1
Q

Causes of oral ulceration

A

trauma
immunological
infections
carcinoma
gastrointestinal

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2
Q

recurrent aphthous stomatitis types

A

minor
major
herpetiform
Behcet’s syndrome

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3
Q

medications which may induce oral ulceration

A

cytotoxic drugs - e.g. methotrexate
NSAID’s
nicorandil

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4
Q

minor aphthous ulcers - features

A

commonest type of recurrent ulcertaion
less than 10mm diameter
last up to 2 weeks
only affect non-keratinised mucosa
heals without scarring
usually a good response to topical steroids

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5
Q

major aphthous ulcers - features

A

can last for months
can affect any part of the oral mucosa
may scar when healing
poor response to topical steroids
- intralesional steroids more effective
usually larger than 10mm

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6
Q

herptiform apthae features

A

rarest form of aphthous ulcers
multiple small ulcers on. non-keratinised or non-keratinised
heals within 2 weeks
can coalesce into larger areas of ulceration

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7
Q

Behcets disease diagnosis

A
  • 3 episodes of mouth ulcers in a year
  • at least 2 of the following: genital sore, eye inflammation, skin ulcers, pathergy
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8
Q

RAS predisposing factors

A

genetics
viral and bacterial infections
systemic disease
stress
hormonal fluctuations
mechanical injuries/trauma
microelement deficiency

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9
Q

aphthous ulcers - investigations

A

blood tests
- haematinic deficiecnies - iron, b12, folic acid
- coeliac disease - TTG
allergy tests
- contact or immediate hypersensitivity

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10
Q

drug prescribing for aphthous ulcers

A

inconvenient lesions
- non steroid topical therapy
disabling lesions
- steroid topical therapy
SEE SDCEP

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11
Q

when to refer to oral medicine for RAS

A

no good result from treatment
children under 12

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12
Q

What is a fibro-epithelial polyp?

A

a localised hyperplastic lesion

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13
Q

fibro-epithelial polyp aetiology

A

overproduction of granulation and fibrous tissue in response to damage or trauma

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14
Q

fibro-epithelial polyp - clinical features

A

commonly presents in buccal mucosa
often in areas of trauma
may be pedunculated or sessile
firm or soft
pink appearance
painless
can be ulcerated and easily traumatised
may have associated frictional keratosis
usually an isolated lesion

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15
Q

fibro-epithelial polyps - histology

A

fibrous tissue in the core
thick interlacing collagen fibres
adjacent normal tissue
covered with squamous epithelium
may have hyperkeratosis
little inflammatory infiltrate

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16
Q

fibro-epithelial polyp - management

A

photos
identify cause and correct if appropriate
consider excisional biopsy

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17
Q

fibro-epithelial polyp - benefits and risks of excisional biopsy

A

benefits
- can confirm diagnosis - useful if uncertain or patient has ssc risk factors
- can remove lesion
risks
- surgical risks
- altered sensation
- recurrence or incomplete excision

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18
Q

denture associated lesions - management

A

consider excision
denture hygiene
candida management
consider making new denture

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19
Q

epulis - meaning

A

a reactive hyperplastic lesion on the gingivae

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20
Q

fibrous epulis - what is it?

A

a fibro-epithelial polyp presenting on the gingiva

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21
Q

fibrous epulis features

A

same colour as gingiva
may be ulcerated
histologically similar to polyps
- more likely to have varying amounts of inflammatory infiltrates

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22
Q

Giant cell epulis features

A

also known as peripheral giant cell granuloma
red/purple appearance
sessile or pedunculated
often inderdentally
more common in children

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23
Q

Giant cell epulis histology

A

vascular stroma
fibrous tissue
multinucleate osteoclast giant cells

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24
Q

Giant cell epulis - management

A

excisional biopsy
OPT and/or CBCT
bone profile
parathyroid hormone assay

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25
Q

vasular epulis/pyogenic granuloma features

A

increase in size due to hormonal changes
if pregnant in pregnancy = pregnancy epulis
soft bright red appearance
may resolve during birth
if removed following birth, inflammation may decrease and resemble a fibrous epulis
may recur if removed during pregnancy

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26
Q

vascular epulis histology features

A

vascular appearance
variable amounts of inflammatory infiltrate

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27
Q

vascular epulis management options

A

in GDP - refer to oral surgery for further advice
keep under observation
- excise following birth
excisional biopsy

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28
Q

drugs linked to generalised gingival overgrowth

A

drug induced
- calcium channel blockers
- ciclosporin
- phenytoin

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29
Q

non drug induced causes of generalised gingival overgrowth

A

chronic hyperplastic gingivitis
- mouth breathing, pregnancy
hereditary gingival fibromatosis
- enlarged, little inflammation, expansion of the tuberosities
- may require repeated gingivectomies to facilitate oral hygiene
granulomatous disease
- OFG
- Oral crohns etc
haematological malignancy
- gingival swelling/periodontal disease rapidly progressing in the presence of good OH?

