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Finals > Oral Medicine > Flashcards

Oral Medicine Flashcards

1
Q

How is oral ulceration managed?

A

Nutritional deficiencies
Avoid sharp or spicy foods
Prevention of superinfection
Symptomatic relieve

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2
Q

What are Bohn’s Nodules?

A

Gingival cysts filled with keratin in the alveolar ridge

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3
Q

What are fibro-epithelial polyps?

A

Localised hyperplastic lesion

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4
Q

What is the aetiology of fibro-epithelial polyps?

A

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

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5
Q

What are the clinical features of fibro-epithelial polyps?

A

Pedunculated or sessile
Firm or soft
Pink appearance
Painless
Can be ulcerated and easily traumatic
May have associated frictional keratosis
Usually an isolated lesion

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6
Q

Where do fibro-epithelial polyps present?

A

Buccal mucosa
Areas of trauma

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7
Q

Describe the histology of a fibre-epithelial polyp:

A

Fibrous core
Thick interlacing collagen
Adjacent normal tissue
Covered with squamous epithelium
May have hyperkeratosis
Little inflammatory infiltrate

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8
Q

What are the clinical considerations in regard to fibro-epithelial polyps?

A

Does it bother the patient?
Do they have risk factors for oral cancer?

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9
Q

What is the name for a fibro-epithelial polyp on the gingiva?

A

Fibrous epulis

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10
Q

What is the management of a fibro-epithelial polyp?

A

Photos
Identify and if appropriate, correct the traumatic cause
Consider excision biopsy

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11
Q

What are the benefits of excision biopsy for fibro-epithelial polyps?

A

Can confirm diagnoses
Can remove the lesion

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12
Q

What are the risks of excision for fibro-epithelial polyps?

A

Surgical risks
Altered sensation- can be permanent
Recurrence or incomplete excision

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13
Q

What are examples of hyperplasticity tissue conditions related to dentures?

A

Leaf fibroma
Denture hyperplasia
Papillary hyperplasia

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14
Q

What is papillary hyperplasia?

A

Granular inflammation of denture bearing surface- more common on palate

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15
Q

What is papillary hyperplasia associated with?

A

Candida

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16
Q

What is the management for denture associated lesions?

A

Consider excision of lesion
Denture hygiene
Candida management
Consider making a new prosthesis

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17
Q

What is an epulis?

A

A reactive hyperplastic lesion on the gingiva

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18
Q

What are the features of fibrous epulis?

A

Fibro-epithelial polyp on the gingiva
Same colour as gingiva
May be ulcerated

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19
Q

What is giant cell epulis also known as?

A

Peripheral giant cell granuloma

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20
Q

Describe the presentation of giant cell epulis:

A

Red/purple appearance
Sessile or pedunculated
Often interdental
Most common in children

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21
Q

What does giant cell epulis have identical histopathological features as?

A

Central giant cell lesion
Hyperparathyroidism (Brown’s Tumour)

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22
Q

What is the histopathological presentation of giant cell epulis?

A

Multi-nucleated osteoclast giant cells
Vascular stroma
Fibrous tissue

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23
Q

What is the pathogenesis of giant cell epulis?

A

Unknown
Reactive to trauma or irritation

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24
Q

What is the management of giant cell epulis?

A

Excisional biopsy
OPT +/- CBCT
Bone profile
Parathyroid hormone assay
Photos and investigation from paeds clinic

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25
Q

What is a vascular epulis the same as?

A

Pyogenic granuloma

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26
Q

What is the name of a vascular epulis that presents in pregnancy?

A

Pregnancy epulis

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27
Q

Why do pregnancy epulis present/increase in size?

A

Hormonal changes- may resolve following birth and result in a fibrous epulis
May recur if removed during pregnancy

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28
Q

What is the presentation of a vascular epulis?

A

Soft-bright red appearance
Gradual increase in size

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29
Q

What is the histological appearance of a vascular epulis?

A

Vascular appearance
Variable amounts of inflammatory infiltrate

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30
Q

What are the management options for a vascular epulis?

A

Keep under observation
Refer to oral surgery in GDP
Excisional biopsy
Excise after birth (pregancy epulis)

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31
Q

What drugs are associated with generalised gingival overgrowth?

A

Calcium channel blockers
Ciclosporin
Phenytoin

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32
Q

What is the management of gingival overgrowth?

A

Gingivoplasty
Ask GP to consider alternative medications
Plaque control
Are there risk factors for other disease
Consider referral to Oral Medicine to exclude other causes

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33
Q

What is chronic hyperplastic gingivitis associated with?

A

Mouth breathing
Pregnancy

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34
Q

How does hereditary gingival fibromatosis present?

A

Enlarged gingiva
Little inflammation
Expansion of the tuberosities

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35
Q

What is a sign of haematological malignancy associated with gingival overgrowth?

A

Rapid progression in presence of good OH

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36
Q

What is squamous cell papilloma also referred to as?

A

Benign growth (tumpur)
Wart

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37
Q

How does squamous cell papilloma present?

A

Pedunculated or sessile
Cauliflower appearance
Often keratinised surface
Single or multiple lesions

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38
Q

What is the aetiology of squamous cell papilloma?

A

Viral- HPV infection (HPV: 2,4,6,11 and 40)
May present in immunocompromised

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39
Q

What is the management of squamous cell papilloma?

A

Excisional biopsy
Observation: if no red flag signs, symptoms or OSCC risk factors

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40
Q

What is the histological presentation of squamous cell papilloma?

A

Finger like processes of hyperplastic squamous epithelium
Thin cores of vascular connective tissue

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41
Q

What is a pyogenic granuloma?

A

Reactive vascular lesion

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42
Q

Where do pyogenic granulomas present?

A

Gingiva usually

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43
Q

What is the cause of pyogenic granulomas?

A

Response to local irritation/trauma

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44
Q

What is the histological presentation of a pyogenic granuloma?

A

Vascular proliferation
Oedematous fibrous stroma
Variable inflammatory infiltrate

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45
Q

What is the management of pyogenic granulomas?

A

Remove irritant- plaque/overhangs/denture/trauma
Excisional biopsy
Photos

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46
Q

What is the pathophysiology of black hairy tongue?

A

Hyperplasia of filiform papillae
Build up of commensal bacteria, food debris
Pigment inducing fungi and bacteria

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47
Q

What are factors associated with the development of black hairy tongue?

A

Smoking
Antibiotics
Chlorhexidine mouthwash
Poor oral hygiene

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48
Q

What is the management of black hairy tongue?

A

Re-assure
Stop smoking
Stay hydrated
Lightly brush the tongue
Gently exfoliate tongue surfaces- peach stones
Eating fresh pineapple

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49
Q

What are fordyce spots?

A

Sebaceous glands

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50
Q

What do fordyce spots present as:

A

Yellowish bumps on the buccal mucosa and lips
Symmetrical distribution
Greater prominence later in life

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51
Q

What % of adults have fordyce spots?

A

60-75%

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52
Q

What is geographic tongue also called?

A

Benign migratory glossitis
Erythema migrans

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53
Q

What % of adults have geographic tongue?

A

1-3%

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54
Q

What is geographic tongue associated with?

A

Psoriasis

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55
Q

What is geographic tongue?

A

Loss of filiform papillae- areas of tongue atrophy and hyper keratinisation

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56
Q

What are the symptoms of geographic tongue?

A

Asymptomatic
Sensitivity to hot and spicy foods and toothpaste

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57
Q

What is the management of geographic tongue?

A

Reassurance
Biopsy not indicated
If symptomatic- consider difflam mouthwash
Ask about skin changes (psoriasis)
Consider avoiding trigger foods if painful

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58
Q

What are mucoceles?

A

Cysts

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59
Q

What are mucoceles caused by?

A

Damage to salivary ducts or minor salivary glands

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60
Q

What is a ranula?

A

Mucocele on floor of mouth

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61
Q

Where do mucoceles present?

A

Lower lip mainly
If upper lip- treat as malignancy until proven otherwise

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62
Q

How do mucoceles present?

A

Blue/translucent lump
Sessile

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63
Q

How are mucoceles classified?

A

Mucous retentive
Mucous extravasation

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64
Q

What age group are mucoceles most common in?

A

Under 30

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65
Q

What is the management of mucoceles?

A

Excision- blunt dissection to remove full capsule of cyst and damaged minor salivary gland
Paeds- watchful wait

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66
Q

What happens if a mucocele is incompletely excised?

A

Increased chance of reoccurrence

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67
Q

What is a lingual tonsil?

A

Lymphoid tissue

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68
Q

Where is a lingual tonsil found?

A

Postero-lateral aspect of tongue

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69
Q

What is a varice?

A

Blood vessel

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70
Q

When are varices more prominent?

A

Increasing age
Smokers
CVD patients

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71
Q

What is a hamartoma?

A

Disorganised vascular tissue

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72
Q

Where do hamartomas present?

A

Head and neck

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73
Q

What is a haemangioma?

A

Common, benign growth made of a collection of small blood vessels that form a lump under the skin

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74
Q

What are the histological subtypes of haemangioma?

A

Capillary- smaller capillary vessels
Cavernous- large thin walled vessels

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75
Q

What groups are haemangiomas most common in?

A

Children
Females

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76
Q

What is a vascular malformation?

A

Congenital lesion due to abnormal blood vessel development

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77
Q

What are vascular malformations associated with?

A

Larger arteries and veins
Stuge-weber syndrome

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78
Q

When do vascular malformations present?

A

Birth
Different times of life

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79
Q

What is the management of vascular malformations?

A

No treatment
Ultrasound
Cryotherapy
Cauterisation
MRI +/- Angiogram (large lesions)
May require extensive excision and free-flap reconstruction

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80
Q

What is the histological presentation of tori and exostoses?

A

Thicker epithelium
Broad rete process

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81
Q

What is linea alba?

A

Horizontal, asymptomatic white lesion along the occlusal

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82
Q

What is the histological appearance of linea alba?

A

Parakeratosis
Prominent or reduced granular layer
Acanthuses

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83
Q

What is fissured tongue?

A

Variation of normal anatomy
Occurs later in life
No treatment needed
Associated with geographic tongue

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84
Q

What is the management of fissured tongue?

A

Encourage good oral hygiene
Consider lightly brushing tongue

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85
Q

What is a bony exostosis?

A

Usually benign overgrowth of calcified bone
Associated with parafunction

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86
Q

What % of the population have bony exostosis?

A

30-40%

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87
Q

Where do bony exostosis present?

A

Palate: torus palatinus
Mandible: torus mandibularis (typically lingual)

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88
Q

What is the management of bony exostosis?

A

Monitoring: photos, study models, x-rays

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89
Q

What should be considered with patients with physiological pigmentation?

A

Addisons disease
Smokers melanosis
Drug-related pigmentation

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90
Q

What are the systemic risk factors for oral candida infection?

A

Immunocompromised: medication, medical conditions
Deficiency states: anaemia
Extremes of age

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91
Q

What are the local factor that influence oral immunity or ecology and are associated with increased oral candida infection risk?

A

Hyposalivation
Smoking
Broad-spectrum antimicrobials
Corticosteroids
Dental appliances
Irradiation involving the mouth or salivary glands

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92
Q

What is candida infection also known as?

A

Thrush/Yeast/Fungal infection

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93
Q

What is the management of oral candidiasis?

A

Antifungal therapy
Local measures
Investigations to exclude systemic disease

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94
Q

What anti fungal therapy can be provided to patients with oral candida?

