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Oral Medicine > Facial Pain, OFG, Vesiculobullous Diseases > Flashcards

Facial Pain, OFG, Vesiculobullous Diseases Flashcards

1
Q

What is Oral Dysaesthesia known as?

A

Burning Mouth Syndrome

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2
Q

C/O: burning pain, dry mouth, tingling, altered taste.
Differential diagnosis?

A

oral dysaesthesia/burning mouth syndrome

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3
Q

What is burning mouth syndrome?

A

Oral dysaesthesia.
Burning mucosal pain with no clinical signs.

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4
Q

Management of oral dysaesthesia/bms?

drugs

A

Anxyiolytic-based medications:
1. Nortriptyline
2. Mirtazepine
3. Vortioxetine

Neuropathic medication:
1. Gabapentine/Pregabalin
2. Topical Clonazepam

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5
Q

What is oral dysaesthesia/bms usually associated with?

A

haematinic deficiency

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6
Q

What are the clinical features of oral dysaesthesia/BMS?

A
  • usually anterior two-thirds of tongue
  • spontaneous onset
  • lasts from months to several years
  • altered taste (dysguesia) / metallic
  • tingling
  • GI problems
  • dry mouth
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7
Q

What is Persistent Idiopathic Facial Pain (PIFP)?

A

Persistent facial and/or oral pain, with varying presentations but recurring daily for >2 hours per day over >3 months, in the absence of cliical neurological deficit.

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8
Q

How is PIFP managed?

persistent idiopathic facial pain

A
  • believe the patient
  • multidisciplinary approach
  • patient education (discourage from further invasive interventions aimed at pain relief in the absennce of a clear associated pathology e.g. tooth extractions)
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9
Q

What are the clinical features of PIFP?

persistent idiopathic facial pain

A
  • usually deep, but can be superficial
  • poorly localised, radiating, and mostly unilateral
  • aching, burning, throbbing, stabbing pain
  • persistent, long lasting (years) daily pain
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10
Q

C/O: unilateral pain, poorly localised and radiating. Aching, burning, throbbing, stabbing pain. Persistent and ongoing everyday for years.
Had took taken out but still pain.
Differential diagnosis?

A

Persistent Idiopathic Facial Pain (PIFP)

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11
Q

C/O: pain in face, head and neck that is worse in mornings/evenings + parafunctional clenching.
Differential diagnosis?

A

TMD pain

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12
Q

Management of TMD Pain?

A
  • patient education/self-help advice
  • physical therapy (CBT education and exercises. Soft diet and analgesia. Bite splint)
  • biochemical manipulation (tricyclic)
  • physiotherapy
  • acupuncture
  • clinical psychology
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13
Q

How would you investigate TMD pain?

A

Imaging:
* ultrasound scan - to assess functional visualisation of disc movement
* OPT/CBCT - to assess bone (if bony problem suspected)
* MRI (best image of disc)

Arthroscopy - to directly visualise the disc

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14
Q

How to assess TMJ?

clinical examination

A

Assess:
* muscles of mastications (any tenderness)
* sternomastoid and trapezius muscles (any tenderness)
* palpate TMJ (any tenderness)
* mouth opening (range of motion and deviation)
* TMJ clicking/crepitus
* dental occlusion

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15
Q

What is the difference between TMJ clicking and crepitus?

A

Clicking suggests disc displacement, while crepitus suggests a degenerative problem.

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16
Q

C/O: sharp, shooting pain on one side of the face.
Differential diagnosis?

A

Trigeminal Neuralgia

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17
Q

What are the causes of trigeminal neuralgia?

A
  • idiopathic
  • vascular compression of trigeminal nerve
  • multiple sclerosis
  • space-occupying lesion
  • skull-base bone deformity
  • connective tissue diseSe
  • arteriovenous malformation
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18
Q

What are the clinical features of TN?

trigeminal neuralgia

A
  • unilateral maxillary/mandibular division pain (> opthalmic division)
  • stabbing pain
  • 5-10 seconds duration
  • triggers: cutaneous, wind/cold, touch, chewing
  • sudden pain or concomitant continuous pain
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19
Q

General management of TN.

trigeminal neuralgia

A

medications
pain diary
LA

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20
Q

Surgical management of TN.

trigeminal neuralgia

A

**microvascular decompression (MVD)
**
destructive central procedures:
* balloon compression
* radiofrequency thermocoagulation

sterotactic radiosurgery (gamma knife)

destructive peripheral neurectomies

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21
Q

First-line drug therapy for TN.

trigeminal neuralgia

A

Carbamazepine
100mg tablets 2x daily for 10 days

Oxcarbamezapine

Lamotrigine

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22
Q

Carbamezapine is a first-line drug for trigeminal neuralgia.

