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Oral surgery > 4th year mucosal disease > Flashcards

4th year mucosal disease Flashcards

1
Q

Define leukoplakia

A

A white patch plaque of questionable risk with no other histological diagnosis

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2
Q

What is the prevalence of leukoplakia?

A

1-2%

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3
Q

In smokers, how much does the prevalence of leukoplakia increase?

A

x6

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4
Q

What are the 2 different forms of leukoplakia?

A

Speckled
Verrucous

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5
Q

Define erythroplakia

A

Red patch that cannot be classified as any other disease and is associated with an increased risk of malignancy

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6
Q

What is the malignant transformation rate of erythroplakia?

A

> 80%

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7
Q

List the 8 risk factors for progression of red/white patches

A

Female gender
Long duration of leukoplakia
Leukoplakia in non-smokers/drinkers
Location on the tongue and/or floor of the mouth
Size > 200 mm²
Non-homogeneous type
Presence of Candida
Presence of epithelial dysplasia

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8
Q

Define an ulcer

A

A break in the oral mucosa

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9
Q

What should be done if an ulcer is not healing?

A

Create red flag referral to be seen within 2 weeks

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10
Q

What are the 2 common locations for ulcers?

A

Edge of tongue
Buccal mucosa

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11
Q

Name the 4 classifications of ulcers based on size

A

Minor (<1cm)
Major (>1cm)
Herpetiform (pin point ulcers)
Large erosive areas

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12
Q

List 5 topical treatments for ulcers

A

Corsydyl
Difflam
Topical steroids (Betamethasone, Predsol, Flixonase)
Antibiotics (Doxycycline)
Triple mouthwash

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13
Q

What are features of suspicious oro-mucosal lesions? (8)

A

Solitary ulcer present for >3 weeks
Unintended weight loss
Rolled margins
Bleeding on light touch
Firm or fixed lesions
Numbness
Red or speckled lesions
Severe or extensive ulceration

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14
Q

What are 6 potential causes of oral ulceration?

A

Neoplasia (SCC)
Trauma
Recurrent aphthous stomatitis
Oral infections (syphilis)
Drugs
Systemic disease (IBS, leukaemia, agranulocytosis, Langerhans cell histiocytosis)

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15
Q

What is recurrent aphthous stomatitis (RAS)?

A

A condition characterized by recurrent, painful ulcers in the oral cavity

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16
Q

What is the epidemiology of oral lichen planus?

A

Affects 2% of the population, more common in females and older adults

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17
Q

What are the 6 clinical forms of lichen planus?

A

Reticular
Papular
Plaque-like
Atrophic
Erosive
Bullous

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18
Q

What are the 4 treatment options for oral lichen planus?

A

No active treatment
Remove trigger
Topical/intralesional/systemic steroids
Other immunomodulatory agents

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19
Q

What is oral squamous cell carcinoma (OSCC)?

A

The commonest intraoral cancer, accounting for 90% of intraoral malignancies

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20
Q

What are 6 risk factors for OSCC?

A

Tobacco
Alcohol
UV-light/sun exposure
Malnutrition
Infections: syphilis, candida, HPV
Immunosuppression

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21
Q

What are 3 clinical features of OSCC?

A

Lump: firm, not very mobile
White patch: thickened warty plaque
Ulcer: raised, rolled, everted edge

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22
Q

What is the survival rate for early-stage and late-stage OSCC?

A

Early: 80% three-year survival
Late: 50% three-year survival

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23
Q

What are 7 important features requiring referral?

A

Ulcer with granular floor
Traumatic ulcer unhealed after 3 weeks
Indurated swelling
Thickened white patch esp. if speckled
Spontaneously loosed teeth
Non-healing socket
Neurological symptoms

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24
Q

Define potentially malignant oral lesions

A

Lesions that are not malignant but have a risk of developing into OSCC

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25
Q

What are the 2 classifications of leukoplakia?

A

Homogeneous leukoplakia: lowest risk of OSCC
Non-homogeneous leukoplakia: higher risk of OSCC

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26
Q

What are 3 causes of white patches in the oral cavity?

A

Thicker keratin (hyperkeratosis)
Thicker epithelium (hyperplasia)
Fibrosis in the lamina propria

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27
Q

What is dysplasia?

