Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

My BDS4 > Oral cancer - Dysplasia > Flashcards

Oral cancer - Dysplasia Flashcards

1
Q

What are the two classifications of head and neck cancers?

A

oral cavity cancer

oropharyngeal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List high risk areas for oral cancer. (7)

A

● Floor of the mouth – increased risk to this site in drinkers and smokers

● Lateral border of the tongue - increased risk to this site in drinkers and smokers

● Retromolar regions

● Soft palate - increased risk to this site in drinkers and smokers

● hard palate
● Gingivae
● Buccal mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for oral cancer? (9)

A

Smoking
Drinking
smoking and drinking
Socioeconomic status
Diet
Betel quid (paan)
oral health
family history
sexual activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How much does smoking increase your risk of OCC?

A

X2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How much does drinking (3-4 drinks/day) increase your risk of OCC?

A

x2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How much does smoking and drinking increase your risk of OCC?

A

x5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How much does Betel paan increase your risk of OCC?

A

x3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How much does SE status increase your risk of OCC?

A

x2
(even without other risk factors you have the sane risk as those who smoke or drink)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What specific type of cancer has the greatest risk of developing if a px smokes?

A

larynx cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What specific type of cancer has the greatest risk of developing if a px drinks? (2)

A

oral cavity

oropharyngeal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What factors contribute to the OCC risk from smoking? (3)

what patter of use increases the risk?

A

Quantity
duration
frequency

fewer cigarettes for longer duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What factors contribute to the OCC risk from drinking? (1)

what patter of use increases the risk?

A

Frequency
(more important than duration) – more drinks each day key

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do we reduce the risks of OCC? (3)

A

Stop smoking

stop drinking

Healthy diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

when are the benefits of stopping smoking seen?

A

benefits of quitting smoking are seen one to four years after stopping

  • After quitting for 20 years: you’re at the same risk as someone who has never smoked
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when are the benefits of stopping drinking alcohol seen?

A

Benefits of quitting heavy alcohol consumption emerge 20 years after quit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what advice would you give px’s regarding reducing the risk of OCC if only a limited health education message can be conveyed?

A

In the short term, if a px is going to change either their smoking or drinking habits, they are going to get an improvement in oral cancer risk quickest by reducing their smoking (rather than drinking) however should be encouraged to reduce/stop both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In terms of diet how can we reduce our OCC risk (by 1/2) ?

A

high intake of fresh fruits and vegetables

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is the incidence of oropharyngeal cancer increasing?

A

Due to the HPV epidemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are potentially malignant lesions? (6)

A
  • White lesions - leukoplakia
  • Red lesions - erythroplakia
  • Lichen planus
  • Candidal Leukoplakia
  • Chronic Hyperplastic Candidiasis
  • Oral Submucous Fibrosis
20
Q

describe the risks associated with leukoplakia.

A
  • Higher risk of malignant transformation compared to normal healthy mucosa
    (however most OCC arise from healthy mucosa)
  • not all white patches have the same level of risk
21
Q

Describe what colour of lesion is more commonly associated with malignant transformation.

A

Erythroplakia
- More Commonly associated with malignant change, erythema due to the vascular changes that occur as a consequence to malignant change

22
Q

What is the criteria for dysplasia based on? (2)

A

Cellular atypia

epithelial architectural organisation

23
Q

How do we categorise dysplasia? (3)

A
  • Low grade
  • high grade
  • carcinoma-in-situ

based on the cellular atypia and epithelial architectural organisation

24
Q

What cytological changes are associated with dysplasia? (8)
Not all have to be present to mean its dysplastic

A

Abnormal variation in nuclear size

Abnormal variation in nuclear shape

Abnormal variation in cell size

Abnormal variation in cell shape

increased/altered nuclear/cytoplasmic ratio

atypical mitosis figures

increased number and size of nucleoli

nuclear hyperchromatism

25
Q

What epithelial architectural changes are associated with dysplasia? (8)
Not all have to be present to mean its dysplastic

A

irregular epithelial stratification

loss/disturbed of polarity basal cells

drop-shaped rete ridges

increased and abnormal mitoses

premature keratinisation in single cells

abnormal keratinisation

keratin pearls within rete ridges

loss of epithelial cell cohesion or adhesion

26
Q

List the criteria for a low grade dysplasia. (8)

A
  • Easy to identify that the tumour originates from squamous epithelium
  • Architectural change into lower third
  • Cytological atypia or dysplasia may not be prominent
  • Shows a considerable amount of keratin production
  • Evidence of stratification (2 or more cell layers)
  • Well formed basal cell layer surrounding the tumour islands
  • Tumour islands are usually well defined and are often continuous with the surface epithelium
  • Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT
27
Q

List the criteria for a high grade dysplasia. (5)

A
  • Show little resemblance to a normal squamous epithelium
  • Architectural change reaches the upper third
  • Usually show considerable atypia
  • Invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CT
  • Mitotic figures are prominent and many may be abnormal
28
Q

How do we classify a dysplasia which has changes in the middle 1/3rd?

