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Y2 DERMATOLOGY > disease profiles > Flashcards

disease profiles Flashcards

1
Q

what is the aetiology of acne

A

Lesions arise in the pilsebasceous follicle, which becomes blocked due to abnormal keratinisation and increased production of altered sebum, leading to comedones. Blockage of pilosebaceous duct is followed alteration in its microbiome, especially involving Cutibacterium acnes. Leading to activation innate immunity. This causes an inflammatory response with influx of neutrophils that release elastase, causing connective tissue damage.

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2
Q

what are clinical features of acne

A
  • non inflammatory: open comedones (blackheads) or closed comedones (white heads)
  • inflammatory: papules, pustules, nodules and cysts
  • scars
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3
Q

what is the management for acne

A
  • Topical retinoids, azeliac acid, salicylic acid are keratolytic and help unblock pores but also cause dry flakey skin which can be combated by non-comedogenic moisteriser
  • Tetracycline and erythromycin are used orally for acne
  • combined oral contraceptive pill
  • Oral Isotretinoin is effective for severe inflammatory acne, especially with scarring
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4
Q

what is rosacea

A

Common inflammatory rash that predominantly affects the central face. More common on fair skin. Usually starts mid adult life

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5
Q

what does the pathogenesis of rosacea involve

A
  • chronic sun damage
  • increased innate immune response triggered by the commercial mite Demodex folliculorum and leading to synthesis of pro-angiogenic and proinflammatory mediators
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6
Q

what are clinical features of rosacea

A
  • diffuse erythema and inflammatory papules and pustule
  • flushing and telangiectasia may be early feature
  • papules and pustules but with no comedones
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7
Q

what is the management of rosacea

A

Supressive rather than curative

  • Topical metronidazole, azelic acid or ivermectin may be used for long time control
  • intermittent use of oral tetracyclines
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8
Q

what is the aetiology of atopic eczema

A
  • chronic inflammatory skin disease that arises from a combination of genetic, immunological and environmental factors that lead to skin barrier dysfunction and altered skin microbiome
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9
Q

what is events that lead to atopic eczema

A
  • fillagrin gene mutation: fillagrin deficiency leads to impaired skin barrier function and dry skin allowing antigens and microbes to penetrate the skin
  • IgE is a key mediator of itch
  1. Activation of TH2 CD4 lymphocytes in the skin
  2. increased IL-4-5-13 levels that lead to raised IgE and IL-31
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10
Q

what are clinical features of atopic eczema

A
  • elbows, knees, ankles and wrists and around the neck
  • Itch.
  • Dry, sensitive skin.
  • Inflamed, discolored skin.
  • Rough, leathery or scaly patches of skin.
  • Oozing or crusting.
  • Areas of swelling.
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11
Q

what is common with a secondary infection of eczema

A
  • Usually by staph aureus in moist flexural areas

- pustules, oedema and golden crusted inflamed papules strongly suggest secondary infection

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12
Q

what is eczema herpeticum

A
  • caused by herpes simplex virus

- Appears as multiple small blisters or punched out crusted papules that are associated with malaise and pyrexia

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13
Q

what investigations are done for atopic eczema

A
  • diagnosed on history and clinical features

- raised total IgE and allergen-specific IgE and mild eosinophilia

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14
Q

how do you manage atopic eczema

A
  • avoidance of irritants/allergens
  • emollients
  • topical therapies: steroids, immunomodulators
  • adjunct therapies: oral antibiotics, sedating antihistamiens, bandaging
  • phototherapy
  • systemic therapy
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15
Q

what are clinical features of seborrhoeic eczema

A
  • affects greasy areas
  • on the face it presents with scaling and erythema around the nose, medial eyebrows, hairline and ear canals
  • ## itch is variable
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16
Q

what is the aetiology of seborrhoeic eczema

A

lipophilic commensal yeast, Malassexia triggers the inflammatory response

17
Q

how do you manage seborrhoeic eczema

A
  • treatment is suppressive rather than curative
  • topical azalea anti-fungal creams
  • short term use of mild to moderate potency steroids
18
Q

what is the aetiology of psoriasis

A

Appears to be polygenic with epigenetic and environmental triggers

19
Q

what are clinical features of chronic plaque psoriasis

A
  • pink/red
  • well demarcated plaques
  • silver/white scales
  • extensor surfaces of the knees and elbows
20
Q

what are clinical features of flexural psoriasis

A
  • older adults with a raised BMI
  • well demarcated, shines plaques with little, if any scaling affecting large flexures of the groin, natal cleft, axillae and submammary area
21
Q

what are clinical features of guttate psoriasis

A
  • ‘raindrop’ like pattern of psoriasis
  • most common in children and young adults
  • develops over days and consist of small circular ir oval plaques on the torso
  • triggered by step throat infection
22
Q

how do you manage psoriasis

A

No curative treatment
1- topical therapy ie vit D analogues, corticosteroids, coal tar
2- phototherapy
3- systemic therapy ie methotrexate, Ciclosporin
4- biological therapy

23
Q

what is urticaria

A

short lived itchy ‘wheals’ that clear within minutes to ours without residual drying or skin flaking

24
Q

what causes urticaria

A

dermal mast cell degranulation and release of pro inflammatory mediators that cause vasodilation and increased capillary permeability

25
Q

what is impetigo

A
  • Highly contagious infection that usually affects children and spread by direct contact
  • infected areas appear as inflamed plaques with golden crusted surface, typically around the mouth and nose
26
Q

how do you manage impetigo

A
  • Topical fusidic acid
  • Mupirocin should be reserved for cases cashed by MRSA
  • Topical antibiotic retapamulin is effective but expensive so used as secondary treatment
  • Widespread infection or bulls impetigo should be treated with oral antibiotics for 7 days (flucloxacillin or erythromycin or clarithromycin)
  • Avoid school or work until the lesions are dry for 48 hours after starting antibiotics
27
Q

what causes necrotising fasciatis

A

group A streptococcus

28
Q

what are clinical features of necrotising fascitis

A
  • severe pain that’s out of proportion to the apparent signs of skin inflammation
  • infection tracts rapidly
  • spreading erythema, swelling, pain and sometimes tissue crepitus
  • febrile and severally unwell
29
Q

what are clinical features of scabies

A
  • Widespread intensely itchy, excoriated, eczema’s rash that is triggered by a hypersensitivity response to mite antigens
  • Pruritis is worse at night
  • small red papules or vesicles and occasionally pustules
  • The diagnostic sign is fine linear or curved burrows a few millimetres ling
30
Q

how do you confirm scabies

A

demonstrating the mite and/or eggs on the microscopy of potassium hydroxide-treated skin scrapings from the top of a burrow, but this time consuming and treatment is usually based on clinical features and risk factors

31
Q

how do you treat scabies

A
  • Topical scabicide is applied overnight
  • Treat all the skin below the neck, including the genitals, palms and soles and under the nails
  • Treat all close contacts at the same time even if they are asymptomatic
  • wash recently worn clothes at 60 degrees to avoid reinfection

Y2 DERMATOLOGY (21 decks)

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