A

Fluconazole
Miconazole
Nystatin

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95
Q

What local measures of management can be provided to patients with oral candida?

A

Rinse after inhalers
Use a spacer
Denture hygiene
Smoking cessation

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96
Q

What is traumatic keratosis?

A

Increased keratin deposition at a site of trauma
Protective response

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97
Q

What is the management of traumatic keratosis?

A

Encourage smoking cessation
Take photographs

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98
Q

What are the six types of oral lichen planus and oral lichenoid reactions?

A

Reticular
Atrophic
Papular
Erosive
Plaque like
Bullous

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99
Q

What is oral lichen planus?

A

CD8+ T Cell mediated destruction of basal keratinocytes
Chronic inflammatory condition

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100
Q

How does oral lichen planus present?

A

Asymptomatic or burning/stinging sensation

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101
Q

What is the difference between oral lichen planus and oral lichenoid tissue reactions?

A

Oral lichen planus is generalised and idiopathic
Oral lichenoid tissue reactions are localised and may be a response to medicines/allergens

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102
Q

What is the malignant potential of oral lichenoid reactions?

A

1% over 10 years

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103
Q

What should you ask a patient with oral lichen planus/oral lichenoid reactions about?

A

Systemic symptoms or recent cancer therapy

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104
Q

What drugs can cause oral lichenoid reactions?

A

Antihypertensives
Antimalarials
NSAIDs
Allopurinol
Lithium

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105
Q

What materials can cause oral lichenoid reactions?

A

Metals (gold, nickel)
Composite resin

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106
Q

What is the management of oral lichen planus/ oral lichenoid reactions?

A
  1. Simple mouthwash (HSMW)
  2. Local anaesthetic (Benzydamine or lidocaine)
  3. Avoid trigger factors (spicy foods, fizzy drinks)
  4. Steroid mouthwash (Betamethasone MW, Beclometasone inhaler or hydrocortisone oromucosal tablets
  5. Change restorations (composite causative?)
  6. Onward referral- biopsy, inform of increased cancer risk, stop the cause
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107
Q

What is hairy leukoplakia?

A

Non-removable white patch
Acanthotic and para-keratinised tissue
Finger-like projections of para keratin

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108
Q

Where is hairy leukoplakia usually?

A

Lateral borders of tongue

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109
Q

What are the risk factors for hairy leukoplakia?

A

Triggered by EBV
Immunocompromised

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110
Q

What % of HIV patients have hairy leukoplakia?

A

20-25%

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111
Q

What is leukoplakia?

A

Diagnosis of exclusion
No obvious cause for white patch
Has malignant potential
Can be dysplastic: group of abnormal cellular changes associated with malignancy

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112
Q

What is a red patch with no clear cause associated with?

A

A high likelihood of being dysplastic or malignant

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113
Q

What is granulomatosis with polyangitis also known as?

A

Wegner’s granulomatosis

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114
Q

What is granulomatosis with polyangitis?

A

Systemic vasculitis
May present with fever and weight loss

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115
Q

How is granulomatosis with polyangitis managed?

A

Immunosuppressants

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116
Q

What % of patients with granulomatosis with polyangitis have ear, nose or throat manifestations?

A

92%

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117
Q

What is erythroplakia?

A

Velvety, fiery, red patch
High malignant transformation

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118
Q

How is erythroplakia diagnosed?

A

Diagnosis of exclusion

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119
Q

What is the management of erythroplakia?

A

Urgent referral (high malignant transformation)
Consider urgent biopsy for histopathology

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120
Q

What is OFG and Oral Crohn’s?

A

Non-necrotising granuloma formation

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121
Q

What is the management of OFG and Oral Crohn’s?

A

Topical steroids
Avoidance diets
Intralesional steroid
Biologics for crohns disease
Infliximab, adalimumab (anti TNF), ustekinumab (Anti IL21/23), Vedolizumab (Anti-a4b7)

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122
Q
A
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123
Q

How many oral cancer cases are diagnosed per year?

A

500

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124
Q

What is the % survival for an early diagnosis of oral cancer?

A

50%

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125
Q

What is the % diagnosis for a late diagnosis oral cancer?

A

50%

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126
Q

What are the red flags for oral cancer?

A

> 3 week duration
50 years old
Smoking
High alcohol consumption
History of oral cancer
Non-homogenous
Non-healing ulceration (with no cause)
Indicated
Exophytic
Tethering of tissue
Tooth mobility
Non-healing extraction sockets
Difficulty speaking/swallowing
Cervical lymphadenopathy
Weight loss/appetite loss
Numbness/altered sensation

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127
Q

How can we increase early detection?

A

Soft tissue exam for every patient
Patient education and empowerment
Recognition of complex social, cultural, public health reasons behind risk behaviours, poor attendance and access to dental practices

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128
Q

What are the risk factors of oral cancer?

A

Smoking
Poor OH
HPV
Alcohol
Chewing tobacco/betel/areca nut
Socio-economic background
Low fruit/veg

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129
Q

What is oral epithelial dysplasia?

A

Abnormal growth

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130
Q

How is oral epithelial dysplasia diagnosed ?

A

By histology

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131
Q

What are the risk factors of oral epithelium dysplasia?

A

Smoking
Alcohol
HPV
Genetics

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132
Q

How does Oral epithelium dysplasia present?

A

Patches of red/white

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133
Q

What are the four factors of describing lesions?

A

Site
Size
Colour
Texture

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134
Q

What is a higher risk site of an oral lesion?

A

Ventrolateral tongue and FoM

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135
Q

What should you look at when considering the texture of a lesion?

A

Can you feel it when palpating?
Is it thickened/rough/corrugated/firm/rubbery?

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136
Q

What should you look at when considering the texture of a lesion?

A

Can you feel it when palpating?

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137
Q

What are the architectural features of oral epithelial dysplasia?

A

Irregular epithelial stratification
Loss of polarity of basal cells
Drop-shaped rete ridges
Increased number of mitotic figures
Abnormally superficial mitoses
Premature keratinisation in single cells (dyskeratosis)
Keratin pearls with rete ridges
Loss of epithelial cell cohesion

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138
Q

What are the cytological features of oral epithelial dysplasia?

A

Abnormal variation in nuclear size
Abnormal variation in nuclear shape
Abnormal variation in cell size
Abnormal variation in cell shape
Increased nuclear-cytoplasmic ratio
Atypical mitotic figures
Increased number and size of nucleoli
Hyperchromasia

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139
Q

What are the molecular markers for Oral Epithelial Dysplasia?

A

Signalling pathways: EGFR
Cell cycle: Ki67, p53, pRB
Immortalisation: Telomerase
Apoptosis: p53, p21
Angiogenesis: VEGF
COX-1&2 enzymes
Proliferation and differentiation markers
Viruse: HPV + and HPV-
Loss of heterozygosity (LOH): 3p, 9p, 13q (retinoblastoma), 17p

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140
Q

How does basal hyperplasia present?

A

Increased basal cell numbers
Regular stratification and basal compartment is larger (architecture)
No cellular atypia

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141
Q

How does mild dysplasia present?

A

Architecture; changes in the lower third
Cytology: mild atyppia
Pleomorphism, hyperchromatism

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142
Q

How does moderate dysplasia present?

A

Architecture: change extends into the middle third
Cytology: moderate atypia

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143
Q

How does severe dysplasia present?

A

Architecture: changes extend to the upper third
Cytology: several atypia and numerous mitoses, abnormally high

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144
Q

How does carcinoma in situ present?

A

Malignant but not invasive:
Architecture: Abnormal, full thickness (or almost full) of viable cells
Cytology: pronounce cytological atypia- mitotic abnormalities frequent

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145
Q

How is oral epithelial dysplasia managed?

A

Mild or low grade- monitored (minimum 5 years)
Moderate or severe/high grade- considered for removal by OMS

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146
Q

What is the definition of oral potentially malignant disorders?

A

Any mucosal abnormality that is associated with statistically increased risk of developing oral cancer

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147
Q

What are examples of oral potentially malignant disorders?

A

Leukoplakia
Proliferative verracous leukoplakia
Erythroplakia
Oral submucous fibrosis
Oral lichen planus
Oral lichenoid lesion
Actinic cheilitis/keratosis
Palatal lesions in reverse smokers
Oral lupus erythematosus
Dyskeratosis congenital
Oral graft vs host disease

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148
Q

What is the definition of leukoplakia?

A

Predominantly white patch, not attributed to another disorder

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149
Q

What are the two types of leukoplakia?

A

Homogenous- typically well demarcated
Non-homogenous- diffuse borders, red/nodular components

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150
Q

What could leukoplakia be?

A

Frictional keratosis
Biting habits
Oral lichen planus
Pseudomemranous candidiasis (can be scraped off)
Leukoedema (bilateral, disappears on stretching)
Nicotinic stomatitis
Papilloma

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151
Q

What is proliferative Verrucous leukoplakia?

A

Distinct form of multi-focal oral leukoplakia
Progressive

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152
Q

What Oral potentially malignant condition has the highest risk of malignant change?

A

Proliferative verrucous leukoplakia

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153
Q

What is erythoplakia?

A

Predominantly fiery red patch that cannot be characterised clinically or pathologically as any other definable disease
Solitary lesion, typically well demarcated

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154
Q

What can distinguish erythroplakia from widespread conditions?

A

Solitary nature

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155
Q

What is oral submucous fibrosis?

A

Progressive condition leading to the loss of elasticity which progresses to fibrosis of the lamina propria
Function limiting

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156
Q

What may a patient with oral submucous fibrosis present with?

A

Burning sensation with spicy food
Later restricted mouth opening

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157
Q

What habits are associated with oral submucous fibrosis?

A

Paan- areca nuts, slaked lime, betel leaves

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158
Q

What is oral lichen planus?

A

Inflammatory condition of the oral mucosa,
Usually Idiopathic

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159
Q

What does erosive oral lichen planus lead to?

A

Ulceration and erthemaotous erosions

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160
Q

What do oral lichenoid lesions include?

A

Atypical OLP/unilateral lesions
Lichenoid tissue reactions
Lichenoid drug reactions

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161
Q

What factors are considered in regard to risk vs benefit of removing amalgam restorations in oral lichenoid lesions

A

Potential for tooth to become symptomatic
Requiring larger restoration
Requiring crown
Unrestorable
No resolution

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162
Q

What is actinic cheilitis?

A

Diffuse, patch with dryness and thickening associated with solar radiation exposure

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163
Q

How is actinic cheilitis prevented?

A

Smoking cessation
UV protection

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164
Q

What is often the cause of a palatal lesion in a reverse smoker?

A

Burning end of cigarette held in mouth

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165
Q

What is dyskeratosis congénita?

A

Rare hereditary condition
Leukoplakia and hyperpigmentation of skin and nail dystrophy

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166
Q

What is oral systemic erythematosus?

A

Autoimmune inflammatory condition
Clinically similar to OLP- starburst appearance on hard palate

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167
Q

What % of systemic lupus erythematosus have oral lesions?

A

20%

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168
Q

What is an example of a previously included oral potentially malignant disorder?

A

Chronic hyperplasticity candidiasis

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169
Q

What is chronic hyperplastic candidiasis?

A

Occurs in smokers

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170
Q

What is the treatment of chronic hyperplastic candidiasis?

A

Antifungal treatment

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171
Q

What are the causes of oral ulcers?

A

Trauma
Metabolic/nutritional
Allergic/hypersensitive
Infective
Inflammatory
Immunological
Drug Induced (iatrogenic)
Neoplastic
Idiopathic

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172
Q

What factors should be considered when assessing the aetiology of an ulcer?