A

depending on the level of cytological atypia = will be classified into low grade or high grade

29
Q

Describe a carcinom - in - situ dysplasia. (4)

A

A lesion which the pathologist strongly suggests a carcinoma is present but cant provide evidence that invasion through the basement membrane has occurred;

  • Cytologically malignant but not invading
  • Abnormal architecture
  • Full thickness (or almost full)
  • Severe cytological atypia
    *Mitotic abnormalities frequent
30
Q

What factors determine how cancer should be managed? (4)

A
  1. Pattern of Invasion
  2. Depth of Invasion
  3. Perineural Invasion
  4. Invasion of Vessels
31
Q

Describe pattern of invasion in relation to cancer prognosis.

A

Good prognosis = Bulbous rete pegs infiltrating at same level is considered

poor prognosis = widely infiltrating small islands and single cells

32
Q

Describe depth of invasion in relation to cancer prognosis.

A

Risk of metastases for a tumour which is greater than 4mm in size = 4x greater than for a tumour less than 4mmm

33
Q

Describe invasion of vessels in relation to cancer prognosis.

A

poor prognosis = thought to be associated with lymph node metastaes

34
Q

Describe field cancerisation of the oral cavity.

A

Where the cancer has developed in the mouth Is not the only area which has been subject to the cellular changes and to the environmental stimuli which have caused the cancer
– the same changes progress in other parts of the mouth at a slower rate but can also produce OCC in the future = a new primary and not reoccurrence.

35
Q

Why should we continue to review not only the site of the oral cancer but the whole mouth in patients who have a history of OCC?

A

Field cancerisation tells us that patients presenting with an OCC in one area have a risk of developing other tumours in other parts of the mucosa
- High cancer risk in 5cm radius of original primary = that’s most of the mouth/pharynx.
Therefore we consider the whole mouth as a risk and the whole mouth should be reviewed each time.

36
Q

What is the cure rate of a stage 1 early lesion?

A

80% cure rate

37
Q

what is the cure rate for stage 2?

A

65% cure rate

38
Q

what is the cure rate for stage 3 or worse?

A

less than 30% cure rate

5 year survival is < 50%

39
Q

what is the survival time (in months) for an untreated lesion with metastases?

A

around 4 months

40
Q

How do we determine how to treat the cancer?

A

Based on the TNM staging and findings
- N&M cannot be fully assessed until excised and sent for pathological examination

41
Q

Does lip cancer come under OCC or OPC

A

none - separate type

42
Q

How does lip cancer present? (2)

A

as a on-healing ulcer or swelling

43
Q

what can cause lip cancer? (2)

A
  • Sunlight UV-B
  • Smoking
44
Q

Describe the behaviour of a lip cancer. (5)

A
  • slow growth
  • local invasion
  • rarely metastasise to nodes
  • Good prognosis as usually detected early
  • Responds well to surgery
45
Q

What methods do we use to screen for oral cancer? (5)
which is the most effective?

A
  • HPV16 screening
  • Toluidene blue
  • VELscope – (Autofluorescence of tissues with blue light) Loss of fluorescence = ‘change’, Change may be cancer but can be other changes
  • Photodynamic Diagnosis (PDD)
  • Clinical judgement of experienced clinician – most efficient
46
Q

what is an advantage of using toluidene blue for oral cancer screening?

A

Can detect areas within lesions which are more likely to become maliganant – determines biopsy site

47
Q

What is a GDP’s role in relation to oral cancer? (7)

A
  • Smoking cessation advice
  • Alcohol reduction advice
  • Healthy diet promotion
  • Dentist has to make decision about their referral threshold for potentially malignant lesions
  • Monitor with photographs
  • Remove local factors where ulcer may be due to trauma, then review
  • Monitor PML & if they undergo changes = refer

My BDS4 (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions