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My BDS4 > BAMS - Potentially malignant lesions > Flashcards

BAMS - Potentially malignant lesions Flashcards

1
Q

What is the gold standard for diagnosing potentially malignant lesions?

A

histopathology/biopsy

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2
Q

How do we stage potentially malignant lesions? what do we use?

A

Via clinical examination

T - tumour size (width)
N - lymph node involvement
M - distant metastesis

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3
Q

How do we grade potentially malignant lesions? what do we use?

A

histopathology/biospy

  • well differentiated
  • moderately differentiated
  • poorly differentiated
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4
Q

What does the term potentially malignant disorder encompass? (2)

A
  • Potentially malignant lesion
  • Potentially malignant conditions
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5
Q

What is a potentially malignant lesion?

A

An area of altered tissue in which cancer is more likely to form

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6
Q

What is a potentially malignant condition?

A

Generalized systemic condition that a patient has that increases cancer risk

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7
Q

What are systemic conditions which increase the risk of oral cancer? (4)

A
  • lichen planus – erosive/ulcerative variant especially on tongue and gingivae
  • oral submucous fibrosis - chewing of beetlenut
  • iron deficiency – due to the oral epithelium being thinner, this is an important pathogen/carcinogen barrier
  • tertiary syphilis (rare)
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8
Q

What types of lichen planus increases the oral cancer risk?

A

erosive/ulcerative variant especially on tongue and gingivae

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9
Q

How much more likely is it for leukoplakia to undergo malignant change than normal mucosa?

A

Leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa

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10
Q

What indicators are used to predict malignant change to leucoplakia? (5)

A
  • age– OC risk increases with age
  • gender - females more at risk of OC
  • idiopathic
  • site - floor of mouth, tongue and gingivae = high risk
    sublingual keratosis = extremely high risk of OC
  • clinical appearance - non-homogeneous verrucous, ulcerated, leuko-erythroplakia
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11
Q

What are the disadvantages of biopsy? (2)

A

Can’t screen patients = unpleasant/painful and invasive

Can’t monitor tissue response to treatment

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12
Q

What are biopsied samples asssessed for? (3)

A
  • dysplasia
  • atrophy (thinning)
  • candida infection – chronic hyperplastic candidiasis/candida leukoplakia has malignant potential
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13
Q

Why is leucoplakia tested for candida infection?

A

candidiasis/candida leukoplakia has malignant potential

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14
Q

What is the function of a p53 gene?
what is the relationship between this gene and cells that undergo malignant change?

A

gene helps prevents cell division in cells where there is irreparable cellular damage

In a larger percentage of malignant cells, this gene has been deleted/ inactivated = allows the defective cells to proliferate

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15
Q

What protein degrades the p53 gene and in which circumstances is this gene present?

A

Those with HPV 16&18

HPV16&18 Produces E6 protein which degrades p53

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16
Q

What is the difference between epithelial dysplasia and cellular atypia?

A

Dysplasia is disordered maturation (growth) in a tissue

changes that occur at an individual cellular levels (not the tissues)

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17
Q

What is the criteria for diagnosis (via histopathology) of a PM lesion? (2)

A
  1. Assess architectural changes
    - boundaries between categories not well defined
    - architectural changes = abnormal maturation and stratification
  2. Cytological abnormalities
    - individual cells – look for atypia
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18
Q

List the grades of epithelial dysplasia. (5)

A
  1. hyperplasia
  2. mild
  3. moderate
  4. severe
  5. carcinoma-in-situ
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19
Q

What occurs in basal hyperplasia (grade 1 epithelial dysplasia).

A

Increased basal cell numbers in the basal cell compartment.

20
Q

Describe the architectural changes and the cytological abnormalities of a grade 1 epithelial dysplasia/basal hyperplasia.

A

Architecture:
- regular stratification
- basal compartment is larger

No cytological changes - Only affects the basal cell numbers, No basal cell atypia

21
Q

Describe the architectural changes and the cytological abnormalities of a grade 2 mild epithelial dysplasia. (3 + 1)

A

Architecture:
changes in lower third only
- pleomorphism: variety of shapes and sizes in nucleus and/or cell
- hyperchromatisim: has an increased DNA content = nucleus stains darker
- basal cell hyperplasia (increased no.s)

cytology:
mild atypia of cells

22
Q

How much of the cell layers are involved in grade 2 mild epithelial dysplasia.

A

the lower 1/3rd only

23
Q

Describe the architectural changes and the cytological abnormalities of a grade 3 moderate epithelial dysplasia. (3)

A

Architecture:
changes in 2/3rds of cell layers
- pleomorphism
- hyperchromatisim

cytology:
moderate atypia of cells

24
Q

How much of the cell layers are involved in grade 3 mild epithelial dysplasia.