A

Site
Onset
Duration
Number
Texture
Appearance
Size
Pain
Predisposing factors
Relieving factors

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173
Q

How does a traumatic ulcer present?

A

White (keratotic) borders
Clear causative agent
Surrounding mucosa normal and ulcer soft

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174
Q

What is the most common ulcerative condition?

A

Aphthous ulcers

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175
Q

How does an aphthous ulcer present?

A

Painful
Red border
Yellow/white centre

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176
Q

What % of the population experience aphthous ulcers?

A

20%

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177
Q

How does a major recurrent aphthous ulcer present?

A

Greater than 1cm
Long time to heal

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178
Q

How does a minor recurrent aphthous ulcer present?

A

Less than 1cm
Heals in 2-3 weeks

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179
Q

How does a herpetiform recurrent aphthous ulcer present?

A

Multiple small ulcers that may coalesce

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180
Q

What are the triggers for aphthous ulcers?

A

Stress
Trauma
Allergy
Sensitivity

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181
Q

What are the metabolic/nutritional causes of ulcers?

A

Associated with growth in children/teens
Adults with occult GI/GU pathology
Malnourishment
Anaemia

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182
Q

What are inflammatory/immunological causes of ulcers?

A

Behcet’s
Necrotising sialometaplasia
Lichen planus ]
Vesiculobullous disease
Connective tissue disease

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183
Q

Where does behcet’s affect?

A

Aphthous appearance ulcers on mouth, skin, genitals and eyes

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184
Q

What are examples of connective tissue diseases?

A

Systemic Lupus Erythematous
Rheumatoid Arthritis
Scleroderma

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185
Q

What questions should you ask when you suspect a GIT cause for ulcerations?

A

Abdominal pain
Post rectal blood/mucous
Altered bowel motions
Unintentional weight loss

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186
Q

What questions should you ask when you suspect a connective tissue disease cause for ulcerations?

A

Joint pain and stiffness
Photosensitive rashes
Xerophthalmia/xerostomia
Fatigue

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187
Q

What are infective causes of ulceration?

A

Primary or recurrent herpes simplex virus infection
Varicella-zoster virus
Epstein-barr virus
Coxsackie virus
Echovirus
Treponema pallidum
Mycobacterium tuberculosis
Chronic mucocutaneous candidiasis
HIV

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188
Q

What age group is commonly affected by primary herpes simplex virus infection?

A

2-5 years

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189
Q

How does primary herpes simplex virus infection present systemically?

A

Fever
Headache
Malaise
Dysphagia
Cervical lymphadenopathy

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190
Q

How does primary herpes simplex virus infection present in the oral cavity?

A

Short lasting vesicles on the tongue, lips, buccal, palatal and gingival mucosa which then form ulcers

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191
Q

Explain the pathway of the varicella-zoster virus?

A

Primary varicella-zoster infection: Chicken Pox
Virus remains latent in sensory ganglion
Reacrivation of latent virus results in VCZ infection: Shingles

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192
Q

How does the varicella-zoster infection present?

A

Distributed over a dermatome
Reactivated due to immunocompromisation or acute infection

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193
Q

How are patients with varicella-zoster managed?

A

Lisa with GP
May need further investigations, provide analgesia and difflam if painful

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194
Q

What are iatrogenic causes of ulceration?

A

Chemotherapy
Radiotherapy
Graft vs Host disease
Drug Induced Ulceration

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195
Q

What drugs are associated with drug induced ulceration?

A

Potassium channel blockers
Bisphosphonates
NSAIDs
DMARDs

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196
Q

How do neoplastic ulcers present?

A

Exophytic
Rolled borders
Raised
Hard to touch
Non moveable
Not always painful
Sensory disturbance

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197
Q

What is the local management pathway of ulceration?

A

If suspicion of malignancy- refer to OMFS
Reverse the reversible
Refer to GP for FBC/Haemantics/Coeliac Screen (aphthous appearance)

  1. Simple Mouthwash (HSMW)
  2. Antiseptic mouthwash (hydrogen peroxide or CHX or doxycycline)
  3. Local anaesthetic (Benzydamine spray or mouthwash)
  4. Steroid mouthwash (betamethasone)
  5. Steroid inhaler (beclometasone)
  6. Onward referral
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198
Q

What are the three types of pain?

A

Nociceptive
Inflammatory
Pathological

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199
Q

What is the cause of pathological pain?

A

Abnormal functioning of the nervous system

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200
Q

What are the causes of mucosal non-odontogenic intra-oral pain?

A

Ulcers
Lichen planus
Vesticulobullous disorders
Salivary gland pain

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201
Q

What are the causes of non-odontogenic intra-oral pain?

A

Neuropathic pain
Trigeminal neuropathic pain
Persistent idiopathic dentoalveolar pain

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202
Q

What are examples of neuropathic pain?

A

Non-diseased dento-alveolar structure
Presents with burning/shooting/shot-like/allodynia/hyperalgesia

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203
Q

How does oral dysesthesia (burning mouth syndrome) present

A

Pain/burning sensation
Altered sensation ]
Perception of dry or excess saliva

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204
Q

What can cause trigeminal neuralgia?

A

Tumour
MS
Neurovascular conflict

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205
Q

How does trigeminal neuralgia present?

A

Electric shock/shooting/stabbing
Unilateral
Severe 10/10
Short lasting
Episodic

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206
Q

How should you manage suspected trigeminal neuralgia?

A

MRI

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207
Q

Why do oral lesions appear white?

A

The epithelium has thickened

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208
Q

What conditions are associated with white lesions?

A

Congenital
Lichen Planus
Infections
Neoplastic/potentially neoplastic
Keratosis

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209
Q

What are organic material causes of white lesions?

A

Candida infection
Food debris

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210
Q

What are physiological causes of white lesions?

A

Tongue coating
Desquamation
Leukoedema

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211
Q

How does leukoedema present?

A

Faint white lines (typically buccal mucosa)
Fade or disappear on starching mucosa

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212
Q

What ethnicity is leukoedema common in?

A

African heritage

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213
Q

What are the genetic associations with White Sponge Naevus?

A

Inherited Autosomal dominant
Mutation of genes that code for keratins 4 and 13

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214
Q

How does white sponge naevus present?

A

Affects oral mucosa (commonly buccal)
Presents in adolescence or childhood
Poorly defined border
Benign

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215
Q

What is the histology of white sponge naevus?

A

Acanthotic- thickening of epithelium (especially stratum spinosum)
Hyperkeratosis
Intra-cellular oedema in stratum spinosum and parakeratinised layers
No inflammatory changes

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216
Q

How does Darier disease present?

A

Rare autosomal dominant disorder
Hyperkeratosis papules affecting seborrheic areas on head, neck, skin folds and thorax
Crusted papules
Oral manifestations rare but affect palatal and alveolar mucosa
Asymptomatic

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217
Q

How does focal palmoplantar and oral mucosa hyperkeratosis syndrome present and genetic aspect?

A

Autosomal dominant
Affects soles, palms and oral mucosa- mainly keratinised tissue
Rare

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218
Q

What restorative materials are associated with lichen planus and lichenoid tissue reactions?

A

Amalgam
Gold
Polymerised plastics

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219
Q

What medications are associated with lichen planus and lichenoid tissue reactions?

A

Anti-malarials
Oral hypoglycaemic
NSAIDs

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220
Q

What food and food additives are associated with lichen planus and lichenoid tissue reactions?

A

Flavouring- cinnamon and derivatives

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221
Q

How does hairy leukoplakia present?

A

Presents on lateral aspects of tongue
Bilateral

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222
Q

What are the causative factors of hairy leukoplakia?

A

EBV infection in immunocompromised; HIV (decreases CD4+ T cell count), diabetes, steroid use

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223
Q

What are examples of neoplastic and potentially malignant white patches?

A

Squamous cell carcinoma
Leukoplakia
Submucous fibrosis
Actinic Chelitis

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224
Q

What are the red flags associated with squamous cell carcinoma?

A

> 3 week duration
50 years old
Smoking
High alcohol consumption
History of oral cancer
Non-homogenous
Non-healing ulceration
Induration
Exophytic
Tethering of tissue
Tooth mobility
Non-healing extraction sockets
Difficulty speaking/swallowing
Cervical lymphadenopathy
Weightless/appetite loss/fatigue
Numbness/altered sensation

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225
Q

How is suspected squamous cell carcinoma managed?

A

Urgent cancer referral to oral and maxillofacial surgery
Follow local guidelines
Be honest with patient and explain concerns and that a biopsy should be taken promptly

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226
Q

How does homogenous leukoplakia present?

A

Uniformly white, flat and thin
Smooth surface
May exhibit shallow cracks

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227
Q

What is the definition of leukoplakia?

A

A white patch or plaque that cannot be characterised clinically or pathologically
Diagnosis of exclusion
Cannot be rubbed away

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228
Q

How does verrucous leukoplakia present?

A

Surface is raised, exophytic, wrinkled or corrugated

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229
Q

What % of leukoplakia will become malignant in ten years?

A

2-5%

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230
Q

What % of leukoplakias are displastic?

A

5-20%

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231
Q

What % of leukoplakia showing dysplasia progress to carcinoma in 10 years?

A

10-35%

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232
Q

What are the clinical features of a leukoplakia that is likely to become malignant?

A

> 200mm2
Non-homogenous texture
Red or speckled colour
Sited on tongue/ FoM
Female
50 years
Smoker

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233
Q

What are the histological features of a leukoplakia that is likely to become malignant?

A

Severe/high risk of dysplasia
HPV-16 +
Aneuploidy DNA content
Loss of heterozygosity (many genes involved)

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234
Q

What disorders should be excluded for a leukoplakia diagnosis?

A

Leukoedema
White sponge naevus
Frictional keratosis
Chemical injury
Acute pseudomembranous candidiasis
Hairy leukoplakia
Lichen planus (plaque like variant)
Lichenoid reaction
Discoid lupus erythematous

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235
Q

What % of proliferative verrocous leukoplakia undergo malignant transformation?

A

85%

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236
Q

How does proliferative verrucous leukoplakia present?

A

Warty surface with white/yellow appearance
Palate and gingiva common sites
Enlarge overtime

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237
Q

How does oral sub mucous fibrosis present?

A

Pale in colour
Firm to palpate
Fibrous band develops
Buccal mucosa and soft palate typically affected
Mouth opening diminishes overtime

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238
Q

What % of oral submucous fibrosis becomes malignant?

A

5%

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239
Q

What is the general management of oral potentially malignant disorders?

A

Smoking cessation
Increase fruit and veg intake
Mapping biopsies
Observation with clinical photos
Consider excision if evidence of dysplasia
Monitor

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240
Q

What is a keratose?

A

Response to trauma- frictional, thermal or chemical

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241
Q

What are frictional causes of keratoses?

A

Sharp teeth
Restorations
Dentures
Occlusion

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242
Q

What are thermal causes of keratoses?

A

Smoking
Hot food/drinks

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243
Q

What are chemical causes of keratoses?

A

Aspirin
Acid
Bleach
Chlorhexidine

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244
Q

What is the management of linea alba/frictional keratosis?

A

Identify cause
Correct cause and review 2-3 weeks later
If no improvement, consider referral or biopsy

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245
Q

What is the general management of white patches?

A

Thorough history and systems enquiry
Exclude red flags
Clinical photos
Correct obvious causes
If no improvement- refer
Consider need biopsy

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246
Q

Why do oral lesions appear to be red?

