Inflammatory Skin Conditions Flashcards

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1
Q

What is Eczema?

A
  • Eczema (or dermatitis) is a chronic skin condition common in children but also prevalent in adults.
  • 20% prevalence in <12 years old in the UK
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2
Q

What are the causes of Atopic Eczema?

A

Not fully understood, but

  • Positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present
  • Primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema
  • Exacerbating factors such as infections, allergens (e.g. chemicals, food, dust, pet fur), sweating, heat, occupation and severe stress
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3
Q

What is the presentation of Atopic Eczema?

A
  • Acute presentation consists of itchy papules and vesicle often weepy (exudative)
  • Chronic lesions: dry scaly itchy patches can be erythematous in paler skin or grey/ brown in richly pigmented skin
  • More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults
  • In richly pigmented skin eczema may present as brown, grey or purple bumps (papular eczema or follicular eczema)
  • Chronic scratching/rubbing leads to lichenification
  • Across of skin types eczema can lead to pigmentary changes such as hypopigmentation (reduced pigmentation) and hyperpigmentation (increased pigmentation)
  • Nail may show pitting and ridging of the nails
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4
Q

What is the management of Atopic Eczema?

A
  • General measures: avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute
  • Topical therapies: topical steroids for active areas; topical immunomodulators (e.g. tacrolimus, pimecrolimus) for maintenance therapy as steroid-sparing agents
  • Oral therapies: antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. aciclovir) for secondary herpes infection
  • Phototherapy and immunosuppressants (e.g. azathioprine, ciclosporin, methotrexate) for severe non-responsive cases, biologic therapy
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5
Q

What are complications of Atopic Eczema?

A
  • Secondary bacterial infection (crusted weepy lesions)
  • Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum
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6
Q

What is Acne?

A
  • An inflammatory disease of the pilosebaceous follicle
  • Over 80% of teenagers aged 13- 18 years
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7
Q

What are the causes of Acne Vulgaris?

A
  • Hormonal (androgen)
  • Contributing factors include
    • Increased sebum production
    • Abnormal follicular keratinization
    • Bacterial colonization (Propionibacterium acnes)
    • Inflammation
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8
Q

What is the presentation of Acne Vulgaris?

A
  • Non-inflammatory lesions (mild acne): open and closed comedones (blackheads and whiteheads)
  • Inflammatory lesions (moderate and severe acne): papules, pustules, nodules, and cysts
  • In richly pigmented skin:
    • Inflammatory lesions’ may not be so apparent, instead hyperpigmented lesions (‘acne hyperpigmented macules’) are seen.
    • Hyperpigmented lesions may also signify ongoing inflammation
    • Non-erythematous nodules may be present and detected by palpation

Commonly affects the face, chest and upper back

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9
Q

What is the management of Acne Vulgaris?

A
  • General measures: no specific food has been identified to cause acne, treatment needs to be continued for at least 6 weeks to produce effect
  • Topical therapies (for mild acne): benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties)
  • Oral therapies (for moderate to severe acne) - oral antibiotics, and anti-androgens (in females)
  • Oral retinoids (for severe acne)
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10
Q

What are complications of Acne Vulgaris?

A
  • Post-inflammatory hyperpigmentation
  • Scarring
  • Deformity
  • Psychological and social effects
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11
Q

What is Psoriasis?

A

A chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration

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12
Q

What are types of Psoriasis?

A
  • Chronic plaque psoriasis (most common type)
  • Guttate (raindrop lesions)
  • Seborrhoeic (naso-labial and retro-auricular)
  • Flexural (body folds)
  • Pustular (palmar-plantar)
  • Erythrodermic (total body redness)
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13
Q

What is the cause of Psoriasis?

A
  • Complex interaction between genetic, immunological and environmental factors
  • Precipitating factors include trauma (which may produce a Köebner phenomenon), infection (e.g. tonsillitis), drugs, stress, and alcohol
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14
Q

How does Psoriasis present?

A
  • Well-demarcated erythematous scaly plaques
  • In richly pigmented skin psoriasis can present as dark brown, grey or purple patches or plaques
  • Lesions can sometimes be itchy, burning or painful
  • Common on the extensor surfaces of the body and over scalp
  • Auspitz sign (scratch and gentle removal of scales cause capillary
  • bleeding)
  • 50% have associated nail changes (e.g. pitting, onycholysis)
  • 5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans (flexion deformity of distal interphalangeal joints)
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15
Q

What is the management of Psoriasis?

A
  • General measures: avoid known precipitating factors, emollients to reduce scales
  • Topical therapies (for localised and mild psoriasis): vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations
  • Phototherapy (for extensive disease): phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA
  • Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement): methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters,and biological agents (e.g. etanercept, adalimumab, ustekinumab)
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