Psoriasis, acne, rosacea, pemphigoid and pemphigus Flashcards

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1
Q

Describe the lesions and likely diagnosis. Where are these lesions often found?

A

Sharply demarcated scaly erythematous plaques

Psoriasis

Extensors, scalp, sacrum, hands, nails

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2
Q

Briefly describe the pathology of psoriasis.

A

Epidermal hyperplasia and increased turnover

(possibly a complement-mediated attack on keratin layer)

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3
Q

What is the Koebner phenomenon?

A

Lesions that appear on “trauma lines”

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4
Q

What is the mainstay of psoriasis treatment?

A

Topical theraipies: vitamin D analogues (e.g. calcitriol), steroids, coal tar

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5
Q

In severe or refractory cases of psoriaris, what treatments can be tried under specialist supervision?

A

Phototherapy, systemic treatments (immunosuppressants, retinoids, anti-TNF and other biologics)

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6
Q

What is often found in the history of patients with guttate psoriasis?

A

Strep infection 2-3 weeks previous

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7
Q

Where is acne most often seen?

A

Across the distribution of sebaceous glands

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8
Q

How is acne treated?

A

Most resolve themselves

Topical- benzoyl peroxide, Vit A derivatives, antibiotics

Systemic- antibiotics, isoretinoin (can also cause severe flare-ups)

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9
Q

Which skin condition does the picture show? Describe the lesions.

A

Rosacea

Erythematous lesion with papules and pustules and no comedones

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10
Q

What can rosacea be aggravated by?

A

Topical steroids

UV

Spicy food

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11
Q

What role does the Demodex mite have in rosacea?

A

Rosacea may be caused by an allergic reaction to demodex

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12
Q

How is rosacea managed?

A

Trigger avoidance

Antibiotics (topical metronidazole, oral tetracycline)

Isoretinoin (refractory cases)

Telangiectasia

Surgery/laser shaving for rhinophyma

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13
Q

What is the primary feature of the immunobullous disorders?

A

Blisters caused by autoantibodies

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14
Q

How are bullous pemphigoid and pemphigus distinguished?

A

Pemphigoid- the ‘split’ is deeper, within the DEJ

Pemphigus- the ‘split’ is superficial, within the epidermis

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15
Q

Outline the immunopathogenesis of bullous pemphigoid.

A

Autoantibodies (IgG) against hemidesmosome proteins anchoring the basal cell layer to the basement membrane

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16
Q

Describe the clinical features of bullous pemphigoid (how it initially presents and how this develops)

A

May present as itchy, erythematous plaques, progressing to large, tense, fluid-filled blisters

17
Q

What is the Nikolsky sign? How does this relate to immunobullous disorders?

A

Nikolsky +ve = slight rubbing of the skin elicits blisters.

Pemphigoid is Nikolsky -ve

Pemphigus is Nikolsky +ve

18
Q

Which is the more common, bullous pemphigoid or pemphigus vulgaris?

A

Pemphigus vulgaris

19
Q

What is acantholysis?

A

Loss of connection between keratinocytes

20
Q

How does pemphigus vulgaris present?

A

Thin-roofed blisters, prone to rupture and infection, typically found on axillae, face, scalp, groin

21
Q

What is the prognosis of pemphigus vulgaris?

A

Chronic course, high mortaility if left untreated

22
Q

How is pemphigus treated?

A

Systemic steroids, immunosuppresants

23
Q

How is pemphigoid treated?

A

Topical/oral steroid

Immunosuppressants

May also add tetracycline antibiotics, nicotinamide