A

Architectural and cytological changes in epithelium resembling cancer without invasion

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28
Q

What is frictional keratosis?

A

A condition characterized by a thickening of the epithelium due to chronic friction or irritation

Often seen in areas of the oral cavity subjected to repeated trauma.

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29
Q

What is a candidal infection?

A

An infection caused by the overgrowth of Candida species, most commonly Candida albicans

It can affect various mucosal surfaces, including the oral cavity.

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30
Q

Is leukoplakia homogeneous or non-homogeneous?

A

It can be either homogeneous or non-homogeneous

The classification depends on the appearance and texture of the lesions.

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31
Q

What does palpation check for in oral examinations?

A

Any change in the feel of the underlying tissues, especially induration

Induration refers to the hardening of soft tissue.

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32
Q

What are the types of laboratory investigations for oral lesions?

A

Microbiological, haematological, histopathological

These investigations help in diagnosing infections and abnormalities.

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33
Q

Define dysplasia

A

Architectural and cytological changes in epithelium resembling cancer but without invasion of tissues

It indicates a tissue disturbance that looks like cancer but does not behave like it.

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34
Q

What are features of epithelial dysplasia? (10)

A

Distorted rete peg architecture
Irregular stratification
Dyskeratosis
Basal cell hyperplasia
Loss of adherence
Loss of polarity
Hyperchromatism
Anisocytosis
Pleomorphism
Abnormal mitotic figures

N:C refers to the nuclear-to-cytoplasmic ratio.

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35
Q

What is the risk factor increase for OSCC with the presence of dysplasia?

A

Increases the risk by a factor of 10

OSCC stands for oral squamous cell carcinoma.

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36
Q

What are the grades of dysplasia and their associated risks?

A

Mild: less than 5%
Moderate: 10-20%
Severe: 15-50%

Higher grades of dysplasia correlate with increased risk for cancer.

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37
Q

What are the 5 types of surgical treatments for dysplasia?

A

Scalpel excision
Laser excision
CO2 laser ablation
Photodynamic therapy
Cryotherapy

These methods aim to remove or destroy abnormal tissues.

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38
Q

What are the advantages of medical treatment approaches for dysplasia?

A

Topical drugs can be directed at abnormal tissues
Less overall destruction
Systemic medications may help manage other sites

Medical treatments may include retinoids and EGFR inhibitors.

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39
Q

What are the 3 disadvantages of treatment for dysplasia?

A

Local side effects: pain, infection, slow healing
Systemic side effects
None of the therapies prevent new lesions or OSCC

Ongoing monitoring is essential.

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40
Q

Define fibrous hyperplastic nodules

A

Overgrowth of tissue

They are often caused by chronic minor trauma or low-grade infection.

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41
Q

What is the aetiology of fibrous hyperplastic nodules?

A

Chronic minor trauma or chronic low-grade infection

These factors contribute to the development of these lesions.

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42
Q

What are the 5 clinical features of papilloma?

A

Usually painless
Single or multiple
Occur at any oral site
Exophytic
Cauliflower-like appearance due to keratin

Caused by HPV types 6 and 11.

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43
Q

2 managements of papilloma

A

Excision
Cryotherapy

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44
Q

What are the 4 clinical features of pyogenic granuloma?

A

Painless
Pedunculated lesion
Red and inflamed
Commonly found on the gingiva

Often associated with pregnancy gingivitis.

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45
Q

3 causes of pyogenic granuloma

A

Local low-grade irritation
Hormonal changes
Trauma

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46
Q

3 managements of pyogenic granuloma

A

Excision
Remove causative factors
Improve oral hygiene as often calculus/plaque causative

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47
Q

Define giant cell granuloma

A

Uncommon benign lesion commonly at tooth bearing areas of unknown aetiology

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48
Q

2 classifications of giant cell granulomas and where they are found

A

Central: within bone
Peripheral: on gingiva

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49
Q

What are the 6 clinical features of central giant cell granuloma?

A

May be asymptomatic
Bony swelling
Can erode through cortical plate
Loosening of teeth
Purple gingival swelling
Ulceration/inflammation of overlying mucosa

This condition can be diagnosed through radiographic imaging.

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50
Q

What are the 5 radiographic features of central giant cell granuloma?

