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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
name three adverse effects of Dapsone
nausea difficulty breathing loss of appetite
26
what is Prednisolone
glucocorticoid steroid that has anti-inflammatory and immunosuppressive effects
27
how does Prednisolone work
binds to glucocorticoid receptor which mediates change in gene expression inhibits neutrophil apoptosis promotes anti-inflammatory genes (interleukin)
28
what dose of Prednisolone is prescribed
1-1.5mg/kg/day
29
name three side effects of Prednisolone
weight gain due to alteration in glucose tolerance hypertension bone resorption
30
what is Azathioprine
adjuvant immunosuppressive medicine
31
name four aspects of management of MMP and PV in primary dental setting
analgesic mouthwash topical corticosteroids SLS free toothpaste antiseptic mouthwash
32
name four aspects of management of MMP and PV in secondary dental setting
systemic therapy with corticosteroids biologic medication adjuvant topical corticosteroids
33
what are biologic drugs
recombinant proteins that intervene in immunological processes
34
give two two examples of biologic agents
etanercept rituximab
35
how does rituximab work
binds to B cells and inhibits production of anti-desmosomal igG antibodies
36
what is erythema multiforme
cutaneous and mucosa type III and IV hypersensitivity reactions h
37
what drug is used to stimulate saliva in Sjogren's syndrome
pilocarpine
38
what is a neuralgia
intense stabbing pain that is usually brief pain extends along the course of the affected nerve
39
what are the three potential causes of trigeminal neuralgia
1) idiopathic 2) vascular compression of trigeminal nerve 3) multiple sclerosis, connective tissue disease, space occupying lesion
40
how does trigeminal neuralgia present
unilateral maxillary or mandibular division pain stabbing pain lasts 5-10 seconds
41
name three triggers of trigeminal neuralgia
wind/ cold touch chewing
42
what features of presentation would make you more concerned than usual for trigeminal neuralgia patient
less than 40 sensory deficit in facial region other cranial nerve lesions
43
what are the three first line drugs for treatment of trigeminal neuralgia
carbamazepine oxacarbazepine lamotrigine
44
what are three examples of second line drug therapy for trigeminal neuralgia
gabapentin pregabalin phenytoin
45
how should trigeminal neuralgia be managed
use of carbamazepine often difficult to control pain first thing in morning - avoid triggers at this time pain diary responsive to local anaesthesia
46
name side effects of carbamazepine
thrombocytopenia neutropenia pancytopenia skin reactions
47
when would surgery be considered for trigeminal neuralgia treatment
when approaching maximum tolerable medical management even if pain controlled younger patients with significant drug use
48
what are four surgical options for trigeminal neuralgia
microvascular decompression (MVD) destructive central procedures sterotactic radiosurgery destructive peripheral neurectomies
49
name complications after trigeminal neuralgia surgery
sensory loss motor deficits
50
what are trigeminal autonomic cephalagias
unilateral head pain predominantly over CN V1
51
what are prominent features of trigeminal autonomic cephalagias that occur on the same side as the headache
conjunctival injection nasal congestion eyelid oedema ear fullness miosis and ptosis (Horner's syndrome)
52
what is ptosis
drooping or falling of the upper eyelid
53
what is miosis
a constricted pupil
54
what are cluster headaches
pain occurring mainly orbital and temporal regions attacks unilateral can last 15 mins to 3 hours rapid cessation of pain
55
how do cluster headaches present
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
how is circadian periodicity related to cluster headaches
attacks occur at same time each day bouts occur at same time each year
57
what is a chronic cluster headache
bouts lasting more than 1 year without remission remission lasts less than 1 month
58
what is the difference between paroxysmal hemicrania and cluster headaches
pain lasts shorter in paroxysmal hemicrania paroxysmal hemicrania not affected by circadian rhythm
59
what are examples of abortive medications for cluster headaches
subcutaneous sumatriptan oral prednisolone
60
name preventative medications for cluster headaches
verapamil lithium CGRP monoclonal antibodies
61
what is the treatment options for paroxysmal hemicrania
no abortive treatment prophylaxis is with indomethacin or COX-II inhibitors
62
what is oral dysaesthesia
abnormal sensory perception in absence of abnormal stimulus
63
name sensations a patient with oral dysesthesias might experience
burning or nipping feeling dysgeusia dry mouth
64
name predisposing factors for oral dysaesthesia
haematinic deficiencies fungal/ viral infections anxiety and stress
65
what is dysgeusia
bad taste/ smell/ halitosis
66
what must be ruled out when investigating dysaesthesias
infection tumours
67
how is dysaesthesia managed
explain condition to patient assess anxiety drug therapy - anxiolytic vs neuropathic
68
what are examples of anxiolytic medication used for dysaesthesia
nortiptyline vortioxetine
69
name two examples of neuropathic medication used to treat oral dysaesthesia
gabapentin/ pregabalin clonazepam topical mouthwash
70
how are patients classified with TMD
if it is disease or disfunction
71
name four causes of TMD
occlusion grinding clenching stress stress
72
what signs should be looked for in TMD
clicking joint locking with reduction limited mouth opening tenderness of MOM parafunction signs
73
what investigations are used for TMD pain
ultrasound CBCT MRI arthroscopy
74
name five management strategies for TMD
CBT bite splint and soft diet tricyclic antidepressants physiotherapy acupuncture/ botox
75
name five possible non-dental causes of facial pain
oral malignancy mucosal lesions BMS salivary gland pathology
76
what aspect of social history is thought to make TMD pain worse
smoking
77
what assessments can be used for facial pain
quality of life scores HAD questionnaire
78
what is CRPS
chronic regional pain syndrome delocalised pain spreads around anatomical boundaries bilateral
79
why may you experience shingle vesicles in the ear
CN VII supplies sensory part of the ear

FINALS (25 decks)

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