A

Inflammation
Mucosal atrophy
Increased vascularisation
Mucosal/submucosa bleeding

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247
Q

What are the differential diagnoses for red patches?

A

Viral infection
Candidal infection
Iatrogenic- mucositis secondary to chemo or radiotherapy
Lichen planus/lichenoid reactions
Granulomatous disease
Blistering diseases- vesticulobullous disorders
Allergy
Psoriasis
Geographic tongue
Leukaemia
Purpura
Trauma
Deficiency states
Erythroplakia

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248
Q

What is erythroplakia?

A

Atrophic lesion
Localised/focal
Well defined borders
Velvety/red texture
Speckled appearance (erythroleukoplakia)
Commonly affects soft palate/buccal mucosa/ FoM
Strong association with tobacco use

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249
Q

What % of erythoplakia showed invasive carcinoma?

A

51%

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250
Q

What % of erythroplakia showed carcinoma in situ?

A

40%

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251
Q

What % or erythroplakia showed moderate dysplasia?

A

9%

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252
Q

What is the % of malignant transformation rate of erythroplakia?

A

50%

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253
Q

What mutation is associated with erythroplakia?

A

p53

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254
Q

What is the management of erythroplakia?

A

Refer urgently to OMFS or OM

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255
Q

How does erythroleukoplakia present?

A

Speckled red/white patches
Heterogenous appearance
Highly suspicious for SCC or severe dysplasia

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256
Q

What is the management of red patches?

A

Through history and examination
Exclude red flags
Get photos
Correct obvious cause
Consider biopsy

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257
Q

What are exogenous causes of pigmented oral lesions?

A

Amalgam
Chlorhexidine
Tobacco
Heavy metals

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258
Q

What are endogenous causes of pigmented oral lesions?

A

Melanin

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259
Q

How doe amalgam tattoos present?

A

Amalgam fragments introduced into soft tissues
Blue/grey appearance
Consider radiograph or biopsy

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260
Q

What are examples of foreign bodies that can cause oral pigmentation?

A

Grit/dirt from road traffic accidents
Tattoos

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261
Q

What is peutz-jeghers syndrome?

A

Developmental hypermelanosis
Autosomal dominant disorder
Associated with STK11 (tumour suppressor gene mutation)
Resembles freckles; affects buccal mucosa and lips
Presents in infancy

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262
Q

What are the investigations for peutz-jeghers syndrome?

A

FBC
Endoscopy
STK11 gene

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263
Q

What is the treatment of peutz-jeghers syndrome?

A

Manage polyps
Regular MRI/CT

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264
Q

What is the effect of inflammation on melanocyte activity?

A

Stimulation causing increased melanin in areas of infection

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265
Q

What is the effect of Addisons disease on the oral cavity?

A

ACTH stimulates melanocytes leading to patchy hyperpigmentation

266
Q

What medications are associated with oral pigmentation?

A

Antimalarials
Zidovudine- antiretroviral
Busulphan- chemotherapy
Gold
Minocycline- antibiotics
Heavy metal

267
Q

What is a melanotic macule?

A

Single brown lesion compromised of melanin containing cells
Flat, non-raised, <1cm, no rapid change, painless
Common on vermillion border,

268
Q

How should you manage a melanotic macule?

A

Consider excision biopsy to exclude melanoma

269
Q

How does melanocytes naevi present?

A

Blue/black lesions
Focal proliferations of melanocytes
Appears during childhood
<1cm
Papular appearance
No rapid change
Clinically resemble melanoma

270
Q

Where is melanoma in the oral cavity most common?

A

Palate or maxillary gingival

271
Q

What factors are associated with suspected melanoma?

A

Asymmetry
Border Irregularity
Colour Irregularity
Diameter >6mm
Evolving (size, shape, colour, elevation)

272
Q

What should you do with a suspected melanoma?

A

Refer urgently to OMFS

273
Q

How common is melanoma?

A

1.2 cases per 10 millon per year
1-2% of oral malignancies
Average age 60
More common in more pigmented populations

274
Q

What is the 5YS of melanoma?

A

25.5%

275
Q

What is Kaposi’s Sarcoma?

A

Vascular neoplasm associated with HHV8
Disorganised epithelial cell growth resulting in cleft containing erythrocytes
Redish-blue or brown foci
Presents on skin, oral mucosa and GI tract

276
Q

What groups does Kaposi’s Sarcoma most commonly affect?

A

Immunocompromised
Predilection for men who have sex with men
50% present in patients with untreated aids
Older Italian and eastern european jewish populations without imunodeficiency

277
Q

What is the management of Kaposi’s Sarcoma

A

Surgery
Radiotherapy
Chemotherapy
Immunotherapy
Manage underlying immunodeficiency (HAART)

278
Q

What factors should be considered in the history of a patient with Kaposi’s Sarcoma?

A

Onset of pigmentation
Appearance change
Symptoms
Other sites
PMH/Surgical History
Drug Hx
Tobacco/Betel use
Family history
Symptoms of systemic disease

279
Q

What factors should be considered in the examination of a patient with Kaposi’s Sarcoma?

A

Number of lesions
Diffuse or localised
Size/Borders/Colour
Variation in pigment
Inflammation/Ulceration
Lymphadenopathy
General examination

280
Q

What blood tests should be carried out in secondary care for diffuse pigmented lesions?

A

FBC
U+E
LFT
Glucose
TFT
Cortisol/ACTH/Adrenal Antibodies
Ferritin
Bone Profile
HIV
Coeliac screen

280
Q

What investigations can be carried out in secondary care for diffuse pigmented lesions?

A

Clinical photos
Lying/Standing BP - to exclude Addisons
Blood tests
Biopsy
Chest Xray- to exclude TB/Sarcoidosis (can cause adrenal insufficiency)
Endoscopy

281
Q

What are the characteristics of viruses?

A

Small size
Simple chemical composition
No intracellular organelles
Genetic information kept in DNA or RNA

282
Q

What are the stages of viral replication of herpes simplex?

A
  1. Binding
    2a/2b. Entry
  2. Release and Nuclear Transport
  3. Nuclear Entry
  4. Gene Expression
  5. DNA Replication
  6. Packaging
  7. Egress
283
Q

What are the factors to consider in the history and examination in regard to laboratory diagnosis?

A

Ability to write referral letter or communicate via phone call

284
Q

What are the features of a viral swab?

A

Flocked swab
Placed in molecular sample solution
After immersion the swab is removed

285
Q

What tube is used for a blood sample?

A

EDTA (purple topped)

286
Q

What can a blood sample be used for?

A

Serology or Molecular

287
Q

What should be included on a virology request form?

A

Patient details and clinician details
Clinical details and provisional diagnosis
Date of onset
Patient DOB or CHI no
Specify tesy

288
Q

What must specimens be transported in?

A

Approved containers

289
Q

What are examples of common muculo papular/erythematous viral pathogens?

A

Enterovirus
HHV6
HHV7
Measles
Rubella

290
Q

What type of specimen is taken for a maculo papular erythematous virus?

A

Mouth swap

291
Q

What test is carried out for a maculo papular erythematous virus?

A

DNA/RNA detection

292
Q

What are examples of common vesicular pathogens?

A

HSV1
HSV2
V2V
Enterovirus

293
Q

What is the appropriate specimen for a vesicular pathogen?

A

Mouth swab

294
Q

What is the appropriate test for a vesicular pathogen?

A

DNA/RNA detection

295
Q

What are examples of common pathogens associated with ulcers?

A

HSV
Enterovirus

296
Q

What is the appropriate specimen for ulcers?

A

Mouth swab

297
Q

What is the appropriate test for ulcers?

A

DNA/RNA detection

298
Q

What does serology detect?

A

Nucleic acid amplification or antibody levels

299
Q

In regard to serology of a maculo papular/ erythematous lesion what are the common pathogens associated?

A

B19
CMV
EBV

300
Q

What is the appropriate serology sample for maculo papular/ erythematous lesions?

A

EDTA blood

301
Q

What is the appropriate serology test for maculo papular/ erythematous lesions?

A

DNA/RNA detection or serological markers

302
Q

What Ig are CMV/EBV associated with?

A

IgM

303
Q

What is VZV

A

Varicella Zoster Virus

304
Q

What is HSV?

A

Herpes Simplex Virus

305
Q

What are examples of oral viral infections?

A

Herpes simplex type 1
Herpes simplex type 2
Varicella zoster
Epstein barr
Cytomegalovirus
HHV-6
HHV-7
HHV-8 (Kaposi’s sarcoma associated virus)

306
Q

What are the common features of human herpes viruses?

A

Primary infection
Latency period
Recurrent infection

307
Q

What are the clinical features of HHV 1 &2?

A

Gingivo stomatitis
Herpes labials
Keratoconjunctivitis
Herpetic whitlow
Bell’s palsy
Genital herpes

308
Q

What are the stages of herpes simplex pathogenesis?

A

Acute infection
Latency
Reactivation: Cold sores, viral shedding, epithelial cell death

309
Q
A
310
Q

What is the reservoir of HSV?

A

Saliva

311
Q

What is the route of transmission of HSV?

A

Direct by close person to person contact

312
Q

How can a lab diagnosis be made from vesicle/ulcer fluid?

A

Swab and molecular sample for PCR

313
Q

What is the prevention of HSV?

A

Chemoprophylaxis: Aciclovir to prevent recurrent infection in difficult cases (200mg x5 daily)

314
Q

What is the treatment of HSV?

A

Topical therapy with Aciclovir (5% cream)
IV therapy for severe and immunocompromised

315
Q

What are the clinical features of varicella zoster virus?

A

Incubation period of 10-21 days

316
Q

What are the signs and symptoms of shingles?

A

Vesicles appear in dermatome, representing cranial or spinal ganglia where the virus has been dormant
The affected area may be intensely painful with associated paraesthesia

316
Q

What are the complications of varicella zoster virus? (chicken pox)

A

Secondary bacterial infections
Pneumonia
Problems in pregnancy; Congenital, perinatal/neonatal

317
Q

What are the complications of varicella zoster virus? (shingles)

A

Post herpetic neuralgia
Secondary bacterial infection
Ophthalmic zoster
Ramsay Hunt Syndrome

318
Q

What is the pathogenesis of varicella zoster?

A

Primary infection- varicella zoster virus (chicken pox)
Latency- sensory ganglion (trigemina)
Recurrent Infection: Reactivation of latent virus from sensory ganglion

319
Q

What is the epidemiology of varicella zoster?

A

Very common >90%

320
Q

What is the mode of transmission of varicella zoster?

A

Contact with varicella or zoster

321
Q

What is the varicella form?

A

Chicken pox

322
Q

What are the features of varicella?

A

Highly infections especially the respiratory secretions, the vesicles are also infectious
48 hours before symptoms

323
Q

What is zoster?

A

Shingles

324
Q

How is shingles developed?

A

From the latent virus in the sensory ganglion

325
Q

What is the rate of transmission of zoster from vesicle fluid?

A

Low

326
Q

What is the route of transmission of VZV?

A

Direct contact
Droplet or airborne spread

327
Q

What is the occurrence of varicella?

A

Highest in children

328
Q

What is the occurrence of zoster?

A

Highest in elderly and immunocompromised

329
Q

How many cases of zoster is there per year in Scotland?

A

7000

330
Q

How many people develop post herpetic neuralgia from zoster in Scotland per year?

A

700-1400

331
Q

How many people are admitted to hospital from complications with post herpetic neuralgia in Scotland per year?

A

600

332
Q

What sample should be taken for zoster?

