Dermatology Flashcards
Erythema multiforme epidemiology
Adults 20-40yo
Can affect any age group
Erythema multiforme distribution
Symmetrical, typically on extremities
< 10% TBSA
Erythema multiforme development
Quickly over a 24 hour period
First appear on dorsums of hands and feet –> spread along limbs –> trunk
Clinical erythema multiforme
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
Erythema multiforme forms
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)
Erythema multiforme aetiology
90%: infection
- MC = HSV1 esp. affecting lip
- mycoplama pneumonia
- VZV, Hep viruses, HIV, CMV, poxvirus
- dermatophyte infections
Drugs
- NSAIDs, barbituates, penicillins, sulphonamides, antiepileptics, phenothiazines
Dx Erythema multiforme
clinical
may be supported by skin biopsy histology
Ix to ID causative infection
Tx of Erythema multiforme
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
Prognosis Erythema multiforme
Good
Self limiting: 2-3 weeks for minor and 6 weeks for major
recurrence possible esp. if assoc. with HSV
Dx not to miss as DDx for Erythema multiforme
toxic epidermal necrolysis (TEN) or Stevens-Johnson syndrome (SJS) can present with target lesions in early cause of disease
What is cutaneous vasculitis
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.
Mechanisms of cutaneous vasculitis
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
Large vessel vasculitis e.g.,
Takayasus arteritis
Giant cell arteritis
Medium vessel vasculitis
Polyartheritis nodosa
Kawasaki disease
ANCA-associated
Small vessel vasculitis
Microscopic polyangiitis, livedo vasculitis, Henoch-Schonlein purpura, and cryoglobulinaemic vasculitis