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30
Q

squamous cell papilloma features

A

benign growth - tumpur/wart
any aspect of oral mucosa
pedunculated OR sesile
cauliflower appearance
often keratinised surface
result from viral infection
- typically HPV
not associated with malignant transformation
single or multiple lesions
may present in immunocompromised patients

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31
Q

squamous cell papilloma histology

A

finger like processes of hyperplastic squamous epithelium
thin cores of vascular connective tissue

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32
Q

squamous cell papilloma - management

A

excisional biopsy
observation
- if no red flag sign, symptoms or oral cancer risk factors

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33
Q

black hairy tongue pathophysiology

A

hyperplasia of filiform papillae
build up of commensal bacteria, food debris
pigment inducing fungi and bacteria

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34
Q

black hairy tongue cause

A

specific cause unknown
linked to
- smoking
- antibiotics
- chlorhexidine mouthwash
- poor oral hygiene

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35
Q

black hairy tongue management

A

reassure
stop smoking
stay hydrated
lightly brush tongue
gentle exfoliation of tongue surfaces
- peach stones
eat fresh pineapeale

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36
Q

White patches - potential causes (CLINK)

A

congenital
lichen planus
infections
neoplastic/potentially neoplastic
keratosis

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37
Q

Give examples of neoplastic and potentially malignant white patches

A

squamous cell carcinoma
leukoplakia
sub mucous fibrosis
actinic chelitis

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38
Q

Squamous cell carcinoma red flags

A

> 3 week duration
50 years old
smoking
high alcohol consumption
history of oral cancer
non-homogenous
non-healing ulceration
tooth mobility
non-healing extraction sockets
difficulty speaking or/and swallowing
weight loss
fatigue
appetite loss
cervical lymphadenopathy
numbness/altered sensation

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39
Q

squamous cell carcinoma management

A

urgent suspected cancer referral to oral and maxillofacial surgery
be honest with patient and explain concern
explain that they will need to get a biopsy/sample promptly

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40
Q

Leukoplakia - define

A

a white patch or plaque that cannot be characterised clinically or pathologically
- can’t be rubbed away

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41
Q

proliferative verrucous leukoplakia features

A

up to 85% undergo malignant transformation
warty surface with white/yellow appearance
common sites palate and gingiva
will enlarge over time
often very extensive and impractical to remove

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42
Q

oral submucous fibrosis features

A

related to paan use
pale in colour
firm to palpate
fibrous bands develop
typically affects buccal mucosa and soft palate
mouth opening over time diminishes

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43
Q

oral sub mucous fibrosis malignant transformation rate

A

5%

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44
Q

erythroplakia features

A

atrophic lesion
localised
well defined borders
can have speckled appearance - erythroleukoplakia
strong association with tobacco use
50% malignant transformation rate

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45
Q

melanotic macule features

A

single brown lesion
- comprised of a collection of melanin containing cells
flat
non raised
typically <1cm diameter
no rapid change
painless
common on vermillion border

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46
Q

melanoma features

A

rare
may arise from a pigmented naeuvus
palate or maxillary gingiva most common
refer if suspected melanoma

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47
Q

melanoma - warning signs (ABCDE)

A

asymmetry
border irregularity
colour irregularity
diameter >6mm
evolving
- shape, size, colour, elevation

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48
Q

Kaposi’s sarcoma features

A

vascular neoplasm/tumour
human herpes virus 8 associated
disorganised epithelial cell growth
mainly presents in immunocompromised
Reddish-blue or brown foci
can present on skin, oral mucosa or GI tract

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49
Q

Kaposi’s sarcoma management

A

surgery
radiotherapy
chemotherapy
immunotherapy
managing underlying immunodeficiency

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50
Q

oral candidosis local risk factors

A

xerostomia
poor oral hygiene
dentures
smoking
mouth piercings
irradiation to the mouth or salivary glands
inhaled/topical corticosteroids e.g. asthmatics