What are the side effects of carbamezapine?

A
  • blood dyscrasias (thrombocytopenia, neutropenia, pancytopania)
  • electrolyte imbalance
  • neurological deficits (paraesthesia, vestibular problems)
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23
Q

C/O:
orbital/temporal pain that is one-sided (unilateral). Rapid onset. Lasts for 15 mins to 3 hours. Feels like a migraine.
Assoc. symptoms: nausea, vomiting, photophobia, phonophobia.

Differential diagnosis?

A

Cluster headache

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24
Q

C/O:
orbital/temporal pain that is one-sided (unilateral). Rapid onset. Lasts for 2-30 mins. About 2-40 attacked per day.

Differential diagnosis?

A

Paroxysmal Hemicrania

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25
Q

Management of Cluster headache.

drug

A

Preventive:
* verapamil
* lithiun
* topiramate

Attack:
* subcutaneous sumatriptan 6mg or nasal zolmatriptan 5mg
* low O2 7-12 L/min via a non-rebreathing mask

Occipital lidocaine injection
Oral prednisolone

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26
Q

Management of paroxysmal hemicrania.

drug

A

indometacin (usually absolute response)

alternative: COX-II inhibitots, topiramate

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27
Q

What are the clinical features of Orofacial Granulomatosis (OFG)?

A
  • perioral erythema
  • perioral swelling
  • lip swellinng (can cause lip fissures and dry, cracking lips)
  • angular cheilitis
  • proliferative erythematous gingivitis
  • oedema of floor of mouth (staghorn sign)
  • linear fissured ulcer in labial sulcus
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28
Q

What are the histological features of OFG?

orofacial granulomatosis

A

non-caseating granulomatous inflammation within the tissues.
giant cells obstructing lymphatics, no swelling.

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29
Q

C/O: swelling of the face, lips and oral tissues.
Differential diagnosis?

A

Orofacial granulomatosis
Crohn’s disease

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30
Q

Pathogenesis of OFG.

orofacial granulomatosis

A

blockage of lymphatic drainage due to immune reaction - type IV hypersensitivity

angio-oedema which settles down faster is a type I hypersensitivity

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31
Q

OFG symptoms are similar to that of Crohn’s disease.

How can you screen for Crohn’s disease?

crohn’s screening

A
  1. Parental awareness of importance of altered bowel habits of abdominal pain
  2. Growth and GI function monitoring
  3. Faecal calprotectin assay
32
Q

Management of OFG.

initial management (primary care)

A

Identify possible cause of swelling. OFG or Crohns.
Monitor growth and GI symptoms. Faecal calprotectic assay.

Diet history for possible allergens.

3 months diet exclusion.
No benzoic acid, sorbic acid, cinnamon, chocolate, E10-E19

non-specialist treatment

33
Q

Management of OFG in a specialist setting.

A
  1. Topical treatment to angular cheilitis/fissure (miconazole or hydrocortisone cream)
  2. Topical treatment to lip swelling or facial erythema (tacrolimus ointment 0.03%)
  3. Intralesional steroid injection (triamcinolone, weekly for 3 weeks)
  4. Pulsed azithromycin 3 months (3days/week)
  5. Prednisolone
  6. Azathioprine
34
Q

Types of Pemphigus?

(5)

A
  1. Pemphigus Vulgaris (PV)
  2. Pemphigus Foliaceous
  3. Paraneoplastic pemphigus
  4. Drug-induced pemphigus
  5. IgA pemphigus
35
Q

What is the type of pemphigus that causes oral lesions?

the common one

A

Pemphigus Vulgaris (PV)

36
Q

What is the main antibody involved in PV?

pemphigus vulgaris

A

IgG polyclonal antibodies

37
Q

What type of reaction is pemphigus?

hypersensitivity

A

Type II hypersensitivity immune reaction as it is antibody-mediated.

