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BDS4 Oral Medicine > Potentially malignant disorders and oral cancer > Flashcards

Potentially malignant disorders and oral cancer Flashcards

1
Q

What is the WHO definition of Potentially malignant lesions?

A
  • Altered tissue in which cancer is more likely to form
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2
Q

What is the WHO definition of potentially malignant condition?

A
  • Generalised state with increased cancer risk
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3
Q

What are some potentially malignant conditions (systemic conditions)?

A
  • Lichen planus (erosive or ulcerative on gingiva and tongue increased)
  • Oral submucous fibrosis
  • Iron deficiency
  • Tertiary syphilis
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4
Q

Why does a person with iron deficiency at higher risk of developing cancer?

A
  • Iron deficiency leaves oral epithelium thinner
  • Oral epithelium vital part of proetcting against pathogens and carcinogens
  • When barrier is decreased - increased risk of infections of carcinogens
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5
Q

What are some potentially malignant lesions?

A
  • Leukoplakia
  • Erythroplakia
  • Chornic hyperplastic candidiasis
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6
Q

What mucosa do most carcinoma in the UK arise from?

A
  • Clinically normal mucosa
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7
Q

Where in the world does most cancer arise from potentially malignant lesions?

A
  • High incidence arease
  • e.g. India
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8
Q

How many more time is leukoplakia likely to progress to cancer than clinically normal mucosa?

A
  • 50 to 100 times
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9
Q

What is the most common type of white patch that can be scraped off?

A
  • Acute pseudomembranous candidosis
  • aka thrush
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10
Q

What is leukoplakia?

A
  • White patch which cannot be attributed to any other diagnosis
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11
Q

What is erythoplakia?

A
  • Red patch that cannot be attributed to any other diagnosis
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12
Q

What are the predictors of malignancy in leukoplakia?

A
  • Age (incidence increases with age)
  • Females more likely
  • Idiopathic (no risk factors ass with oral cancer more likely to become malignant)
  • Floor or mouth , tongue and gingivae have high risk
  • buccal mucosa has low risk
  • Non homogenous e.g. verrucous, ulcerated leuko-erythroplakia have higher risk than homogenous
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13
Q

What is it called when there is a white patch on the floor of mouth?

A
  • Sublingual keratosis
  • Extremely high risk of developing into oral cancer
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14
Q

What is the gold standard for assessing malignant change in a lesion? What are we assessing?

A
  • Histopathology
  • Dysplasia
  • Atrophy (thinner)
  • Candida infection (presence of candida hyphae - chronic hyperplastic candidiasis or aka candidal leukoplakia )
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15
Q

There is a new way being researched to assess malignant change by histopathology, what is it termed and what are we assessing?

A
  • Biological markers
  • DNA content in leukoplakia showing hallmarks for future maligancy
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16
Q

What gene whether it has been mutated or other can be a strong indicator that the lesion is on its way to becoming malignant?

A
  • p53
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17
Q

What is a risk factor of oropharyngeal cancer? What prognosis does this give?

A
  • HPV
  • Presence of HPV gives better prognosis
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18
Q

What is dysplasia?

A
  • Disordered maturation (growth) in a tissue
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19
Q

What is atypia?

A
  • Changes in cells
  • Different to dysplasia
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20
Q

What are the two categories of criteria for diagnosis of epithelial dysplasia from histopatholgy?

A
  • Assess Architectural changes first (abnormal maturation and stratification)
  • Then assess Cytological changes (cellular atypia)
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21
Q

What is the WHO 2005 grading of epithelial dysplasia?

A
  • Done via microscope !
  • Hyperplasia
  • Mild
  • Moderate
  • Severe
  • Carcinoma-in-situ
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22
Q

What is basal hyperplasia in terms of histopathology?

A
  • Increased basal cell numbers
  • Architecture has regular stratification and basal compartment is larger
  • No cellular atypia

*arrow shows basal compartment being larger

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23
Q

What is mild dysplasia in regard to histopathology?

A
  • Architectural changes in lower third
  • Cytological changes of mild atypia
  • Mild atypia such as pleomorphism, hyperchromatism
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24
Q

What is pleomorphism ?

A
  • Variety of shapes and sizes
  • Can be from nucleus or cell or both together
25
Q

What is hyperchromatism?

A
  • Increased in DNA content therefore taking up more staining so appears darker purple on histopathologucal analysis
26
Q

What are some factors that can contribute to mild dysplasia and what is likely to happen if these factors are removed?

A
  • Trauma
  • Infection
  • Smoking
  • Removal of these factors likely to cease the mild dysplasia
27
Q

What is moderate dysplasia in terms of histopathology?

A
  • Architectural change extends into middle third of epithelium
  • Cytology : moderate atypia (plemorphism or hyperchromatism)
28
Q

What is severe dysplasia in terms of histopathology?

A
  • Architectural changes extend to upper third epithelium
  • Cytology: Severe atypia and numerous mitoses , abnormally high up in epithelium, loss of polarity, pleomorphism and hyperchromatism
29
Q

Where does mitoses usually happen?

A
  • At basal cell layer
30
Q

What is carcinoma-in-situ?