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51
Q

systemic risk factors for oral candidosis

A

extremes of age
- neonates, elderly
malnutrition
diabetes
HIV/AIDS
Haematinic deficiency
broad-spectrum antibodies
chemotherapy
haematological malignancy

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52
Q

Miconazole oral gel contraindications (same as fluconazole capsules)

A

warfarin
- increases anti-coagulant effect
statins
- risk of rhabdomylosis and myopathy with some statins

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53
Q

Acute pseudomembranous candidosis features

A

‘thrush’
- white flecks resemble breast of thrush bird
commonly seen in neonates
in adults - “disease of the diseased”

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54
Q

acute pseudomembranous candidosis appearance

A

white slough on mucosa surface
- easily wiped off
underlying erythematous base

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55
Q

acute pseudomembranous candidosis (oral thrush) management

A

predisposing factors need to be investigated and dealt with
oral hygiene
topical
- miconazole oral gel
- nystatin oral mouthwash
systemic if topical ineffective or infection is extensive or severe
- fluconazole capsules

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56
Q

chronic hyperplastic candidosis clinical signs (candidal leukoplakia(

A

usually occur on buccal mucosa
- at labial commissure/corner of the mouth
often bilaterally
white or speckled red/white appearance
can occur on tongue - less common

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57
Q

chronic hyperplastic candidosis diagnosis

A

incisional biopsy with PAS stain
- is there dysplasia?

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58
Q

Why would you give fluconazole before a biopsy for a patient with chronic hyperplastic candidosis?

A

to allow pathologist to see potential dysplasia more clearly
fungal-related inflammation can give false positives for dysplasia

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59
Q

chronic hyperplastic candidosis management

A

predisposing factors - treat
systemic antifungal
stop smoking
careful clinical follow up in oral med clinic or GDP
- management of dysplasia as required

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60
Q

denture-related stomatitis features

A

candida infection of mucosa beneath a dental appliance
common in patients in care facilities
- elderly, dry mouth, high sucrose diet, poor OH
common upper complete denture
- micro-environment

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61
Q

denture related stomatitis clinical signs and symptoms

A

pain or discomfort
bad breath
dryness
burning sensation in mouth
redness

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62
Q

acute erythematous candidosis clinical features

A

aka atrophic candidosis
most commonly presents with associated ‘burning’
palate most commonly affected

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63
Q

acute erythematous candidosis predisposing factors

A

recent broad spectrum antibiotics
corticosteroids
diabetes
HIV
nutritional factors

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64
Q

acute erythematous candisosis diagnosis and management

A

diagnosis
- clinical
- oral rinse or swab
management
- medical referral
- topical antifungal
- systemic antifungal

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65
Q

angular chelitis signs and symptoms

A

soreness
erythema
fissuring
crusting
bleeding
at corners of mouth

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66
Q

angular chelitis management

A

predisposing factors
- may require new dentures
- underlying disease or deficiency?
denture hygiene
OHI
topical antifingal - miconazole cream - effective against fungus and some bacteria
topical antibacterial - sodium fusidate ointment
- when clearly bacterial in nature e.g. non-denture wearer

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67
Q

primary herpetic gingivostomatitis symptoms

A

fever
malaise
red, fiery oedamatous gingiva
vesicles - ulcers

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68
Q

primary herpetic gingivostomatitis management

A

largely supportive
- fluids
- soft diet
- chlorhexidine to prevent secondary infection of oral lesions
- difflam mouthwash
- paracetamol

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69
Q

When would urgent specialist care with systemic antivirals be indicated for primary herpetic gingivostomatitis patients?

A

in pregnant women and neonates

70
Q

Factors which can cause reactivation of HSV

A

sunlight
- UV radiation
unwell
- fever
tissue injury
stress
immunosuppression
hormones
- menstrual cycle

71
Q

recurrent herpes simplex virus management

A

avoidance of triggers
antivirals in prodrome period
- acyclovir 5% cream every 2 hour (herpes labialis)
- acyclovir 200mg tablets 5x per day for 5 days (intra-oral herpes)
immunocompromised - specialist referral

72
Q

varicella signs and symptoms

A

mainly children
- complication risk in adults
highly contagious
- via respiratory droplets or lesion
fever
malaise
truncal rash
- itch, papules, vesicles, scabs
oral ulcers