38
Q

What are the main target antigens in PV?

pemphigus vulgaris

A

desmoglein3 (Dsg3)
desmoglein1 (Dsg1)

39
Q

Which antigen gives rise to oral lesions in PV?

pemphigus vulgaris

A

desmoglein3 (Dsg3)

40
Q

Which antigen gives rise to skin lesions in more severe cases of PV?

pemphigus vulgaris

A

desmoglein1 (Dsg1)

41
Q

What is the difference between pemphigus vulgaris and pemphigoid?

A

PV: suprabasal clefts, intraepithelial clefts
Pemphigoid: sub-epithelial clefts

42
Q

Pathogenesis of PV.

pemphigus vulgaris

A

IgG4 polyclonal antibodies attack Dsg3,
thus damaging desmosomes,
which results in the loss of cell-cell adhesion, leading to vesiculations, erosions, or ulcers.

43
Q

How can PV be diagnosed?

A

Direct and Indirect immunofluorescnece.
Biopsy.
Test for presence of acantholytic cells.
Nikolsky sign (occasionally helpful).

44
Q

What is the Nikolsky sign?

A

A somewhat helpful diagnostic test.
Rub mucosa to induce bulla.

45
Q

What is Pemphigus?

A

A vesiculobullous disease.

Intraepithelial blisters, resulting in bullae that easily rupture (within hours), resulting in ulceration of mucosal and/or cutaneous sites (oral cavity, conjunctiva, genitalia and upper respiratory tract).

46
Q

Histological features of PV.

pemphigus vulgaris

A

Acantholysis with intraepithelial bullae formation.
Serum IgG, IgM, sometimes IgA autoantibodies to Dsg.

Suprabasilar clefts annd separation of the epithelium from the basal cell layer.
Within the blister/bullae separated area, acantholytic cells present.

Basket-weave-like pattern on IF.

47
Q

C/O:
erosions and ulcers in buccal mucosa, palate and lips.
slow-healing, no scarring.
severe desquamative or erosive gingivitis.
ulcers not well-defined.
persistent ulcers.

Differential diagnosis?

A

pemphigus vulgaris

48
Q

Local management of PV.

pemphigus vulgaris

A

Betamethasone phosphate tablets 0.5mg
Dissolve in 10ml water. Hold 2mins. 4x/day

Prednisolone 5mg tablets

49
Q

First-line management of PV. (systemic meds)

pemphigus vulgaris

A

oral prednisolone starting at 1mg/kg/day
(increase on 50-100% increments every 5-7 days if blistering continues)

consider pulsed IV corticosteroids.
assess osteoporosis risk.
corticosteroids + aduvant immunosuppressant (remission maintenance stage):
* azathioprinne 2-3mg/kg/day
* mycophenolate motefil 2-3g/day
* rituximab 1g x 2 infusions, 2 weeks apart

50
Q

Second-line management of PV. (systemic meds)

pemphigus vulgaris

A

azathioprine
mycophenolate motefil
rituximab

51
Q

Third-line management of PV. (systemic meds)

pemphigus vulgaris

A

methotrexate
IVIg
plasmaphoresis

52
Q

C/O:
itchy, urticated erythematous rash,
blisters which appear weeks to months after initial puritis,
lesions are localised to limbs or may be generalised

oral lesions are mild, transient. lesions heal without scarring

Differential diagnosis?

A

Bullous Pemphigoid

53
Q

What are the types of Pemphigoid?

(3)

A
  1. Bullous Pemphigoid
  2. Mucous Membrane Pemphigoid
  3. Cicatritial Pemphigoid
54
Q

What are the main target antigens in bullous pemphigoid?

A

BP180 and BP230

55
Q

How can BP be diagnnosed?

bulloud pemphigoid

A

biopsy
DIF
IIF
serology
clinical presentation

56
Q

What are the histological features of BP?

bullous pemphigoid

A

subepidermal blister with an inflammatory infiltrate (lymphocytes and eosinophils).

DIF shows linear BMZ (basement membrane zone) deposition of IgG and/or complement.

57
Q

Management of BP.

A

mild/localised:
* topical corticosteroids

moderate/severe:
* oral prednisolone with or without adjuvant therapy (immune modulating agents) (azathioprine, mycophenolate motefil).

steroid ± immune modulating agents

58
Q

What is mucous membrane pemphigoid?