A
  • Theoretical concept
  • Malignant but not invasive (still contained within basement membrane of epithelium)
  • Abnormal architecture (full thickness of viable cell layers)
  • Pronounced cytological atypia with mitotic abnormalities frequent
  • Needs full removal if found in a pt
31
Q

What is present in the underlying connective tissue if a pt has a malignancy?

A
  • Inflammation
  • Shows pts has a immune response
  • If dysplasia present but no inflammation then pt is immunocompromised
32
Q

Histopathology is the gold standard for malignancy prediction. What are some negatives hitsopathology?

A
  • Invasive
  • Can’t monitor tissue response to txt effectively as can’t repeatedly take tissue samples to test response to txt
  • Not suitable for mass screening
33
Q

What future technique are available for predicting malignancy?

A
  • Salivary biomarkers
  • Next generation sequencing
  • Artificial intelligence
34
Q

What are the two main factors of carcinogenesis?

A
  • Genetics
  • Environmental damage
35
Q

What is the very basic molecular basis of cancer?

A
  • Damage to cells
  • Lead to altered gene expression
  • Lead to altered cell function
36
Q

What are the 4 stages of carcinogenesis?

A
  • Initiation where there is a change to gene such as carcinogen
  • Promotion of the cell via cell multiplication
  • Transformation of the cell via genetic change (mutation) into a malignant cell
  • Progression of the malignant cell via genetic change into malignant tumour
37
Q

What are some examples of changes to genes that can occur?

A
  • Change to chromosomes
  • Change to genes
  • Epigenetic changes
38
Q

Give examples of changes to chromosomes

A
  • Aneuploidy (extra or missing chromosome)
  • Translocations (rearrangement of chromosome)
  • Amplification
39
Q

Give examples of changes to genes that can occur

A
  • Mutations
  • Deletions
  • Amplifications
40
Q

Give examples of epigenetic changes

A
  • Chemical changes in DNA
    like methylation and modification of histone that package DNA
41
Q

What types of HPV have oncological ability?

A

HPV 16 and HPV 18

42
Q

Give the oral cancer genetic broad overview

A
  • Oncogenes which produce normal growth factors
  • Tumour suppressor genes which suppress the growth of cells
  • growth of cells in body is in equilibrium between oncogenes and tumour supressor genes
  • Most active tumour suppresor gene is Tp53 either mutated or inactivated (in about 50-80% of head and neck cancer pt)
  • Genes that regulate apoptosis (cell death) if not done then cell continues lifespan
  • Genes involved in DNA repair
  • MiRNA (can play a role in neoplastic transformation) - chemo targets these
43
Q

What is Knudson’s two-hit hypothesis of carcinogenesis?

A
  • Need both Tp53 tumour suppressor genes on the chromosome (pair) mutated or inactivated in order for carcinogenesis to occur
44
Q

Do you need both of the oncogenes on a chromsome to be mutated or inactivated for malignant progression to occur?

A
  • No oncogenes only need one to be mutated or inactivated for malignancy to occur
  • Tumour suppressor Tp53 requires both!
45
Q

What are the 6 hallmarks of cancer? *KNOW

A
  • Evading apoptosis
  • Self sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Tissue invasion and metastasis
  • Limitless replicative potential
  • Sustained angiogenesis
46
Q

What is the filed change theory (field cancerisation)?

A
  • If the area that the cancer was present has been removed this does not reduced the risk of oral cancer devloping in another area
  • there is genetic instability increasing the poss of devloping cancer
  • Clincally may appear normal and it is diff to estimate the extend of field
  • But multiple primaries of 15-20%
  • Can be synchronous or metachronous
47
Q

What does synchronous mean?

A
  • Primary malignancy that arise within 6 months of first maligancy
48
Q

What does metachronous mean?

A
  • Primary malignancy that arise more than 6 months apart
49
Q

What are the important points that come back when oral cancer pathology report is performed?

A
  • Diagnosis of squamous cell carcinoma
  • Differentiation and grading
  • Pattern of invasive front related to nodal spread
  • Local extension of disease
50
Q

This image shows a cohesive front of dysplasia. What is meant by the term cohesive front?

A
  • Cells advancing at the same rate and same time (sim to a wave)
51
Q

What is meant by the term non-cohesive front?

A
  • Cells advancing in clumps or strains at different rates
  • Positive correlation with lymph node involvement
52
Q

How is the spread of oral cancer described?

A
  1. Local extension of disease
    - Varies according to site i.e. mucosal extension, muscle (tongue), bone or nerve
  2. Lymphatic spread
  3. Haematogenous spread
53
Q

How can tumour spread into bone?

A
  • If pt is edentulous then via gaps in the cortex
  • If pt is dentate via periodontal ligament - bone destruction and increased mobility
54
Q

What is meant by the term perineural spread?

A
  • Involving small nerved at advancing edge predicts nodal spread
  • Extensive spread related to IAN may give recurrence
55
Q

What are 3 ways lymphatic spread of oral cancer can occur?

A
  • Via embolism
  • Via permeation
  • Via tumour involved node with extracapsular spread

Require sentinal node biopsy

56
Q

What is the clinical staging of oral cancer?

A

TNM

57
Q

What are some rare types of OSCC?

A
  • Verrucous carcinoma
  • Basaloid squamous (common in HPV)
  • Spindle cell (aggresive)
58
Q
A

BDS4 Oral Medicine (22 decks)

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