oral cancer - oral lesions + therapy options Flashcards

1
Q

Give 4 examples of potentially malignant lesions

A

White lesions (leukoplakia)
Red lesions (erythroplakia)
Lichen planus
Oral submucous fibrosis

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2
Q

What is the prevalence of oral cancer in white lesions?

A

0.2-0.4% of white lesions become malignant
Most oral carcinomas arise in initially clinically normal mucosa
Most cancer in high incidence areas eg - India, arise from potentially malignant lesions
Leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa

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3
Q

What is dysplasia based on?

A

Cellular atypia
Epithelial architectural organisation

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4
Q

How can dysplasia be categorised?

A

Low grade
High grade
Carcinoma-in-situ

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5
Q

Give 4 examples of cytological changes

A

Abnormal variation in nuclear size
Abnormal variation in nuclear shape
Abnormal variation in cell size
Abnormal variation in cell shape

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6
Q

Give 4 examples of architectural changes

A

Irregular epithelial stratification
Loss/disturbed polarity of basal cells
Drop-shaped rete ridges
Increased and abnormal mitoses

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7
Q

Describe histological changes seen in low grade oral mucosa dysplasia

A

Architectural change into lower third
Evidence of stratification
Considerable amount of keratin production
Well formed basal layer surrounding tumour islands

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8
Q

Describe the histological changes seen in high grade oral mucosa dysplasia

A

Shows little resemblance to a normal squamous epithelium
Architectural change in upper third
Usually shows considerable atypia
Mitotic figures are prominent and many may be abnormal

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9
Q

What is a carcinoma-in-situ?

A

A theoretical concept where there is no evidence of invasion through the basement membrane but pathologists highly suspect there is a carcinoma
Abnormal architecture seen
Mitotic abnormalities frequent

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10
Q

Name 4 histological prognostic factors

A

Pattern of invasion
Depth of invasion - increases risk of metastases
Perineural invasion
Invasion of vessels - associated with LN metastases

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11
Q

Describe the field cancerisation concept

A

Where cancer develops isn’t the only region subject to the changes which lead to cancer formation
There is a high cancer risk in 5cm radius of the original primary
This would be a new primary tumour rather than occurrence

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12
Q

How is oral cancer staged?

A

Size (T)
Nodal involvement (N)
Metastases (M)

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13
Q

What is the prognosis of oral cancer based on the stage?

A

Stage I = 80% cure rate
Stage II = 65% cure rate
If untreated, with metastases, survival is about 4 months

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14
Q

What proportion of oral cancer patients present at stage I or II?

A

1/3

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15
Q

Which tx option has the best outcome for resectable tumours?

A

Primary surgery

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16
Q

What is the aetiology of lip cancer?

A

Sunlight and smoking

17
Q

Describe the behaviour or lip cancer?

A

Slow growth
Local invasion
Rarely metastasise to nodes
Good prognosis as early detection due to visibility

18
Q

Describe the ethics of oral cancer screening?

A

Need to look at benefit vs harm as screening will not pick up everything and it can give false positives
Need to question whether its cheaper to find disease early or to let the disease progress and then treat it

19
Q

What are the 5 methods of oral cancer screening?

A

HPV16 screening
Toluidene blue
VELscope
Photodynamic Diagnosis (PDD)
The clinical judgement of an experienced clinician

20
Q

How does toluidine blue work and when is it used?

A

Dye is applied to the mucosa
Stains certain markers within cells - good for showing areas of change and dysplasia
Causes false positives in inflammatory lesions and trauma cases
Good for already known lesions to select biopsy site

21
Q

How does VELscope work?

A

Autofluorescence of tissue with blue light
Loss of fluorescence equates to change
Change may be cancer but can be other changes
No adequate evidence yet

22
Q

What must a GDP be competent in, in regards to oral cancer?

A

Smoking cessation advice
Alcohol reduction advice
Healthy diet promotion
2 week referral pathway if cancer thoughts