MMP

A

It is a rare type of pemphigoid,
which involves the oral mucosa, conunctiva (symblepharon - leading to impaired vision & blindness), genitalia, upper aerodigestive tract, some skin.

The oral mucosa is most frequently affected, especially the gingiva (desquamative gingivitis).

59
Q

What is the main target antigen for MMP?

mucous membrane pemphigoid

A

BP180

60
Q

What are the main antibodies for MMP?

mucous membrane pemphigoid

A

IgG and/or IgA autoantibodies

61
Q

How is MMP diagnosed?

mucous membrane pemphigoid

A

postive DIF for IgG, IgA, IgM or C3 at BMZ

gold standard diagnostic test

62
Q

What are the histological features of MMP?

mucous membrane pemphigoid

A

subepithelial cleft with mixed inflammatory infiltrate

DIF shows IgG, IgA, IgM and/or C3 at basement membrane

63
Q

What is Erythema Multiforme?

EM

A

Target skin lesions, with oral or ocular involvement.
Can recur.
Associated with HSV infection or drugs.

EM is cytotoxic immunologic attack on keratinocytes exppressing non-self-antigenns due to HSV/drugs (allopuriol, antibiotics, anticonvulsant, NSAIDs).

64
Q

What are the types of EM?

(4)

A
  1. EM minor (affects only 1 mucosa)
  2. EM major (affects 2 or more mucous membranes)
  3. Stevens-Johnson Syndrome (SJS) (extensively skin)
  4. Toxic Epidermal Necrolysis (TEN)
65
Q

Which vesiculobullous disease can be triggered by a HSV infection?

EM type

A

Major/Minor EM

66
Q

Which vesiculobullous disease can be triggered by drugs?

EM type

A

Stevens-Johnsonn Syndrome
Toxic Epidermal Necrolysis

67
Q

C/O:
extensive painful erythmatous and ulcerative lesions of the mucous membranes that leaves scars,
irrefgular shallow ulcers and crusting of the lips

Differential diagnosis?

A

erythema multiforme

68
Q

What is the pathogenesis of EM?

erythema multiforme

A

CD8+ T lymphocytes in epitheliium inducing apoptosis of scattered keratinocytes,
leading to satellite cell necrosis.

69
Q

What are the histologival features of EM?

A
  • lichenoic infiltrate inn basement membrane zone of epithelium.
  • T lymphocytes and monoiuclar cells present in dermis and lamia propia and extend into epithelium.
  • epithelium appears edematous and spongiotic.
  • necrosis of basal and suprabasal epithelial ells, resulting in intra- and subepithelial bullae formation.
  • IF shows granular staining for C3 at BMZ and occasionally within vessels or apoptotic keratocytes.
70
Q

Management of EM.

erythema multiforme

A

urgent medical therapy:
* systemic steroids (up to 60mg/day)
* systemic aciclovir

encourage fluid intake
* may require admission for IV fluid if unable to drink

encourage analgesia

71
Q

What is Angina Bullosa Haemorrhagica?

ABH

A

Benign subepithelial oral mucosal blistera filled with blood in the absence of an identifiable cause or systemic disorder.

72
Q

What causes ABH?

angina bullosa haemorrhagica

A

trauma
long-term steroid inhaler use
zinc deficiency
hypertension

73
Q

What are the clinical features of ABH?

angina bullosa haemorrhagica

A
  • acute, sometimes painful oral blood-filled vesicles and bullae (not due to blood dyscrasia or other known causes)
  • mainly soft palate affected (can develop on buccal mucosa, lip and lateral surface of tongue
  • haemorrhagic bullae spontaneously burst after a short time resulting in ragged, painless, superficial erosions that heal spontaneously within 1 week without scarring
  • intact bullae is red to purple in colour
  • bulla 2-3cm in diameter
  • lesions may recur
74
Q

Management of ABH.

A

no treatment.
reassure patient disease is benign.
explain known triggers and course of disease.

75
Q

What are the histologic features of ABH?

A
  • parakeratotic epithelium with a subepithelial separation from the underlying lamina propria.
  • bullae filled with erythrocytes and fibrin
  • IF shows no IgG, IgM, IgA or C3 antibodies within basement membrane zone or epithelium

Oral Medicine (11 decks)

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