A

May be large/rounded
Radiolucent, may have areas of trabeculation
Soap bubble appearance
Localised but often ill defined edges
May perforate alveolar bone, extend into the mouth and resorb/displace adjacent roots

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51
Q

3 management strategies for giant cell granuloma

A

Excision of soft tissue lesion and curettage underlying bone
Resection may be required in larger lesions
Corticosteroids, calcitonin, interferon alpha and bisphosphonates in children and patients unable to carry out surgery

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52
Q

Define hyperparathyroidism

A

Parathyroid hormone overproduction

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53
Q

What is the management for hyperparathyroidism-related lesions?

A

Correction of the underlying lesion

May involve surgical resection and management of calcium levels.

54
Q

Define vascular malformation

A

An abnormal growth and development of a single type of vessel or a combination of vessels

55
Q

What are the 5 clinical features of vascular malformations?

A

Raised or flat
Soft but can become firm
Deep red/bluish color
Size varies
Usually blanch with pressure

They can be congenital and may impact movement if located on the tongue.

56
Q

5 management strategies for vascular malformations

A

Excision if small
Laser surgery
Cryotherapy
Radiation therapy
Corticosteroids

57
Q

Define haemangioma

A

A benign vascular tumour that usually presents in the first few months of life

58
Q

3 management strategies for haemangioma

A

Leave as can regress with time
Cryotherapy
Excise

59
Q

Define purpura

A

Small blood vessels bleeding into skin or mucous membranes

60
Q

Causes of purpura

A

Underlying platelet or vascular disorders

61
Q

Define herpes group viruses

A

DNA viruses characterized by latency

Herpes simplex viruses include HHV-1 and HHV-2.

62
Q

Define HHV-1

A

A herpes simplex virus that causes primary herpetic gingivostomatitis and may become latent and recur as a cold sore

63
Q

Define HHV-2

A

A herpes simplex virus that causes genital herpes and occasionally causes oral disease that is clinically similar to that of HHV-1 infection

64
Q

Define HHV-3

A

Varicella-zoster virus that causes the primary infection chickenpox and the secondary reactivation herpes zoster

65
Q

Define HHV-4

A

Epstein-Barr virus that causes infectious mononucleosis and is implicated in various diseases, such as oral hairy leukoplakia

66
Q

Define HHV-5

A

Cytomegalovirus (CMV) that causes primary infection of the salivary glands and other tissue, it is believed to have a chronic form

67
Q

What are the 3 clinical features of herpes simplex virus infections?

A

Variable, usually ulcers effecting any mucosal site
Cervical lymphadenopathy
Pyrexia

Severity can vary, especially in immunocompromised individuals.

68
Q

What is the 4 managements for herpes simplex virus infections?

A

Maintain fluid intake
Analgesic therapy
Systemic acyclovir for severe cases
Mouthwash therapy

Preventive measures are crucial to limit spread.

69
Q

4 clinical features of herpes labialis

A

Initial prodrome
Clusters of tiny blisters, which ulcerate
Crusting and healing
Usually effects function vermillion border lip

70
Q

3 management strategies for herpes labialis

A

Preventive measures, e.g sunblocks
Warn patients of infectivity of the lesion
Topical 5% acyclovir cream in prodromal phase

71
Q

Clinical features of shingles

A

Unilateral painful vesicular eruption localised to a single dermatome

72
Q

Management of shingles

A

High dose systemic acyclovir for 7-10 days, 800mg x5 day

73
Q

Mechanism of action of acyclovir

A

Analogue of purine nucleotide
Viral enzymes phosphorylate drug to Acyclo-AMP
Cellular enzymes phosphorylate Acyclo-AMP to Acyclo-GTP
Acyclo-GTP inhibits viral DNA synthesis

74
Q

What are the 5 clinical features of measles virus infections?

A

Respiratory symptoms: cough, runny nose
Inflamed eyes
Pyrexia
Rash
Koplik spots: intra-oral may form before skin rash

75
Q

What are the 2 clinical features of mumps virus infections?

A

Enlarged salivary glands
Flu-like symptoms

Complications can include meningitis and deafness.

76
Q

Define hand foot and mouth disease

A

A common infection that usually effects children causes mouth ulcers plus spots and blisters on the hands and feet

77
Q

What are the transmission methods for human papilloma viruses?