A

Vesicle/ulcer fluid for swab and molecular sample for PCR

333
Q

Who is offered the chicken pox vaccine?

A

People in close contact to someone who is particularly vulnerable to chicken pox or its complications

334
Q

What is the treatment of shingles?

A

Anti viral therapy: Aciclovir 800mg oral x5 daily for 7 days

335
Q

What is the prevention of zoster?

A

Vaccine: Zostavax

336
Q

What type of vaccine is Zostavax?

A

Live attenuated virus

337
Q

Who received zostavax?

A

All people aged over 70

338
Q

What is the efficacy of Zostavax?

A

62%

339
Q

What was the % decrease of post herpetic neuralgia following the Zostavax?

A

70-88%

340
Q

What are the symptoms of hand, food and mouth disease?

A

Fever
Runny nose
Sneezing
Coughing
Skin rash
Mouth blisters
Body and muscle aches

341
Q

What is the pathogenesis of hand, foot and mouth disease?

A

Enterovirus
A large group of virus
Transmitted though nose and throat secretions or fluid from blisters scabs or faeces

342
Q

What is the dentally relevant non-polio enterovirus?

A

Coxsackie virus

343
Q

When is hand, foot and mouth most infectious?

A

1st week of disease

344
Q

What is the epidemiology of hand, foot and mouth disease?

A

Common in children under 5
Very contagious

345
Q

What type of sample can be taken for suspected hand, foot and mouth disease?

A

Oral swab

346
Q

What can be done in the prevention of hand, foot and mouth?

A

Hand hygiene

347
Q

What can be done in the treatment of hand, foot and mouth?

A

Relieve symptoms and prevent dehydration

348
Q

What is the animal equivalent of hand, foot and mouth?

A

Foot and mouth disease

349
Q

What are the signs and symptoms 7-14 days after an exposure to measles?

A

High fever
Cough
Runny nose
Conjunctivitis

350
Q

What are Koplik spots?

A

Tiny white spots inside the mouth
Occur 16-7 days after exposure to measles

351
Q

What are the signs and symptoms 3-5 days after Koplik spots have developed?

A

A rash begins on the face and spreads downwards

352
Q

What are examples of complications of measles?

A

Pneumonia
Brain swelling
Diarrhea
Death
Hearing loss

353
Q

What is the R number of measles?

A

18

354
Q

How long can measles virus live on surfaces?

A

2 hours

355
Q

What is the laboratory diagnosis of measles?

A

PCR from mouth swab

356
Q

What is the incubation period of mumps?

A

12-24 days

357
Q

What are the signs and symptoms of mumps?

A

Headache and fever
Swelling of the parotid glands

358
Q

What type of virus is mumps?

A

Paramyxovirus family
RNA virus

359
Q

How is mumps transmitted?

A

Direct contact with saliva/fomites or aerosol

360
Q

What sample is taken for lab diagnosis of mumps in Scotland?

A

Oral swab for RNA detection

361
Q

What sample is taken for lab diagnosis of mumps in England?

A

Oral fluid samples
Oral fluid IgM antibody tests
PCR

362
Q

What is the epidemiology of mumps?

A

Notable outbreaks in student populations linked to MMR vaccine distribution

363
Q

What is the treatment of mumps?

A

Symptom relief

364
Q

What is the prevention of mumps?

A

Routine vaccination

365
Q

When do symptoms begin for monkeypox?

A

5-21 days after exposure

366
Q

What are the clinical features of monkeypox?

A

Rash 1-5 days post fever
Blistering rash or skin lesions on face and genital area
Most common in males- identifying as gay/bisexual/have sex with other men
Clinical diagnosis is difficult

367
Q

What type of virus is monkey pox?

A

Enveloped DNA virus
Zoonotic disease

368
Q

How is monkeypox transmitted?

A

Close contact with an infected person or animal or contaminated material

369
Q

How many cases of monkey pox has there been worldwide?

A

71,237

370
Q

What is the lab diagnosis method for monkey pox?

A

PCR for viral DNA from swabs

371
Q

What is the prevention of monkeypox?

A

Vaccination: modified vaccinia Ankara (MVA)

372
Q

What is aciclovir?

A

Antiviral medication
An acrylic purine nucleoside

372
Q

What type of vaccine is modified vaccinia Ankara?

A

Live Attenuated

373
Q

How does aciclovir work?

A

Inhibits DNA polymerase in viruses

374
Q

Discuss the steps in the mechanism of action of aciclovir:

A

Viral enzymes add a phosphate group to acyclovir
Human enzymes add two more phosphate groups producing acyclovir triphosphate
During viral DNA replication, acyclovir is added to the growing strand rather than GTP. This halts further elongation of the DNA molecule and stops viral replication

375
Q

What is the viral enzyme (aciclovir)?

A

Thymine kinase

376
Q

What are the uses of aciclovir?

A

Management of herpes simplex and zoster infections

377
Q

How does resistance to aciclovir occur?

A

Mutations in viral thymine kinase

378
Q

What is the definition of a vesicle?

A

<5mm visible accumulation of fluid within or beneath epithelium

379
Q

What is a bullae?

A

> 5mm visible accumulation of fluid within or beneath epithelium

380
Q

What are some examples of vesiculobullous conditions?

A

Mucous membrane pemphigoid
Pemphigus vulgaris
Erythema multiforme
Stevens-Johnson syndrome/toxic epidermal necrolysis

381
Q

What are the oral/lip features of vesiculobullous conditions?

A

Vesicles
Bullae
Ulcers

382
Q

What are the oral/lip features of vesiculobullous conditions?

A

Vesicles
Bullae
Ulcers

383
Q

What is the mucosal involvement associated with vesiculobullous conditions?

A

Oesophageal
Ocular
Nasal
Anogenital

384
Q

What are the features of oral mucosa?

A

Epithelium (keratinocytes): stratified squamous
Basement membrane: Non-cellar interface
Lamina propria: collagen, fibroblasts, nerves, blood vessels
Desmosomes: joins kertainocytes
Hemi-desmosomes: joins basal keratinocytes to basement membrane

385
Q

What are the features mucous membrane pemphigoid?

A

Autoimmune process
50-60 years
1M:2F

386
Q

What are the clinical features of mucous membrane pemphigoid?

A

Oral vesicles/blisters —> ulcers
Desquamative gingivitis
Ocular lesions —> conjunctival scarring
Anogenital lesions
Skin lesions (scalp)
Nasal mucosa

387
Q

What are the clinical features of mucous membrane pemphigoid?

A

Oral vesicles/blisters —> ulcers
Desquamative gingivitis
Ocular lesions —> conjunctival scarring
Anogenital lesions
Skin lesions (scalp)
Nasal mucosa

388
Q

What is the aetiology of mucous membrane pemphigoid?

A

Unknown
Likely genetic predisposition
Autoimmune

389
Q

What is the Pathogenesis of mucous membrane pemphigoid?

A

Antibody (IgG) targeting the basement membrane zone (hemidesmosomes)
Complement activation
Subepithelial splitting- vesicles, blisters, ulcers

390
Q

How is mucous membrane pemphigoid diagnosed?

A

Biopsy:
H&E staining
Direct immunofluorescence microscopy (DIF)- from perilesional tissue

Indirect immunofluorence

391
Q

How is mucous membrane pemphigoid diagnosed?

A

Biopsy:
H&E staining
Direct immunofluorescence microscopy (DIF)- from perilesional tissue

Indirect immunofluorence

392
Q

What is direct immunofluorescence?

A

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

393
Q

What is indirect immunofluorescence?

A

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

394
Q

What is the management of Mucous Membrane Pemphigoid?

A

MDT Approach: Oral medicine, opthamology, gynaecology, dermatogy

Low risk- oral disease only
High risk- multi site

395
Q

What is the management of mucous membrane pemphigoid?

A

Patient education
Oral disease severity score
Symptomatic relief (benzydamine mouthwash)
Oral hygiene
Topical corticosteroids:
Intralesional steroid injection:
Systemic treatment:

396
Q

What are the topical corticosteroid used for mucosal membrane pemphigoid?

A

Mouthwash (betamethasone)
Custom made tray (clobetasol)

397
Q

What are intralesional steroid injection?

A

Triamcinolone

398
Q

What are examples of systemic treatments for mucosal membrane pemphigoid?

A

Prednisone (pulsed)
Dapsone
Doxycycline
Azathioprine
Mycophenolate mofetil
Methotrexate
Rituximab
IV immunoglobulins

399
Q

What is pemphigus vulgaris?

A

Autoimmune condition with a female preponderance

400
Q

What are the clinical features of pemphigus vulgaris?

A

Oral bullae (quickly rupture to leave erosions/ulcers)
Desquamative gingivitis
Ocular involvement
Aerodigestive tract
Anogenital blistering
Skin
Pain
Potentially lethal
Systemically unwell: impaired oral intake, sepsis

401
Q

What are the clinical features of pemphigus vulgaris?

A

Oral bullae (quickly rupture to leave erosions/ulcers)
Desquamative gingivitis
Ocular involvement
Aerodigestive tract
Anogenital blistering
Skin
Pain
Potentially lethal
Systemically unwell: impaired oral intake, sepsis

402
Q

What is the aetiology of pemphigus vulgaris?

A

Autoimmune overlap

403
Q

What is the aetiology of pemphigus vulgaris?

A

Autoimmune overlap

404
Q

What is the Pathogenesis of pemphigus vulgaris?

A

Antibodies (mainly IgG) directed against desmosomes
Loss of cell-cell contact in epithelium- ‘acantholysis’
Intra-epithelial split forms
Flaccid blisters (cf MMP)

405
Q

What is the Pathogenesis of pemphigus vulgaris?

A

Antibodies (mainly IgG) directed against desmosomes
Loss of cell-cell contact in epithelium- ‘acantholysis’
Intra-epithelial split forms
Flaccid blisters (cf MMP)

406
Q

How is pemphigus vulgaris diagnosed?

A

Nikolsky’s sign
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)

407
Q

How is pemphigus vulgaris diagnosed?

A

Nikolsky’s sign
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)

408
Q

What is nikolsky’s sign?

A

Rubbing the mucosa induces a bulla

409
Q

What is nikolsky’s sign?

A

Rubbing the mucosa induces a bulla

410
Q

How does pemphigus vulgaris present in a H&E staining?

A

Intra-epithelial acantholysis

411
Q

How does pemphigus vulgaris present on a direct immunofluorescence (DIF)?

A

Intercellular deposition of IgG and C3- chicken wire appearance

412
Q

How does pemphigus vulgaris present on a direct immunofluorescence (DIF)?

A

Intercellular deposition of IgG and C3- chicken wire appearance

413
Q

How does pemphigus vulgaris present on a indirect immunofluorescence (DIF)?

A

Titre of autoantibody correlates with disease severity

414
Q

How does pemphigus vulgaris present on a indirect immunofluorescence (DIF)?

A

Titre of autoantibody correlates with disease severity

415
Q

What is the MDT management of pemphigus vulgaris?

A

IV fluid resuscitation
Feeding
Management of secondary infection
Analgesia

416
Q

What is the MDT management of pemphigus vulgaris?

A

IV fluid resuscitation
Feeding
Management of secondary infection
Analgesia

417
Q

What are the two main phases of the management of pemphigus vulgaris?

A
  1. Induction of remission
  2. Maintainance
418
Q

What does the induction of remission stage of pemphigus vulgaris treatment involve?

A

Prednisolone (+/- bone/gastric protection)
Commence second agent (Aza, MMF, rituximab)

419
Q

What does the maintenance phase of pemphigus vulgaris treatment involve?

