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BDS4 Oral Medicine > Dysplasia and OC > Flashcards

Dysplasia and OC Flashcards

1
Q

Common red flag sites for oral cancer?

A

Lateral border of Tongue
FOM

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2
Q

What is oral cancer risk increased by in:

  • smokers
  • alcohol
  • alcohol and smoking
A

2x

2x

5s

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3
Q

What are some risk factors for oral cancer?

A

Smoking
Alcohol
DIet
Chewing betel nut
Chewing tobacco

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4
Q

What is a potentially malignant disorder?

A

This is a term for a condition or disease that has an increased risk of becoming malignant (does not mean it will become malignant just higher chance)

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5
Q

What are some examples of potentially malignant disorders?

A

Lichen planus
Leukoplakia
Erythroplakia

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6
Q

What is lichen planus?

A

This is a chronic oral condition affecting mucosal membrane and skin that has 7 diff types:

Reticular
Atrophic
Papular
Plaque
Bullous
Ulcerative/Erosive

EROSIVE AND ULCERATIEV HAVE HIGHEST RISK

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7
Q

What is luekopakia?

A

white patch with no attributable cause, does not rub off, higher risk than normal mucosa

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8
Q

Wha is erythroplakia?

A

Red patch, no attributable cause - rare than leukoplakia but its due to a vascular change which can be a sign of malignancy

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9
Q

Risk if white lesions progressing to cancer?

A

Low - 0.2-0.4% however have to warn pts there is a risk and it must be monitored

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10
Q

What are the clinical predictors of malignancy? 5

A

Age - elder pts higher risk
Gender - females higher risk
Site - FOM, gingiva higher risk
Clinical Appearance - rolled, non homogenous, leuko-erythroplakia, verroucous, ulcerative
Idiopathic = if pt is non smoker, non drinkers etc then more concerned as to why it is therw

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11
Q

What is the gold standard for assessing a lesion?

A

Histopathology

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12
Q

What does histopathology do?

A

Assesses for dysplasia, atrophy and candida infection

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13
Q

What can we also look fo run a tissue sample?

A

Biological markers - such as VEGF (this is a growth factor) and p53 which normally induces cell apoptosis when it notices something is off with cell however in 50% of cancers this is switched off

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14
Q

What is dysplasia?

A

Disordered growth in tissue

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15
Q

What is atypia?

A

Changes in cell at cellular level

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16
Q

How do we diagnosis a potentially malignant lesion?

A

Cytological changes - cell size, cell shape, nuclear hyperchromatism (inc uptake of dye due to inc DNA content), nuclus size, nucleus shape, atypical mitotic figures

Architectural change - loss of epithelial cell adhesion, drop shaped rete ridges, irregular stratification, premature keratin in single cells, increasd and abnormal mitosis

17
Q

What architectural changes dowe look for ?

A

How much ep is involved - low, mid, upper 1/3rd
increased or atypical mitosis
loss of epithelial cell adhesion
dropped shaped rete ridges
irregular stratification
premature keratin in single cells

18
Q

What cytological changes do we look for?

A

Abnormal nucleus size
Abnormal nucleus shape
Abnormal cell size
Abnormal cell shape
Nucleus hyerpchromatism
Inc no and size of nucleus
Atypical mitotic figures

19
Q

What is the WHO classification for histopathological grading of lesions?

A

Hyperplasia
Mild dysplasia
Moderate dysplaisa
Severe dysplasia
Carcinoma in situ

NOW WE TEND TO USE LOW GRADE, HIGH GRADE, CIS

20
Q

Describe basal cell hyperplasia?

A

This is where there is INCREASED BASAL CELL NUMBERS

There is regular stratification

no cellular atypia

21
Q

What is mild dysplasia?

A

This is where there are changes in the lower 1/3rd of the epithelium
Often due to reactive change due to smoking, infection, inflammation, trauma etc
May see nuclear hyperchromatism
Pleomorphism
few cells show atypia (pleomorphism, hyperchromatism)
rest of cells look normal

22
Q

What is moderate dysplasia?

A

This is where there are changes into the mid 1/3rd of epithelium

Architecture - Loss of cohesion of epithelial cells (non cohesive pattern)

cytology - hyperchromaism, pleomorphism

rete pegs more round and bulbous

23
Q

What is severe dysplasia?

A

This is where the upper 1/3rd is affected, so majority of layers are affected and there is little resemblance to the normal Strat squamous ep , non cohesive

cytology = severe atypic of cells (size and shape), pleomorphism, hyperchroatism, presence of mitotic figures further up (should only be in basal layer), inc no of mitotic figures

24
Q

What is severe dysplasia?

A

This is where the upper 1/3rd is affected, so majority of layers are affected and there is little resemblance to the normal Strat squamous ep , non cohesive W

cytology = severe atypic of cells (size and shape), pleomorphism, hyperchroatism, presence of mitotic figures further up (should only be in basal layer), inc no of mitotic figures

25
Q

What is carcinoma in situ?

A

This is a theoretical concept

all layers are involved (including upper third)

sample is malignant but not yet invasive a sit hasn’t breached the connective tissue - needs removal!!

26
Q

What are the 4 histological prognostic factors of cancer?

A

Pattern of invasuon
depth of invasion
perineurial invasion
invasion of vessels

27
Q

What are the main factors in carcinogens?

A

Genetics
Envuronement (alcohol, tobacco, betel nut chewing, diet which promote change from altered cell exp to malignancy and invasion)

28
Q

WHat is the process of carcinogenesis?

A

INITIATION (this is where the DNA mutation occurs and this DNA mutation inactivates the tumour suppression gene)

PROMOTION (this is where the cell proliferations with the mutation and inactivates DNA repair gene)

TRANSFORMATION (this is where cell undergoes further mutations that cant repair

PROGRESSION - cell undergoes further mutations, inactivates several more tumour suppressor genes and has the hallmarks of malignancy

29
Q

What is an oncogene?

A

This is a gene that when normal regulates and promotes cell proliferation

however when it becomes mutated it has the potential to cayse cancer as there is inappropriate proliferation

30
Q

What isa tumour suppressor gene?

A

This supresses cell growth

31
Q

What does Tp53 do?

A

Ptoetein that induces cell apoptosis when mutation is recognised however in50% of cancer its inactivated so mutated cell profilerates

32
Q

What are the hallmarks of cancer? 6

A

Evades apoptosis
Angiogenesis
Insenstive to anti-growth signals
Has its own growth signals
invades tissues and metastasises
replicates uncontrollably

33
Q

What is the fild cancerisation concept?

A

This is the theory that it is no just the tissue that has the malignant change that as been exposed to the changes and stimuli leading to the cancer - the surrounding tissue has also been exposed and may be occurring at a slower rate
there is a big risk in 5cm radio from original primary and may actually get a second new primary tumour rather than as secondary tumour

§

34
Q

What is a synchronous slesion?

A

Second primary within 6 months

35
Q

What is a metachronu lesion?

A

Second primary more than 6 months after first and due to same field change

36
Q

How do we stage cancer?

A

T - tumour primary
T0 = no primary found
T1 = <2cm
T2 = 2-4cm
T3 = >4cm

N - lymph node involvement
N0 = no regional LN involvement
N1 = ipsilateral single, <3cm
N2 = <6cm, ipsilateral single, multiple or bilateral
N3 = >6cm

M = metastasius

N0 = no
M1 = metastasised

37
Q

Risk factors for lip cancer?

A

Sunlight
Smoking

38
Q

What is good about lip cancer ?

A

Slow growth
rarely metastasis to nodes
local invasion
responds well to xt

BDS4 Oral Medicine (12 decks)

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