73
Q

zoster - signs and symptoms

A

rash in one dermatome - scabs
pain before, during and after lesions
vesicles and ulcers intra-orally

74
Q

diseases linked to Epstein bar virus

A

oral hairy leukoplakia
burkitt’s lymphoma
nasopharyngeal cancer

75
Q

oral AIDS defining illnesses

A

oral candidosis
acute necrotising ulcerative gingivitis
kaposi sarcoma
oral hairy laukoplakia
non-hodgkin’s lymphoma
aphthous-like ulcers

76
Q

oral cancer risk factors

A

smoking
poor oral hygiene
alcohol
HPV
chewing tobacco
low fruit/veg consumption
socio economic background

77
Q

what is oral epithelial dysplasia?

A

abnormal growth
can only be diagnosed on histology
carried a higher risk of becoming cancer than ‘normal’ tissue

78
Q

basal hyperplasia histological features

A

increased basal cell numbers
architecture
- regular stratification
- basal compartment is larger
no cellular atypia

79
Q

mild dysplasia histological features

80
Q

moderate dysplasia histological features

81
Q

severe dysplasia histological features

82
Q

What is lichen Planus?

A

a common chronic immune mediated mucocutaneous disease

83
Q

Lichen Planus can commonly effect…

A

oral mucosa
skin
- including nails and scalp
ano-genital mucosa

84
Q

how do oral lichenoid lesions and oral lichen planus differ?

A

oral lichen planus: no specific identifiable aetiological factor

oral lichenoid lesions: an identifiable aetiological factor OR a manifestation of a systemic disease

85
Q

risk factors for OLP and OLL

A

stress
dental materials
SLS
medical conditions
medication
nutritional deficiency
chronic trauma
hypertension

86
Q

conditions which are associated with an increased OLP or OLL risk

A

graft versus host disease
diabetes
lupus
auto-immune diseases

87
Q

types of lesions seen in OLP/OLL

A

reticular
atrophic
papular
erosive
plaque like
bullous

88
Q

OLP and OLL symptomatic relief (first line)

A

0.15% Benzydamine (Difflam) mouthwash or spray
- mouthwash for generalised
- spray for localised lesions

rinse or gargle every 16 hours as required
- usually for no more than 7 days

89
Q

OLP and OLL symptomatic relief - if benzydamine doesn’t work

A

betamethasone 500 mcg soluble tablets
- fully dissolve tablet in 10ml water
- rinse for 5 minutes
- spit after rinsing
- do not swallow
- repeat up to 4x daily

no significant risks or interactions - little systemic absorption
may be associated with oral fungal infection

90
Q

what is required in a referral for OLP/OLL?

A

detailed history
clinical findings
provisional diagnosis
a reason why it needs seen in specialist care
details of treatments tried
excellent clinical photos
referral; to oral medicine or local oral and maxillofacial surgery unit

91
Q

Histological features of OLP/OLL

A

keratosis
hyperplastic epithelium
lymphocytes in epithelium
basal cell destruction
band-like lymphocytic infiltrate
epithelial atrophy or erosion

92
Q

vesicle - define

A

<5mm visible accumulation of fluid within or beneath epithelium
- e.g. a small blister

93
Q

bullae - define

A

> 5mm visible accumulation of fluid within or beneath epithelium
- e.g. a bigger blister

94
Q

Give examples of vesiculobullous conditions

A

mucous membrane pemphigoid
pemphigus vulgaris
Erythema multiform
Stevens-Johnson syndorme/ toxic epidermal necrosis

95
Q

mucous membrane pemphigoid - clinical features

A

oral vesicles/blisters
- ulcers
- robust blisters, sometimes blood filled
heals with scarring
desquamative gingivitis
ocular lesions
- scarring of conjunctiva
anogenital lesions
skin lesions
- scalp
nasal mucosa affected

96
Q

mucous membrane pemphigoid diagnosis

A

clinical/histological/immunopathological

biopsy
- H & E staining from affected tissue
- direct immunofluorescence microscopy - from perilesional tissue
indirect immunofluorescence
- blood sample

97
Q

MMP symptomatic relief

A

benzydamine mouthwash
oral hygiene instruction

98
Q

MMP systemic treatment options

A

prednisolone
doxycycline
methotrexate
azathioprine
rituximab

99
Q

pemphigus vulgaris clinical features

A

blisters, erosions and ulcers
- oral bullae - quickly rupture to leave erosions/ulcers (thin walled blisters that rupture easily)
- heal without scarring
- desquamative gingivitis
- ocular involvement
- aeorodigestive tract
- anogenital blistering
- skin affected
pain
potentially lethal
systemically unwell
- impaired oral intake
- sepsis- secondary infection

100
Q

pemphigus vulgaris pathogenesis

A

antibodies (mainly IgG) directed against desmosomes
loss of cell-cell contact in epithelium
- intra-epithelial split forms
- flaccid blisters

101
Q

pemphigus vulgaris - diagnosis (clinical/histological/immunopathological)

A

Nikolsky’s sign
- rubbing the mucosa induces a bulla
biopsy
- H and e staining from affected tissue
- direct immunofluorescence microscopy from perilesional tissue
indirect immunofluorescence
- blood sample
- more sensitive in pemphigus vulgaris than mucous membrane pemphigoid

102
Q

What is OFG/Orofacial Granulomatosis

A

Chronic inflammatory disease
relapsing and remitting lip swelling
can also involve
- perioral skin
- buccal mucosa
- gingiva
- floor of mouth
- tongue

103
Q

OFG histopathology

A

typically non-caseating granulomas with or without multinucleate giant cells
granulomas deep in oral mucosa
- missed if specimen too shallow
lymphoedema
dilated lymphatics
pervisacular lymphatic infiltrate
indistinguishable from Crohn’s

104
Q

OFG clinical features

A

lip swelling
buccal cobblestoning
gingival enlargement
stag horning
mucosal tags
linear ulceration
skin changes

105
Q

OFG and Crohn’s similarities

A

histopathologically indistinguishable
relapsing and remitting course
clinical features similar

106
Q

OFG investigations

A

FBC, haenatinitics - inflammatory markers
fecal calprotein
oral biopsy - deep
endoscopy and biopsy if abdominal symptoms
serum ACE
patch testing

107
Q

OFG treatment

A

benzoate and cinnamon exclusion diet
- beneficial in 54%-78%
- strict adherence for 3 months and introduce foods one at a time
liquid enteral nutrition 6 weeks
topical steroid for intraoral involvement
- betamethasone 500mcg tablets in water
- flixonase 400mcg nasules in water
- beclomethasone 100mcg inhaler
- clobetasol ointment 0.05%
topical 0.1% tacrolimus for skin involvement and lip swelling
intralesional triamcinolone 40mg/ml

108
Q

What is trigeminal neuralgia?

A

a disorder characterised by recurrent unilateral brief electric shock pains, abrupt in onset and termination
- limited to the distribution of one or more divisions of the trigeminal nerve
- triggered by innocuous (non-harmful) stimuli
- may develop without apparent cause or be a result of another diagnosed disorder

109
Q

trigeminal neuralgia - consequences

A

suicide
- 78% of patients had considerable negative thoughts
depression and anxiety
8% have had irreversible and unnecessary dental treatment
47% have been prescribed 3 medications which have been ineffective

110
Q

name the classifications of trigeminal neuralgia

A

classical
secondary
idiopathic

111
Q

diseases which may cause trigeminal neuralgia

A

multiple sclerosis
space occupying lesion
other
- skull base deformity
- connective tissue disease
genetic causes of neuropathy

112
Q

idiopathic trigeminal neuralgia features

A

unilateral or bilateral pain in the distribution of one or more trigeminal nerve branches
- indicative of neural damage but of unknown aetiology
- purely paroxysmal
- with concomitant continuous pain

113
Q

Classical TN pathophysiology

A

neurovascular conflict of the superior cerebellar artery
compression leads to demyelination
resulting in ectopic firing
- can be observed in asymptomatic patients

114
Q

idiopathic TN pathophysiology

A

no conflict but unregulated sodium ion inflow resulting in depolarisation

115
Q

Trigeminal neuralgia - how might a patient describe the pain?

A

stabbing
electric shock
severe
memorable first episode
scary
10/10

116
Q

common TN triggers

A

eating
washing face
brushing teeth
eating
speaking
smiling
cold wind
stress
temperature change

117
Q

Trigeminal neuralgia - red flag features to ask about

A

sensory motor defects
deafness
loss of balance
optic neuritis
history of cranio-facial malignancy
bilateral TN
systemic symptoms
< 30 years of age

118
Q

Prescribing Carbamazepine - considerations

A

check BNF for interactions
care in elderly
- increases risk of falls
care in those operating heavy machinery or driving or childcare
arrange blood monitoring with GP
- FBC/U+E/LFT

119
Q

Carbamazepine risks

A

hyponatraemia
- low sodium in the blood
- increased with other medications such as bendroflumethiazide
falls
unsteadiness
confusion
rash/skin reaction
- more common in Han Chinese and Thai populations
side effects usually dose dependent
- low risks at 100mg 2x daily

120
Q

why is an MRI taken for trigeminal neuralgia patients?