A

Gradular withdrawal of oral steroids (aim <10mg prednisolone)
Second agent
Regular monitoring (ODSS)
Topical steroids
Benzydamine
Excellent OH

420
Q

What is paraneoplastic pemphigus?

A

Rare variation of PV
Associated with an underlying malignancy (usually haematological malignancy)
Presents with severe mucosal and skin involvement
High mortality

421
Q

What is erythema multiforme?

A

Acute onset
Hypersensitivity reaction (often triggered)
25% recurrence

422
Q

What age group is affected by erythema multiforme?

A

10-40 years

423
Q

What age group is affected by erythema multiforme?

A

10-40 years

424
Q

What are the clinical features of erythema multiforme?

A

Flu-like prodrome (1-2 weeks)
Skin- classical target lesion, itchy
Lip blisters, ulceration and crusting
Oral ulcers (particularly anteriorly)
Other mucosal affected- eyes, genitals

425
Q

What are the clinical features of erythema multiforme?

A

Flu-like prodrome (1-2 weeks)
Skin- classical target lesion, itchy
Lip blisters, ulceration and crusting
Oral ulcers (particularly anteriorly)
Other mucosal affected- eyes, genitals

426
Q

What is the difference between minor and major erythema multiforme?

A

Minor- oral +/- skin targets
Major- oral, skin and other mucosa site

427
Q

What is the aetiology of erythema multiforme?

A

Hypersensitivity
Infective
Drugs
Following BCGs or Hep B immunisations

428
Q

What are the infective aetiological factors associated with erythema multiform?

A

Herpes simplex virus (HSV-1) in 15-20%

429
Q

What are the drug related factors associated with erythema multiform?

A

Allopurinol
Carbamazepine
NSAIDs
Phenytoin

430
Q

What is the Pathogenesis of erythema multiform?

A

Release of cytokines from CD4 cells
Amplified immune response
CD8 T cells attack keratinocytes
Apoptosis and necrosis of keratinocytes

431
Q

How is erythema multiform diagnosed?

A

Clinical history - triggering agent
Biopsy of perilesional tissue- histology: lymphocytic infiltrate, keratinocytes necrosis, intra and sub epithelial splitting
Immunofluorescence
HSV serology/throat swabs for mycoplasma pneumoniae

432
Q

How is erythema multiform managed?

A

MDT approach: feeding/fluids
Stop any obvious precipitating medications
Topical steroids for oral lesions (minor EM), systemic steroids for more serious disease
Adjunctive oral care (hygiene, CHX, comfort measures)
Antihistamines for skin itch

433
Q

How is recurrent erythema multiform managed?

A

Consideration of immunosuppression (Aza, MMF)- risk/benefit
Prophylactic aciclovir (due to HSV implication)

434
Q

What is Steven-Johnson Syndrome (SJS)/ Toxic Epideral necrolysis (TEN)?

A

Rare
Very severe- critical care admission
Spectrum
Wide spread blistering of skin and oral, pharyngeal genital, nasal and conjunctival involvement

435
Q

What is the aetiology of SJS/TEN?

A

Hypersensitivity to medications: allopurinol, carbamazepine, NSAIDs, phenytoin, penicillins
Genetic predisposition
Association with HIV

436
Q

What is the Pathogenesis of SJS/TEN?

A

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)

437
Q

How is SJS/TEN diagnosed?

A

Clinical history and exam
Skin biopsy- epidermal necrosis, detachment from dermis

438
Q

How is SJS/TEN diagnosed?

A

Clinical history and exam
Skin biopsy- epidermal necrosis, detachment from dermis

439
Q

What is the TBSA and mortality rate of SJS?

A

<10% TBSA
1-5% mortality rate

440
Q

What is the TBSA of SJS/TEN overlap?

A

10-30% TBSA

441
Q

What is the TBSA and mortality rate of TEN?

A

> 30% TBSA
30% mortality rate

442
Q

What is the TBSA and mortality rate of TEN?

A

> 30% TBSA
30% mortality rate

443
Q

How is SJS/TEN managed?

A

Urgent assessment in specialist centre- burns unit, ITU
A-E approach
Stop causative agent (medication)
MDT approach

444
Q

How is SJS/TEN managed?

A

Urgent assessment in specialist centre- burns unit, ITU
A-E approach
Stop causative agent (medication)
MDT approach

445
Q

What is the A-E approach in SJS/TEN?

A

A Airway involvement- intubation
B Ventilatory support
C Guided fluid resuscitation
D Sedation/pain management
E Temperature management, secondary infection, NG feeding

446
Q

What is the A-E approach in SJS/TEN?

A

A Airway involvement- intubation
B Ventilatory support
C Guided fluid resuscitation
D Sedation/pain management
E Temperature management, secondary infection, NG feeding

447
Q

What is the MDT approach to SJS/TEN?

A

Dermatology, ophthalmology, ENT, burns team
CHX, oral lubricants, topical steroid
Skin/wound management
Eye care

448
Q

What are examples of fungal oral infectious disease?

A

Candida

449
Q

What are examples of viral infectious diseases?

A

Herpes simplex
Varicella zoster
Human immunodeficiency virus
Hepatitis C
Coxsackie virus

450
Q

What are examples of bacterial oral infectious diseases?

A

Syphilis
Gonorrhoea
Chlamydia
Tuberculosis

451
Q

What is candidosis?

A

Infection of mucosa caused by candida species

452
Q

What % of normal population are carriers of Candida albicans?

A

70%

453
Q

What are local defences to candida?

A

Oral mucosa: physical barrier, innate immunity (lysozyme, T cells, phagocytes)

Oral microbiome: competition and inhibition

Saliva: mechanical cleansing, antimicrobial peptides (mucins, defensins, histatins), IgA antibodies

454
Q

What are systemic defences to candida?

A

Immune system; adaptive immunity

455
Q

What are local risk factors to oral candidosis?

A

Xerostomia
Poor OH
Dental appliances
Mouth piercings
Smoking
Irradiation to mouth/salivary glands
Inhaled/topical corticosteroids

456
Q

What are the systemic risk factors to candidosis?

A

Extremes of age
Malnutrition
Diabetes
HIV/AIDS
Haemantinic deficiency
Broad spectrum antibodies
Chemotherapy
Haematological malignancy

457
Q

How are candidal infections managed?

A

Investigate and manage predisposing factors
Oral hygiene
Topical anti fungal a

458
Q

What questions should you investigate when managing a patient with candida?

A

Does this person have underlying systemic disease or deficiency ?
Do they smoke?
Do they have a dry mouth?
Do they use a steroid inhaler?
Consider dentist hygiene

459
Q

What topical anti fungals are used for candida?

A

Miconazole gel
Nystatin oral mouthwash

460
Q

When should miconazole be avoided?

A

warfarin/ statins

461
Q

What systemic antifungals can be given for candida infections?

A

Fluconazole

462
Q

What systemic antifungals can be given for candida infections?

A

Fluconazold

463
Q

What is the prescription for nystatin in candida patients.

A

20mg/g
Send 80g tube
Apply a pea sized amount after food 4 times daily

464
Q

What is the interaction of warfarin and miconazole?

A

Increases anticoagulant effect (increases INR)

465
Q

What is the interaction between miconazole and statins?

A

Risk of rhabdomyolysis and myopathy with some statins

466
Q

What is the prescription for nystatin oral suspension for candida patients?

A

100,000 units/ ml
Send 30ml
Label 1ml after food 4 times daily for 7 days

Continue use for 48 hours after lesions have healed

467
Q

What is the prescription for fluconazole in candida patients?

A

50mg
Send 7 capsules
Label 1 capsule daily

468
Q

When should you not prescribe fluconazole?

A

Warfarin and statins

469
Q

When should you not prescribe fluconazole?

A

Warfarin and statins

470
Q

What is the interaction of fluconazole and warfarin?

A

Increased anticoagulant effect

471
Q

What is the interaction between fluconazole and statins?

A

Risk if rhabdomyolysis and myopathy

472
Q

What are the types of candidal infections?

A

Acute psuedomembranous candidosis
Chronic hyperplastic candidosis
Denture related stomatitis
Acute erythematous glossitis
Angular cheilitis

473
Q

What is acute pseudonenbranous candidosis also known as?

A

Thrush

474
Q

What age group is most commonly affected by acute pseudomembranous candidosis?

A

Neonates

475
Q

How does acute psuedomembranous candidosis present?

A

White slough on mucosa surface (easily wiped off)
Underlying erythenatous base

476
Q

How is acute psuedomembranous candidosis diagnosed?

A

Clinically
Microbiology investigations: oral rinse, oral swab

477
Q

How is acute psuedomembranous candidosis managed?

A

Predisposing factors investigated and managed
Oral hygiene
Topical: miconazole oral gel , nystatin oral mouth wash
Systemic (if topical ineffective or severe disease)- fluconazole capsules

478
Q

What is chronic hyperplastic candidosis also known as?

A

Candidal leukoplakia

479
Q

What is the risk of chronic hyperplastic candidosis?

A

Potentially malignant disorder

480
Q

How does chronic hyperplastic candidosis present?

A

Usually on buccal mucosa (at labial commissure)
Often bilateral
Can occur less commonly on tongue

481
Q

How is chronic hyperplastic candida managed?

A

Incisional biopsy (with periodic acid schiff stain)

482
Q

Why should you prescribe fluconazole before biopsy of suspected chronic hyperplastic candidosis?

A

To allow pathologist to see potential dysplasia more clearly
Fungal related inflammation can give fake positive for dysplasia

483
Q

How is chronic hyperplastic candidosis managed?

A

Predisposing factors
Systemic antifungals
Stop smoking
Careful clinical follow up
Manage of dysplasia as required

484
Q

What is denture related stomatitis?

A

Candidal infection of mucosa beneath a dental appliance

485
Q

What group is denture related stomatitis most associated with?

A

Care facilities: elderly, dry mouth, high sucrose diet, lack of oral hygiene

486
Q

What type of denture is most associated with denture related stomatitis?

A

Upper complete

487
Q

What % of denture related stomatitis is candida?

A

90%

488
Q

What is involved in a mixed infection of denture related stomatitis?

A

Candida
Staphylococcus
Streptococcus

489
Q

What features of dentures lead to a good habitat for candidal adherence?

A

Acrylic resin
Soft liners

490
Q

How is denture related stomatitis diagnoses?

A

Clinical diagnosis

491
Q

What is newtons class 1?

A

Localised inflammation (pinpoint)

492
Q

What is newtons class 1?

A

Localised inflammation (pinpoint)

493
Q

What is newtons class 2?

A

Generalised erythema covering the denture bearing area

494
Q

What is newtons class 3?

A

Granular type

495
Q

What is the management of denture related stomatitis?

A

Predisposing factors
Denture hygiene
Oral hygiene (brushing palate)
Antifungals (last resort); miconazole to surface of denture

496
Q

What denture hygiene advice should be given to a denture related stomatitis patient?

A

Remove denture at night
Gently daily brushing
Chlorhexidine immersion
Dilute hypochlorite immersion
Microwave disinfection
Alkaline peroxide
Remake if required

497
Q

What is acute erythematous candidiasis also known as?

A

Atrophic candidiasis

498
Q

How does acute erythematous candidiasis present?

A

Burning
Usually affects palate

499
Q

What are examples of predisposing factors to acute erythematous candidiosis?

A

Recent broad spectrum antibiotics
Corticosteroids
Diabetes
HIV
Nutritional factors

500
Q

How is acute erythematous candidiasis diagnosed?

