potentially malignant disorders Flashcards

1
Q

What is a potentially malignant lesion?

A

Altered tissue which cancer is more likely to form

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2
Q

What is a potentially malignant disorder?

A

Generalised state with increased cancer risk

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3
Q

Give 4 examples of potentially malignant systemic conditions

A

Lichen planus
Oral submucous fibrosis
Iron deficiency - anaemia can lead to atrophy of oral epithelium so barrier function is diminished
Tertiary syphilis - can form white patch on tongue

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4
Q

Describe chronic hyperplastic candidosis

A

Caused by C. albicans
Commissures seen at the angles of the mouth
Found in smokers
Dysplasia may be present

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5
Q

How is chronic hyperplastic candidosis treated?

A

Systemic antifungal - fluconazole capsules, 50mg once daily for 14 days
Biopsy
Stop smoking
Observe

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6
Q

Where do most oral carcinomas in the UK arise from?

A

Clinically normal mucosa

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7
Q

How much more likely is leukoplakia to progress to cancer than clinically normal mucousa?

A

50 to 100 times

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8
Q

What are the clinical predictors of malignancy in leukoplakia?

A

Age - older more likely
Gender - differs from country
Site - buccal mucosa is low risk, floor of mouth and tongue is high risk
Clinical appearance - if homogenous and smooth then less likely, non-homogenous, verrucous and ulcerated then mitre likely

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9
Q

What are the histopathological predictors of malignant change?

A

Dysplasia
Atrophy
Candida infection
Biological markers eg - p53, HPV+ and HPV-

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10
Q

What is dysplasia?

A

Disordered maturation (growth) in a tissue
A histopathological diagnosis, not clinical

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11
Q

What is atypia?

A

Changes in cells

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12
Q

What are the predictors for histopathology epithelial dysplasia?

A

Assess architectural changes then cytology
Architectural changes such as maturation (growth) and stratification (more layers)
Cytological abnormalities such as cellular atypia

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13
Q

What is the WHO classification for grading of epithelial dysplasia?

A

Hyperplasia
Mild
Moderate
Severe
Carcinoma-in-situ

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14
Q

How is staging and grading carried out?

A

Grading is done histopathologically
Staging is done clinically

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15
Q

Describe basal hyperplasia

A

Increased number of basal cells, rest of epithelium is normal
Architecture - regular stratification, basal component is larger
No cellular atypia

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16
Q

Describe mild dysplasia

A

Architectural changes in lower third
Cytology - mild atypia, pleomorphism and hyperchromatism

17
Q

What is pleomorphism?

A

Difference in size and shape of a cell

18
Q

What is hyperchromatism?

A

Darker staining of a cell due to more DNA present

19
Q

Describe moderate dysplasia?

A

Architecture changes extends into middle third
Cytology - moderate atypia - hyperchromatism and pleomorphism

20
Q

Describe severe dysplasia

A

Architecture changes extend into upper third
Cytology - severe atypia and numerous mitoses, abnormally high
- hyperchromatism and pleomorphism
- loss of polarity (lack of difference between different layers of cells)

21
Q

Describe a carcinoma-in-situ

A

A theoretical concept
Malignant but not invasive
Abnormal architecture - full thickness or almost full of viable cell layers
Pronounced cytological atypia - mitotic abnormalities frequent

22
Q

How may pathology be confirmed in the future?

A

Salivary biomarkers
Next generation sequencing
AI

23
Q

What common diagnostic tests are used for potentially malignant lesions?

A

Vital staining
Oral cytology
Optical imaging

24
Q

What are the 2 main factors of carcinogenesis?

A

Genetic
Environmental (carcinogens)

25
Q

What is the molecular basis of cancer?

A

Damage leads to altered gene expression which leads to altered cell function

26
Q

What is an oncogene?

A

A gene that has the potential to cause malignancy

27
Q

What are tumour suppressor genes?

A

Genes that regulate cell division

28
Q

What is miRNA?

A

Strands of RNA which can play a role in neoplastic transformation as they control the function of oncogenes and tumour suppressor genes

29
Q

How can oncogene inactivation/mutation lead to malignancy?

A

If 1 of a pair is inactivated/mutated, the others function will not be enough and the cell will become malignant

30
Q

How can tumour suppressor gene inactivation/mutation lead to malignancy?

A

Need both of a pair to be inactivated/mutated for the cell to become malignant
This is called Knudson’s ‘two hit’ hypothesis of carcinogenesis

31
Q

Give an example of a tumour suppressor gene and it’s role

A

Tp53 gene provides instructions for p53 protein

32
Q

Give an example of a viral component in oral cancer genetics?

A

HPV

33
Q

What are the 6 genetic changes of cancer?

A

Evading apoptosis
Self-sufficiency in growth signals
Insensitivity to anti-growth signals
Tissue invasion and metastasis
Limitless replication potential
Sustained angiogenesis

34
Q

What percentage of oral cancer is SCC?

A

95%

35
Q

What is cohesive front and non-cohesive front in cancer spread?

A

Cohesive front - cells are together and advance at the same time
Non-cohesive front - strong possibility of LN involvement even if no clinical signs of enlargement

36
Q

What are the 3 methods of oral cancer spread?

A

Local extension of disease
Lymphatic spread
Haematogenous spread

37
Q

How may oral cancer spread to bone?

A

Gaps in cortex in edentulous patients
PDL if patient is dentate

38
Q

Describe the subtypes of oral SCC?

A

Verrucous carcinoma - has the best outcome
Basaloid squamous - aggressive and associated with HPV
Spindle cell - aggressive and difficult to identify