A

to exclude underlying disease

121
Q

Oxacarbazepine - how does it effects differ from carbamazepine

A

tends to be better tolerated
greater risk of lowering sodium levels

122
Q

trigeminal neuralgia second line medications

A

lamotrigine
baclofen
gabapentin
pregablin

123
Q

burning mouth disorder - definition

A

a chronic orofacial pain with an intraoral burning or dysaesthetic sensation that records for more than 2 hour a day on 50% of the days over more than 3 months
- without evident causative lesions on clinical investigation and examination

124
Q

Burning mouth syndrome is a diagnosis of exclusion. what conditions do you need to exclude?

A

oromucosal diseases
- e.g. oral lichen planus
hypo salivation
tongue parafunction
anaemia
vitamin b12 and b9 deficiency
diabetes mellitus
use of ACE inhibitors

125
Q

burning mouth disorder - symptoms

A

pain of a burning quality affecting the mouth lining
often tongue is the focus
can affect multiple sites
may be associated xerostomia or dysgeusia
often bilateral presentation
often relieved with eating
often worsen as day progresses

126
Q

burning mouth syndrome - common triggers

A

dental procedures
medical procedures
new medications
illness
stressful life events

127
Q

persistant idiopathic facial pain - symptoms

A

poorly localised unilateral pain
- can present bilaterally
usually maxillary region affected
described as dull, nagging, aching, throbbing
can be sharp exacerbations
persistent and daily
aggravated by stress

128
Q

persistent idiopathic dentoalveolar pain symptoms

A

well localised moderate intensity pain
any tooth or mucosa of extraction site
most commonly premolar or molar regions of maxilla
character - dull, pressure like

difficult to distinguish from odontogenic pain

129
Q

Sjogrens - eye symptoms

A

persistent troublesome dry eyes for > 3 months
recurrent sensation of sand/gravel in eyes
tear substitutes used > 3 times a day

130
Q

Sjogrens oral symptoms

A

daly feeling of a dry mouth for > 3 months
recurrent swelling of salivary glands as an adult
frequently drinking liquid to aid swallowing dry foods

131
Q

What gland biopsy is taken to provide histopathological analysis for a sjogrens diagnosis?

A

labial gland
parotid can also be sampled

132
Q

Sjogrens test diagnosis criteria (give scores)

A

Blood test for anti-ro antibodies (score 3)
gland biopsy: focus score of > or = 1 (score 3)
slit lamp examination: abnormal ocular staining score > or = 5 (score 1)
Filter paper: schemer;s test without anaesthetic < or = 5mm/5 min (score 1)
spit in cup: unstimulated salivary flow <0.1ml/min (score 1)

133
Q

A classification of sjogrens disease requires a cumulative score of…

134
Q

Sjogrens histopathology: what can be seen in minor glands?

A

focal lymphocytic sialadenitis
acinar loss
fibrosis

135
Q

Sjogrens histopathology: what can be seen in major salivary glands?

A

lymphocytic infiltrate
epithelial hyperplasia

136
Q

Sjogren’s disease head and neck complications

A

oral infection
caries risk
functional loss
- speech
- swallowing
problems with denture retention
salivary lymphoma

137
Q

Sjogrens disease is a multisystem autoimmune disease. what other systems can it effect? give clinical features

A

CNS
- fatigue
- peripheral and CN neuropathies
skin
- rashes
vascular
- Raynaud’s syndrom e
eyes
- corneal ulcers
respiratory
- cronic cough
GI
- dysphasia
- pancreatic insufficiency
haematological
- anaemia
musculoskeletal
- myalgia, arthralgia
GU
- vaginal dryness

138
Q

How to assess the severity of a dry mouth

A

gland palpation
duct expression
challacombe scale

139
Q

dry mouth management

A

treat underlying cause
preventative care
symptomatic relief
artificial saliva products

140
Q

potential underlying causes of dry mouth

A

dehydration
caffeine
smoking
alcohol
medications
diabetes
somatoform disorder

141
Q

dry mouth preventive care includes…

A

caries prevention
- diet
- fluoride
SLS free toothpaste for sore tongue
candida management

142
Q

give examples of some saliva substitutes

A

sprays
- Glandosane (pH 5.75)
- saliva orthana
- Xerotin
lozenges
- saliva orthana
- Saliva stimulating tablets
saliva stimulants
- pilocarpine
oral care gels
- bioextra gel
- xerostom

143
Q

what saliva substitute should not be used in dentate patients and why?