A

changes in 2/3rds of cell layers

25
Q

How much of the cell layers are involved in grade 4 severe epithelial dysplasia.

A

most cells affected
- changes extend to the upper 1/3rd

26
Q

Describe the architectural changes and the cytological abnormalities of a grade 4 severe epithelial dysplasia. (5)

A

Cytology:
Severe atypia
- Hyperchromatism affecting the majority of cells
- Mitotic cells above the basal cell layer = abnormal = malignant changes
- pleomorphism
- hyperchromatisim

27
Q

Describe a lesion which has carcinoma in situ.

A

A Malignant but non-invasive lesion = Still confined to epithelium however all cells affected (cellular atypia)

28
Q

List the 4 stages of carcinogenesis.

A

initiation
promotion
transformation
progression

29
Q

Describe what occurs in the initiation stages of carcinogenesis.

A

spontaneous change or triggers (carcinogens) causes mutation to occur that isn’t repaired however doesn’t form a malignant cell

30
Q

Describe what occurs in the promotion stages of carcinogenesis.

A

mutated cells continue to grow and reproduce and there is a fault in the repair genes

31
Q

Describe what occurs in the transformation stages of carcinogenesis.

A

malignant conversion of the cell
(preneoplastic to malignancy)

32
Q

Describe what occurs in the progression stages of carcinogenesis. (3)

A

= expression of the malignant phenotype

= genetic instability and uncontrolled growth

= activation of oncogenes and loss of tumour suppressor genes

33
Q

List 3 changes to chromosomes (contain genes) that can occur.

A
  • aneuploidy: missing or extra chromosomes
  • translocations: sections of the chromosome break off and attach to another chromosome
  • amplifications: extra copies of genes
34
Q

List 3 changes to genes (sections of DNA) that can occur.

A
  • mutations
  • deletions
  • amplifications
35
Q

List epigenetic changes that can occur. (2)

A

chemical changes in DNA - such as methylation (silence genes)

modification of the histones that package DNA

36
Q

What is the function of Tp53 gene? What is the relationship between this and carcinogenesis?

A

most important tumour suppressant genes (come in pairs)

in cancer these genes are mutated or inactivated

37
Q

Describe Knudson’s “two-hit” hypothesis of carcinogenesis.

A

2x tumour suppressant genes (come in pairs) e.g. Tp53 must be damaged to become malignant
If only 1 is damaged the cell will remain benign

38
Q

List the 6 hallmarks of cancer.

A

self sufficiency in growth signals

insensitviety to anti-growth signals

tissue invasion and metastasis

limitless replicative potential

sustained angiogenesis

evading apoptosis

39
Q

Describe field change theory.

Which sites are commonly affected. (3)

A

The formation of multiple patches of premalignant disease with a higher-than-expected rate of multiple local second primary tumors forming - not metastasis.

commonly - Pharynx, larynx and respiratory tract.

40
Q

What is included on an oral cancer pathology report? (3)

A
  1. differentiation and grading using histopathology
    - well differentiated
    - moderately differentiated SCC
    - poorly differentiated SCC
  2. pattern of invasive front (related to nodal spread)
    - cohesive (cells advance like a wave)
    - non-cohesive: has correlation with lymph node involvements
  3. local extension of the disease
41
Q

What are the ways in which oral cancer can spread? provide examples. (6)

A

Local extension of disease
- mucosal extension
- muscle (tongue etc)
- bone
- nerve

  1. Lymphatic spread
  2. Haematogenous spread
42
Q

Describe how oral cancer would spread to bone in edentulous patients.

A

via gaps in cortex

43
Q

Describe how oral cancer would spread to bone in dentate patients.

what must we investigate further?

A

along the PDL and into the jaw bone

In patients with good OH and no reason for mobility of teeth

44
Q

In terms of perineural spread, which type of spread can predict nodal spread?

A

If malignancy has spread to small nerves at the advancing edges

45
Q

In terms of perineural spread, which type of spread can predict reoccurence?

A

If there is extensive spread of the malignancy related to the inferior alveolar nerve

46
Q

List and describe haematogenous spread of cancer. (3)

A
  • Permeation = Grow inside vessels
  • Via embolism
  • Via extracapsular spread
47
Q

List 3 types of rare SCC.

A
  • Verrucous - rarely metastasises and better prognosis
  • Basaloid – associated with HPV
  • Spindle cell – aggressive

My BDS4 (57 decks)

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