop into severe sepsis and septic shock
  14. What investigations are useful in septic arthritis?
    • Joint aspirate: gram stain, microscopy for crystals (gout) and cultures
    • Blood cultures: colony and sensitivity testing
    • FBC
    • CRP
    • Imaging: in osteomyelitis
  15. Outline some causative organisms of septic arthritis
    • S. Aureus
    • Strep pyogenes, pneumococcus
    • H. Influenzae
    • N. Meningitidis/gonorrhoeae
    • E.Coli
  16. How is septic arthritis treated?
    • Minimum of two weeks IV antibiotics
    • Afterwards, 3 weeks oral antibiotics
  17. What is the definition of osteoarthritis?
    Progressive infection of bone, characterised by necrosis and sequestra formation
  18. Outline the causes of oseoarthritis
    • Similar organisms to septic arthritis
    • Haematogenous spread
    • Local spread from overlying infection (e.g. cellulitic ulcer)
    • Trauma (compound fracture)
    • Surgical inoculation
  19. How is osteoarthritis investigated and treated?
    • MRI the image of choice
    • Antibiotic choice depends on culture; eithe oral or 4-6 weeks IV
    • Surgery
  20. Outline the use of surgery in osteomyelitis
    • Debulk infection back to healthy bone
    • Manage dead space that remains
    • Stabilise infected fractures
    • Debride sinuses
    • Close wounds
  21. Outline the pathogenesis of prosthetic joint infections
    • Usually caused by coagulase negative Staph aureus; gram negative bacilli, S. Viridans.
    • In local spread, it may be anything
    • Prosthesis has no blood supply, so infections common
    • Biofilms common
  22. How are infections commonly introduced in prosthetic joint infections?
    • Local spread in 60-80%; skin organisms
    • Haematogenous in 20-40%
  23. Outline the clinical presentation of prosthetic joint infections
    • Inflammation; pain, effusion, warmth
    • Fever and systemic symptoms
    • Loosening on radiograph/mechanical dysfunction
  24. What investigations are used in prosthetic joint infections?
    • Macroscopic appearance, histopathology and microbiology
    • Cultures are not definitive due to contamination
    • Tissue, fluid or pus samples preferable to swabs
  25. What prophylaxis is commonly used in preventing PJIs?
    • Given 30mins before incision, for <24 hours
    • Cephalosporins used, unless C.Diff present
    • If MRSA, glycopeptides used (vanco or teico)
  26. What treatments are used in PJIs?
    • DAIR: Debride, antibiotics and implant retained
    • Removal: If infection >30 days after surgery, joint may not be functional. Prosthesis/cement removed
  27. Give the definition of:
    - Arthroplasty
    - Resection arthroplasty
    - Revision arthroplasty
    - Arthrodesis
    - Pseudo arthrosis
    • Putting in an artificial joint
    • Replacing a diseased joint with an artificial one
    • Re-operating on an artificial joint
    • Fusing two bones together
    • Allowing two bones to articulate, without a joint
  28. Define cellulitis
    • Spreading infection of the dermis and subcutaenous tissue
    • Often affects lower limb
  29. Outline the clinical presentation of cellulitis
    • Erythema
    • Heat
    • Bullae
    • Spreading, diffuse edge
    • Often painless
    • Systemic symptoms in 40% (fever, nausea)
  30. Outline the diagnosis of cellulitis
    • Usually clinical, not laboratory
    • If below the waist or in diabetis, expect gram negative
    • In IVDUs, it can be anything
  31. Outline the management of cellulitis
    • Antibiotics: Flucloxacilllin, penicillin V (clinda/vanco if allergy)
    • Mark area of inflammation to monitor progress
    • If refractory, consider; resistance/admission/underlying condition/incorrect diagnosis (e.g. DVT, erysipelas)
  32. Define erysipelas
    • Streptococcus infection of dermis, especially face and eyes
    • Similar to cellulitis
    • Well demarcated edge, raised
  33. Describe impetigo, including treatment
    • Staph infection of epidermis
    • Often peri-oral, honey coloured skin crusting
    • Very transmissible
    • Gentle crust removal, flucloxacillin
  34. Describe methods of reducing surgical infection likelihood
    • MRSA screening
    • Hair removal
    • Prophylactic antibiotics
    • Glucose control
    • Normothermic
  35. Define necrotising fasciitis
    Rapidly spreading infection of subcutaneous fascia, occurs over hours
  36. Outline the pathophysiology of necrotising fasciitis
    • Toxin or mixed mediated
    • Toxins a superantigen; cytokines released + toxic shock syndrome
    • Medical emergency; 70% mortality if untreated
  37. What are the characteristics of necrotising fasciitis?
    • Intitially painful, becomes painless in later stages
    • Dark bullae
    • Very rapid spread of dusty, necrotis skin
    • Systemic upset
    • Skin crepitus can occur, due to air entry into subcutaneous tissue
  38. How is necrotising fasciitis treated?
    • Rapid surgical assessement and debridement of all necrotic tissue
    • Tissue samples sent from theatre for cultures and sensitivity
    • Broad IV antibiotics cover helpful; penicillin, fluclox, clinda, metro, genta
  39. Describe the cause, presentation and treatment of abscesses
    • Causes include IVDU, trauma
    • Presents with pain, swelling
    • Aspirated and cultured
  40. How are burns managed?
    • Cultures rarely sterile, due to rapid colonisation
    • Dressings
    • Topical antimicrobials
    • Topical antibiotics
    • Systemic antibiotics