A

Clinical
Oral rinse/oral swab

501
Q

How is acute erythematous candidiasis managed?

A

Medical referral (?)
Topical antifungal
Systemic anti fungal

502
Q

Where does median rhomboid glossitis?

A

Posterior aspect/midline of tongue dorsum

503
Q

How does median rhomboid glossitis present?

A

Depapillitation in irregular shape
May have a kissing lesion on the palate

504
Q

What is median rhomboid glossitis associated with?

A

Steroid inhalers
Smokers

505
Q

How is median rhomboid glossitis diagnosed?

A

Clinical

506
Q

How is median rhomboid glossitis managed?

A

Predisposing factors
Oral/denture hygiene
Topical antifungal
Systemic antifungal

507
Q

What is angual cheilitis?

A

Infection of mucocutaneous region around corners of mouth, often associated with dermatitis

508
Q

What is involved in a mixed annual cheilitis infection?

A

Candida
Staphylococcus
Streptococcus

509
Q

How does angular cheilitis present?

A

Soreness
Erythema
Fissuring
Crusting
Bleeding

510
Q

What mechanical factors play a role in angular cheilitis?

A

Ageing
Edentulous
Dentures lacking in vertical height (encourages saliva pooling)

511
Q

How is angular cheilitis diagnosed?

A

Clinical diagnosis
Swab for microbiology

512
Q

How is angular cheilitis managed?

A

Predisposing factors (new dentures, underlying disease/deficiency?)
Denture hygiene and oral hygiene
Topical antifungal - micoazole cream
Topical antibacterial- sodium fusidate ointment (when clearly bacterial nature- non-denture wearer)

513
Q

What is the prescription for sodium fusidate?

A

Sodium fusidate ointment 2%
Send 15g tube
Label apply to angles of mouth four times daily

514
Q

Why is sodium fusidate to not be used for longer than 10 days?

A

To avoid the development of resistance

515
Q

What is the treatment of angular cheilitis if there is significant associated dermatitis?

A

Combined miconazole and hydrocortisone cream/ointment

cream for wet surface
ointment for dry surface

516
Q

What is the prescription for miconazole and hydrocortisone cream?

A

Miconazole (2%) and Hydrocortisone (1%)
Send 30g tube
Label apply to angles of the mouth twice daily

maximum of 7 days

517
Q

What are human herpes viruses?

A

Family of DNA viruses
Transmitted in saliva, respiratory secretions and direct contact

518
Q

When do human herpes viruses reactivate?

A

When immunity drops

519
Q

What is the difference between HSV 1 and HSV 2?

A

1- oral
2- anogenital

520
Q

How does the primary HSV1/2 infection present?

A

Lesions in mouth, oropharynx and ano-genital lesions

521
Q

When does primary infection of HSV1 and 2 usually occur?

A

2-4 years

522
Q

How is HSV1 and 2 transmitted?

A

Close contact (saliva)

523
Q

What are the symptoms of primary infection of HSV 1 and 2?

A

Fever
Malaise
Red, fiery oedematous gingival
Vesicles –> ulcers

524
Q

How is primary herpetic gingivostomatitis diagnosed?

A

Clinical (and history)
Viral swab for PCR

525
Q

How is primary herpetic gingivastomatitis managed?

A

Largely supportive: fluids, paracetamol, soft diet, chlorhexidine mw, difflam mw
Pregnant women and neonates- urgent specialist care

526
Q

What % of the population has recurrent herpes simplex virus?

A

15%

527
Q

What is another name for cold sores?

A

Herpes labialis

528
Q

What can reactivate herpes simplex virus?

A

Sunlight (UV radiation)
Unwell (fever)
Tissue injury
Stress
Immunosuppression
Hormonal (menstrual cycle)

529
Q

How does recurrent herpes simplex virus present?

A

Prodromal period- pain, burning, tingling, itching (up to 48 hrs before)
Herpes labialis and intra-oral herpes
Crops of ulcers- scab within 72 hours, resolve by 10 days

530
Q

How is recurrent herpes simplex virus diagnosed?

A

Clinical

531
Q

How is recurrent herpes simplex virus managed?

A

Avoidance of triggers

Antivirals in prodrome period;
5% Aciclovir cream every 2 hours herpes labials
Aciclovir 200mg tablets 5 times a day for 5 day intra-oral herpes

Immunocompromised- specialist referral

532
Q

What antiviral should be prescribed for herpes labialis?

A

Aciclovir 5% every 2 hours

533
Q

What antiviral should be prescribed for intra oral herpes?

A

Aciclovir 200mg

534
Q

What are the complications of recurrent herpes simplex virus?

A

Disseminated herpes infection (immunocompromised)
Bell’s palsy
Erythema multiforme
Herpetic whitlow (fingers)
Eye disease (herpetic keratoconjunctivitis)

535
Q

Where does latent varicella zoster virus lie?

A

In the Doral root ganglion

536
Q

How does varicella zoster spread?

A

Respiratory droplets or lesion

537
Q

How does varicella zoster present?

A

Fever
Malaise
Truncal rash- itchy, papules, vesicles, scabs
Oral ulcers

538
Q

How is varicella zoster managed?

A

Supportive
Immunocompromised, pregnant and neonates- specialist care

539
Q

How does zoster present?

A

Rash in one dermatome –> scabs
Pain before, during and after lesions
Vesicles and ulcers intra-orally

540
Q

How is zoster diagnosed?

A

Clinically

541
Q

How is zoster managed?

A

Aciclovir 800mg tablets (within 72 hours od onset)
Refere to GP
Immunocompromised- to specialist

542
Q

What is the prescription for acyclovir for zoster?

A

Aciclovir 800mg
Send 35 tablets
Label 1 tablet 5 times daily

543
Q

What are the complications of zoster virus?

A

Post herpetic neuralgia
Ramsay hunt syndrome

544
Q

What is post herpetic neuralgia?

A

Burning pain
Persists 6 months after mucocutaneous healing

545
Q

What medication is used to treat post herpetic neuralgia?

A

Gabapentin
Amitriptyline
Nortriptyline
Carbamazepine

546
Q

What is Ramsay Hunt syndrome?

A

Reactivation within geniculate ganglion (CN7)

547
Q

How does Ramsay Hunt syndrome present?

A

Facial nerve palsy
Vesicular rash around ear and oral vesicles

548
Q

What % of the population have Epstein Barr Virus?

A

95%

549
Q

How is Epstein Barr virus transmitted?

A

Saliva

550
Q

What is glandular fever also known as?

A

Infectious mononucleosis

551
Q

Where does Epstein Barr virus lie during latency period?

A

Lymphoid tissue

552
Q

What may Epstein Barr virus reactivate as?

A

Oral hairy leukoplakia
Burkitts lymphoma
Nasopharyngeal cancer

553
Q

What conditions is hairy leukoplakia associated with?

A

HIV positive patients (when CD4 count drops)
Seen in chemotherapy, leukoplakia

554
Q

Where is oral hairy leukoplakia found?

A

Lateral aspect of tongue

555
Q

How is oral hairy leukoplakia diagnosed?

A

Incisional biopsy
Immunohistochemistry for EBV

556
Q

Where is human herpes virus 8 found?

A

Endothelial cells of blood and lymphatic vessels

557
Q

How is human herpes virus 8 diagnosed?

A

Incisional biopsy

558
Q

How is human herpes virus 8 managed?

A

Underlying immunosuppression- HAART in HIV
Excision
Cryotherapy
Intralesional vinblastine
Chemotherapy

559
Q

What is HAART?

A

Highly active antiretroviral therapy

560
Q

What is HIV?

A

Blood borne RNA virus

561
Q

How is HIV transmitted?

A

Sexual transmission
Needle stick injuries
Splashes
Vertical transmission

562
Q

What does HIV do?

A

Enters and destroys CD4 T helper cells

563
Q

What does AIDS stand for?

A

Acquired Immunodeficiency Syndrome (AIDS)

564
Q

What is the treatment of HIV?

A

ART
PrEP
PEP

565
Q

How many people in UK have HIV?

A

105,300

566
Q

What % of HIV patients in UK are virally suppressed?

A

97%

567
Q

What is the testing for HIV?

A

Blood test- look for antibodies and p24 antigen

568
Q

What is ART?

A

Anti retroviral therapy

569
Q

What does ART do?

A

Halts HIV replication
Causes a normal CD4 count and undetectable viral load
Can cause oral hyperpigmentation

570
Q

What are AIDs defining illnesses?

A

Kaposi Sarcoma
Pneumocystis jirovecci pneumonia (PCP)
Cytomegalovirus infection
Candidiasis
Lymphomas
Tuberculosis

571
Q

What are oral AIDS defining illnesses?

A

Oral candidosis
Acute necrotising ulcerative gingivitis
Kaposis sarcoma
Oral hairy leukoplakia
Non-hodgkins lymphoma
Aphthous like ulcers

572
Q

What is Hepatitis C?

A

RNA virus that infects liver leading to chronic infection

573
Q

How is hepatitis C spread?

A

Blood and bodily fluids

574
Q

What are the complications of hepatitis C?

A

Liver cirrhosis
Hepatocellular carcinoma

575
Q

What is the cure for hepatitis C?

A

Antiviral medication for 8-12 weeks

576
Q

What condition is hepatitis C associated with?

A

Oral lichen planus

577
Q

What is coxsackie virus?

A

Family of RNA virus

578
Q

How does coxsackie virus spread?

A

Faecal-oral route
Saliva

579
Q

How does coxsackie virus present?

A

hand, foot and mouth disease
Herpangina

580
Q

Who is affected by coxsackie virus?

A

Young children

581
Q

What are the systemic symptoms of coxsackie virus?

A

Fever
Reduced appetite
Malaise

582
Q

How does coxsackie virus present on hands, feet and mouth?

A

Vesicles/blisters
(labial, buccal and tongue mucosa)

583
Q

How does herpangina present?

A

Numerous vesicles on the soft palate, uvula and sauces

584
Q

How is coxsackie virus diagnosed?

A

Clinical

585
Q

How is coxsackie virus managed?

A

Supportive
Fluids
Paracetamol, ibuprofen
Soft diet
Chlorhexidine to aid OH
Difflam mouthwash

586
Q

What are examples of bacterial infections?

A

Periapical infection
Periodontal infection
Pericoronal infection
Bacterial sialadenitis

587
Q

What are the risk factors for STIs?

A

Previous STI
Under 25 years
New sexual partner
More than one sexual partner in the last year
No condom use
Paying for sex
Socioeconomic deprivation
Chemsex

588
Q

What is syphilis?

A

Sexually transmitted disease

589
Q

What bacteria is syphilis associated with?

A

Spirochete treponema palladium

590
Q

What % of GBMSM account for new syphilis diagnoses?

A

76%

591
Q

How does primary syphilis present?

A

Chancre at site of inoculation
Painless ulcer
Usually genital but can be oral
Self limiting- heals by 8 weeks
Associated lymphadenopathy (80%)
Untreated infection spreads lymphovascular

592
Q

How does secondary syphilis present?

A

4-6 weeks after initial infection
Non-specific symptoms- lethargy, malaise, fever, musculoskeletal pain, rash
Mucosal white patches
Snail track ulcers
Condloma lata

593
Q

How does tertiary syphilis present?

A

Progression from untreated infection
Presents 1-30 years after innoculation
Gummatous lesions (granulomatous infection)
Neurosyphilis (dementia, cranial nerve palsy)
Cardiovascular syphilis (aortic aneurysms)

594
Q

How is syphilis diagnosed?

