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FINALS > Oral Medicine > Flashcards

Oral Medicine Flashcards

1
Q

what is mucous membrane pemphigoid

A

blistering lesions affecting different mucous membranes

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2
Q

why can MMP be considered to be dangerous

A

associated with oesophageal and laryngeal strictures and stenosis

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3
Q

how does MMP occur

A

body’s immune system mistakenly attacks its own mucous membranes
antibodies are produced that attack the proteins within the membrane

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4
Q

what do the antibodies associated with MMP attack in the mucous membranes

A

the proteins involved in anchoring the basement membrane to epithelial cells

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5
Q

what is the immunological mechanism of MMP

A

IgG and IgA bind to BP180 protein which forms an immune complex
activation of complement system
inflammatory cascade activation
influx of immune cells causes blisters to form

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6
Q

name four oral manifestations of MMP

A

bullae formation
ulcerations
erythema
stricture formation (cases of scarring)

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7
Q

name the four most common sites for MMP lesions to be seen on

A

buccal mucosa
gingiva
palate
tongue

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8
Q

name three extra-oral presentations of MMP

A

ocular involvement
skin lesions
nasal, genital or pharyngeal

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9
Q

what is nikolskys sign

A

dislodgement of intact superficial epidermis by a shearing force - inducing a bulla

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10
Q

how do you elicit Nikolskys sign

A

apply lateral pressure with thumbs/ fingers of peri-lesional skin

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11
Q

name two histological features of MMP

A

sub epithelial split with inflammatory cell infiltrate
hemi-desmosome involvement at basement membrane

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12
Q

what is direct immunofluorescence in MMP

A

gold standard for diagnosing MMP
detects linear IgG along basement membrane

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13
Q

what is indirect immunofluorescence in MMP

A

serological testing
IIF - detects for circulating IgG autoantibodies
ELISA - tests for BP180

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14
Q

how does pemphigus vulgaris develop

A

Anti-DSG1 and anti-DSG3 autoantibodies attack proteins on surface of keratinocytes
loss of cell-cell adhesion (acanthosis)

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15
Q

how does pemphigus vulgaris present intra-orally

A

oral erosion

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16
Q

where are biopsies taken for PV investigation

A

from the edge of an early lesion for H&E staining

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17
Q

what are Tzank cells

A

large round keratinocytes with hypertrophic nucleus and abundant basophilic cytoplasm

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18
Q

what is required for diagnosis of PV

A

direct immunofluorescence by testing for presence of autoantibodies in non-affected oral mucosa

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19
Q

why are samples taken peri-lesional when trying to diagnose MMP or PV

A

samples taken from affected sites are more likely to produce false negative result
due to destruction of immunoreactants during the disease process

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20
Q

what would develop if there are anti-dsg1 autoantibodies only

A

develop only skin blisters

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21
Q

what would develop if there are anti-dsg3 autoantibodies only

A

erosions/ ulcerations on mucosal membranes

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22
Q

what would develop if both anti-dsg1 and anti-dsg3 autoantibodies are present

A

both skin and mucosal lesions

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23
Q

what is Dapsone

A

used for mild MMP or PV
inhibits bacterial synthesis of dihydrofolic acid and synthesis of cytokines and chemokines

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24
Q

what dose of Dapsone should be prescribed

A

25-50 mg per day originally
increase monthly by 25-50mg until clinical remission achieved
or maximum of 200mg/ day reached

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25
Q

name three adverse effects of Dapsone

A

nausea
difficulty breathing
loss of appetite

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26
Q

what is Prednisolone

A

glucocorticoid steroid that has anti-inflammatory and immunosuppressive effects

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27
Q

how does Prednisolone work

A

binds to glucocorticoid receptor which mediates change in gene expression
inhibits neutrophil apoptosis
promotes anti-inflammatory genes (interleukin)

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28
Q

what dose of Prednisolone is prescribed

A

1-1.5mg/kg/day

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29
Q

name three side effects of Prednisolone

A

weight gain due to alteration in glucose tolerance
hypertension
bone resorption

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30
Q

what is Azathioprine

A

adjuvant immunosuppressive medicine

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31
Q

name four aspects of management of MMP and PV in primary dental setting

A

analgesic mouthwash
topical corticosteroids
SLS free toothpaste
antiseptic mouthwash

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32
Q

name four aspects of management of MMP and PV in secondary dental setting

A

systemic therapy with corticosteroids
biologic medication
adjuvant topical corticosteroids

33
Q

what are biologic drugs

A

recombinant proteins that intervene in immunological processes

34
Q

give two two examples of biologic agents

A

etanercept
rituximab

35
Q

how does rituximab work

A

binds to B cells and inhibits production of anti-desmosomal igG antibodies

36
Q

what is erythema multiforme

A

cutaneous and mucosa type III and IV hypersensitivity reactions h

37
Q

what drug is used to stimulate saliva in Sjogren’s syndrome

A

pilocarpine

38
Q

what is a neuralgia

A

intense stabbing pain that is usually brief
pain extends along the course of the affected nerve

