Dermatology Flashcards

1
Q

Erythema multiforme epidemiology

A

Adults 20-40yo
Can affect any age group

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2
Q

Erythema multiforme distribution

A

Symmetrical, typically on extremities
< 10% TBSA

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3
Q

Erythema multiforme development

A

Quickly over a 24 hour period
First appear on dorsums of hands and feet –> spread along limbs –> trunk

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4
Q

Clinical erythema multiforme

A

Start: well demarcated red/pink macules, mildly pruritis –> blistering/crusting in centre of lesions

Target lesions with 3 concentric zones
- dark red centre with blister/crust
- raised pink oedematous ring
- bright red ring

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5
Q

Erythema multiforme forms

A

Minor: no prodromal illness or mucous membrane involvement
Major: prodromal Sx (fever, chills, lethargy, GI upset, arthralgia) –> precede lesions by 1-14 days + mucosal involvement (blisters –> break to painful ulcers)

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6
Q

Erythema multiforme aetiology

A

90%: infection
- MC = HSV1 esp. affecting lip
- mycoplama pneumonia
- VZV, Hep viruses, HIV, CMV, poxvirus
- dermatophyte infections

Drugs
- NSAIDs, barbituates, penicillins, sulphonamides, antiepileptics, phenothiazines

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7
Q

Dx Erythema multiforme

A

clinical

may be supported by skin biopsy histology
Ix to ID causative infection

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8
Q

Tx of Erythema multiforme

A

Targeted at possible cause e.g., HSV or mycoplasma pneumoniae or cessation of offending drug

Skin lesions often require no Tx
Symptomatic Tx can be topical corticosteroids and anti-histamines and mouthwashes with LA and antiseptic

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9
Q

Prognosis Erythema multiforme

A

Good
Self limiting: 2-3 weeks for minor and 6 weeks for major

recurrence possible esp. if assoc. with HSV

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10
Q

Dx not to miss as DDx for Erythema multiforme

A

toxic epidermal necrolysis (TEN) or Stevens-Johnson syndrome (SJS) can present with target lesions in early cause of disease

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11
Q

What is cutaneous vasculitis

A

Clinicopathologic process characterised by inflammation of the blood vessels in the skin. With marked involvement, it leads to ischaemia of the overlying or underlying tissues.

can be a part of systemic vasculitis where other organ systems can be involved.

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12
Q

Mechanisms of cutaneous vasculitis

A

Direct injury to vessel wall by infective agent

Indirect injury via deposition of immune complexes activating complement components

Indirect injury by activation of antibodies

Delayed HS reaction

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13
Q

Large vessel vasculitis e.g.,

A

Takayasus arteritis
Giant cell arteritis

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14
Q

Medium vessel vasculitis

A

Polyartheritis nodosa
Kawasaki disease
ANCA-associated

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15
Q

Small vessel vasculitis

A

Microscopic polyangiitis, livedo vasculitis, Henoch-Schonlein purpura, and cryoglobulinaemic vasculitis

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16
Q

Leukoclastic vasculitis (acute) presentation

A

Palpable purpura (bleeding under the skin), petechiae, ulceration and necrosis

Systemic signs can include fever, arthralgia, and gastrointestinal upset.

Symptoms usually resolve after 2-3 weeks.

17
Q

Dx cutaneous vasculitis

A

Diagnosis is made on clinical appearance and confirmed with biopsy. Other investigations focus on identifying systemic involvement and the underlying cause. Kidney function and urine dipstick may indicate involvement of the kidneys by the presence of protein and blood. FBC can detect blood disorders, autoimmune screen (ANA, ANCA, ENA, RF) may indicate SLE or other autoimmune disorders, cryoglobulins detect antibodies that precipitate in the cold, and electrophoresis can detect blood disorders such as multiple myeloma. Anti-streptococcal antibodies and hepatitis B and C serology can detect bacterial and viral infection. Anti-neutrophil cytoplasmic antibodies (ANCA) are increased in patients with systemic vasculitis particularly medium sized vessel vasculitis such as granulomatosis with polyangiitis or eosinophilic granulomatosis with polyangiitis. Up to 75% of cases are idiopathic in nature and no cause is identified.