A

Incisional biopsy- for microscopy and immunohistochemistry
Blood test- IgG and IgM antibodies to Treponema palladium

595
Q

How is syphilis managed?

A

By sexual health specialist (GUM clinic)
STAT doses of IM benzylpenicilin
Screening for other STIs
Contact tracing

596
Q

What bacteria is gonorrhoea associated with?

A

Neisseria gonorrhoea

597
Q

What bacteria is chlamydia associated with?

A

Chlamydia trachomatis

598
Q

Where does gonorrhoea and chlamydia affect?

A

Urethra
Endocervix
Rectum
PharynxWh

599
Q

What are the symptoms of gonorrhoea and chlamydiua?

A

Male- urethral discharge, dysuria
Female- altered vaginal discharge, dyuria

600
Q

What is the oral presentation of gonorrhoea and chlamydia?

A

Pharyngitis

601
Q

How is gonorrhoea and chlamydia diagnosed?

A

Clinical - oral
Specialist- vulvovaginal or urethral swabs (NAAT), swab for microscopy culture and sensitivity

602
Q

How is gonorrhoea and chlamydia managed?

A

By sexual health specialist (GUM clinic)
Gonorrhoea STAT dose of IM ceftriaxone/ Chlamydia 7 days oral doxycycline
Screening for other STIs
Contact tracing

603
Q

What bacteria is associated with tuberculosis?

A

Mycobacterium tuberculosis

604
Q

How many deaths globally due to tuberculosis?

A

1.5m

605
Q

How is tuberculosis transmitted?

A

Respitatory secretions

606
Q

How does tuberculosis present?

A

Fever, weight loss, night sweats
Cough, haemoptysis

607
Q

What are the risk factors of tuberculosis?

A

Close contact with tb patient
Born in high prevalence regions (India, Pakistan, Somalia, Eritrea, Romania)
HIV
Diabetes
Leukaemia
Alcohol excess
Socioeconomic deprivation
Homelessness

608
Q

What are the oral manifestations of tuberculosis?

A

Ulceration
Lip swelling

609
Q

How is tuberculosis diagnosed?

A

Incisional biopsy- H+E, Ziehl-Neelsen staining

610
Q
A
611
Q

What is the prevalence of Recurrent Apthous Stomatitis?

A

5-60% depending on population

612
Q

What is the aetiopathogenesis of recurrent apthous stomatitis?

A

Idiopathic

Strong associations: FH, Nonsmoker or smoking cessation, trauma, haemantinic deficiencies, age >30 years

Weak associations: female, higher SES, high stress, food intolerance, hormonal imbalance, SLS containing toothpaste and drugs

613
Q

What is the aetiopathogenesis of recurrent apthous stomatitis?

A

Idiopathic
Strong associations: FH, Nonsmoker or smoking cessation, trauma, haemantinic deficiencies, age >30 years

614
Q

What knowledge is developing in regard to recurrent apthous stomatitis?

A

Multiple genetically identified HLAs identified
Cytokine polymorphism recently implicated as a predisposing factor

615
Q

What are examples of the immunological response in RAS?

A

Reactivation and hyper-reactivity of neutrophils
Increased number of NK cells
High level of the complement system ingredients
Increased number of B lymphocytes
Decreased activity of regulatory Treg CD4+ CD25+ lymphocytes
Decreased number of CD4+ lymphocytes- disrupted CD4+/CD8+ ratio
Increased number of TyAlpha cells
Decreased expression of HSP
Limited expression of anti-inflammatory Th2-type cytokines and TCF-B
Preponderance of pro inflammatory Th1 type cytokines (Il-2, Il-12, IFN-y, TNF-Alpha)

616
Q

How is recurrent apthous stomatitis diagnosed?

A

Clinical diagnosis (of exclusion)
No single diagnostic test- ulcer history, medical history, medications, systems enquiry

617
Q

What are the factors of an ulcer history?

A

Onset
Number
Duration
Frequency
Pattern
Location
Size
Pain
Prodrome
Associated symptoms
Triggers
Relievers
Previous treatments
Impact on QoL

618
Q

What features of MH are relevant to an ulcer history?

A

Previous medical diagnoses
Current medical problems
Is the patient attending any other hospital specialists

619
Q

What are examples of systems of GI problems?

A

Weight loss
Constipation
Diarrhoea
Bloating
Reflux
Blood in stool

620
Q

How does an aphthous ulcer present clinically?

A

Round/ovoid
Grey base
Erythematous halo

621
Q

How does a minor apthous ulcer present?

A

Less than 1cm
7-10 days
Non-keratinised mucosa
No scarring

622
Q

How does a major apthous ulcer present?

A

Greater than 1cm
Lasts > 2-3 weeks
Can affect all mucosa
Heals with scarring

623
Q

How do herpetiform ulcers present?

A

Multiple tiny ulcers
Resemble herpetic ulcers
Can coalesce
Keratinised and non-keratinised surfaces

624
Q

What investigations can be implemented for patients presenting with oral ulcers?

A

Blood tests- standard (fbc, haemantinics, coeliac screen), additional (ESR, ANA, viral screens)

Referral

Biopsy- to exclude ulcerative condition (+/- direct immunofluorescence

625
Q

What conditions are associated with with Aphthous Like Ulceration (ALU)?

A

Behcet’s syndrome
Inflammatory bowel diseases
Gluten sensitivity enteropathy
Periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis (PFAPA)
Haemantinic deficiencies
Zinc deficiency
Cyclic neutropenia and benign familial neutropenia
Primary and secondary immunodeficiencies (HIV)
Mouth and genital ulcers with inflamed cartilage (MAGIC syndrome)
Sweet’s syndrome
TRAPS (TNF receptor associated to periodic fever)
Food hypersensitivity
Drug reactions

626
Q

What is Behçet’s disease?

A

Chronic relapsing multisystem inflammatory vasculitis
Affects large and small vessels

627
Q

How does Behcets syndrome present?

A

Oral and genital ulcerations
Skin lesions
Uveitis
Inflammatory vascular involvement of the CNS and GIT

628
Q

What is the International criteria for Behçet’s disease?

A

Ocular lesions- 2
Genital aphthosis- 2
Oral aphthosis- 2
Skin lesions- 1
Neurological manifestations- 1
Vascular manifestations -1
Positive pathology test- 1

629
Q

What score on the International Criteria of Behçet’s disease is diagnostic?

A

> 4

630
Q

What is the first line of management for recurrent aphthous ulcers?

A

Diet
Trauma
Toothpaste
Topical- benzydamine, lidocaine, covering agent, chlorhexidine

631
Q

What is the second line of management for recurrent aphthous stomatitis?

A

Topical corticosteroids (creams, gels, sprays, mouthwashes)- beclomethasone
Topical antibiotics - doxycycline
Consider vitamin b12

632
Q

What is the second line of management for recurrent aphthous stomatitis?

A

Topical corticosteroids
Topical antibiotics
Consider vitamin b12

633
Q

What instructions should be given to a patient who is prescribed doxycycline capsules for recurrent aphthous stomatitis?

A

Dissolve contents of capsule in 10ml water
Hold in mouth for 4 minutes over ulcers
Spit out
Do not rinse, eat or drink for 20 mins

634
Q

What instructions should be given to a patient who is prescribed doxycycline capsules for recurrent aphthous stomatitis?

A

Dissolve contents of capsule in 10ml water
Hold in mouth for 4 minutes over ulcers
Spit out
Do not rinse, eat or drink for 20 mins

635
Q

What are examples of holistic treatments for recurrent aphthous stomatitis?

A

Garlic
Coconut
Lavender oil
Aloe vera
Herbal remedies
Silver nitrate
Botox

636
Q

What is the third line of management for recurrent aphthous ulcerations?

A

Corticosteroids
Colchicine
Pentoxyphilline
Thalidomide
Azathioprine
Mycophenolate
Biologics

637
Q

What is the third line of management for recurrent aphthous ulcerations?

A

Corticosteroids
Colchicine
Pentoxyphilline
Thalidomide
Azathioprine
Mycophenolate
Biológicos

638
Q

What does TUGSE stand for?

A

Traumatic ulcerative granuloma with stromal eosinophilia

639
Q

What is TUGSE?

A

Rare, benign and self limiting form of oral ulceration
Uncertain aetiology (associated with complex MH, dry mouth and persistent oral ulcers)
Resolution after biopsy common
Topical/intra-lesional steroid tx may provide benefit

640
Q

What medications/factors may be associated with TUGSE?

A

Cytotoxic drugs- methotrexate
NSAIDs
Nicorandil- potentially inhibits cell migration necessary to repair mucosal micro trauma
Age; co-morbidities; other medications

641
Q

What should be avoided in the diet of patients with RAS

A

Benzoates

642
Q

What is oral lichen planus?

A

An inflammatory condition of the mouth that may occur on its own or with skin, nail, or genital lichen planus. Affects 1-2% of the population, predominantly middle-aged and elderly women.

It can also affect men, but children are rarely impacted.

643
Q

What is the cause of oral lichen planus?

A

The cause is largely unknown but likely related to the immune system. It is not an infection and is not contagious.

Some cases may link to chronic hepatitis C virus infection or certain medications and dental materials.

644
Q

Is oral lichen planus hereditary?

A

It may have a genetic basis, but it is uncommon for multiple family members to be affected.

645
Q

What are the symptoms of oral lichen planus?

A

Symptoms may include burning or stinging discomfort, especially with spicy foods, citrus fruits, and alcohol. Mild cases may be symptom-free.

Ulcers (erosions) can occur and cause significant pain.

646
Q

What does oral lichen planus look like?

A

Typically presents as a white, lace-like pattern; can also appear as white and red patches or ulceration. Gum involvement is known as desquamative gingivitis.

This causes gums to appear red and shiny.

647
Q

How is oral lichen planus diagnosed?

A

Diagnosis can often be based on appearance, but a biopsy may be needed for microscopic examination.

648
Q

Can oral lichen planus be cured?

A

Generally, it cannot be cured but may resolve spontaneously. Treatments can help manage symptoms.

Changes in medications or dental materials may improve oral lichenoid lesions.

649
Q

Is oral lichen planus serious?

A

It is usually not serious, but there is a small risk (about 1%) of cancerous change over 10 years.

650
Q

What are the treatments for oral lichen planus?

A

Topical treatments include:
* Anaesthetic mouthwashes
* Topical steroids
* Topical tacrolimus
* Good oral hygiene practices

Systemic treatment may be required in severe cases.

651
Q

What can patients do to manage oral lichen planus?

A

Patients should:
* Avoid spicy, acidic, or salty foods
* Maintain oral hygiene
* Use mild-flavored toothpaste
* Regularly see a dentist for check-ups
* Avoid smoking and limit alcohol intake.

652
Q

Fill in the blank: Oral lichen planus affects primarily _______.

A

middle-aged and elderly women.

653
Q

True or False: Oral lichen planus is contagious.

A

False

654
Q

What are common triggers for discomfort in oral lichen planus?

A

Spicy foods, citrus fruits, and alcohol.

655
Q

What is desquamative gingivitis?

A

Gum involvement in oral lichen planus that causes gums to become red and shiny.

656
Q

What is the risk of cancer associated with oral lichen planus?

A

About 1% risk over a period of 10 years.

657
Q

What are the systemic treatment options for severe oral lichen planus?

A

Oral corticosteroids, azathioprine, and mycophenolate mofetil.

Regular blood tests are required to monitor for drug toxicity.

Finals (20 decks)

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