A

Via skin-to-skin contact

HPV types 6 and 11 are commonly associated with benign lesions.

78
Q

What are the 3 transmission methods for herpes simplex virus

A

Direct contact with infective lesion
Contact with infected saliva from individual shedding the virus
Transfer via inanimate objects

79
Q

What are the transmission method for Varicella-Zoster virus

A

Through direct contact, coughing, sneezing

80
Q

What are the transmission method for measles virus

A

Primarily air borne

81
Q

What are the transmission methods for mumps virus

A

Airborne
Inanimate objects

82
Q

Aetiology of human papilloma viruses

A

HPV 6 and 11

83
Q

Define actinomycosis

A

A rare, chronic suppurative granulomatous disease caused by filamentous anaerobic Gram-positive bacilli

It is often linked to poor oral hygiene and trauma.

84
Q

What are 6 predisposing factors for Actinomycosis?

A

Poor oral hygiene
Trauma
Poorly controlled diabetes mellitus
Immunosuppressed
Alcoholism
Malnutrition

85
Q

What are 4 common clinical presentation of Actinomycosis?

A

Cervicofacial slow growing painless, indurated swelling
Abscesses with sinus discharge to oral mucosa or skin
Discharge contains visible granules “sulphur like”
Pain and trismus in advanced stages

86
Q

What are 3 diagnostic methods for Actinomycosis?

A

Imaging
Aspiration and culture
Histopathology

87
Q

3 management strategies for Actinomycosis

A

Removal of dental focus
Antimicrobials: penicillin, clarithromycin
Surgical debridement

88
Q

Define Cat Scratch Disease

A

Regional lymphadenopathy and fever resulting from the scratch or bite of an infected cat caused by Bartonella henselae

89
Q

What are 4 clinical features of Cat Scratch Disease?

A

Papule/pustule at site of inoculation
Regional lymphadenopathy
Surrounding tissue changes
Suppuration

90
Q

What is the management for Cat Scratch Disease?

A

Avoidance of infected cat as self-limiting
Antimicrobial therapy: erythromycin

91
Q

Define impetigo

A

Common contagious superficial bacterial skin infection caused by Staphylococcus aureus, Streptococcus pyogenes

92
Q

What is the most common form of Impetigo?

A

Non-bullous impetigo

93
Q

4 clinical features of non-bullous impetigo

A

Erythematous macule/papule
Becomes pustuler before rupture
“Honey-coloured” yellow crust on skin after rupture
Lesions expand and coalesce

94
Q

4 clinical features of bullous impetigo

A

Vesicles or bullae
Blister formation
Rupture and shed to produce an erythematous moist base that oozes serum
Systemic symptoms

95
Q

Management of impetigo

A

Spontaneous resolution
Antimicrobial agents: Mupirocin

96
Q

Define Lyme Disease

A

Bacterial infection caused by Borrelia burgdorferi

97
Q

What are the three stages of Lyme Disease?

A

Stage 1: Spreading annular rash
Stage 2: Cardiac, neurological abnormalities
Stage 3: Chronic skin, CNS or joint abnormalities

98
Q

What is the characteristic rash of Lyme Disease called?

A

Erythema migrans, a red rash that increases in size may have a central clearing and presents at site of bite

99
Q

Define Syphilis

A

Common sexually transmitted infection caused by Treponema pallidum

100
Q

What are the four main clinical stages of Syphilis?

A

Primary syphilis
Secondary syphilis
Latent syphilis
Tertiary syphilis

101
Q

What is a common manifestation of primary syphilis?

A

Solitary chancre that develops at site of inoculation, usually lips which heals within 8 weeks

102
Q

What are the symptoms of secondary syphilis?

A

‘Flu-like’ constitutional symptoms
Mucocutaneous manifestations: skin rash, mucous patches
Generalised lymphadenopathy

103
Q

What are common complications of tertiary syphilis?

A

Cardiovascular syphilis
Neurosyphilis

104
Q

What is the main transmission route for Congenital Syphilis?

A

Mother to child

105
Q

What is the causative bacteria of Tuberculosis?

A

Mycobacterium tuberculosis

106
Q

What are common predisposing factors for Tuberculosis?

