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BDS4 ORAL MED > blistering disorders of oral cavity > Flashcards

blistering disorders of oral cavity Flashcards

1
Q

what is a vesicle

A

<5mm visible accumulation of fluid within or beneath epithelium i.e. small blister

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2
Q

what is a bullae

A

> 5mm visible accumulation of fluid within or beneath epithelium i.e. bigger blister

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3
Q

what are some vesiculobullous conditions

A
  • mucous membrane pemphigoid
  • pemphigus vulgaries
  • erythema multiforme
  • stevens-johnson syndrome / toxic epidermal necrolysis
  • linear igA disease
  • epidermolysis bullosa
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4
Q

what is the distinct immune mechanism in vesiculobullous conditions

A
  • attack epithelium/basement membrane
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5
Q

where can vesiculobullous conditions affect

A
  • oesophageal
  • ocular
  • nasal
  • anogenital
  • skin
    -oral
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6
Q

explain normal oral mucosa histology

A
  • epithelium (keratinocytes)
    • stratified squamous
  • basement membrane
    • non cellular interface
  • lamina propria
    • collagen, fibroblasts, nerves,blood vessels etc.
  • desmosomes
  • joins keratinocyte-keratinocyte
  • cell junction

hemidesmosomes
- joins basal keratinocytes to basement membrane
- only between bottom layer and basement membrane

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7
Q

what is mucous membrane pemphigoid

A
  • autoimmune process
  • 50-60 yr old
  • 1:2 male to female ratio
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8
Q

what is clinical features of MMP

A
  • oral vesciles/blisters → ulcers
  • “desquamitive gingivitis”- outer layers of epithelium starts to peel off
  • ocular lesions → conjunctival scarring
  • anogenital lesions
  • skin lesions (scalp)
  • nasal mucosa
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9
Q

what can be seen histologyically in MMP

A

sub-epithelial splitting = between epithelium and lamina propria

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10
Q

what is the important of desmosomes and semi-desmosomes in vesiculobullous conditions

A

If these structures are targeted by a disease process we get breaches in the integrity of mucosa/skin

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11
Q

what is pathogenesis of MMP

A
  • Antibody (IgG) targeting the basement membrane zone (hemidesmosomes)
    -Complement activation
    -Subepithelial splitting = vesicles, blisters, ulcers
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12
Q

what is aetiology of MMP

A

Unknown
Likely genetic predisposition
Autoimmune

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13
Q

how is MMP diagnosed

A
  • Clinical / histological / immunopathological

Biopsy
H+E staining - from affected tissue
Direct immunofluorescence microscopy (DIF) – from perilesional tissue

Indirect immunofluorescence
Blood sample

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14
Q

what type of biopsy for MMP diagnosis

A

H+E staining - from affected tissue
Direct immunofluorescence microscopy (DIF) – from perilesional tissue

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15
Q

what is direct immunofluorescence

A
  • Tissue (biopsy) is put onto slide and processed
  • Antibody (bound to fluorophore) - specific to IgG, IgA and C3 are applied to the tissue
  • Examined with UV microscope
  • Fluorescence at areas of binding

“Linear deposition of IgG along the basement membrane”

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16
Q

what is indirect immunofluorescence

A

Blood sample taken (containing the primary disease antibody)
Incubated with normal mucosa (monkey oesophagus)
Addition of (secondary) antibody + fluorophore
Tissue examined
If antibodies present in serum, will show in tissue

Less sensitive in MMP
Positive in 50-80%

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17
Q

management of MMP

A

-MDT approach

  • patient education
  • oral disease severity score
  • symptomatic relief (benzydamine mouthwash)
  • oral hygiene
  • topical corticosteroid
  • intralesional steroid
  • systemic treatment
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18
Q

name some medications used to treat MMP

A

topical corticosteroid
- mouthwash (betamethasone)
- via custome-made tray (clobetasol)

intralesional - triamcinonlone

systemic - prednisolone, doxycycline, azothioprine, methotrexate, rituximab

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19
Q

what is pemphigus vulgaris

A
  • autoimmune condition
  • blisters, erosions and ulcers
  • potentially lethal
20
Q

what is clinical features of pemphigus vulgarise

A

blisters , erosions and ulcers

  • oral bullae (which quickly rupture to leave erosions/ulcers)- often first clinical feature
  • desquamitive gingivitis
  • ocular involvement
  • aerodigestive tract
  • anogenital blisteing
  • skin
21
Q

what is a complication of pemphigus vulgaris

A
  • sepsis (secondary bacterial/viral/fungal infection)
  • systemically unwell
22
Q

pathogenesis of PV

A
  • antibodies (mainly IgG) directed against desmosomes
  • loss of cell-cell contact in epithelium = “acantholysis”
  • intra-epithelial split forms
  • “flaccid” blisters (cf MMP)
  • sub epithelial
23
Q

aetiology of PV

A
  • autoimmune overlap
24
Q

how to diagnose PV

A

Nikolsky’s sign (rubbing the mucosa induces a bulla)