39
Q

what are the three potential causes of trigeminal neuralgia

A

1) idiopathic
2) vascular compression of trigeminal nerve
3) multiple sclerosis, connective tissue disease, space occupying lesion

40
Q

how does trigeminal neuralgia present

A

unilateral maxillary or mandibular division pain
stabbing pain
lasts 5-10 seconds

41
Q

name three triggers of trigeminal neuralgia

A

wind/ cold
touch
chewing

42
Q

what features of presentation would make you more concerned than usual for trigeminal neuralgia patient

A

less than 40
sensory deficit in facial region
other cranial nerve lesions

43
Q

what are the three first line drugs for treatment of trigeminal neuralgia

A

carbamazepine
oxacarbazepine
lamotrigine

44
Q

what are three examples of second line drug therapy for trigeminal neuralgia

A

gabapentin
pregabalin
phenytoin

45
Q

how should trigeminal neuralgia be managed

A

use of carbamazepine
often difficult to control pain first thing in morning - avoid triggers at this time
pain diary
responsive to local anaesthesia

46
Q

name side effects of carbamazepine

A

thrombocytopenia
neutropenia
pancytopenia
skin reactions

47
Q

when would surgery be considered for trigeminal neuralgia treatment

A

when approaching maximum tolerable medical management even if pain controlled
younger patients with significant drug use

48
Q

what are four surgical options for trigeminal neuralgia

A

microvascular decompression (MVD)
destructive central procedures
sterotactic radiosurgery
destructive peripheral neurectomies

49
Q

name complications after trigeminal neuralgia surgery

A

sensory loss
motor deficits

50
Q

what are trigeminal autonomic cephalagias

A

unilateral head pain predominantly over CN V1

51
Q

what are prominent features of trigeminal autonomic cephalagias that occur on the same side as the headache

A

conjunctival injection
nasal congestion
eyelid oedema
ear fullness
miosis and ptosis (Horner’s syndrome)

52
Q

what is ptosis

A

drooping or falling of the upper eyelid

53
Q

what is miosis

A

a constricted pupil

54
Q

what are cluster headaches

A

pain occurring mainly orbital and temporal regions
attacks unilateral
can last 15 mins to 3 hours
rapid cessation of pain

55
Q

how do cluster headaches present

A

sharp burning or piercing pain on one side of face at same time of day
can happen multiple times a day
usually occurs in periods of 1-3 months with at least 1 month of remission in between

56
Q

how is circadian periodicity related to cluster headaches

A

attacks occur at same time each day
bouts occur at same time each year

57
Q

what is a chronic cluster headache

A

bouts lasting more than 1 year without remission
remission lasts less than 1 month

58
Q

what is the difference between paroxysmal hemicrania and cluster headaches

A

pain lasts shorter in paroxysmal hemicrania
paroxysmal hemicrania not affected by circadian rhythm

59
Q

what are examples of abortive medications for cluster headaches

A

subcutaneous sumatriptan
oral prednisolone

60
Q

name preventative medications for cluster headaches

A

verapamil
lithium
CGRP monoclonal antibodies

61
Q

what is the treatment options for paroxysmal hemicrania

A

no abortive treatment
prophylaxis is with indomethacin or COX-II inhibitors

62
Q

what is oral dysaesthesia

A

abnormal sensory perception in absence of abnormal stimulus

63
Q

name sensations a patient with oral dysesthesias might experience

A

burning or nipping feeling
dysgeusia
dry mouth

64
Q

name predisposing factors for oral dysaesthesia

A

haematinic deficiencies
fungal/ viral infections
anxiety and stress

65
Q

what is dysgeusia

A

bad taste/ smell/ halitosis

66
Q

what must be ruled out when investigating dysaesthesias

A

infection
tumours

67
Q

how is dysaesthesia managed

A

explain condition to patient
assess anxiety
drug therapy - anxiolytic vs neuropathic

68
Q

what are examples of anxiolytic medication used for dysaesthesia

A

nortiptyline
vortioxetine

69
Q

name two examples of neuropathic medication used to treat oral dysaesthesia

A

gabapentin/ pregabalin
clonazepam topical mouthwash

70
Q

how are patients classified with TMD

A

if it is disease or disfunction

71
Q

name four causes of TMD

A

occlusion
grinding
clenching stress
stress

72
Q

what signs should be looked for in TMD

A

clicking joint
locking with reduction
limited mouth opening
tenderness of MOM
parafunction signs

73
Q

what investigations are used for TMD pain

A

ultrasound
CBCT
MRI
arthroscopy

74
Q

name five management strategies for TMD

A

CBT
bite splint and soft diet
tricyclic antidepressants
physiotherapy
acupuncture/ botox

75
Q

name five possible non-dental causes of facial pain

A

oral malignancy
mucosal lesions
BMS
salivary gland pathology

76
Q

what aspect of social history is thought to make TMD pain worse

A

smoking

77
Q

what assessments can be used for facial pain

A

quality of life scores
HAD questionnaire

78
Q

what is CRPS

A

chronic regional pain syndrome
delocalised pain
spreads around anatomical boundaries
bilateral

79
Q

why may you experience shingle vesicles in the ear

A

CN VII supplies sensory part of the ear

FINALS (25 decks)

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