A
  • Overcrowded living situations
  • Poor health and hygiene
  • Poverty
  • Drug abuse
  • Immunosuppression
107
Q

What are the oral manifestations of Tuberculosis?

A

Single, painful ulcers on the dorsum of the tongue

108
Q

What is the most common oral fungal infection in humans?

A

Oral candidosis

109
Q

What is the most common species causing oral candidosis?

A

C. albicans

110
Q

What are the clinical presentations of Pseudomembranous candidosis?

A
  • Semi adherent white/creamy patches
  • Wiped off to reveal an erythematous base
111
Q

What is a characteristic feature of Angular cheilitis?

A

Inflammation, fissuring and pain of the skin at commissure

112
Q

What is the management for oral candidosis?

A
  • Control predisposing factors
  • Anti-fungal therapy: topical and systemic
113
Q

What are the two forms of Candida as a dimorphic yeast-like fungus?

A
  • Blastospore
  • Hyphae
114
Q

What is the treatment for oral candidosis using Nystatin?

A

100,000 units qds for 1-2 weeks

115
Q

What is the risk associated with Azole antifungal drugs like Miconazole?

A

Significant drug interactions

116
Q

List 3 systemic treatments for ulcers

A

Colchicine
Dapsone
Azathioprine

117
Q

Define white sponge naevus

A

Hereditary condition present from birth/early childhood causing thick bilateral symmetrical white plaques mainly on the buccal mucosa

118
Q

Define lichen planus

A

A clinically distinctive maculopapular mucocutaneous rash with a characteristic distribution that eventually heals without scar but may leave hyperpigmented macules with a tendency to develop at sites of trauma

119
Q

4 sites commonly presenting with oral lichen planus

A

Buccal mucosa(e)
Lateral border(s) of tongue
Dorsum of tongue
Attached gingiva

120
Q

Define lichenoid reaction

A

Something that resembles lichen planus clinically and histologically but is caused by an identifiable agent, e.g. a drug

121
Q

Describe the pathogenesis of lichen planus

A
  1. Something alters the protein signature of the basal keratinocyte
  2. Langerhans’ cells detect the new antigen(s)
  3. Antigen(s) presented by Langerhans’ cells to T-cells
  4. Cell mediated immunity develops
  5. Activated T-cells infiltrate back to the altered epithelium and kill individual basal cells
  6. The epithelium reacts by proliferating
122
Q

5 conditions that mimic oral lichen planus/lichenoid reaction

A

Frictional keratosis
Lupus erythematosus
Tobacco-related keratosis
Potentially malignant oral lesion
Chronic graft-versus-host disease

123
Q

3 common sites for OSCC

A

Tongue: lateral border and ventral surface
Floor of mouth
Lower gum including retromolar pad

124
Q

3 treatment options for OSCC

A

Surgery: remove all tumour with a 5mm periphery of non-tumour tissue
Radiotherapy
Chemotherapy

125
Q

Define leukoplakia

A

White patch that cannot be classified as any other disease and is associated with an increased risk of malignancy

126
Q

What are 3 causes of red patches

A

Thinner keratin
Thinner epithelium (atrophy)
Vascularity in the lamina propria

127
Q

3 classifications of potentially malignant oral lesions

A

Homogeneous leukoplakia: lowest risk of OSCC
Non-homogeneous leukoplakia: higher risk of OSCC
Erythroplakia: highest risk of OSCC

128
Q

What are the 5 medical treatments for dysplasia?

A

Retinoids
EGFR inhibitors/antagonists
COX2 antagonists
Cell cycle interruption, e.g., p53 modulators
Topical anti-cancer agents, e.g., Bleomycin

129
Q

What is the advantage of surgical management of dysplasia

A

The most abnormal-looking tissue can be removed or destroyed

130
Q

What are the 3 clinical features of fibrous hyperplastic nodules

A

Usually well circumscribed
Solid and raised
Can form on mucosa close to line of occlusion

131
Q

What are the 3 presentations of fibrous hyperplastic nodules

A

Fibroepithelial polyp (FEP)
Fibrous epulis at gingiva
Denture induced hyperplasia

132
Q

2 management strategies for fibrous hyperplastic nodules

A

Remove stimulus
Excisional biopsy under LA, can recur if causative factor not removed

Oral surgery (4 decks)

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