OM- Potentially malignant disorders Flashcards

1
Q

Compare a potentially malignant lesion to a potentially malignant disorder?

A

Potentially malignant lesion- altered tissue in which cancer is more likely to form.
Pottentially malignant disorder- a generalised condition which puts patients at greater risk of cancer.

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2
Q

List some potentially malignant conditions

A

Leukoplakia (undiagnosed white patch)
Erythroplakia (undaiagnosed red patch)
Lichen planus- erosive and ulcerative type are higher risk.
Chronic hyperplastic candidasis
Tertiary syphillis-
Iron deficiency- causing thinning of oral epithelium.
Oral submucous fibrosis- abnormal collagen produced inthe submucosa which causes limited mouth opening (caused by chewing the betel nut)
Iron deficiency.

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3
Q

What clinical test do we complete with a white patch and what does the result tell us?

A

Try and scrape the lesion off.
If it scrapes off it is a candidal lesion.
If it does not scrape off it is leukoplakia.

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4
Q

What is leukoplakia?

A

A white patch that cannot be diagnosed clinically. It is a pottentially malignant lesion which is 50-100 x more likely to progress into cancer than clinically normal mucosa.

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5
Q

Give some clinical predictors of malignancy

A

Age (more likely when older)
Gender (females are more likely)
Idiopathic (patients without risk factors are more likely)
Site (floor of mouth & tongue = high risk. Buccal mucosa = low risk. Sublingual keratosis= very high risk.
Clinical appearance- Non-homogeneous e.g. verrucous/ ulcerated leuko-erythroplakia = increased risk.

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6
Q

What are we looking for when taking a biopsy of a suspected leukoplakia?

A

Dysplasia
Atrophy
Candida infection

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7
Q

What is chronic hyperplastic candidiasis?

A

This is candidal leukoplakia which is associated with smoking and has an increased risk of progressing into oral cancer.

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8
Q

Compare epithelial dysplasia and cellular atypia?

A

Dyplasia is disordered growth in the tissue.
Atypia is disorded growth in the cell.

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9
Q

What architectural changes are we looking for in the biopsy ?

A

How much of the epithelium is involved (1/3? 2/3?)
Stratification- are the cells arranged normally?
Any spaces between the cells
Atypia (pleomorphism and hyperchromatism)

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10
Q

Compare hyperchromatism and pleomorphism

A

Pleomorphism - change in nuclei size.
Hyperchromatism- change in cell staining as a result of DNA retention in the cell.

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11
Q

Name and grade this type of dysplasia?

A

Basal cell hyperplasia
Increase in the number of basal cells causing a larger basal compartment.
Architecture- regular stratification
Cytology- no atypia.

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12
Q

Name and grade this type of dysplasia?

A

Mild dsyplasia
architecture- changes in the lower 1/3 (Basal cell hyperplasia)
Cytology- Mild atypia. Pleomorphism. Hyperchromatism

Removal of the cause can help it regress.

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13
Q

Name and grade this type of dysplasia?

A

Moderate dyplasia
Architecture-change extends in to the middle third. There are spaces between the cells. The rete ridges become rounder.
Cytology- Pleomorphism and hyperchromatism.

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14
Q

Name and grade this type of dysplasia?

A

Severe dysplasia
Architecture- changes extend to the upper third (we have loss of stratification)
Cytology- Severe atypia and numerous mitoses (mitoses are not at the bottom which is abnormal)

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15
Q

Name and grade this type of dysplasia?

A

Carcinoma in situ
Theoretical- Malignant but not invasive (all cells have shown malignant change but haven’t spread to the underlying connective tissue)
The connective tissue should show inflammation (good immuen response)

Archiecture- abnormal all viable cell layers involved
Cytology- Pronounced cytological atypia with mitotic abnormalities.

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16
Q

How do we detect oral cancer?

A

Clinically then histopathologically for confirmation (Biopsy)

17
Q

What are the two main factors involved in carcinogenesis?

A

Genetic and carcinogens (environmental factors)

18
Q

Name the 6 hallmarks of cancer?

A

Self-sufficency in growth signals

19
Q

What important information is provided with a biopsy

A

Grading and differentiation (is it a well/moderately or poorly differentiated carcinoma)
Pattern of invasive front (Can help predict if lymph nodes are involved)
Spread (local extension/ Lymphatic spread/ haematogenous spread )

20
Q

What type of cancer are the majority of oral cancer?

A

Oral squamous cell carcinoma

21
Q

Compare cohesive and non-cohesive front’s in terms of oral cancer patterns?

A

Cohesive front- the malignant lesion progresses as one.
Non-cohesive front (The malignant lesion progresses in small clumps- this has a positive correlation with lymph node involvement)

22
Q

Why do we biopsy a leukoplakia?

A

To exclude carcinoma and assess for candida colinization.

23
Q

What do we use to grade dysplasia?

A

Cytological changes
-Abnormal variations in nuclear size, nuclear shape, cell size, cell shape, Atypical mitotic figures.
Architectural changes
-How much of the epithelium is involved? Irregular epithelial stratification.Loss. disturbed polarity. Drop shaped rete ridges. Increased and abnormal mitoses. Premature keratinisation in single cells. Abnormal keratinisation. Keratin pearls within the rete ridges.

24
Q

What is the most common malignancy related to oral cancer?

A

Oral squamous cell carcinoma

25
Q

What histological factors can be used to predict prognosis?

A
  • Pattern of the invasive front (helps us predict if lymph nodes are involved)
  • Spread
26
Q

What are we looking to find out about the spread of a malignancy?

A

Is there local extension (to the mucosa/tongue/bone nerve)
What is the depth of invasion (greater risk for tumours >4mm depth)
Has it spread to lymphatics
Any haematogeneous invasion (Widely associated with lymph node metastases and a poor prognosis)
Any perineural invasion (especially if found in nerves far away from the cancer site.

27
Q

What is chronic hyperplastic candidasis?

A

This is a white lesion associated with the candidal organism and smoking. (pottentially malignant condition)