Inflammatory Skin Disease Flashcards

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1
Q

Define dermatitis/eczema [1]

A

itchy inflammatory disorder of the skin

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2
Q

Describe the causes/general pathogenesis of dermatitis [4]

A
  1. Combination of genetic, immune and reactivity to a variety of stimuli
  2. Inflammation in eczema primarily due to inherited abnormalities in skin, so called “barrier defect”.
    • Leads to increased permeability and reduces its antimicrobial function
  3. An inherited abnormality in Filaggrin expression considered a primary cause of disordered barrier function.
    • Filaggrins are proteins which bind to keratin fibres in the epidermal cells.
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3
Q

What are the different types of dermatitis? [9]

A
  1. Endogenous:
    • Atopic
    • Seborrhoeic
    • Discoid
    • Varicose
    • Pompholyx
  2. Exogenous:
    • Contact (allergic, irritant)
    • Photoreaction (allergic, drug)
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4
Q

What conditions are typically associated with atopic eczema? [4]

A
  1. asthma,
  2. allergic rhinitis,
  3. conjunctivitis,
  4. hay fever (atopy)
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5
Q

What are the causes of atopic eczema? [2]

A
  1. High lgE immunoglobulin antibody levels
  2. Genetic and immune aetiology
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6
Q

What are the clinical features of infant atopic eczema? [6]

A
  1. Itchy
  2. Occasionally vesicular (small blisters)
  3. Often facial component
  4. Secondary infection
  5. < 50% still have eczema by 18 months
  6. Occasionally aggravated by food (i.e. milk)
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7
Q

What are the potential complications of atopic eczema? [5]

A
  1. Bacterial infection
    • Staph. aureus
  2. Viral infection
    • Molluscum
    • Viral warts
    • Eczema herpeticum
  3. Tiredness
  4. Growth reduction
  5. Psychological impact
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8
Q

What are the management options for atopic eczema? [9]

A
  1. Emollients
  2. Topical steroids
  3. Bandages
  4. Anti-histamines
  5. Antibiotics/anti-viral medication
  6. Education for parents/child
  7. Avoidance of exacerbating factors
    • rarely dietary avoidance/house dust mite etc.
  8. Systemic drugs e.g.
    • ciclosporin,
    • methotrexate
  9. Newest biologic agent:
    • IL4/13 blocker - Dupilumab
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9
Q

Define Seborrhoeic Dermatitis [1]

A

Chronic, scaly inflammatory condition

Often thought to be “dandruff’

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10
Q

Where can seborrhoeic dermatitis be found? [4]

A
  1. face
  2. scalp
  3. eyebrows
  4. occasionally upper chest
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11
Q

What is the cause of seborrhoeic dermatitis? [1]

A

overgrowth of Pityrosporum Ovale yeast

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12
Q

What are the management options for seborrhoeic dermatitis…

  1. in the scalp? [2]
  2. on the face? [3]
  3. in what conditions does it often improve? [1]
A
  1. Scalp - medicated anti yeast shampoo
    • i.e. Antifungal ketoconazole - Nizoral, Selsun
  2. Face - anti-microbial, mild steroid
    • i.e. Daktacort cream → simple moisturiser
  3. Often improves with UV/sunlight
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13
Q

Describe the pathogenesis of venous (varicose) dermatitis [4]

A
  1. Due to underlying venous disease
  2. Affects lower legs
  3. Incompetence of deep perforating veins
  4. Increased hydrostatic pressure
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14
Q

What are the management options of venous (varicose) dermatitis? [4]

A
  1. Emollients
  2. Mild/moderate topical steroid
  3. Compression bandaging/stockings
  4. Consider early venous surgical intervention
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15
Q

What are the causes of contact dermatitis? [3]

A
  1. Precipitated by an exogenous agent
    • Irritant - direct noxious effect on skin barrier
    • Allergic - Type IV hypersensitivity reaction
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16
Q

What are the common allergens associated with contact dermatitis? [5]

A
  1. Nickel
    • jewellery,
    • zips,
    • scissors,
    • coins
  2. Chromate
    • cement,
    • tanned leather
  3. Cobalt
    • pigment/dyes
  4. Colophony
    • glue,
    • adhesive tape,
    • plasters
  5. Fragrance
    • cosmetics
    • creams
    • soaps
17
Q

What is psoriasis? [1]

A

Chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin

18
Q

Describe the causes/pathogenesis of psoriasis [6]

A
  1. T cell mediated autoimmune disease
  2. Abnormal infiltration of T Cells
    • release of inflammatory cytokines incl. interferon, interleukins and TNF (tumour necrosis factor)
    • increased keratinocyte proliferation
  3. Environmental and genetic factors
    • PSORS genes (e.g. PSORSI, Chromosome 6) and HLA - Cw0602 associated in certain subtypes
19
Q

What are the types of psoriasis? [7]

A
  1. Plaque
  2. Guttate
  3. Pustular
  4. Erythrodermic
  5. Flexural/Inverse
  6. ?palmar/plantar pustulosis
  7. Psoriasis at sites of trauma/scars → Koebner phenomenon (not Auspitz)
20
Q

What is the potential complication of psoriasis that affects up to 20% of patients? [1]

A

Up to 20% of patients with psoriasis develop arthritis

21
Q

Describe the management options for psoriasis [21]

A
  1. Topical creams and ointments
    • Moisturisers → help reduce dryness, flaking
    • Steroids (reduce autoimmune response, redness, itching, inflammation)
    • Salicylic Acid (to dissolve thick dead skin)
    • Slow down keratinocyte proliferation
      • Vitamin D analogues
      • Coal Tar
      • Dithranol
  2. Phototherapy light treatment
    • Non specific immunosuppressant therapy
    • Can reduce T cell proliferations
    • Encourages Vitamin D and reduces skin turnover)
    • UV-B light most commonly used
    • UV-A with psoralen photosensitiser
    • Risks
      • Short term burning
      • Longer term skin cance
  3. Systemic drugs/immunosuppressants
    • Immunosuppressants
      • Methotrexate
      • Ciclosporin
    • Acitretin (oral retinoid / vitamin A)
    • Dimethyl Fumarate
    • Apremilast
  4. Biologics:
    • Adalimumab (anti TNF)
    • Ustekinumab (anti IL12/23)
    • Most drugs have potent side effects (i.e. liver dysfunction, hypertension, risk of infection) so need to be tailored to patient