A

glandosane
- acidic

144
Q

simple lifestyle measures to manage sjogrens

A

moist oily foods and sauces
humidify home environment
regular exercise
omega 3 supplements
glasses/goggles to reduce tear evaporation
warm eye compress 10 mins daily

145
Q

What are the major salivary glands?

A

parotid
submandibular
sublingual

146
Q

obstructive sialadenitis symptoms

A

intermittent swelling of salivary glands
usually unilateral
may or may not have inflammation
usually painful
often associated with mealtimes
can be chronically obstructed
most common in the submandibular gland

147
Q

obstructive sialadenitis is also known as…

A

mealtime syndrome

148
Q

obstructive sialadenitis potential causes

A

sialoiths - duct calculi
stricture in the salivary duct
salivary duct oedema
- trauma
neoplasm
mucous plug

149
Q

obstructive sialadenitis history -questions to ask

A

pain history if needed
ask if associated with eating/food
coming and going or persistent
swallowing problems
bad taste or pus
generally unwell
- to exclude acute infection

150
Q

obstructive sialadenitis clinical examination

A

extra oral exam
bimanual palpation of floor of mouth
express saliva from ducts
- pus?
- obstruction?

151
Q

obstructive sialadenitis investigations in primary care

A

lower occlusal x ray or OPT to identify calcification

152
Q

obstructive sialadenitis investigations in secondary care

A
  • ultra sound scan
  • sialography
  • MRI or CT may be indicated in some cases
153
Q

obstructive sialadenitis conservative measures

A

massage gland and duct
heat application
sucking on citrus fruits or sugarfree sweets
stay hydrated
excellent oral hygiene
simple analgesia

154
Q

sialadenitis - define

A

inflammation of the salivary glands

155
Q

acute viral sialadenitis clinical features

A

painful parotid swelling
usually bilateral
- can sometimes be a single gland
no hyposalivation
10% have submandibular gland involvement
- very rare to only involve sm gland
malaise, fever and feeling generally unwell
- likely precedes parotid swelling
swelling lasts approximately 7 days
trismus

156
Q

mumps management

A

no specific antivirals

supportive management
- hydration
- analgesia
- pyrexia management
- isolation for 6-10 days may be advisable
- contact public health

157
Q

salivary gland swelling - other extra oral features which would indicate referral; to OM or GP

A

shortness of breath
cough
chest pain
macroglossia
peripheral neuropathy
bruising
peripheral oedema
GI symtoms
fatigue
weight loss

158
Q

Mucocele - define

A

a cystic lesion of the minor salivary glands

159
Q

mucoceles commonly present in…

A

lower labial mucosa
floor of mouth

160
Q

mucocele appearance

A

fluctuant
blue swelling

161
Q

give the 2 types of mucocele

A

mucous extravasation (90%)
mucous retention (10%)

162
Q

mucous extravasation aetiology and features

A

caused by trauma to minor salivary duct
not lined by epithelium
- therefore not a true cyst
termed ranula if on floor of mouth
most commonly present in lower lip/labial mucosa
most common under age of 30
- peak incidence 2nd decade

163
Q

mucous retention cyst aetiology and features

A

saliva being retained in duct/gland
- more common over age of 50
- never seen in lower lip
- cystic dilation of the duct

164
Q

excision of mucocele - risks

A

high recurrence rate
potential damage to neighbouring structures

165
Q

most common salivary gland neoplasm

A

Pleomorphic adenoma (PSA)

166
Q

sublingual gland neoplasms are..

A

uncommon and usually malignant

167
Q

parotid gland neoplasms are…

A

usually pleomorphic adenomas

168
Q

submandibular gland neoplasms are..

A

usually pleomorphic adenomas
1/3 are malignant

169
Q

minor salivary gland neoplasms are..

A

50% malignant
50% pleomorphic adenomas

170
Q

neoplasms management if benign

A

surgical excision
(facial nerve injury risk)