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BDS4 Oral Medicine > Pathology 2 - Potentially malignant lesions > Flashcards

Pathology 2 - Potentially malignant lesions Flashcards

1
Q

Define a potentially malignant lesion.

A

Altered tissue in which cancer is more likely to form

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2
Q

Define a potentially malignant condition.

A

Generalised state with increased cancer risk

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3
Q

Give examples of potentially malignant conditions.

A
  • lichen planus
  • oral submucous fibrosis
  • iron deficiency
  • tertiary syphilis
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4
Q

Why is an iron deficiency a potentially malignant condition?

A

Iron deficiency thins the mucosa which makes it easier to carcinogens to penetrate

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5
Q

Which lesions have a higher transformation rate?

A
  • leukoplakia
  • chronic hyperplastic candidiasis
  • proliferative verrucous leukoplakia
  • erythroplakia
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6
Q

What is chronic hyperplastic candidiasis also known as?

A

Candidal leukoplakia

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7
Q

Where is chronic hyperplastic candidiasis typically found?

A

Commissures of smokers

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8
Q

How is chronic hyperplastic candidiasis managed?

A
  • systemic antifungal (fluconazole)
  • biopsy
  • smoking cessation
  • observation
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9
Q

From where do most oral carcinomas arise in the UK?

A

Clinically normal mucosa

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10
Q

What is the transformation risk of leukoplakia?

A

50-100x risk than clinically normal mucosa

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11
Q

What factors increase the risk of transformation of leukoplakia?

A
  • age
  • female
  • FOM or tongue are high risk sites
  • non-homogeneous appearance
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12
Q

What does altered or missing p53 indicate as a molecular marker?

A
  • p53 is a tumour suppressor gene
  • changes indicate progression of a lesion
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13
Q

What impact does a positive result for HPV in a tumour have?

A

Tumours that are positive for HPV have a better prognosis than those that are negative

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14
Q

Define dysplasia.

A

Disordered maturation in a tissue

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15
Q

Define atypia.

A

Changes within cells

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16
Q

What can be observed in histopathology slides to aid diagnosis?

A
  • architectural changes
  • cytological abnormalities
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17
Q

What are the grading of epithelial dysplasia?

A
  • hyperplasia
  • mild
  • moderate
  • severe
  • carcinoma-in-situ
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18
Q

Can you grade epithelial dysplasia clinically?

A

No - a microscopic diagnosis

19
Q

Describe basal hyperplasia.

A
  • increased basal cell numbers
  • regular stratification but basal compartment is larger
  • no cellular atypia (!)
20
Q

Describe mild dysplasia.

A
  • changes to architecture in lower third
  • mild cellular atypia (not all cells show changes)
21
Q

Define pleomorphism.

A

Variety of shapes and sizes of cells or cellular components

22
Q

Define hyperchromatism.

A

Cells stain darker due to increase in DNA

23
Q

Describe moderate dysplasia.

A
  • changes to architecture extending into middle third
  • moderate atypia
24
Q

Describe severe dysplasia.

A
  • architectural changes extend into more than 2/3 of epithelium
  • most cells are affected by atypia
  • numerous mitoses, loss of polarity and mitotic figures
25
Q

Describe carcinoma-in-situ.

A
  • theoretic concept
  • malignant but not invasive (ie confined within epithelium)
  • full thickness changes to architecture
  • pronounced cellular atypical with frequent mitotic abnormalities
  • degree of inflammation
26
Q

What is the gold standard for detection and diagnosis of oral cancer?

A
  • visual detection
  • histopathology for diagnosis
27
Q

What are screening tools that may be used in the future?

A
  • salivary biomarkers
  • NGS
  • AI
28
Q

What are the two main factors in carcinogenesis?

A
  • genetics
  • environmental (carcinogens)
29
Q

What is the molecular basis of cancer?

A
  • damage
  • altered gene expression
  • altered cell function
30
Q

What genes are involved in the progression of cancers?

A
  • oncogenes
  • tumour suppressor genes (eg p53)
  • genes that regulate apoptosis
  • genes involved in DNA repair
  • miRNA
31
Q

Define aneuploidy.

A

Changes in number of chromosomes

32
Q

Define translocation.

A

DNA strands break and reattach in different location

33
Q

Define amplification.

A

Extra copies of genes or chromosomes

34
Q

What are epigenetic changes?

A
  • chemical changes in DNA
  • modification of histones
35
Q

What are the six hallmarks of cancer?

A
  • evading apoptosis
  • self-sufficiency in growth signals
  • insensitivity to anti-growth signals
  • tissue invasion and metastasis
  • limitless replicative potential
  • sustained angiogenesis
36
Q

What is the difference between a cohesive front and a non-cohesive front?

A
  • cohesive front, all cells advance at the same rate
  • non-cohesive front see cells advancing at different rates and is more likely to involve nodes
37
Q

How can oral cancer spread?

A
  • local extension
  • lymphatic spread
  • haematogenous spread
38
Q

Describe local extension of oral cancer.

A
  • depends on site
  • can extend further into mucosa
  • can spread to muscle, bone or nerves
39
Q

How does oral cancer spread into bone?

A
  • in edentulous patients can spread via gaps in cortex
  • in dentate patients can spread via PDL
40
Q

What prognosis does perineural spread have?

A
  • spread at small nerves it predictive of nodal spread
  • extensive spread via IAN can predict recurrence
41
Q

What are the different types of lymphatic spread of oral cancer?

A
  • embolism
  • extracapsular spread
  • permeation (growth within nodes)
42
Q

What is a sentinal node biopsy?

A

Principle draining lymph node is biopsied

43
Q

What are the OSCC subtypes?

A
  • verdurous carcinoma
  • basaloid squamous (HPV)
  • spindle cell (aggressive)
44
Q

What is the haematogenous spread of oral cancer?

A
  • spread via blood vessels
  • late stage feature
  • can spread to lungs, spine etc

BDS4 Oral Medicine (31 decks)

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