Biopsy
H+E staining - from affected tissue
Direct immunofluorescence microscopy (DIF) – from perilesional tissue

Indirect immunofluorescence
Blood sample
More sensitive in PV than in MMP

25
management of PV
- MDT - lethal - iv fluid, feeding, analgesia 2 phases of management - induction of remission and maintenance
26
what is induction of remission in PV
Prednisolone (+/- bone protection, gastric protection) Commence second agent (e.g. Aza, MMF, rituximab)
27
maintenance phase in PV
Gradual withdrawal of oral steroids (aim <10mg prednisolone) Second agent Regular monitoring (using ODSS***) Topical steroids Benzydamine Excellent oral hygiene
28
what is pareneoplastic pemphigus
A rare variation of PV Associated with an underlying malignancy (usually haematological malignancy) Causes immune system disarray Severe mucosal and skin involvement Typically systemically unwell High mortality
29
what is erythema multiform
Acute onset Hypersensitivity reaction – often identify a trigger Ulceration and blistering of oral mucosa and lips Skin rash
30
who does erythema multiforme affect
- 10-40 years old
31
clinical features of erythema
Flu-like prodrome (1-2 weeks) Skin – classical target lesion, itchy Lip blisters, ulceration and crusting Oral ulcers (particularly anteriorly) Other mucosae – eyes, genitals Minor (oral +/- skin targets) Major (oral, skin + other mucosa site)
32
aetiology of erythema multiform
Hypersensitivity Infective – Herpes simplex virus (HSV-1) in 15-20% Drugs – allopurinol, carbamazepine, NSAIDs, phenytoin Following BCG or Hep B immunisations
33
pathogenesis of erythema multiform
Release of cytokines from CD4 cells Amplified immune response CD8 T cell attack keratinocytes Apoptosis and necrosis of keratinocytes
34
diagnosis of erythema multiform
Clinical history - ?triggering agent Biopsy of perilesional tissue Histology = lymphocytic infiltrate, keratinocyte necrosis, intra- and sub-epithelial splitting Immunofluorescence – non-specific HSV serology / throat swab for Mycoplasma pneumoniae
35
management of erythema multiform
MDT approach (consider need for inpatient admission) Feeding/fluids Analgesia Stop any obvious precipitating medication Topical steroids for oral lesions (minor EM) Systemic steroids for more severe disease Adjunctive oral care (hygiene, CHX, comfort measures) Antihistamines for skin itch Recurrent EM Consideration of immunosuppression (Aza, MMF) – risk/benefit Prophylactic aciclovir (due to HSV implication)
36
what is SJS/TEN
- rare -severe -critical care admission - widespread blistering of skin + oral, pharyngeal , genital, nasal and conjunctival involvement
37
what is mortality rate for SJS and TEN
1-5% SJS 30% TEN
38
aetiology of SJS/TEN
Most cases = hypersensitivity reaction to medications Allopurinol, carbamazepine, NSAIDs, phenytoin, penicillins (>200) Genetic predisposition 100x more common in people with HIV
39
pathogenesis of SJS/TEN
Antigens (medication) presented to T lymphocytes Dysregulated immune reaction CD8 cells, macrophages and neutrophils into epithelium Release of granulysin – pore-forming peptide Apoptosis, necrosis of keratinocytes Breach of skin/mucosa – “skin failure”
40
histology of SJS/TEN
- epidermal necrolysis, detachment from dermis
41
management of SJS/TEN
- urgent assessment in specialist care - ABCDE - stop causative agent MDT approach
42
what is Linear IgA disease
- blistering condition similar to MMP triggered by meds - NSAIDS DIF = IgA deposits in basement membrane of skin and mucosa (hence “linear”) with subepithelial split
43
whais is management of linear IgA disease
Removal of any triggers MDT approach Topical steroids (mouthwash, ointment) Second-line: dapsone, sulfapyridine
44
what is epidermolysis bullosa acquisita
Rare Middle-aged patient Autoimmune DIF = IgG antibodies targets collagen (type VII) in basement membrane, destabilise the epithelial/connective tissue junction Friction/trauma - blister formation – erosions, ulceration, scarring
45
management of epidermal bullosa acquisita
MDT approach Topical steroids (mouthwash, ointment) Systemic immunosuppression (prednisolone, Aza, MTX, MMF)

BDS4 ORAL MED (12 decks)

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