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BDS4 Oral Medicine > Vesiculobullous Disorders > Flashcards

Vesiculobullous Disorders Flashcards

1
Q

What can immunogenic diseases be divided into based on their pathogenesis

A
  • cell mediated
  • antibody mediated (pemphigus and pemphigoid)
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2
Q

Why do many immunological skin conditions also effect the oral mucosa

A

they share common antigens

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3
Q

What tissues does erythema multiforme involve

A
  • skin and mucous membranes
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4
Q

What type of hypersensitivity reaction is erythema multiforme

A

type 3

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5
Q

What is the possible aetiologies of erythema multiforme

A
  • drugs
  • oral herpes simplex virus
  • mycoplasma
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6
Q

Describe the pathogenesis of erythema multiforme

A

Large antibody antigen immune complexes get stuck in capillaries and organs and they activate complement

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7
Q

Which antibody complexes get stuck in oral EM

A

IgM

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8
Q

Is the onset of erythema multiforme usually acute or chronic

A

acute

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9
Q

How does erythema multiforme appear on the skin

A

as target lesions

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10
Q

How does erythema multiforme appear on the mucosa

A
  • erythematous patches
  • followed by vesiculobullous eruptions
  • bullous eruptions breakdown rapidly into erosions as the bullae disintegrate
  • erosions on lip accompanied by crusting
  • v painful, may find it hard to eat and drink
  • may resemble primary herpetic gingivostomatits
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11
Q

Which age group is erythema multiforme most common in

A

young males

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12
Q

What is recurrent erythema multiforme associated with

A

recurrent herpes simplex

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13
Q

What are the management strategies for erythema multiforme

A
  • urgent medical therapy
  • encourage fluids
  • encourage analgesia
  • manage recurrance
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14
Q

What urgent medical therapy should be provided for EM

A
  • high dose systemic steroids
  • systemic aciclovir
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15
Q

How should we manage recurrence

A

consider daily aciclovir for prophylaxis
allergy testing
consider mycoplasma cause

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16
Q

What is the presentation of angina bullosa haemorrhagia

A
  • blood blister in the mouth
  • rapid onset - tends to appear within a few minutes and only last an hour then burst
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17
Q

What is the possible aetiology for ABH

A

trauma

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18
Q

Where are the common sites for ABH

A
  • buccal mucosa
  • soft palate
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19
Q

What does a biopsy of ABH show

A

non-specific ulceration

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20
Q

What is the management of ABH

A
  • CHX/difflam spray for healing
  • no tx available
  • reassure that disease is benign
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21
Q

What type of hypersensitivity reaction is pemphigoid

A
  • type 2 hypersensitivtiy
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22
Q

What is pemphigoid

A
  • group of immune mediated blistering diseases
  • characterized by production of autoantiibodies to various components of hemidesmosomes
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23
Q

What are hemidesmosomes

A
  • attach epithelium to underlying connective tissue
24
Q

What type of vesicles are formed in pemphigoid

A
  • sub-epithelial
25
Q

What type of antibodies develop in pemphigus/pemphigoid

A

IgG

26
Q

What are the types of pemphigoid

A
  • bullous
  • mucous membrane
  • cicatritial
27
Q

What is bullous pemphigoid

A

involves skin alone

28
Q

What is mucous membrane pemphigoid

A
  • involves all mucous membranes e.g eye, genitals, oral
29
Q

What is cicatritial pemphigoid

A

mucosal scarring
can lead to blindness

30
Q

What does histopathology for pemphigoid show

A

subepithelial bulla
can see neutrophils, eosinophils, macrophages and lymphocytes

31
Q

What is direct immunofluorescence

A
  • antibody is bound to tissue
  • manufactured antibody has fluorescein attached
  • binds to bound antibody
  • requires biopsy (perilesional - not of lesion)
32
Q

What is indirect immunofluorescence

A
  • circulating antibody not yet bound to tissue
  • detected using plasma sample
  • not always useful for diagnosis but useful for monitoring disease
33
Q

What does direct IF show for pemphigoid

A
  • linear staining along BM
  • C3, IgG +/- IgA
34
Q

What does indirect IF show for pemphigus/pemphigoid

A

should be positive

35
Q

What happens if the pemphigoid scars

A
  • can cause blindness - called ocular cicatritial pemphigoid
  • eventually can result in symblepharon where eyelids become attached to eye
36
Q

What is the most common pemphigus

A
  • pemphigus vulgaris
37
Q

Describe the epidemiology of pemphigus vulgaris

A
  • usually middle aged
  • f>m
  • genetic link? commoner in ashkenazi jews
38
Q

What sites are involved in pemphigus vulgaris

A
  • skin
  • mucosa - often first site
  • eventually both
39
Q

What is the presentation of pemphigus

A
  • intrapeithelial bullae
  • bullae are fragile and readily rupture forming crusted/weeping areas of denudation on the skin as well as irregular ragged ulcers
  • possible desquamative gingivitis
40
Q

What are the common oral sites for pemphigus vulgaris

A
  • soft palate
  • buccal mucosa
  • lips most frequently effected
41
Q

How are the bulla produced in pemphigus vulgaris

A
  • acantholysis (loss of desmosomes)
  • process extends laterally into surrounding epithelium for considerable distance
42
Q

What is Nikolsky’s sign

A
  • mostly used for pemphigus
  • gentle lateral pressure to mucosa
  • leads to formation of bulla
43
Q

What does the histology of pemphigus show

A
  • splitting of epithelium
  • changes occur in stratum spinosum above basal cell layer
  • tzanck cells
44
Q

What are tzanck cells

A
  • single small clumps of cells free within blister fluid
45
Q

What does direct IF show for pemphigus vulgaris

A
  • basket weave appearance
  • C3 + IgG
46
Q

How is pemphigus managed

A
  • systemic corticosteroids especially for acute phase
  • reduce weekly
  • if no response, look at mycophenolate or azathioprine
47
Q

What are the long term risks of pemphigus

A
  • infection
  • paraneoplasm malignancy
  • chronic inflammation
  • swallowing issues
48
Q

If further testing past direct and indirect IF are required, what can be done

A

ELIZA
shows us what autoantibodies are targetting

49
Q

What are the long term risks of pemphigoid

A
  • blindness
  • no real mlaignant potential but tx can have malignant potential
50
Q

How does HSV1 result in erythema multiforme

A
  • virus taken up by monocytes and macrophages
  • cells migrate to mucosal site/skin and deposit the virus in these skin areas resulting in antigen/antibody complexes which dont phagocytose well so the response lingers
51
Q

What is the multiorgan condition of erythema multiforme called

A

steven johnson syndrome

52
Q

What is steven johnson syndrome

A

widespread involvement of the skin, oral, genital and ocular mucosae (erythema multiforme)

53
Q

What is linear IgA disease

A
  • C3 & IgA antibody subepidermal blistering disease of skin
  • overlaps wit bullous pemphigoid
  • linked to gluten intolerance
54
Q

What is dermatitis herpetiformis

A
  • chronic, intensely pruritic subepidermal autoimmune blistering condition
  • granular IgA, C3
  • oral presentation: ranges from small symptomless erythematous areas to extensive erosions
55
Q

How many biopsies do we need for pemphigus/pemphigoid

A

two
one for histopathology
one for direct IF

BDS4 Oral Medicine (17 decks)

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